high blood pressure 1 Flashcards
how is systolic pressure different from diastolic pressue
sysolic is the maximum blood pressure during contractions between ventricles
diastolic is the minimum pressure recorded prior to the next contraction (ventricular relaxation)
What is the correct classification of blood pressure in a person with systolic pressure of 142 mmHg and diastolic pressure of 92 mmHg, according to the JNC7 guidelines?
A. Normal blood pressure
B. Prehypertension
C. Stage 1 hypertension
D. Stage 2 hypertension
According to the JNC7 classification (shown on Slide 4), Stage 1 hypertension is defined as SBP 140–159 or DBP 90–99 mm Hg.
which of the following contributes to hypertension?
a. low phosphate
b. low magnesium
c. low sodium
d. high sodium
e. low phosphatre
hgih sodium and low potassium
Which of the following is a primary determinant of blood pressure as described by the equation in the slides?
A. Blood viscosity × hematocrit
B. Stroke volume × peripheral resistance
C. Heart rate × venous return
D. Cardiac output × peripheral vascular resistance
Cardiac output × peripheral vascular resistance
cardiac output=amount of blood pumped out by each ventricle per min
perpheral=resistance in the circulatory system that is used to create blood pressure
what is blood pressure mainly regulated by and does vasocontriction or vasodilation increase blood pressure
blood pressure is regulated by the sympathetic nervous system
higher blood pressure is due too a narrow radius=vasconstriction (the heart has to work harde to pump blood throughout the body)
Which of the following drug classes acts primarily on the heart to reduce blood pressure?
A. Alpha-1 blockers
B. Beta-blockers
C. Aldosterone antagonists
D. ACE inhibitors
Beta-blockers reduce blood pressure by decreasing cardiac output through actions on the heart.
what are the cirtical sites that drugs work on in the body to reduce hypertension?
- heart by beta blockers and diuretics
- resistance vessels by alpha blockers
- RAAS/aldosterone system (no drug stated)
Which of the following is NOT a primary component of the Renin-Angiotensin-Aldosterone System (RAAS)?
A. Kidney
B. Adrenal gland
C. Pulmonary artery
D. Vasculature
The RAAS includes the kidneys, adrenal gland, and vasculature. The pulmonary artery is not listed as a key RAAS component.
why does fluid regulation occur in the distal convoluted tube?
Fine-tunes electrolyte balance, especially sodium (Na⁺) and chloride (Cl⁻) reabsorption via the Na⁺/Cl⁻ co-transporter.
it is also the main site for diuretics
Which of the following best explains how thiazide diuretics help in managing hypertension?
A. They increase renin secretion, leading to vasodilation
B. They inhibit aldosterone receptors, reducing sodium reabsorption in the loop of Henle
C. They block Na⁺/Cl⁻ transporters in the distal tubule, reducing blood volume
D. They enhance calcium excretion, lowering vascular resistance
They block Na⁺/Cl⁻ transporters in the distal tubule, reducing blood volume
Thiazide diuretics lower blood pressure primarily by blocking Na⁺/Cl⁻ symporters in the distal convoluted tubule, leading to natriuresis and a reduction in extracellular fluid volume, which decreases blood pressure
these durgs increase urine production in the kidneys, which lowers blood volume.
state 3 thiazide drugs:
hydrochlorothiazide
chlorothiazide
indapamide
Which of the following best describes the mechanism by which thiazide diuretics lower blood pressure?
A. Inhibit Na⁺/K⁺-ATPase pump in the proximal tubule, reducing blood volume
B. Block Na⁺/Cl⁻ co-transporter in the distal convoluted tubule, decreasing plasma volume
C. Inhibit renin secretion in the juxtaglomerular apparatus, decreasing angiotensin II
D. Stimulate aldosterone receptors in the collecting duct, promoting natriuresis
Thiazide diuretics lower blood pressure by blocking the Na⁺/Cl⁻ co-transporter in the distal convoluted tubule, leading to increased sodium and water excretion, reducing plasma volume and thereby blood
what is the importance of adrenergic receptors?
a. they lower blood volume in the body bly blocking NA+/Cl- co-transporters
b. they are important in increasing K+ in the urine
c. they are important for regulating blood pressue
important for refulating blood pressure
which is true about adrenergic receptors?
a. the are activated catecholamines: ephinephrine, norephinephrine, dopamine, and glutamate
b. they are GPCR’s
c. they contain alpha, beta, and gamma receptors
d. they are activated by acetylcholine, norepinephrine, and epinephrine
B is the only correct answer
a- they are activated by catecholamines dopamine, norephinephrine, ephinephrine but NOT GLUTAMATE
c-they only have alpa and beta recpetors
d- completely false
receptors in the heart that are responsible for increasing hear rate and causing the heart to pump harder during a fight or flight response:
a. alpha receptors
b. adrenergic receptors
c. beta 2 receptors
d. beta 1 receptors
beta 1 receptors
Which of the following components are involved in the β1-adrenergic receptor signaling cascade in cardiac muscle, leading to enhanced contractility?
A. IP3 and DAG activation via Gq-coupled α1-receptors → smooth muscle contraction
B. Inhibition of adenylate cyclase → decreased cAMP → reduced cardiac output
C. L-type voltage-gated Ca²⁺ channels → increased Ca²⁺ influx; Ryanodine receptors → increased Ca²⁺ release from SR; SERCA pumps → increased Ca²⁺ reuptake
D. β2-mediated MLCK inhibition → smooth muscle relaxation via increased cAMP
β1 receptors in cardiac muscle are Gs-coupled, leading to:
↑ cAMP → activation of PKA
PKA phosphorylates:
L-type Ca²⁺ channels → more Ca²⁺ influx
Ryanodine receptors (RyRs) → more Ca²⁺ release from the sarcoplasmic reticulum (SR)
SERCA pumps → faster Ca²⁺ reuptake into SR, improving relaxation and readiness for the next beat
C
what will the enzyme phosphorylations cause in B1 adrenergic receptors?
- calcium influx
- release of calcium by ryanodine receptors (RYR’s)
- Calcium reuptake increases
What is the main physiological outcome of β1 activation in the heart?
A. Vasodilation of coronary arteries
B. Increase in calcium reuptake by SERCA
C. Inhibition of MLCK leading to relaxation
D. Decreased cAMP and reduced contractility
Increase in calcium reuptake by SERCA
hich of the following accurately compares the downstream signaling of β1 and β2 adrenergic receptors?
A. Both are coupled to Gi proteins, leading to inhibition of PKA
B. β1 increases intracellular Ca²⁺ in cardiac muscle, while β2 activates MLCK in vascular smooth muscle
C. β1 enhances calcium handling to increase contraction, whereas β2 inhibits MLCK to induce relaxation
D. β1 and β2 both cause smooth muscle relaxation via SERCA pump activation
β1 receptors (cardiac) enhance contraction via PKA-mediated activation of L-type Ca²⁺ channels, RyRs, and SERCA pumps,
while β2 receptors (smooth muscle) activate PKA, which inhibits MLCK, promoting muscle relaxation.
Both are coupled to Gs
c
receptors located in the lungs that cause bronchodilation and enhace blood flow to skeletal muscles during a fight or flight response
a. alpha receptors
b. adrenergic receptors
c. beta 2 receptors
d. beta 1 receptors
beta 2 receptors
phosphorylation of ______ promotes contractions, and _____ is dependant on protein kinase
MLCK (this happens in beta 2)
MLCK
NOTE: this only occurs when no beta 2 receptors bind because binding of beta 2 receptors inhibit MLCK
what occurs in the cell for beta 2 receptors during smooth muscle contraction?
B2 agonists increase cAMP levels, which inhibit MLCK, leading to no contractions
besides b1 and b2 being Gs GPCR’s, why are they different?
they have different downstream signalling activities or effects
b1; use L-type volted gated calcium channels, ryanodine receptors, and serca pumps to transport calcium ions from the cytosol back into the sarcoplasmic reticulum
b2: uses MLCK (proetin that aids in muscle contraction) and phosphorylation of PKA (helps smooth muscles to relax)
Which statement correctly describes a major side effect concern when using non-selective β-blockers?
A. Hyperkalemia due to β2-mediated potassium channel blockade
B. Bronchoconstriction due to inhibition of β2-mediated smooth muscle relaxation
C. Reflex tachycardia caused by α1 receptor stimulation
D. Sodium retention due to β1 blockade in the nephron
Non-selective β-blockers, like propranolol, block both β1 and β2 receptors. β2 blockade in bronchiolar smooth muscle prevents relaxation, potentially causing bronchoconstriction, which is contraindicated in asthma patients.
this is because in regular conditions b2 receptors cause muscle relaxation by preventing bronchoconstriction
