Which of the following statements are correct? I. Diastole- relaxation of the ventricles, expands II. Systole- contraction, pushed blood out III. Aorta - largest vein IV. Chronotropy - number of beats per min

Which of the following statements are correct? I. CO – all events that occur at one heartbeat including both atrial and ventricular contraction II. Cardiac cycle - capacity of heart to pump out blood per minute, usually 4-8 liters circulated per minute III. SV – the amount of blood ejected per beat IV. CO = HR x SV where hr is 60-90 normally

Which of the following statements are correct? I. Preload - workload required by the heart before contraction II. Afterload - force generated by the interplay between the blood flow and the resistance to blood flow. III. Inotropy - contractility or the of the heart to change its force of contraction without changing its resting length IV. AVP - tension work of the heart presented after contraction; force needed to completely pump the blood out of the heart.

Which of the following statements are correct? I. TPR/VPR - amount of force placed on the blood while moving through the blood vessels. Arteriolar constriction decreases TPR and DBP II. Pulse pressure is difference between sbp and dbp III. MAP (1/3 sbp + 2/3 dbp) pressure throughout the cardiac cycle of contraction. IV. BP is sbp/dbp in mmHG

category of hpn psychosomatic in the clinical environment?

category of hpn high systole with normal diastole?

category of hpn does not respond to any therapeutic interventions?

category of hpn with fluctuating BP?

category of hpn age-related with no underlying cause, unknown, asymptomatic, no s/s?

category of hpn results from other conditions?

category of hpn precipitated by hypertensive crisis which can either be emergency mins/hrs (accompanied by target organ damage) or urgency (without organ damage) hrs/days?

category of hpn with sustained high blood pressure often leads to vascular wall damage and surrounding tissues that results to inflammatory reactions?

Based on JNC for the detection and intervention of HPN, normal is ___

Based on JNC for the detection and intervention of HPN, pre-hypertension is ___

Based on JNC for the detection and intervention of HPN, stage 1 hypertension is ___

Based on JNC for the detection and intervention of HPN, stage 2 hypertension is ___

Identify which of the following are correct? I. BP = CO x PVR II. CO = HR x SV III. HR is affected by action of PANS and SANS IV. SV is affected by blood volume V. PVR is affected by blood viscosity

Inotropy is the force of contraction. Ach (M2) causes the decrease in inotropy and increased by NE (B1). True or False?

True or false? Low BP – retain sodium and water High BP – excrete sodium and water

Damaged kidney =

Changes in the BP causes these receptors to send signals to the brain

True or False? ▪ LowBP→activateshypoglossalnerve→ signals the brain and the ANS in the hypothalamus to release epinephrine ▪ High BP → activates vagus nerve → releases Ach

Alpha-2 adrenoceptors causes negative feedback mechanism

Alpha-1 adrenoceptor activation in the blood vessels causes constriction

Beta-1 adrenoceptor activation in the blood vessels causes (+) inotropy, chronotropy, bathmotropy, and dromotropy, and release of renin

Controls sodium and potassium concentration in the blood

Free flowing substrate from the liver ✓ Renin

Converted from angiotensinogen once renin is released ✓ Angiotensin converting Enzyme / Human Chymase

Strong vasoconstrictor, increases PVR ✓ AT-1 receptors

AT-1 Receptors found on the brain, kidney, heart and blood vessels

AT-2 RECEPTORS Found on the brain and uterine cells

Anti diuretic hormone, prevents the release of water and sodium ✓ Na+ and Water Retention

Intermediary product and weak vasoconstrictor

Strong vasoconstrictor and causes (-) feedbac/ heterotropic modulation to renin release

Stimulates aldosterone secretion that causes water retention

Causes release of plasminogen activator inhibitor-1 which prevents clot formation by inhibiting PT function

T or F? Angiotensin I & II = clinical significance in blood pressure Angiotensin I, II, III & IV = can bind to either AT1 or AT2 receptors

Inhibits Na+/K+ ATPase

present in the BV and described as the most potent vasoconstrictor

Specific to smooth muscles. Activation causes vasoconstriction, bronchoconstricti on, and stimulation of aldosterone hormone

Specific to vascular endothelium Activation causes vasodilation and inhibition of ex- vivo PT aggregation

Produced by arachidonic cascade, COX pathway ✓ Antithrombotic ✓ Prevents excessive formation of blood clot

• Released during inflammation and tissue injury of the BV • Helps in restoration

Powerful vasodilator activates guanylyl cyclase

Electrolyte concentration – alteration would result to changes in BP

Cotton wool patch edema Papilledema Microanurism Jugular vein distention Cyanosis Cold Clammy extremities

The following are risk factors of primary hpn except: a. smoking, alcoholism b. DM, obesity, CVDs c. Pregnancy, stress, age d. Dyspilidemia, racial predisposition

The following drugs are risk factors for hpn. T or F? NSAIDs – COX inhibitors Corticosteroids Anorexiants Ephedrine Oral nasal decongestants • Cocaine Contraceptives

Secondary hpn. Would result to higher level of cortisol andinduce inflammatory responses in the body? Cortisol= stresshormone

A tumor on the adrenal gland = enhances the production of epinephrine Inc.EPI=High BP

Secondary hpn. Damaged kidneys can affect the sodium and water levels High sodium and water = HPN

Secondary hpn. Narrowing of the renal artery

Secondary hpn. Excessive amount of aldosterone in the body

Secondary hpn. Causes an increase in inotropy (force of contraction) because the blood cannot pass through

Secondary hpn. Damage in the thyroid gland result to HPN

Secondary hpn. Difficulty breathing during sleep

Cause of death for secondary hpn except: a. Ischemia b. Graveyard disease c. Cerebrovascular accidents d. Renal failure

T or F? Treat for secondary hpn are: 1. To decrease morbidity/mortality in least obstructive method. 2. To lower target organ disease. 3. To improve quality of life.

Risk stratification. Which category? Initially with lifestyle modification for 1 year No major risk factors No target organ disease

Risk stratification. Which category? Lifestyle modification for 6 months > 1 risk factor but not DM No target organ disease

Risk stratification. Which Category Immediate pharmacologic treatment with lifestyle modification No target organ disease or several Presence of DM as risk factor

Non Pharmacologic treatment: • Lifestyle modification • Exercise – cardiologist approved • Dietary Approach to Stop HPN (DASH) diet Weight reduction • Smoking cessation • Reduction of alcohol intake - <1 ounce • Active lifestyle • Relaxation / Meditation

Pharmacologic treatment: a. For patients under Category _ and _, diuretics and beta-adrenergic blockers. b. For patients under Category _, the other classifications are added in the therapy. c. T or F? To enhance the effect 2 additional drug at a time d. T or F? Partnership of drugs can always include a diuretic except when it is contraindicated like Not effective for latino and black patient e. T or F? Drug combination should not include duplication of therapy to maximize benefits. f. T or F? There are 11 drug classes that can be used in HPN.

Drug classes. - Initial treatment for patients with adequate renal functions - Can also cause vasodilation due to they are chemically related to diazoxides. - Possess vasodilatory effect - Can target blood vessels to lower BP

Site for the action of thiazides

The following are adrs of Thiazides except: a. Hypokalemia - low level of K b. Hypercalcemia - retained Ca c. Hyphophastemia - Ca correlates Phospates d. Hyperglycemia - high glucose level, Patient is dehydrated e. Metabolic alkalosis - bicarbonate ion retained inc in pH f. Allergic reactions - contains Sulfur common allergen

Contraindication of Thiazides: Anuria (minimal to no urine) Oliguria (low urine output) Kidney failure/Glomerulonephritis (inflammation of nephron for kidney)

Class of drugs. - Different pharmacophore compared to true thiazides, but the same MOA - Not derived from diazoxide = no vasodilatory effect

Class of drugs. Have ceiling effects/maximal output to urine but short duration of action (6 hours)

Prototype for loop is furosemide

Loop are CI with combination of thiazides because it may cause severe ADRs

ADR of loop not present in thiazides except: a. Hypercalcemia b. Edema c. Hyperuricemia d. electrolyte imbalance

Class of drugs. - Promotes excretion of sodium but prevents the excretion of potassim - Possess weaker diuretic effects as compared to the first two types. - Cannot be used to lower down the blood pressure. Instead, they are used as adjunct therapy to correct hypokalemia.

Effect of K sparing diuretics?

- Inhibit/suppress aldosterone (anti- diuretic hormone) which inhibit exchange of sodium and potassium, thereby sodium is excreted and potassium is retained. - Mineralocorticoids functions for sodium and water retention in exchange for potassium - Can inhibit the binding of aldosterone to its receptor, therefore sodium will be excreted while potassium is retained

ADRs of K sparing diuretics: a. Hyperkalemia b. GI Disturbances - no action potential c. Gynecomastia - enlargement of breast in men related to spironolactone d. lethargy and acute renal failure

Other therapeutic uses o Adjunct in the treatment of CHF o Adjunct in the treatment of edema o Secondary aldosteroidemia

Other therapeutic use o Nephrogenic diabetes insipidus o Congestive heart failure o Hypercalciuria o High calcium levels in the urine o To lower down the level of calcium in the urine

Drugs that block the action of catecholamines on beta- adrenoceptors

Beta-adrenergic blockers are all true except: a. Catecholamines: Dopamine, Epinephrine, NE b. Effects causes (-) inotropy, chronotropy, bathmotropy, and dromotropy c. Indirectly it can block the release of renin from the kidneys d. Renin release is caused by alpha activation e. Has the suffix -olol

Beta-blockers that only acts on the beta-1 adrenoceptors. Can be used in patients with COPD, asthma, and Reynaud’s disease.

Metropolol is the prototype drug for cardioselective

Esmolol use in hospital settings

- Possess partial sympathomimetic activity - Not complete beta blockers • Used for patients with sinus bradycardia (low HR) and Reynaud’s disease, but can cause MI.

Pindolol is protype drug for ISA (INTRINSIC SYMPATHOMIMETIC ACTIVITY)

-Possess anesthetic-like effects on cardiac muscles which is useful for patients with arrhythmias - Relaxation effects on the cardiac muscle and can rest the action potential to correct the heart rhythm

DOC for arrythmia is propranolol

Can inhibit both alpha and beta adrenoceptors

• Can also inhibit beta-adrenoceptors in other parts of the body. • These are not recommended if the patient has underlying many conditions that requires beta- adrenoceptor activation.

• Can also inhibit beta-adrenoceptors in other parts of the body. • These are not recommended if the patient has underlying many conditions that requires beta- adrenoceptor activation.