Exam II: RAAS, Diabetes drugs Flashcards
Dipines like amlodipine are ?
Calcium channel blockers
Two types of calcium channel blockers based on chemical structure? (Give an example of each)
- Dihydropyridines (DHPs) - amlodipine etc.
2. Non-Dihydropyridines (non-DHPs) - diltiazem, verapamil
Name three differences between DHPs and non-DHPs as far as their effects on the body.
- Dihydropyridine (DHP) CCBs tend to be more potent vasodilators
- Non-dihydropyridine (non-DHP) agents have more marked negative inotropic effects (lower heart rate)
- Non-DHPs more advantageous for patients with chronic kidney disease and diabetic nephropathy.
How do Calcium Channel Blockers (CCBs) control blood pressure?
CCBs regulate Ca2+ influx into cells. This hinders heart contractility, relaxes smooth muscle in the arterial wall and lowers blood pressure.
In addition to vasodilation, what effects do non-DHPs have on the heart?
Decrease the heart rate by depressing atrioventricular (AV) node conduction
What is Raynaud’s Prevention? What medication drug class can treat this disorder?
Raynaud’s Prevention - an idiopathic condition affecting the hands and fingertips, causing them to become cold, spastic, numb and ulcerated.
Dipines can treat this disorder.
This drug class can treat angina (chest pain), afib, tachycardia can migraines.
CCBs
Dipines
Adverse Drug Reactions: Peripheral edema, Orthostasis, Heart block. Name the drug class. (Hint: Treats hypertension)
Non-DHP CCBs
Diltiazem and verapamil
What type of drugs should be used with caution when a patient a taking a CCB? (2)
- Drugs metabolized by Cytochrome P450 3A4
2. Non-DHPs taken with beta blockers
Cautions to take when giving CCBs with these two type of patient populations. (Hint: think age and heart failure)
- Do not use non-DHPs for patients with a a left ventricular ejection fraction of <40%
- Initiate at lower doses in older patients
“RAAS” drugs stands for?
Renin Angiotensin Aldosterone System Antihypertensives
Types of RAAS inhibitors (3)? Give brief description for each.
- ACE inhibitors - Prevents Angiotensin I from being converted to angiotensin II which prevents vasoconstriction and activation of aldosterone
- Angiotensin II receptor blockers (ARBs) - Angiotensin II cannot bind to its receptor
- Direct Renin Inhibitors – Target renin coming directly from the kidneys (prevents the RAAS pathway from occurring to increase BP)
Briefly describe the RAAS pathway.
Lower blood pressure sensed in the kidneys
- Renin released from the kidneys to the blood
- Renin cleaves angiotensin in to angiotensin I (inactive) in the liver
- Angiotensin converting enzyme (ACE) converts Ang I to Ang II (active)
4a. Ang II acts on adrenal cortex - stimulates aldosterone release - Water and sodium retention
5a. Ang II acts on various AT receptors throughout the body to cause cause vasoconstriction, decrease urine output and fluid retention.
Blood pressure increased
Difference between “pril” and “prilat”? ie. Enalapril vs Enalaprilat
Enalaprilat - active metabolite, poorly absorbed, must be admin IV
Enalapril - prodrug (inactive), can be given PO
What type of RAAS drug are “pril” drugs like Benazepril? Also describe mechanism of action.
ACE inhibitors
Prevents conversion of angiotensin I to angiotensin II (potent) by competitive inhibition of ACE
ACE inhibitors AND ARBs are first line therapies for hypertension in what cases? (Name the common factors between the two) –> 6
- Non-African American patients
- Patients with albuminuria
- HF or LVEF less than or equal to 40%
- Coronary Artery Disease
- Post Myocardial Infarction
- Recurrent stroke prevention
Contraindications for ACE inhibitors AND ARBs.
- Bilateral renal artery stenosis (narrowing of renal arteries)
- Pregnancy
- Angioedema (swelling between skin and mucosa typically in the lips) –> most common in African American patients
Adverse reactions for ACE inhibitors AND ARBs. (4)
- Increases in serum creatinine (limited increase as much as 30% okay)
- Hyperkalemia
- Angioedema (occurs 2-4x more in African Americans)
- Dry cough
Angioedema and cough is much less common in ACE inhibitors or ARBs?
Less common in ARBs
What must be monitored when a patient is taking an ACE I or ARB?
Reassess SCr (serum creatine) and potassium K in 1-2 weeks after initiation or dose titration
Much more frequently in patients with renal impairment
Potassium Supplements and other medications that can increase potassium
Cause drug interactions with what type of RAAS drugs?
All three types
ACE I (pril)
ARB (sartan)
DRI (kiren)
Four drug-drug interactions present for ACE inhibitors. (Besides potassium increasing meds)
- Lithium carbonate (ACE I drugs increase lithium levels)
- K+ sparing diuretics like Triamterene + HCTZ - increased risk of hyperkalemia
- NSAID - both drugs affect the kidneys
- Food
What type of RAAS drug are “sartan” drugs like Olmesartan? Also describe mechanism of action.
Angiotensin II Receptor Blockers (ARB)
Inhibits the binding of Angiotensin II to receptors, making the Angiotensin II ineffective as a vasoconstrictor
Also no Na+ retention effect.
What type of RAAS drug are “kiren” drugs like Aliskiren Hemifumarate (Tekturna®)? Also describe mechanism of action.
Direct Renin Inhibitor
Directly inhibits the RAAS at its point of activation; reduces the production of Angiotensin I and Angiotensin II
Therapeutic indication (1) for Aliskiren Hemifumarate (Tekturna®) –> Direct Renin Inhibitor.
Hypertension
Contraindications for Aliskiren Hemifumarate (Tekturna®) –> Direct Renin Inhibitor. (4)
- Pregnancy
- Concomitant use of ACE I and ARBs in diabetic patients - risk of hypotension, renal impairment and hyperkalemia.
- Concomitant use of ACEI or ARBS in patients with a Creatinine Clearance (CrCl) of <60 mL/min/1.73m2 - tests kidney function
- Concomitant use of cyclosporine or itraconazole
High fat meals increase absorption of Aliskiren Hemifumarate (Tekturna®) –> Direct Renin Inhibitor.
True/False
False
High-fat meals decrease absorption substantially
Patients with renal insufficiency should avoid this RAAS drug?
Aliskiren Hemifumarate (Tekturna®) –> Direct Renin Inhibitor.
All hypoglycemic drugs do what? Other names to describe these drugs (2)
Reduce blood glucose
Antidiabetic drugs = antihyperglycemic drugs = hypoglycemic drugs
Where is insulin produced and secreted? What stimulates its release?
Islets of Langerhans β cells in pancreas
Stimulated by increased blood glucose
Two goals of therapy in diabetes mellitus?
- Regulate levels of blood glucose/maintain normal glucose levels
- Avoid ketoacidosis and hypoglycemia
Percentage of patients with DM in the US. Are most diagnosed? More males or females?
14.3% with DM in US
Most undiagnosed in this percentage
Slightly higher percentage of males
Symptoms/signs of DM?
- Polydipsia (Great thirst)
- Polyuria (Frequent dilute urination)
- Polyphagia (Great hunger)
- Weight Loss (Typically Type I)
What sign gives a definitive diagnosis of DM?
HbA1c above 6.5%
Five comorbidities associated with DM.
- Cardiovascular
- Diabetic peripheral neuropathy
- Amputation of Limbs
- Renal [nephropathies]
- Ocular damage [retinopathy]
What is diabetes insipidus?
Caused by a deficiency of the pituitary hormone vasopressin
Failure of renal absorption that leads to larger amounts of dilute urine
What are the levels of blood glucose for pre-diabetic patients (fasting mg/dL and HbA1c)?
Fasting blood glucose 100-125 mg/dL
HbA1c 5.7-6.4%
IDDM (insulin dependent diabetes mellitus)
JODM (juvenile onset diabetes mellitus - insulin deficiency)
Type I or Type II DM?
Type I DM