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