Final- Old Stuff Flashcards
Dixogin
MOA-
- inhibits Na/ K/ ATPase pump.
- Intracellular Na+ & Ca+ increases.
- Increase Ca+→ increased contractility (+ inotrope).
- Intracellular Na+ & Ca+ increases.
- Increase vagal efferent efferent
- redueces SA firing→ decreased HR,
- slows conduction velocity in AV mode
Renal clearnace
DDI- quinidine, verapamil, amioarone
Hypokalemia can cause toxicity (watch for duretic use)
- GI- nausea/ vomitting
- confusion/ neurological changes
- visual changes cardiac toxicity
Lidocaine
Anti-arrhythmic Class 1b- Na channel blockers- short refractory period
Ventricular arrhythmia ONLY
ONLY IV
CNS toxicity- paresthesia, confusion, seizure, tremor
Hydrocholorothiazide
Thiazide diuretic- inhibt Nacl luminal synporter
Inital therapy for hypertention not goog for renal disease but good for kidney stones caused by hypercalciuria
ADR- Hypokalemia, hypercalcemia, hypomagnesemia, hyperuricemia
Glyburide
Sulfonylureas (oral)- first generation
MOA- initally bind to high affinity 140-kDa SU receptor and block K channel in beta cell in increase insulin release , works on pancreas in the K channels in the beta cells
Works independent of glucose load- insulin porduced even if glucose is not present so take with food
ADR- Hypoglycemia (highest in class), weight gain
Use in caution in older patients and those with renal impairment
Esmolol
Class 2- Beta blockers
MOA- supression of abnormal pacemaker activity by cloking sympathetic (beta 1- receptor) activity in SA/ AV node
IV- short acting acute arrhythmia
Preferred for rate control
ADR
- Bronchospasm, AV block, Hypotension, exercise intolerance, sexual dysfunction, masking hyperglycemia
Nateglinide
Glinide
MOA- initally bind to high affinity 140-kDa SU receptor and block K channel in beta cell in increase insulin release , works on pancreas in the K channels in the beta cells
Works independent of glucose load- insulin porduced even if glucose is not present so take with food
Rapid onset of action best for post prandial glucose- take before meal
ADR- Hypoglycemia, weight gain (both less then SU)
Use in caution in older patients and those with renal impairment
Metformin
Biguanide
MOA- Activatio of AMP- Kinase (supress hepatic glucose production (gluconeogenesis)- mean mechanism, increase insulin sensitivity of peripheral tissue (increase number of Glut-4 receptor), works on liver, muscle adipose tissue (AMP-K), Glut-4
ADR- Diarrhea, anorexia, metallic taste, GI (titrate to minimize GI effect), increse plasma lactate( lactic acidosis), less B12 absorption
NO hypoglycemia with monotherapy
causes weight loss or neutral
Renal consideration- eGFR < 30 no not use
Titrate- 500 mg BID with meals to start then increase 500 mg increment every 5-6 days
MAX dose- 2000 mg daily
Ethacrynic Acid
Loop diuretic- inhibits luminal Na/K/2Cl
DOC diuretic class for renal disease, can be used in sulfa allergy
ADR- Hypokalemia, hypocalemia, hypomagnesemia, hyperuricemia
Nisoldipine
DHP CCB
Can be used in HF but only treats the hypertension in HF
Potenial reflex tachycardia so combine with Beta blockers (beta 1- antagonist)
ADR- Peripheral edema (dose- related), flushing (dose-related), palpitations (dose- related), reflex tachycardia (give with beta blocker)
Chlorthalidone
Thiazide diuretic- inhibt Nacl luminal synporter
Inital therapy for hypertention not goog for renal disease but good for kidney stones caused by hypercalciuria
ADR- Hypokalemia,hypercalcemia,hypomagnesemia, hyperuricemia
Lispro U-100
Rapid- Acting Insulin
MOA- stablized in hexamer
Less hypoglycemia then short acting
used in insulin pump
Lixisenatide
GLP-1 receptor agonist- incretin mimetic (injectable)
MOA-
- slows gastic empty which reduces post-pradial rise in blood glucoe (feels fuller longer)
- Decreases in appetitie- WEIGHT LOSS
- Increase insulin secretion by activating beta cells
- glucose dependent (safer then SU)
- Supresses glucagon release
ADR- Nausea (less nausea with weely formulations),mide hypoglycemia, pancretitis, weight loss
Clevidipine
DHP CCB
Can be used in HF but only treats the hypertension in HF
Potenial reflex tachycardia so combine with Beta blockers (beta 1- antagonist)
ADR- Peripheral edema (dose- related), flushing (dose-related), palpitations (dose- related), reflex tachycardia (give with beta blocker)
Adenosine
Adenosine receptors found in AV nodal tissue and vascular smooth mucle
- Slows AV nodal conduction
ADR-
- Vasodilation→ flushing hypotension
- Chest pain
- Dyspnea
Chlorothiazide
Thiazide diuretic- inhibt Nacl luminal synporter
Inital therapy for hypertention can use for renal disease (only one in class) but good for kidney stones caused by hypercalciuria
ADR- Hypokalemia,hypercalcemia,hypomagnesemia, hyperuricemia
Repaglinide
Glinide
MOA- initally bind to high affinity 140-kDa SU receptor and block K channel in beta cell in increase insulin release , works on pancreas in the K channels in the beta cells
Works independent of glucose load- insulin porduced even if glucose is not present so take with food
Rapid onset of action best for post prandial glucose- take before meal
ADR- Hypoglycemia, weight gain (both less then SU)
Use in caution in older patients and those with renal impairment
Linaglipton
DPP-4 Inhibitor
MOA- inhibits the action of the DPP-4 enzyme which inhibits the breakdown of endogenous GLP-1. Inhibits incretin breakdown
Useful in patients with low levels of incretin/ GLP-1
ADR- Headache, nasopharyngitis, rash, URI, joint aches
Renal adjustment NOT required- only one in class
Not replacing incretin- just inhibiting the thing thats breaking down incretin (DPP-4)
Verapamil
Class 4- Ca+ channel blockers (non DHP- CCB)
MOA- slows conduction in AV node by blocking Ca channels (phase 2),
Good for asthma and COPD patients for rate control
DO NOT USE IN HF
ADR- Constipation, hypotension, AV block,
Ramipril
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Disopyramide
Anti-arrhythmic Class 1A- Na channel blockers
MOA- blocks Na+ channel moderately and K+
Negative inotrope
Antimuscarinic effects (Hot, dry fast crazy), exacerbates, heart failure, increases digoxin toxicity
All 1a drugs can precipitate new arrhythmia
Benzepril
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Eprosartan
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Canagliflozin
SGLT-2 inhibitor
MOA-inhibitrs SGLT-2 transporter in kidney to decrease reabsorption of glucose thus increasing urinary glucose excretion
ADR- Polyuria, increased risk of genital myoctic infection and UTI, increased LDL, volume depletion ( with diuretis double the risk), increased risk of amputations
NPH- Humulin, Novolin
Intermediate acting
MOA- recombinant human insulin complexed with zinc and protamine to delay absorption and extend action
Often combined with rapid acting insulin
Highest rate of hypogylcemia
Dulaglitide
GLP-1 receptor agonist- incretin mimetic (injectable)
MOA-
- slows gastic empty which reduces post-pradial rise in blood glucoe (feels fuller longer)
- Decreases in appetitie- WEIGHT LOSS
- Increase insulin secretion by activating beta cells
- glucose dependent (safer then SU)
- Supresses glucagon release
ADR- Nausea (less nausea with weely formulations),mide hypoglycemia, pancretitis, weight loss
Novolin
Short- Acting (regular insulin)
MOA- hexamer complex with zinc
IV in-patient for diabetics for DKA
Higer risk of hyopglycemia then rapid acting
Glipizide
Sulfonylureas (oral)- second generation
MOA- initally bind to high affinity 140-kDa SU receptor and block K channel in beta cell in increase insulin release , works on pancreas in the K channels in the beta cells
Works independent of glucose load- insulin porduced even if glucose is not present so take with food
ADR- Hypoglycemia, weight gain
Use in caution in older patients and those with renal impairment
Captopril
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia,AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Metolazone
Thiazide diuretic- inhibt Nacl luminal synporter
Inital therapy for hypertention can use for renal disease (only one in class) but good for kidney stones caused by hypercalciuria
ADR- Hypokalemia,hypercalcemia,hypomagnesemia, hyperuricemia
Propranolol
Class 2- Beta blockers
MOA- supression of abnormal pacemaker activity by cloking sympathetic (beta 1- receptor) activity in SA/ AV node
thyrotoxicosis induce arrhythmia
Preferred for rate control
ADR
- Bronchospasm, AV block, Hypotension, exercise intolerance, sexual dysfunction, masking hyperglycemia
Telmisartan
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Sacubitril; Valsartan (entresto)
Neprilysin inhibitor- stops the breakdown down of vasodilators
ADR- hyperkalemia, cough/angioedema/ ARF/ AKI/ hypotension (more then enalapril)
Demonstrated superiority to enalapril
Dronedarone
Class 3- K+ channel blocker
MOA- block K+ channelsto delay repolarization (phase 3) (increase AP duration, Increase the refractory period), Na+, Ca+
Strong CYP 34A interactions
ADR
- GI intolerence,
- lacks pulmonary, thyroid, or hepatic effects vs amiodarone
LESS ADRs then amiodarone but not as effective
CANNOT USE IN HF
All Class 3 drugs can increase the risk of subsequent arrhythmias, most notably torsades (QTc prolongation)
Olmesartan
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Afrezza
Inhaled insulin- rapid acting
MOA- absorb onto technosphere microparticles for pulmonary administation, dissoves in neutral pH
Good for people who dont want to inject themselves, bad for asthma/ COPD
less hypoglyemia then aspart
ADR- cough, sore throat, hypoglycemia, bronchitis, weight gain
Monitor- PFT- ar baseline, 6 months and anually
Alogliptin
DPP-4 Inhibitor
MOA- inhibits the action of the DPP-4 enzyme which inhibits the breakdown of endogenous GLP-1. Inhibits incretin breakdown
Useful in patients with low levels of incretin/ GLP-1
ADR- Headache, nasopharyngitis, rash, URI, joint aches
Increased HF admissions with someone already with HF
Renal adjustment required
Not replacing incretin- just inhibiting the thing thats breaking down incretin (DPP-4)
Empagliflozin
SGLT-2 inhibitor
MOA-inhibitrs SGLT-2 transporter in kidney to decrease reabsorption of glucose thus increasing urinary glucose excretion
ADR- Polyuria, increased risk of genital myoctic infection and UTI, increased LDL, volume depletion ( with diuretis double the risk),
Indapamide
Thiazide diuretic- inhibt Nacl luminal synporter
Inital therapy for hypertention can use for renal disease (only one in class) but good for kidney stones caused by hypercalciuria
ADR- Hypokalemia,hypercalcemia,hypomagnesemia, hyperuricemia
Flecainide
Anti-arrhythmic Class 1c- Na channel blockers
Dizziness
Metallic taste
NORMAL HEARTS ONLY
Saxagliptin
DPP-4 Inhibitor
MOA- inhibits the action of the DPP-4 enzyme which inhibits the breakdown of endogenous GLP-1. Inhibits incretin breakdown
Useful in patients with low levels of incretin/ GLP-1
ADR- Headache, nasopharyngitis, rash, URI, joint aches
Increased HF admissions with someone already with HF
Renal adjustment required
CYP 3A4 interacts CYP 3A4 inhibitors
Not replacing incretin- just inhibiting the thing thats breaking down incretin (DPP-4)
Bromocriptine
Prefferable for Parkinson and Diabetes
Pramlintide
Amylin Analog
MOA- supression of high postprandial hyperglycemia, slows gastic emptying, and increased satiety
Indicated for use with mealtime insulin but must reduce inulin dose by 50% to avoid hypoglycemia (BLACK BOX WARNING)
ADR- Nausea, vomiting, anorexia, increased risk of insulin-induced hypoglycemia
Used in Type 1 DM
Procainamide
Anti-arrhythmic Class 1A- Na channel blockers
MOA- blocks Na+ channel moderately and K+
IV
Hypotension, lupus-like syndrome, arganulocytosis, nasuea, diarrhea
Cleared though kidneys
All 1a drugs can precipitate new arrhythmia
Most likely to cause torsades
Valsartan
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Mexilteine
Anti-arrhythmic Class 1b- Na channel blockers- short refractory period
Ventricular arrhythmia ONLY
IV and PO
Longer duration of action
CNS toxicity- paresthesia, confusion, seizure, tremor (sign of toxicity), GI upset
Perindopril
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Sotalol
Class 3- K+ channel blocker
MOA- block K+ channelsto delay repolarization (phase 3) (increase AP duration, Increase the refractory period), K+and Beta receptors
Treatment of ventricular arrhythmias and afib
Do not use if LVEF <25%
Renally cleared
All Class 3 drugs can increase the risk of subsequent arrhythmias, most notably torsades (QTc prolongation)
Liraglutide
GLP-1 receptor agonist- incretin mimetic (injectable)
MOA-
- slows gastic empty which reduces post-pradial rise in blood glucoe (feels fuller longer)
- Decreases in appetitie- WEIGHT LOSS
- Increase insulin secretion by activating beta cells
- glucose dependent (safer then SU)
- Supresses glucagon release
ADR- Nausea, mide hypoglycemia, pancretitis, weight loss
Requires dose titration to reduce nausea
Quinapril
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia,AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Quinidine
Anti-arrhythmic Class 1A- Na channel blockers
MOA- blocks Na+ channel moderately and K+
Most toxic in the class
HA, vertigo, tinnitus, GI distrubance, thrombocytopena, hemolyic anemia, hepatitis
All 1a drugs can precipitate new arrhythmia
Losartan
ARB- Blocks recepotrs for angiotension II
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (lower then ACE ), Angioedema, Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Amlopdipine
DHP CCB
Can be used in HF but only treats the hypertension in HF
Potenial reflex tachycardia so combine with Beta blockers (beta 1- antagonist)
ADR- Peripheral edema (dose- related), flushing (dose-related), palpitations (dose- related), reflex tachycardia (give with beta blocker)
Moexipril
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Felodipine
DHP CCB
Can be used in HF but only treats the hypertension in HF
Potenial reflex tachycardia so combine with Beta blockers (beta 1- antagonist)
ADR- Peripheral edema (dose- related), flushing (dose-related), palpitations (dose- related), reflex tachycardia (give with beta blocker)
Nifedipine
DHP CCB
Can be used in HF but only treats the hypertension in HF
Potenial reflex tachycardia so combine with Beta blockers (beta 1- antagonist)
ADR- Peripheral edema (dose- related), flushing (dose-related), palpitations (dose- related), reflex tachycardia (give with beta blocker)
Spironolactone
K- sparring diuretic- collecting duct- Na excretion and K reabsorbtion
Aldosterone antagonist- can be used for acne, Increases the expression of Na channels
DO not use with diabetics with protein in their urine, can use in sulfa allergy
least likely to cause gout
ADR- Hyperkalemia, gynecomastia (adrogen recepotor blockade),
Lisinopril
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics) and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia,AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Acarbose
Alpha- Glucosidase Inhibitor
MOA- inhibits enzymes in small intestine that hydrolyze polysaccharides (starches) into simple sugars→ delays the absorption of dietary CHO→ reduced post parandial glucose
Taken at the start of each meal- before meal because drug must be available in the intestine
ADR- poor absorption, flatulence, bloating, abdominal pain
Humulin
Short- Acting (regular insulin)
MOA- hexamer complex with zinc
IV in-patient for diabetics for DKA
Higer risk of hyopglycemia then rapid acting
Fosinopril
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Pioglitazone
Thiazolidinediones (TZD)
MOA- Activate PPAR- gamma in muscle, liver and fat
- increase GLUT1 and GLUT4 transpsporter expression
- Increases insulin sensitivity
- Decrease gluconeogenesis
- Decrease TG in ciruclation (increase lipoprotein lipase)
ADR- WEIGHT GAIN, edema→ exacerbate CHF, increased LFTs, increase bone fracture, anemia
Delayed clinical effect- 8-12 weeks combine with metformin
Increased risk of bladder cancer if use over 1 year
Degludec
Ultra- Long acting
MOA- forms multihexamer upon injection, resulting in a large depot. Gradual remocal of zinc leads to slow dissociaion into dimers and monomers
Glargine
Ultra- Long acting
MOA- same as insulin glargine U-100; given at one thrid of volume
Diltiazem
Class 4- Ca+ channel blockers (non DHP CCB)
MOA- slows conduction in AV node by blocking Ca channels
Good for asthma and COPD patients for rate control
DO NOT USE IN HF
ADR- Constipation, Flushing hypotension, AV block
Colesvelam
Approved for pregnancy weight lowering
Amiodarone
Class 3- K+ channel blocker
MOA- has class 1, 2 & 4 electrophysiologix properties
Lowest risk of torsades in class 3
Long half life
DDI (MANY)- digoxin, warfarin, etc
Lipophilic
Monitor- TFTs, LFTs, PFTs/ CXR (yearly)
ADR
- Pumonary fibrosis, hepatic dsyfunction, grey-blue skin, corneal deposits, hypo/hyperthyroidism (iodine based)
All Class 3 drugs can increase the risk of subsequent arrhythmias, most notably torsades (QTc prolongation)
Aliskiren
Direct Renin Inhibitor- prevents the generation of angiotension I
DO NOT COMBINE WITH ACE/ARB
ADR- hypotension, hyperkalemia, AKI/AKF, rare angioedema, teratogenic
Propafenone
Anti-arrhythmic Class 1c- Na channel blockers
Mild Beta blocking properties
NORMAL HEARTS ONLY
Furosemide
Loop diuretic- inhibits luminal Na/K/2Cl
DOC diuretic class for renal disease
ADR- Hypokalemia, hypocalemia, hypomagnesemia, hyperuricemia
Amiloride
K- sparring diuretic- collecting duct- Sodium channel blockers Na excretion and K reabsorbtion
DO not use with diabetics with protein in their urine, can use in sulfa allergy
ADR- Hyperkalemia,
Miglitol
Alpha- Glucosidase Inhibitor
MOA- inhibits enzymes in small intestine that hydrolyze polysaccharides (starches) into simple sugars→ delays the absorption of dietary CHO→ reduced post parandial glucose
Taken at the start of each meal- before meal because drug must be available in the intestine
ADR- poor absorption, flatulence,bloating, abdominal pain
Glulisine
Short- Acting (regular insulin)
MOA- hexamer complex with zinc
IV in-patient for diabetics for DKA
Higer risk of hyopglycemia then rapid acting
Azilsartan
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Glargine
Long acting
MOA- soluable at & injected as an acidic solution (pH-4). After injection the acidic solution is neutralized leading to formation of mcroprepitates. Small amount of glargine are slowly released from assportion
Asoart
Short- Acting (regular insulin)
MOA- hexamer complex with zinc
IV in-patient for diabetics for DKA
Higer risk of hyopglycemia then rapid acting
Torsemide
Loop diuretic- inhibits luminal Na/K/2Cl
DOC diuretic class for renal disease
ADR- Hypokalemia, hypocalemia, hypomagnesemia, hyperuricemia
Rosiglitazone
Thiazolidinediones (TZD)
MOA- Activate PPAR- gamma in muscle, liver and fat
- increase GLUT1 and GLUT4 transpsporter expression
- Increases insulin sensitivity
- Decrease gluconeogenesis
- Decrease TG in ciruclation (increase lipoprotein lipase)
ADR- WEIGHT GAIN, edema→ exacerbate CHF, increased LFTs, increase bone fracture, anemia
Delayed clinical effect- 8-12 weeks combine with metformin
Nimodipine
DHP CCB
Can be used in HF but only treats the hypertension in HF
Potenial reflex tachycardia so combine with Beta blockers (beta 1- antagonist)
ADR- Peripheral edema (dose- related), flushing (dose-related), palpitations (dose- related), reflex tachycardia (give with beta blocker)
Ibutilide
Class 3- K+ channel blocker
MOA- block K+ channels to delay repolarization (phase 3) (increase AP duration, Increase the refractory period), Na+ and Beta receptors
Treatment of acute afib- most effective when given within seven days of onset
All Class 3 drugs can increase the risk of subsequent arrhythmias, most notably torsades (QTc prolongation)
Nicardipine
DHP CCB
Can be used in HF but only treats the hypertension in HF
Potenial reflex tachycardia so combine with Beta blockers (beta 1- antagonist)
ADR- Peripheral edema (dose- related), flushing (dose-related), palpitations (dose- related), reflex tachycardia (give with beta blocker)
Defetilide
Class 3- K+ channel blocker
MOA- block K+ channelsto delay repolarization (phase 3) (increase AP duration, Increase the refractory period)
Must be strated inpatient; provider must be registered to perscribe& pharmacy to dispense
DDI- HCTZ, verapamil
All Class 3 drugs can increase the risk of subsequent arrhythmias, most notably torsades (QTc prolongation)
Metoprolol
Class 2- Beta blockers
MOA- supression of abnormal pacemaker activity by cloking sympathetic (beta 1- receptor) activity in SA/ AV node
Preferred for rate control
ADR
- Bronchospasm, AV block, Hypotension, exercise intolerance, sexual dysfunction, masking hyperglycemia
Isradipine
DHP CCB
Can be used in HF but only treats the hypertension in HF
Potenial reflex tachycardia so combine with Beta blockers (beta 1- antagonist)
ADR- Peripheral edema (dose- related), flushing (dose-related), palpitations (dose- related), reflex tachycardia (give with beta blocker)
Enalapril
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia,AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Semaglutide
GLP-1 receptor agonist- incretin mimetic (injectable)
MOA-
- slows gastic empty which reduces post-pradial rise in blood glucoe (feels fuller longer)
- Decreases in appetitie- WEIGHT LOSS
- Increase insulin secretion by activating beta cells
- glucose dependent (safer then SU)
- Supresses glucagon release
ADR- Nausea (less nausea with weely formulations),mide hypoglycemia, pancretitis, weight loss
Trandolapril
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Exenatide
GLP-1 receptor agonist- incretin mimetic (injectable)
MOA-
- slows gastic empty which reduces post-pradial rise in blood glucoe (feels fuller longer)
- Decreases in appetitie- WEIGHT LOSS
- Increase insulin secretion by activating beta cells
- glucose dependent (safer then SU)
- Supresses glucagon release
ADR- Nausea (less nausea with weely formulations), mide hypoglycemia, pancretitis, weight loss
Eplerenone
K- sparring diuretic- collecting duct- Na excretion and K reabsorbtion
Aldosterone antagonist- can be used for acne, Increases the expression of Na channels
DO not use with diabetics with protein in their urine, can use in sulfa allergy
least likely to cause gout
ADR- Hyperkalemia, gynecomastia (adrogen recepotor blockade)
Sitagliptin
DPP-4 Inhibitor
MOA- inhibits the action of the DPP-4 enzyme which inhibits the breakdown of endogenous GLP-1. Inhibits incretin breakdown
Useful in patients with low levels of incretin/ GLP-1
ADR- Headache, nasopharyngitis, rash, URI, joint aches
Renal adjustments
Not replacing incretin- just inhibiting the thing thats breaking down incretin (DPP-4)
Chlorpropamide
Sulfonylureas (oral)- first generation
MOA- initally bind to high affinity 140-kDa SU receptor and block K channel in beta cell in increase insulin release, works on pancreas in the K channels in the beta cells
Works independent of glucose load- insulin porduced even if glucose is not present so take with food
ADR- Hypoglycemia , weight gain
Use in caution in older patients and those with renal impairment
Candesartan
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Glimeperide
Sulfonylureas (oral)- second generation
MOA- initally bind to high affinity 140-kDa SU receptor and block K channel in beta cell in increase insulin release , works on pancreas in the K channels in the beta cells
Works independent of glucose load- insulin porduced even if glucose is not present so take with food
ADR- Hypoglycemia, weight gain
Use in caution in older patients and those with renal impairment
Detemir
Long- Acting
MOA- Neurtral pH. Has stron molecular association once injected, 98% bound to albumin once in circulation to slow distrubution into tissue
In hypoalbuminemia causes hypoglycemia becase there is more free drug
Irbesartan
ACE- inhibits the conversion of angiotension I to II, increase bradykinin (dry cough)
Diminish proteinura (good for diabetics)and stabilize renal funtion
Uses- hypertension, post MI, LV systolic dysfunction, systolic heart failure, CKD,
Potential increase in SCr initially then declines- CAN CAUSE AKI
ADR- Dry cough (change to ARB), Angioedema (cannot switch to ARB), Hyperkalemia, AKF, tetratogenic, Redued efficiacy in African Americans (use HCTZ)
Bumetanide
Loop diuretic- inhibits luminal Na/K/2Cl
DOC diuretic class for renal disease
ADR- Hypokalemia, hypocalemia, hypomagnesemia, hyperuricemia
Dapagliflozin
SGLT-2 inhibitor
MOA-inhibitrs SGLT-2 transporter in kidney to decrease reabsorption of glucose thus increasing urinary glucose excretion
ADR- Polyuria, increased risk of genital myoctic infection and UTI, increased LDL, volume depletion ( with diuretis double the risk), increased risk of amputations
Triamterene
K- sparring diuretic- collecting duct- Sodium channel blockers Na excretion and K reabsorbtion
DO not use with diabetics with protein in their urine, can use in sulfa allergy
ADR- Hyperkalemia,