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92 Cards in this Set

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  • Back
Explain the Renin-Angiotensin system
1. Angiotensinogen is synthesized in the Liver
2. Angiotensinogen is converted to Anngiotensin I by Renin (secreted from Kidneys)
3. ACE converts Angiotensin I (decapeptide) ➡ Angiotensin II (octapeptide)
Cells that secrete Renin

Cells that regulate Renin secretion
Juxtaglomerular cells

Macula densa
List the 3 mechanisms in which Renin secretion can be inhibited
1. increased NaCl flux thru chemoreceptors in Macula Densa

2. Elevated BP thru baroreceptors in Afferent Arteriole wall

3. Beta-adrenergic blockade by inhibiting symathetic stimulation via B1-adrenergic receptors
What are the 2 major effects of Angiotensin II?
1. Increases Peripheral Resistance = increases Afterload

2. Increases Aldosterone secretion = Increases Fluid retention = increased Preload
What 2 actions do ACE inhibitors cause?
Decrease in Preload and Afterload

*Afterload = via vasodilation from loss of AT-II
*Preload = via loss of Aldosterone
What do ACE inhibitors protect against after Myocardial Infarcts?
Subsequent failure by slowing the remodeling
What common ending do all ACE inhibitors share?

**i.e. Benza-pril, Capto-pril
This is the only intrinsically active ACE inhibitor
Other than Capto-pril, what must all ACE Inhibitors be converted to to be active?
T or F: All ACE Inhibitors are equally effective in blocking conversion of Antiotensin I to Angiotensin II, have the same clinical uses and adverse effects, and there is no compelling reason to favor one over another
What is the mechanism of action of ACE inhibitors?
Inhibit ACE = reduce formation of Angiotensin II = Lower BP
List the 3 mechanisms in which ACE inhibitors lower Blood Pressure
1. reduced Angiotensin II Vasoconstriction = vasodilation lowers BP by reducing peripheral vascular resistance

2. Reduced Angiotensin II will decrease Aldosterone release from Adrenal Medulla = decreases fluid volume = decreases Cardiac Output

3. Reduced destruction of Bradykinin = increases Bradykinin Levels = Vasodilation to enhance BP lowering
When administering ACE Inhibitors,what explains the Blood Pressure lowering in hypertensives whose Renin levels are low or normal?
Elevated Bradykinin levels

**the BP lowering is not due to reduced Angiotensin II formation
What causes the side effects of Coughing and Angioneurotic edema when administering ACE inhibitors?
Elevated Bradykinin levels
What plasma product may increase when administering ACE Inhibitors?
Unlike other vasodilators, what do ACE inhibitors not elicit? Why?
Reflex tachycardia

Concurrent baroreceptor resetting or parasympathetic activation
ACE inhibitors lower BP without compromising blood supply to these 3 organs


ACE inhibitors are most effective in what type of Hypertensives?
those with elevated plasma Renin levels

**BUT will still lower BP even when renin levels are not high (via Bradykinin)
What is the advantage of ACE Inhibitors over other Antihypertensive drugs like Diuretics or B-adrenergic blockers?
have milder and fewer side-effects without chaning blood lipids or glucose
ACE Inhibitor
1. administration
2. lower BP in what % of patients with mild-moderate HTN
1. Oral for monotherapy

2. 50%
What groups of patients are ACE inhibitors most effective? Less Effective?
Young to Middle-age Caucasians

Elderly Blacks
ACE Inhibitors are the 1st choice Antihypertensive drugs for treatment of Hypertensives with these 3 conditions
1. Diabetes
2. Chronic Renal Disease
3. LVH
How do ACE Inhibitors enhance the antihypertensive efficacy of Diuretic drugs?
attenuate (diminish) Aldosterone secretion = natriuresis induced by the diuretic is unopposed
What are the common adverse effects of ACE Inhibitors? (3)
1. Dry, hacking, non-productive cough (5-20%)
2. Angioedema and anaphylaxis (due to Bradykinin)
3. Hyperkalemia (due to inhibited Aldosterone secretion, especially in patients with renal insufficiency)
When are ACE Inhibitors contraindicated?
During last 2 trimesters of Pregnancy due to fetal risks of:
-Renal Failure
What is the common ending for Angiotensin II Antagonists?
Which Angiotensin receptors predominate in vascular smooth muscle and cause most of the known actions of Angiotensin II?
AT1 receptors

**AT2 receptors exist in Fetal Tissues
Where do AT2 receptors mainly occur?
Fetal tissues, with fxn being uncertain
T or F: All the currently available Angiotensin II antagonists act by blocking both AT1 and AT2 receptors
False = they selectively block AT1
What side-effect may the Angiotensin II Antagonists cause, especially in patients with Renal Insufficiency?

*potentially fatal arrhythmias
What is the major difference between Angiotensin II Antagonists and ACE Inhibitors?
Angiotensin II Antagonists are more specific in blocking Angiotensin effects b/c they do not affect Bradykinin metabolism = no coughing or angioedema
What are the 2 main uses of A-II Antagonists?
1. Lower BP in HTN patients

2. Slow morphologic changes (remodeling) after myocardial infarction and thus protect against subsequent development of heart failure
Kinins are potent __1__ formed by enzymes called __2__ acting on protein substrates called __3__
1. Arteriodilators

2. Kallikreins

3. Kininogens

= Kallikreins convert Kininogens to Kinins
Where are Kallikreins present?

Where are Kininogens present?
Plasma and many tissues (kidneys, pancreas, intestine, sweat and salivary glands)

Plasma, lymph, interstitial fluid
There are 2 kinin receptors, which one is widely distributed and causes the biologic effects?
B2 receptors
When Kininogens are released in inflammation, what do they cause?
Redness, pain, swelling, heat
What are B2 receptor Antagonists used for?
Experimentally to evaluate kinin involvement in pain, hyperalgesia, and inflammtion

**none are available yet for clinical use
What may B2 receptor agonists (Bradykinin) be useful for treating? Why?

b/c they produce vasodilation = decrease peripheral vascular resistance
What catalyzes Kinin degradation? How is this knowledge used clinically?

ACE inhibitors reduce Bradykinin destruction -> Vasodilation = contribute to anti-HTN effect of ACE inhibitors
Alternate name for Vasopressin-1
Antidiuretic hormone (ADH)
Vasopressin-1 (ADH) is synthesized in the __1__ together with __2__ and then secreted or released from the __3__
1. Hypothalamus
2. Oxytocin
3. Posterior Pituitary
What 3 receptors does Vasopressin-1 act on? What are the effects?
1. V(1a) receptors in vascular smooth muscle -> Vasoconstriction

2. V(1b) receptors -> potentiate release of ACTH by anterior pituitary corticotropes

3. V2 receptors in Renal Cells produce Antidiuresis by increasing water permeability and reabsorption in Collecting Tubules
Long-acting analog of Vasopressin with minimal V1 activity
Desmopressin = Vasopressin-2
What is the major function of Desmopressin?
Antidiuretic = fluid retention in the kidney
What is the antidiuretic-to-pressor ratio of Desmopressin compared to Vasopressin-1?
4000 times = much more potent at Antidiuresis than Vasoconstriction
What does ADH deficiency result in ?
Diabetes Insipidus = secretion of large amounts of severely diluted urine
What 2 drugs are used to treat Diabetes Insipidus?
Vasopressin & Desompressin
Which would you give to a patient with Coronary Artery Disease when trying to treat Diabetes Insipidus, Vasopressin or Desmopressin? Why?

b/c Vasopressin may constrict Coronary blood vessels
Describe the derivation of the word "Eicosanoid"
Eicosa = 20 = all Eicosanoids are synthesized from Fatty Acids that are 20 Carbon atoms in length
Eicosanoids refers to a large family of __1__ products of __2__ widely distributed in many plants and animal tissues
1. Oxygenation

2. Polyunsaturated long chain fatty acids
If Eicosanoids cause a release of cAMP, what will happen?

If Eicosanoids cause release of IP3, what will happen?
cAMP -> Vasodilation

IP3 -> Vasoconstriction by increasing intracellular Ca++
What is the most abundant and important precursor of Eicosanoids?
Arachidonic acid

**mobilized from the cell membrane phospholipids by PLA2
What Eicosanoids do COX enzymes produce?
What Eicosanoids do Lipoxygenases lead to?
What do the P450 Epoxygenases lead to the formation of?
Which COX is constitutively expressed, widely distributed, and has "housekeeping functions"?
Which COX is inducible and is an immediate early response gene product whose expression is stimulated by Growth Factors, Tumor promoters, and Cytokines?
2 NSAIDs that are equipotent on COX-1 and COX-2

NSAIDs that preferentially inhibit COX-2

Eicosanoids have Smooth Muscle effects in what 4 places?
1. Vascular
2. GI
3. Airway
4. Reproductive sites
What effects does Thromboxane have on Smooth Muscle?

What effects do PGE2 and PGI2 have on Smooth Muscle
Vasodilation by decreasing intracellular Ca++
What are the GI effects of Eicosanoids? Which ones cause it?
Longitudinal muscles contract & Circular muscles relax

PGE2 & PGF2-alpha cause Colicky cramps

** "F"eelings of "E"mesis
What Eicosanoids cause Bronchial Smooth Muscle to be relaxed?

DIE-2, E1
What Eicosanoids cause Bronchial Smooth Muscle contraction?
Thromboxane (TXA2)

What is the major source of the Prostaglandins found in semen?
Seminal Vesicle

**different from the original thought that they came from the Prostate
Explain the difference of prostaglandin concentration in fertile and infertile men
High PG in Fertile

Low PG in Infertile
Prostaglandin production in human semen is enhanced by __1__ and reduced by __2__

What Eicosanoid relaxes Smooth Muscles in the Corpus Cavernosum to enhance Penile erection?
PGE1 = Alprostadil

*E1 = erection
*"Al-the-PRO-STUD = gets the ladies with his erection
What 2 Eicosanoids have potent Oxytocic actions and will end pregnancy by promoting Uterine Contractions?
PGE2 & PGF2-alpha

**End Fetus = E2 & F2a
Oral PGE1 analog used for 1st and 2nd Trimester abortions
Other than actually causing abortion, what are PGE2 and PGF2-alpha used for?
Priming or ripening the Cervix before abortion; softens the cervix by increasing Proteoglycan content & chaning biophysical properties of Collagen
What are the common adverse effects of PGE2 and PGF2-alpha when using them for abortion?
Hypo- or Hypertension
Eicosanoid that is given vaginally for abortion
PGE2 = Dino-pro-stone

**Dino-saur abortion
Platelet aggregation is enhanced by __1__ and inhibited by __2__ & __3__
1. TXA2

2. PGE1
3. PGI2
What cells in the blood have high Prostaglandin synthesis capacity?

What parts of the kidney can synthesize Prostaglandins?
Cortex = PGE2 & PGI2

What 3 PG's increase GFR by causing vasodilation?


What drugs stimulate COX activity to increase PG synthesis in the kidney? Why is this important?
Loop Diuretics

Concurrent administration of COX inhibitors may diminish loop diuretic effects = don't take Aspirin when taking Loop Diuretics
Prostaglandins that are effective at initiating and stimulating labor
PGE2 and PGF2-alpha
Facilitation of labor:
-__1__ is one-tenth as potent, but has more GI toxicity than __2__
1. PGF2-alpha

2. PGE2
Prostaglandins that are both as effective as Oxytocin for inducing labor, but with more GI side effects of NVD

Dysmenorrhea may result from increased Endometrial synthesis of these 2 PG's

What would be the treatment?
PGE2 & PGF2-alpha

NSAIDs = inhibit PG formation
-Aspirin is also effective
Orally effective PGE1 synthetic analog that increases production and secretion of gastric mucosa barrier
Drug apporved for prevention of NSAID-induced peptic ulcers

What is it an analog of?

Current drug of choice for inducing labor
Oxytocin is synthesized in the __1__ together with __2__ and secreted from the __3__
1. Hypothalamus
2. Vasopressin
3. Posterior Pituitary
Explain the mechanism of Oxytocin in inducing labor
1. binds to Oxytocin receptors in Uterine Smooth Muscle
2. alters transmembrane ionic currents to activate voltage-sensitive Ca++ channels
3. sustained uterine contractions
Why does Uterine sensitivity to Oxytocin increase during pregnancy?
b/c the # of Oxytocin receptors increases markedly in late gestation
Aside from Inducing labor, what is Oxytocin's other effect?
Causes Milk ejection by contracting myoepithelium in mammary alveoli

Normal lactation cannot occur w/out Oxytocin-induced contraction
What are the 4 clinical uses of Oxytocin?
1. Induce labor in uterine inertia, incomplete abortion, or conditions requiring early vaginal delivery (maternal diabetes)
2. control Postpartum hemorrhage
3. induce Milk ejection
4. Diagnose placental circulatory reserve
Although adverse rxns to Oxytocin are rare, what are the possible ones?
1. Maternal death due to:
-Uterine rupture
-water intoxication

2. Fetal death