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48 Cards in this Set

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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
We cant detect changes in ICF only in
ECF (in plasma not ISF
Patients with heart failure despite normal plasma volume or even increase plasma volume the system is responding as if patients are actually
hypovolumic because not only plasma volume being monitored, but the effective circulating volume
Volume is detected by baroreceptors they detect
the effective circulating volume depedent on blood volume, CO and total peripheral resistance
In a patient with cardiac failure, CO decreases and carotid sinus and baroreceptors detect changes in
arterial filling (decreased) system detects this as low volume. A patient with vasodilation is detected as low effective circulating volume
Effective Circulatin Volume is affected by
Blood Volume, CO, Total Peripheral Resistance
What are the regulators of effective circulating volume
Baroreceptors, low and high pressure. Low pressure secrete ANP and BNP
Low pressure regulators
Cardiac Chambers (ANP, BNP)
Pulmonary Vasculature
High Pressure receptors
Carotid Sinus
Aortic Arch
Juxtaglomerular Apparatus
Renin Secretion altered by:
Perfusion Pressure
Sympathetic Nerves
Macula Densa signaling
High Pressure Sensors
Liver
CNS
Other Large Systemic Arteries
A decrease in low and high pressure receptors signaling causes
compensatory changes in the cardiovascular and renal systems to increase volume
Sympathetic input causes in renin release
Increase
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
Decreased detectioon in volume..signal to brain to
increase para causing vasoconstriction so MAP goes up. Increase in para influences tubule transport in kidney and affects release of renin
Renal baroreceptors detect decrease in EABV and renin
released
a decrease in GFR triggers further
renin released
Renin triggers Ang 2 which affects
hemodynamics in tubule transport or can cause aldosterone release It can also cause cardiac fibrosis and worsening cardiac failure
Baroreceptors trigger release of ADH
Cardiac tree releases less ANP
Compensatory Responses to a decrease in EABV
1) Activate RAAS System
2) Sympathetic Drive
3) Release ADH
4) Inhibit ANP Release
Renin is released due to decreased in
pressure in kidney
Ang2 causes contraction of smooth muscle so pressure
goes up, it also triggers release of ADH. Thirst centers are also triggered by Ang2 and it increases aldoesterone secretion (NaCl reab increases).
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
Increase Smooth Muscle Contractility via α Adrenergic
Signaling (increases sympa activity) Effect is greater on
Afferent Arterioles, RBF goes down and GFR
Increased sympa activity increases renin secretion causing
Ang2 and aldosterone release to increase
Increase NaCl Reabsorption
pressure increase in efferent arteriole pressure may cause back up of blood into glomerulus increasing filtration, this also would cause a decrease in
hydrostatic pressure in the peritubular capillaries which would lead to better reab of H2O and NaCl in these capillaries
Increased sympa increases NaCl reabsorption of the nephorn by signaling primarily
proximal tubules
Natriuretic Peptides
ANP, BNP an Urodilatin
High levels of right atrial distension, ANP is
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.
ANP increase affects the kidney to
Inhibit NaCl reab
Inhibit Renin Secretion
ANP increase affects the smooth muscle to
Vasodilate (afferent)
Vasoconstriction (efferent)
High ANP stimulates the brain to
inhibit ADH secretion
ANP increase causes adrenal cortex to
inhibit aldosterono secretion. Directly and by reducing Renin
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
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
In a healthy personAs a consequence of Na intake, ECF osmolarity increases leading to water
retention (ADH), as person starts to retain water, ECBV goes up, leading to enhancement of excretion of Na
Excretion of Na lags behind uptake of Na and change in osmolarity meaning
Na would be excreted until theres a volume change
During the period that takes to generate volume response, Na load in body is
increasing aka Positive Na Balance, so volume response to secrete Na lags behind the osmoregulatory response to retain water
So osmoregulatory response first (retention of water) and then
volume response (excretion of Na) eventually Na intake equals Na excretion.
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
Takes a much longer time to start excreting Na so Volume overload (expansion) is even greater
So what are the systems involved in regulation of Na balance that respond to osmotic challenge
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.
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
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
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.
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
): Increase excretion of K+, but
decrease the excretion of Ca++ . These are useful then in treating
cases of idiopathic hypercalciuria.
Distal Tubule Diuretics (Thiazide
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):
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
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