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
- Six years later, you round on Fran in the hospital. She is so happy to see you! She is four days post-op from coronary bypass surgery.
The urine output has been 10 ml during past hour. Creatinine has increased from 3.4 mg/dl to 4.2 in 12 hours.
- She is hypotensive; there is no edema and she is draining copious amount of sanguinous fluid from her chest tube.
You dutifully ‘spin the urine’ and you find just a few hyaline casts, but no muddy brown granular casts.
What is the problem, and what would you do?
A. She has tubular necrosis and steroids should be given.
B. She has tubulointerstitial nephritis and steroids are indicated
C. She is in a pre-renal state and intravenous fluids should be given
D. She is in a pre-renal state and she needs furosemide to increase her urine output
What is the problem, and what would you do?
A. She has tubular necrosis and steroids should be given.
B. She has tubulointerstitial nephritis and steroids are indicated
C. She is in a pre-renal state and intravenous fluids should be given
D. She is in a pre-renal state and she needs furosemide to increase her urine output
- Last week, Joe developed an E. Coli urinary tract infection and was prescribed Bactrim (trimethoprim-sulfamethoxazole).
- He is on day 5 of therapy and now presents with a rash, eosinophilia, and his serum creatinine increased from 1.6 to 2.5. He has bilateral CVA tenderness.
The urinalysis is depicted below.
What is the cause of his AKI?
A. Acute tubular necrosis due to urosepsis
B. Acute tubulo-interstitial nephritis due to sulfa drug
C. Acute urinary obstruction due to sulfa drug induced crystal precipitation
D. Post-infectious glomerulonephritis due to the bacteria
E. Pyelonephritis from an infected cyst
What is the cause of his AKI?
A. Acute tubular necrosis due to urosepsis
B. Acute tubulo-interstitial nephritis due to sulfa drug
C. Acute urinary obstruction due to sulfa drug induced crystal precipitation
D. Post-infectious glomerulonephritis due to the bacteria
E. Pyelonephritis from an infected cyst
Joe returns to your office several years later with 1 day of severe left flank pain and hematuria. The urinalysis is depicted below.
His underlying kidney disease puts him at increased risk for this common condition
A. Renal cell carcinoma
B. Ca oxalate stones
C. Uric acid stones
D. Struvite stones
His underlying kidney disease puts him at increased risk for this common condition
A. Renal cell carcinoma
B. Ca oxalate stones
C. Uric acid stones
D. Struvite stones
Joe has Autosomal Dominant Polycystic Kidney Disease; it is the 4th leading cause of ESRD. This genetic disease affects other organs.
Which associated condition might you find on your patient?
A. Cysts in the Liver
B. Hyperlipidemia
C. Peripheral Vascular Disease
D. Peyronie’s Disease
Which associated condition might you find on your patient?
A. Cysts in the Liver
B. Hyperlipidemia
C. Peripheral Vascular Disease
D. Peyronie’s Disease
- Joe eventually recovers from this episode and when he returns to your clinic 1 year later (at steady state) his serum creatinine is stable at 1.7 mg/dl. He is now 45 years old.
- He is 70 kg and normal body habitus. You load him with a drug and now wish to calculate the maintenance dose of this drug. It is 75% excreted through the kidney.
- Using the Crockroft-Gault equation and assuming normal non-kidney excretion (25%), what % of the drug (assume normal CrCl of 100 ml/min) should you give?
A. 32.5%
B. 48.5%
C. 68%
D. 100%
- Using the Crockroft-Gault equation and assuming normal non-kidney excretion (25%), what % of the drug (assume normal CrCl of 100 ml/min) should you give?
A. 32.5%
B. 48.5%
C. 68%
D. 100%
Assume that other routes of clearance are normal (feces, tears, etc.): 25% by other routes + (56% of 75%) or 41.5% = 68%. The dose should be 68% of original
Mr. Johnson is passing a kidney stone and he has been unable to eat food or drink water for several days. He presents to the emergency room with a blood pressure of 105/65, depressed skin turgor, and a pulse of 120.
What IV fluid would you give this patient?
A. Dextrose-Water (D5W)
B. ½ Normal Saline (0.45%)
C. Normal Saline (0.9%)
D. Hypertonic Saline (3%)
What IV fluid would you give this patient?
A. Dextrose-Water (D5W)
B. ½ Normal Saline (0.45%)
C. Normal Saline (0.9%)
D. Hypertonic Saline (3%)
- He has classic signs of hypovolemia (depressed skin turgor)
- Want something that will stay extracellular
Mr. Johnson remains on the Ace-inhibitor Lisinopril to slow the growth of renal cysts and to control his blood pressure. One side effect of this drug is hyperkalemia.
How does this occur?
A. Results in potassium release (from muscle cells)
B. Blocks production of Angiotensin I
C. Suppresses Angiotensin II therefore reducing the level of Aldosterone
D. Increases the appetite for high-potassium foods
How does this occur?
A. Results in potassium release (from muscle cells)
B. Blocks production of Angiotensin I
C. Suppresses Angiotensin II therefore reducing the level of Aldosterone
D. Increases the appetite for high-potassium foods
What is the result of ang II action on AT1 receptor?
- Heart: remodeling
- Kidneys: Na reabsorption; aldosterone release
- Vasculature: vasoconstriction
- CNS: NE release
Mr. Johnson is taken to the emergency room after an drinking an unknown liquid. He has altered mental status and unable to give any history.
The following lab values are given:
Na 140, K 4.5, Cl 105, HCO3 12, BUN 25, Cr 1.2, glucose 72, osmolarity 320, pH 7.28, pCO2 28.
- You look at the urine and find several crystals.
What is the most likely acid base disturbance and diagnosis?
A. Pure Anion Gap Metabolic Acidosis from Ethylene Glycol
B. Anion Gap Metabolic Acidosis with Respiratory Acidosis from Ethylene Glycol
C. Pure Anion Gap Metabolic Acidosis from Methanol
D. Non-Gap Metabolic Acidosis from Renal Tubular Acidosis
What is the most likely acid base disturbance and diagnosis?
A. Pure Anion Gap Metabolic Acidosis from Ethylene Glycol
B. Anion Gap Metabolic Acidosis with Respiratory Acidosis from Ethylene Glycol
C. Pure Anion Gap Metabolic Acidosis from Methanol
D. Non-Gap Metabolic Acidosis from Renal Tubular Acidosis
- AGMA because low bicarb and pH with resp compensation resulting in low pCO2
- AG = 140 - 105 - 12 = 23
- Methanol pt may come in with blurry vision
- Ethylene glycol toxicity may present with calcium oxalate stones
