Hypertension Flashcards
(168 cards)
These are strong, independent risk factors for hypertension.
Obesity
weight gain
Low dietary intakes of ___ and ____ also may contribute to the risk of hypertension.
calcium
potassium
The two determinants of arterial pressure
Cardiac output
Peripheral resistance
Cardiac output is determined by ____ and ______
stroke volume
heart rate
The most common etiology of secondary hypertension
Primary renal disease
_____ is predominantly an extracellular ion and is a primary determinant of the extracellular fluid volume.
Sodium
Which of the following mechanisms is primarily responsible for kidney-related hypertension?
A) Excessive sodium excretion
B) Overactivity of parasympathetic nervous system
C) Diminished capacity to excrete sodium
D) Increased calcium absorption in the renal tubules
C
In the early stages of vascular volume expansion, how does blood pressure initially increase?
A) Increased peripheral resistance
B) Decreased peripheral resistance
C) Increased cardiac output
D) Decreased cardiac output
C
Which of the following is true regarding the relationship between sodium intake and blood pressure?
A) All salts of sodium significantly increase blood pressure
B) Sodium chloride (NaCl) intake is more strongly associated with increases in blood pressure
C) Sodium intake has no effect on blood pressure
D) Non-chloride salts of sodium have the strongest effect on blood pressure
B
What is the effect of increased arterial pressure on sodium excretion?
A) Decreases urinary sodium excretion
B) Increases urinary sodium excretion
C) Has no effect on sodium excretion
D) Decreases glomerular filtration rate
B
When arterial pressure rises in response to increased sodium intake, urinary sodium excretion increases to restore sodium balance. This process is known as “pressure-natriuresis.”
Which factor is least likely to contribute to hypertension in patients with end-stage renal disease (ESRD)?
A) Increased vascular volume
B) Overactivity of the renin-angiotensin system
C) Increased sodium reabsorption
D) Decreased sympathetic nervous system activity
D
Which of the following best describes the “pressure-natriuresis” phenomenon?
A) The body’s capacity to excrete sodium decreases as arterial pressure increases
B) Sodium balance is maintained through decreased glomerular filtration rate
C) As arterial pressure increases, urinary sodium excretion increases
D) Sodium excretion decreases in response to high NaCl intake
C
What is the most likely consequence in individuals with an impaired ability to excrete sodium?
A) Lower arterial pressure is needed to maintain sodium balance
B) Blood pressure remains unaffected by sodium intake
C) Greater increases in arterial pressure are required to achieve sodium balance
D) Sodium balance is maintained without an increase in arterial pressure
C
In patients with end-stage renal disease (ESRD), how is blood pressure most commonly controlled?
A) Increased potassium intake
B) Salt restriction
C) Pharmacologic blockade of the renin-angiotensin system
D) Adequate dialysis
D
Which of the following is NOT a mechanism through which the kidney affects blood pressure?
A) Excessive renin secretion
B) Overactivity of the parasympathetic nervous system
C) Sympathetic nervous system overactivity
D) Impaired sodium excretion
B
Which of the following catecholamines has a greater affinity for α-adrenergic receptors?
A) Epinephrine
B) Norepinephrine
C) Dopamine
D) Serotonin
B
α receptors: Norepinephrine > Epinephrine
β receptors: Epinephrine > Norepinephrine
What is the primary function of α1 receptors?
A) Vasodilation of smooth muscle
B) Inhibition of norepinephrine release
C) Vasoconstriction of smooth muscle
D) Relaxation of vascular smooth muscle
C
> α1 Receptors:
Location: Postsynaptic smooth muscle cells
Function: Vasoconstriction, increases renal tubular sodium reabsorption
α2 Receptors:
Location: Presynaptic membranes of postganglionic nerve terminals
Function: Inhibit norepinephrine release (negative feedback)
β1 Receptors:
Function: Increase cardiac contraction rate and strength, increase cardiac output, stimulate renin release in the kidney
β2 Receptors:
Function: Relax vascular smooth muscle, leading to vasodilation
Activation of which receptor type is associated with increased renin release from the kidney?
A) α1
B) α2
C) β1
D) β2
C
What is the primary effect of β2 receptor activation?
A) Vasoconstriction of smooth muscle
B) Increased cardiac output
C) Vasodilation of vascular smooth muscle
D) Sodium reabsorption in the kidney
C
Which of the following conditions may result in tachyphylaxis due to adrenergic receptor downregulation?
A) Chronic low levels of catecholamines
B) Chronic high levels of catecholamines
C) Chronic use of adrenergic antagonists
D) Intermittent use of adrenergic antagonists
B
A patient with pheochromocytoma presents with orthostatic hypotension. What is the most likely cause?
A) Increased β2 receptor activation
B) Increased norepinephrine release
C) Lack of norepinephrine-induced vasoconstriction in response to standing
D) Overactivation of α2 receptors
C
What is the primary mechanism by which clonidine, a centrally acting α2 agonist, lowers blood pressure?
A) Inhibition of renin release from the kidney
B) Decreased sympathetic outflow
C) Increased cardiac output
D) Vasoconstriction of peripheral blood vessels
B
Which reflex mechanism primarily buffers acute fluctuations in blood pressure during postural changes?
A) Sympathetic outflow from the spinal cord
B) Arterial baroreflex mediated by stretch-sensitive receptors
C) Chemoreceptor reflex in the brainstem
D) β2 receptor activation by circulating catecholamines
B
A patient treated with clonidine abruptly stops the medication and experiences a significant spike in blood pressure. What is the most likely cause of this rebound hypertension?
A) Upregulation of α1 receptors
B) Downregulation of β1 receptors
C) Increased renin release
D) Decreased norepinephrine levels
A
Abrupt cessation of clonidine, a centrally acting α2 agonist, can cause rebound hypertension due to upregulation of α1 receptors, leading to increased sensitivity to sympathetic stimuli.