MT Flashcards
Drug types used to increase insulin sensitivity
a
Bigunaides
Thiazolidinediones
Bigunaides
Decreases the hepatic production of glucose and reducing insulin resistance.
Does not promote insulin release from the pancreas.
Most side effects are minor, and GI related.
Does not cause hypoglycemia or weight gain.
Can cause lactic acidosis in those with decreased liver function.
Ex Metformin
Long acting insulin
Glargine (Lantus, Basalgar), Detemir (Levemir)
Onset 90 min
NK peak
Duration up to 24 hours
Often given at bedtime, regardless of meals. (QD or BID)
Intermediate acting insulin time action profile
Humulin N/NPH
Onset 1-3 hour
Peak 5-8hrs
Duration up to 18hours
Often given at bedtime, not given in regard to meals
(QD or BID)
Short acting insulin time action profile
Humulin R/Toronto
Onset 30 min
2-3 hr peak
6.5 hr Duration
Given with one or more meals per day, admin’d 30-45 mins before start of meal
Rapid action insulin time/onset profile
Novorapid, Apidra, Lispro
10-15 min onset
1-2 hr peak
3-5 hr duration
To be given 0-15 minutes before (or after meals)
Therapeutic and adverse effects of sulfonylurea
Lowers blood glucose levels in patients with type 2 diabetes
Stimulates release of insulin from pancreatic beta cells
Prototype: Glyburide
Incretin enhancers
Incretins are hormones secreted by the intestine in response to a meal and signal the pancreas to release insulin and the liverto stop producing glucagon.
Ex: Sitagliptin (Januvia)
Main 3 Pharmacological Management of Angina Pectoris (2 of 3)
Nitrates:
Dialation of coronary arteries to reduce O2 needs
- Relaxes venous muscle reducing preload
- Relaxes coronary arteriole muscle, reducing pain and increasing o2
Beta-adrenergic blockers
Prevent anginal episodes by reducing CO and O2 demand
Ca Channel Blockers
Prevent angina episodes by either reducing CO (decrease O2 demand) dilating coronary arteries (increase O2 demand) or both
Indications for the use of Nitro
Acute angina
Acute congestive heart failure
Acute pulmonary edema
Acute myocardial infarction
Severe / emergency hypertension
Ca Channel Blockers
Therapeutic Uses
Stable angina
Atrial dysrhythmias
Hypertension
Mechanism of action
Blocks cardiac calcium channels
Decreases HR and force of contraction, decreasing O2 demand of myocardium
Blocks vascular smooth muscle channels
Increases O2 supply in coronary arteries (vasodilation)
Decreases O2 demand by decreasing afterload (decreased HR anf contraction)
Beta Adrenergic Blockers
Therapeutic effects and uses
Angina, MI
Hypertension
Some dysrhythmias
Some cases of congestive heart failure
Migraines
Mechanism of action
Selectively blocks beta ____receptors causing decreased HR and contractility which decreases myocardial O2 demand
Thrombolytics
Indicated for MI, CVA
Stimulates formation of plasmin, an enzyme that breaks down fibrin, causing active clots to dissolve
Coronary artery opens allowing perfusion of myocardium
Drug classes used in MI
Thrombolytics
Beta Blockers
Ace inhibs
Anticoagulatns
Antiplatlet
Prototype drug and therapeutic effect, mech of action, and adverse effects for Statins
Used in response to hypercholesterolemia or Family hx of it
Inhibits enzyme in liver producing LDL cholesterol
Liver removes LDL cholesterol from blood
Adverse effects:
Headache
Abdom discomfort Diarrhea/Const
Muscle pain
Elevated liver enzymes
Rhabdomyolosis
Can cause fetal abnormalities
Drugs for Heart Failure - Phosphodiesterase III Inhibitors
Block the enzyme phosphodiesterase in cardiac and smooth which increases the amount of calcium available for myocardial contraction
Used with patients with heart failure who have not responded to other therapiesIncreased force of myocardial contraction increasing cardiac output.
Only given IV
Cardiac Glycosides
Used in HF
Can stablize some dysrhythmiads
Cardiac glycosides are negative chronotropes and positive inotropes
Improve symptoms by _________ heart rate while _________ force of contraction
Require digitalizstion to be effective (becomes effective once a suitable concentration of drug has built up in tissues)
Ex. Digitalis
Adverses effects of digoxin (digital toxicity)
Nausea, vomiting
Visual disturbances
Atrial dysrythmias
Bradycardia
Heart block
Vent dysrythmias
Digoxin mech of action
Blocks Na+ / K+ ATPase the critical enzyme responsible for pumping sodium out of the myocardial cell in exchange for potassium. As Na+ accumulates in myocytes calcium ions are released from their storage areas in the cell which produces a more forceful contraction.
Suppresses the SA node and slows electrical conduction through the AV node.
Drugs used for HF
ACE inhibitors, angiotensin receptor blockers
Adrenergic agents, cardiac glycosides
Vasodilators, diuretics,
Isosorbide Dinitrate
Vasodialotor
Angina pectoris
Heart failure
Donates NO molecules which promote relaxation of vascular smooth muscle cells leading to vasodialotrs
HOTN, headache, dizziness, reflex tachycardia .
medications that are used in the acute TX of MI (thrombolytics in text and PP) the prevention of MI and TX of symptoms associated with an MI and their therapeutic action according to the FH guidelines for a STEMI in your Power Point
Anti platelets -ASA chewable, then either ticagrelor or clopidogrel.
Dramatically reduces mortality in the coming weeks.
Clopidogrel and ticlopidine (ticid) antiplatelet drugs usen in the prevention of MI
Anticoagulants- Heparin IV
Other medications;
Atropine- for symptomatic bradyarrhythmia’s
Dimenhydrinate ?
Fentanyl?
Lorazepam?
Metoclopramide?
Morphine?
Indications for the use of diuretics
Hypertension, Heart failure
Renal failure
Liver failure or cirrhosis
Pulmonary edema
Types of diuretics
Loop Diuretics
Thiazides
Potassium sparing
Osmotic diuretics
Carbonic anhydrase inhibitors
What is unique abt thiazide diuretics
Block Na+ reabsorption at distal tubule, reducing reabsorption of water
Indications
Hypertension
Edema
Adverse effects similar to loop diuretics, but thiazides do not promote ototoxicity
Less diuresis than lasix
Potassium-Sparing Diuretics mech of action
Aldosterone antagonists – aldosterone promotes reabsorption of Na+ and secretion of K+; blocking aldosterone receptors prevents reabsorption of water by preventing reabsorption of Na+, retaining K+
Spironolactone (Aldactone)
K+ sparing diuretic
Used for mild HTN
K+ is etaned
Inhibits action of aldosterone in distal tubule and collecting ducts of nephron
Adverse effect is Hyperkalemia
Osmotic Diuretics
Raise osmolality of plasma thereby drawing fluid from ICF and interstitium
Osmotic diuretics are freely filtered by kidney but not reabsorbed; water follows the diuretic, and is not reabsorbed; Na+ is not reabsorbed
Indications
Increased intracranial pressure
High intraocular pressure
Acute renal failure
