9/25- Review 2: Midterm Exam, Acid Base and Electrolytes Flashcards
Ms. Jones is discharged from the hospital after her bypass surgery. She is started on a diuretic to control her hypertension and increased total body volume.
You start her on furosemide.
What is the site of action for this drug?
A. Thick Ascending loop of Henle
B. Proximal Convoluted Tubule
C. Thin Descending loop of Henle
D. Collecting Duct
You start her on furosemide.
What is the site of action for this drug?
A. Thick Ascending loop of Henle
B. Proximal Convoluted Tubule
C. Thin Descending loop of Henle
D. Collecting Duct
Site of action of acetazolamide?
- Uses?
PCT
- Not very strong use as diuretic
- More for altitude sickness (excrete bicarbonate to induce metabolic acidosis and cause hyperventilation to achieve higher oxygen)
Site of action of osmotic agents (mannitol)?
- Mechanism
PCT (also tDLH and CD?)
- Mannitol is an inert starch; pulls out fluid
Site of action of Lasix?
- Mechanism
TALH
- Furosemide/loop diuretics
- Inhibit Na/Cl/K co-transport (reab) so that medulla is less hyperosmotic; this impairs water absorption in CD
Site of action of thiazide?
- Mechanism
DCT
- Go to diuretic; 1st drug of choice for HTN
- Block Na Cl reabsorption
Site of action of aldosterone antagonists?
- Mechanism
CD
- Ex) Spironolactone
- Blocks epithelial Na channel (ENaC)
- Normally, Na is reabsorbed while K is secreted (into negative lumen)
- By blocking ENaC, preventing Na reabsorption and decreasing K secretion (K sparing)
Site of action of ADH antagonists?
- Mechanism
CD
- Insert aquaporins into CD
- Insert UT1 transporters in CD - ?
Because Mrs. Jones has advanced CKD, what is expected for her levels of:
- Phosphorus
- PTH
- FGF-23
Treatment?
- Phosphorus: increased
- PTH: increased
- FGF-23: increased
Treatment
- Decrease dietary PO4 (TUMS?)
- Give Vitamin D to antagonize PTH
What is Vitamin D’s effect on:
- Bone
- Gut
- Kidney
Bone:
- Increased FGF23
Gut:
- Decreased phosphate absorption -> Decreased serum phosphate
Kidney
- Increased urinary phosphate excretion
- > Decreased serum phosphate
Ms. Jones later presents to your clinic with the following lab results.
Na 140, K 4.5, Cl 105, HCO3 18, BUN 60, Cr 4.5, glucose 100, measured osmolarity 310
What is the most likely acid-base disturbance and etiology?
A. Metabolic alkalosis after vomiting
B. Metabolic acidosis due to alcohol ingestion
C. Metabolic acidosis secondary to kidney disease
D. Metabolic alkalosis from Bartter’s syndrome
What is the most likely acid-base disturbance and etiology?
A. Metabolic alkalosis after vomiting
B. Metabolic acidosis due to alcohol ingestion
C. Metabolic acidosis secondary to kidney disease
D. Metabolic alkalosis from Bartter’s syndrome
Metabolic acidosis (known)
- AG = Na - (Cl + HCO3) = 140 - 105 - 18 = 17 (high)
- Calc Osmolality = 2(Na) + BUN/2.8 + glucose/18
What are some agents that increase osmolar gap?
ME DIE
- Methanol
- Ethylene glycol
- Diuretics (osmotic diuretics like mannitol)
- Isopropyl alcohol
- Ethanol
You start Fran on Losartan, a medication that blocks the Angiotensin II Receptor (ARB). This class of medication is used like the ACE-inhibitors.
Two weeks later, creatinine increases from 2 mg/dL -> 3 mg/dl.
She has no specific complaints and did not make any other changes to her medications.
Why did her serum creatinine increase?
A. Pre glomerular arteriole (afferent) constriction
B. Post glomerular arteriole (efferent) vasodilatation
C. Decrease in glomerular surface area
D. Stimulation of proximal nephron creatinine absorption
Why did her serum creatinine increase?
A. Pre glomerular arteriole (afferent) constriction
B. Post glomerular arteriole (efferent) vasodilatation
C. Decrease in glomerular surface area
D. Stimulation of proximal nephron creatinine absorption
Why are ACEIs contraindicated in bilateral renal artery stenosis?
Ang II is the major determinant of efferent vasoconstriction. The Ang II effect helps to maintain GFR when renal perfusion is low (e.g. bilateral renal artery stenosis, volume depletion, and elderly pts with CHF). Blocking the effect of Ang II with ACEIs and ARBs in these situations can cause acute renal failure
How can NSAIDs be harmful to kidney??
PGs are the major determinant of afferent vasodilation. By inhibiting PG production NSAIDs can cause afferent arteriole vasoconstriction and reduce GFR
Two years later, Fran has a myocardial infarction. She undergoes emergent cardiac catheterization with placement of a bare metal stent.
Within 48 hours of the procedure, her serum creatinine increases from 3.0 mg/dl to 4.8 mg/dl.
The urinalysis is pictured below.
What is the most likely cause of her acute kidney injury (AKI)?
A. Pre renal azotemia
B. Contrast induced ATN
C. Interstitial nephritis
D. Diabetic nephropathy
What is the most likely cause of her acute kidney injury (AKI)?
A. Pre renal azotemia
B. Contrast induced ATN
C. Interstitial nephritis
D. Diabetic nephropathy