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48 Cards in this Set
- Front
- Back
A 62 year old male with idiopathic cardiomyopathy and low-output heart failure (ejection fraction of 15%) is being treated in the hospital while waiting for a heart transplant. The patient has marked pulmonary and systemic edema, for which he is treated with a number of drugs.
We want to understand the physiologic basis for the volume retention and the mechanism of action and potential side effects of drugs. Which of the following is causing the edema in this patient? a) increased plasma osmolality b) decreased plasma volume c) increased arterial pressure d) decreased effective circulating blood volume e) increased tubuloglomerular feedback |
Patient has a volume overload. How does the heart and kidney interplay to regulate volume.
Answer is D |
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We cant detect changes in ICF only in
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ECF (in plasma not ISF
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Patients with heart failure despite normal plasma volume or even increase plasma volume the system is responding as if patients are actually
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hypovolumic because not only plasma volume being monitored, but the effective circulating volume
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Volume is detected by baroreceptors they detect
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the effective circulating volume depedent on blood volume, CO and total peripheral resistance
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In a patient with cardiac failure, CO decreases and carotid sinus and baroreceptors detect changes in
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arterial filling (decreased) system detects this as low volume. A patient with vasodilation is detected as low effective circulating volume
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Effective Circulatin Volume is affected by
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Blood Volume, CO, Total Peripheral Resistance
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What are the regulators of effective circulating volume
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Baroreceptors, low and high pressure. Low pressure secrete ANP and BNP
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Low pressure regulators
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Cardiac Chambers (ANP, BNP)
Pulmonary Vasculature |
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High Pressure receptors
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Carotid Sinus
Aortic Arch Juxtaglomerular Apparatus Renin Secretion altered by: Perfusion Pressure Sympathetic Nerves Macula Densa signaling |
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High Pressure Sensors
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Liver
CNS Other Large Systemic Arteries |
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A decrease in low and high pressure receptors signaling causes
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compensatory changes in the cardiovascular and renal systems to increase volume
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Sympathetic input causes in renin release
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Increase
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Which of the following changes are triggered by a detected
decrease in effective circulating blood volume in this patient? a) a decrease in sympathetic tone to the afferent arterioles b) an increase in plasma aldosterone c) an increase in plasma atrial natriuretic factor d) a decrease in plasma arginine vasopressin e) a decrease in parasympathetic tone to the kidney |
Answer is B.
Its not C because Atrial natriuretic factor antagonizes the renin system so it would lead to decrease |
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Decreased detectioon in volume..signal to brain to
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increase para causing vasoconstriction so MAP goes up. Increase in para influences tubule transport in kidney and affects release of renin
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Renal baroreceptors detect decrease in EABV and renin
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released
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a decrease in GFR triggers further
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renin released
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Renin triggers Ang 2 which affects
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hemodynamics in tubule transport or can cause aldosterone release It can also cause cardiac fibrosis and worsening cardiac failure
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Baroreceptors trigger release of ADH
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Cardiac tree releases less ANP
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Compensatory Responses to a decrease in EABV
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1) Activate RAAS System
2) Sympathetic Drive 3) Release ADH 4) Inhibit ANP Release |
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Renin is released due to decreased in
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pressure in kidney
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Ang2 causes contraction of smooth muscle so pressure
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goes up, it also triggers release of ADH. Thirst centers are also triggered by Ang2 and it increases aldoesterone secretion (NaCl reab increases).
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Increase Aldosterone Secretion
Increase NaCl reabsorption by the thick ascending loop, distal tubule and collecting duct what are the channels involve? |
ENaC, NKCC2, NaCl symport, Na/KAtpase
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Increase Smooth Muscle Contractility via α Adrenergic
Signaling (increases sympa activity) Effect is greater on |
Afferent Arterioles, RBF goes down and GFR
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Increased sympa activity increases renin secretion causing
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Ang2 and aldosterone release to increase
Increase NaCl Reabsorption |
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pressure increase in efferent arteriole pressure may cause back up of blood into glomerulus increasing filtration, this also would cause a decrease in
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hydrostatic pressure in the peritubular capillaries which would lead to better reab of H2O and NaCl in these capillaries
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Increased sympa increases NaCl reabsorption of the nephorn by signaling primarily
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proximal tubules
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Natriuretic Peptides
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ANP, BNP an Urodilatin
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High levels of right atrial distension, ANP is
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is released to antagonize Renin
Vasodilation (afferent) and vasoconstriction(efferent) caused by ANP lead to increase filtration pressure in the glomerulus therefore increasing GFR, therefore increasing Na load and H20 load so that we are able to excrete more Na and H20. |
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ANP increase affects the kidney to
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Inhibit NaCl reab
Inhibit Renin Secretion |
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ANP increase affects the smooth muscle to
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Vasodilate (afferent)
Vasoconstriction (efferent) |
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High ANP stimulates the brain to
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inhibit ADH secretion
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ANP increase causes adrenal cortex to
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inhibit aldosterono secretion. Directly and by reducing Renin
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The heart failure patient has been on a low Na+ diet for three years. He
is unable to resist the allure of a bag of salty chips. He goes on a week long binge of salt consumption. Which of the following do you expect to occur at the end of the week? a) He exhibits an increase in the extracellular fluid compartment and a decrease in the intracellular fluid compartment b) He exhibits an increase in both the extracellular and intracellular fluid compartments c) He exhibits a decrease in the extracellular fluid compartment and an increase in the intracellular fluid compartment d) He exhibits an increase in the extracellular fluid compartment and no change in the intracellular fluid compartment e) He exhibits an increase in the intracellular fluid compartment and no change in the extracellular fluid compartment |
Answer is D
Answer is not A because he is not eating a pound of NaCl at once. Eating NaCl for a week would lead to responses like drinking water and body would see this as an isosmotic osmolarity |
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The volume expansion that occurs as a result of the increased
Na+ intake in the heart failure patient is most likely _______ the volume expansion that a healthy individual would experience. a) less than b) equal to c) greater than |
C
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In a healthy personAs a consequence of Na intake, ECF osmolarity increases leading to water
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retention (ADH), as person starts to retain water, ECBV goes up, leading to enhancement of excretion of Na
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Excretion of Na lags behind uptake of Na and change in osmolarity meaning
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Na would be excreted until theres a volume change
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During the period that takes to generate volume response, Na load in body is
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increasing aka Positive Na Balance, so volume response to secrete Na lags behind the osmoregulatory response to retain water
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So osmoregulatory response first (retention of water) and then
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volume response (excretion of Na) eventually Na intake equals Na excretion.
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Heart failure patient who already has a system detecting a decrease in EFbCV which turns on Na retention system, so osmoregulatory systems retain water to keep osmotic balance
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Takes a much longer time to start excreting Na so Volume overload (expansion) is even greater
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So what are the systems involved in regulation of Na balance that respond to osmotic challenge
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ECF [Na] ultimately determines extracellular fliud volume which corresponds to ECBV=effective arterial blood volume (EABV). Increase in Na intake, ECV goes up, symp activity is turned off.
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As Na intake increases, ECBV increases leading to changes in
Sympa activity ANP Na absorption in PT Renin system |
Decrease
Increase Decrease Decrease.. All of these leads to increase of Na excretion |
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In order to counteract the patient’s declining pulmonary function,
he is started on an intravenous loop diuretic (lasix) to increase free water excretion and reduce edema. Which of the following side effects might be seen in subsequent blood work? a) hypokalemia b) hypercalcemia c) hypermagnesemia d) hypophosphatemia e) hyperchloremia |
Answer is A
May have hypocalcemia and hypomagnesemia No effect on phosphate because it is regulated in PT |
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What is the most likely mechanism for the occurrence of hypokalemia in the patient?
a) enhanced Na+ delivery to principal cells of the collecting tubules increases K+ secretion? b) impaired K+ reabsorbtion by the thick ascending limb of the loop of Henle c) decreased urinary flow rate inhibits K+ reabsorbtion in distal tubule cells d) a decrease in GFR reduces the K+ filtered load and K+ reabsorbtion in the proximal tubule by through the paracellular pathway e) inhibition of NKCC2 in the thick ascending limb increases luminal Cl- , trapping K+ and increasing excretion |
Answer is A
Not E because inhibition of NKCC2 doesn’t generate a charge changes so K wouldn’t be. trapped. Loop diuretics inhibit Na and Cl reab in the thick ascending limb, so Na load that reaches later parts is greater, hence Na reab increases through Enac which leads K out of cell leading to excretion of K. |
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Increase the excretion of K+, Ca++,
and Mg++. Treatment with loop diuretics can lead to hypokalemia, hypercalciuria, and hypomagnesemia. Useful in treating cases of hypercalcemia. |
Loop Diuretics (Furosemide
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): Increase excretion of K+, but
decrease the excretion of Ca++ . These are useful then in treating cases of idiopathic hypercalciuria. |
Distal Tubule Diuretics (Thiazide
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Decrease excretion of K+. Useful
in treating patients using loop or Distal Tubule Diuretics to offset the K+ loss in these patients. |
K+ Sparing Diuretics (Amelioride):
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The patient has normal renal function upon entering the hospital. Laboratory reports on the patient’s blood would most likely reveal which of the following sets of values for blood urea nitrogen (BUN) and blood creatinine? (Hint: normal BUN between 7 and 20 mg/dL and normal creatinine is between 0.7 and 1.2 mg/dL).
a) BUN = 4 mg/dL; creatinine = 3.0 mg/dL b) BUN = 15 mg/dL; creatinine = 3.0 mg/dL c) BUN = 15 mg/dL; creatinine = 0.9 mg/dL d) BUN = 45 mg/dL; creatinine = 1.2 mg/dL e) BUN = 45 mg/dL; creatinine = 3.0 mg/dL |
Answer is D
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One of the drugs that the patient is being treated with is an angiotensin
converting enzyme (ACE) inhibitor to treat hypertension. The dose of the ACE inhibitor is increased and new laboratory results show that the patient’s plasma creatinine has increased from within the normal range to 3.3 mg/dL. Which of the following is most likely the cause of the patient’s decrease in GFR and renal function? a) The resulting decrease in AngII levels cause a decrease in renal blood pressure and therefore a decrease in GFR. b) The resulting decrease in AngII levels cause a decrease in aldosterone, resulting in hyperkalemia, cardiac arrhythmias, a decrease in cardiac output, decreased renal blood flow, and therefore a decrease in GFR c) The resulting decrease in AngII levels trigger a decrease in the release of antidiuretic hormone causing dehydration, and there a decrease in GFR. d) The resulting decrease in Ang II levels cause a preferential dilation of efferent arterioles and therefore a decrease in GFR |
Answer is D
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