Renal Tubular
Give 3 causes of Type 1 RTA
Define respiratory acidosis
Accumulation of CO₂ in the blood, causing a decrease in blood pH (making it more acidic) due to a respiratory cause.
T or F : Acidosis causes CNS vasodilation
True
What is the winters formula and what does it tell you?
Expected PaCO2 = (1.5 x serum HCO3)+(8±2)
Expected PaCO2 is approximately equal to the last two digits of the pH ± 2.
Order the renal tubular diseases from most common to least
Type 4 > Type 1 > Type 2 > Type 3
When type 2 includes generalized dysfunction of the PCT it is often referred to as
Fanconi Syndrome
Name 3 causes of hypoventilation that can result in respiratory alkalosis
Lung Disease (COPD, PNA, asthma)
Narcotics
Respiratory muscle weakness
- Myasthenia gravis
- Amyotrophic lateral sclerosis
- Guillain-Barré syndrome
- Muscular dystrophy
Hyperalimenation
Addison's Disease
RTA
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
Define Acidosis/alkalosis vs Acidemia/alkalemia.
Which RTA usually presents with nephrolithiasis
Type 1
What is the pathophysiology of Type 1 RTA (must provide the correct cell type)
How can high altitude acutely lead to a respiratory alkalosis
• Lower atmospheric pressure --> Lower pO2 --> Hypoxia --> hyperventilation --> ↓pCO2 respiratory alkalosis (pH rises)
What test is used to differentiate between a saline resistant and saline responsive metabolic alklaosis
Urine Cl-
What are treatment options for aspirin overdose (3 please)
What is the pathophysiology of Type 2 RTA
Dysfunctional proximal convoluted tubule (PCT) that is unable to reabsorb HCO3-
Describe at least 3 clinical features of type 2 RTA
HCO3- decreases by [blank] mEq/L for every [blank] mm Hg decrease in PCO2 below 40 mm Hg: suggests acute respiratory alkalosis
HCO3- decreases by 2 mEq/L for every 10 mm Hg decrease in PCO2 below 40 mm Hg: suggests acute respiratory alkalosis
A 57-year-old man is brought to the emergency department after being found with an empty pill bottle at his bedside. He has diffuse abdominal pain. He has a history of depression and past suicide attempts. He also has a history of type 2 diabetes mellitus, currently managed with medication. His vital signs are stable. Laboratory studies show:
Na+: 140 mEq/L
K+: 4.8 mEq/L
Cl–: 100 mEq/L
HCO3–: 18 mEq/L
Glucose: 110 mg/dL
Blood urea nitrogen: 30 mg/dL
Serum creatinine: 3.5 mg/dL
Which of the following is the mechanism of the drug most likely causing this patient’s findings?
A: Decreased glucagon release
B: Directly binds insulin receptors
C: Inhibts gluconeogenesis
D: Inhibits intestinal alpha-glucosidases
E: Triggers insulin release
C: inhibits gluconeogenesis
Describe the change in disorders associated with acute vs. chronic aspirin overdose.
Why does it change? Need at least two reasons for chronic pathophysiology
Shortly after ingestion: respiratory alkalosis as salicylates stimulate the medulla --> hyperventilation
Hours after ingestion: AG metabolic acidosis as Salicylates ↓lipolysis, uncouple oxidative phosphorylation, Inhibits citric acid cycle , Accumulation of pyruvate, lactate, ketoacids
Type 3 RTA is a mix of which two RTAs
Type 1 and Type 2
Main Etiology:
Pathophysiology:
A 17-year-old boy is brought to the physician by his father because of a 7-month history of fatigue, recurrent leg cramps, and increased urinary frequency. His pulse is 94/min and blood pressure is 118/85 mm Hg. Physical examination shows dry mucous membranes. Laboratory studies show:
Serum
Na+130 mEq/L
K+2.8 mEq/L
Cl-92 mEq/L
Mg2+1.1 mg/dL
Ca2+10.6 mg/dL
Albumin5.2 g/dL
Urine Ca2+ 70 mg/24
hCl-375 mEq/24h (N = 110–250)
Arterial blood gas analysis on room air shows a pH of 7.55 and an HCO3- concentration of 45 mEq/L. Impaired function of which of the following structures is the most likely cause of this patient's condition?
A: Ascending loop of Henle
B: Distal Convoluted tubule
C: Descending loop of Henle
D: Collecting duct
E: Proximal convoluted tubule
B: Distal Convoluted tubule
Gitelman syndrome is an autosomal recessive renal tubular defect caused by the impaired functioning of the Na+-Cl- cotransporters in the distal convoluted tubule. Symptoms such as fatigue, muscle cramps, polyuria, and chondrocalcinosis typically arise in late childhood and can be attributed to the associated electrolyte abnormalities (hyponatremia, hypomagnesemia, hypokalemia, hypercalcemia, and hypocalciuria). In addition, Gitelman syndrome causes metabolic alkalosis due to mild RAAS activation that occurs in response to natriuresis and volume depletion. Treatment for Gitelman syndrome consists of potassium supplementation and a potassium-sparing diuretic (e.g., spironolactone, amiloride).
Because thiazide diuretics target the Na+-Cl- cotransporters in the distal convoluted tubule, patients with Gitelman syndrome have a blunted response to these agents, with the response being measured as the fractional clearance of chloride. Alternatively, these patients will have a normal response to loop diuretics, which target the Na+-K+-2Cl- cotransporters in the thick ascending loop of Henle.
A 21-year-old man is brought to the emergency department by the police because of altered mental status. The police found him covering his ears and shouting near a highway rest area. Upon questioning, he was unable to look directly at the police and answer coherently. On the way to the hospital, he reported feeling nauseous and vomited twice. His temperature is 38.2°C (100.8°F), pulse is 100/min, respirations are 28/min, and blood pressure is 110/77 mm Hg. He is admitted to the hospital for evaluation. Three hours after admission, he has a tonic-clonic seizure. Laboratory studies show:
Na 140
Cl 102
ABG (On admission. --> 3 hrs later)
Ph 7.47 --> 7.39
paCO2 24 --> 31
pO2 84 --> 82
HCO3 20 --> 18
A. Opioid overdose
B. Salicylate toxicity
C. DKA
D. Recurrent vomiting
E. Adrenal insufficiency
B: Salicylate toxicity
In early toxicity, salicylates directly stimulate the medullary respiratory center and cause tachypnea and hyperpnea, both of which manifest with respiratory alkalosis. Later, the accumulation of organic acids (due to salicylates inhibiting citric acid cycle enzymes) causes a high anion gap metabolic acidosis, which leads to a mixed acid-base disorder. Features of salicylate toxicity include tinnitus, nausea, vomiting, mental status changes, hyperthermia (due to uncoupling of mitochondrial oxidative phosphorylation), pulmonary edema, seizures, and, ultimately, coma.
A 14-year-old girl is brought to the emergency department because of vomiting and disorientation. The patient has a history of asthma and had an exacerbation 1 week prior, which was treated with prednisone. Respirations are 24/min. Physical examination reveals dry mucous membranes and a fruity breath smell. Laboratory tests show a serum creatinine level of 0.8 mg/dL and serum glucose of 413 mg/dL.
A: Metabolic acidosis with increased anion gap
B: Metabolic acidosis with normal aniong gap
C: Metabolic Alkalosis
D: Respiratory Acidosis
E: Respirarory alkalosis
A: Metabolic acidosis with increased anion gap
This patient has a history of recent corticosteroid use, altered mental status, hyperglycemia, and a fruity odor to the breath and is likely experiencing diabetic ketoacidosis (DKA). DKA is a serious complication in patients with type 1 diabetes mellitus and may be the initial presentation of the disease, as seen in this case. It may be triggered by stressors that cause increased insulin requirements (such as infections) or corticosteroid use. The stress and lack of insulin seen in type 1 diabetes mellitus lead to the buildup of glucose and ketones in the blood. Fruity-smelling breath is due to the excess acetone that is exhaled.
A 65-year-old woman is admitted to the emergency department with alcohol withdrawal. The patient is given lorazepam intravenously but shortly afterward exhibits a decrease in urine output despite the intravenous fluids. The serum creatinine rises from 1.2 mg/dL to 1.9 mg/dL. Blood pH is 7.28, anion gap is 24 mEq/L, and serum osmolar gap is 20 mmol/L.
Which of the following is the most likely diagnosis?
A: Dexmedetomidine toxicity
B: Haloperidol toxicity
C: Ketamine toxicity
D: Propofol-related infusion syndrome
E: Propylene glycol toxicity
Propylene glycol is the solvent used to administer intravenous infusions of benzodiazepines (eg, lorazepam, diazepam), and at toxic levels, it can cause elevated serum osmolar gap (>10 mmol/L), anion-gap metabolic acidosis, and acute kidney injury.
A 40-year-old man comes to the physician because of a 4-week history of generalized weakness. He also reports increased urination and thirst. He has type 2 diabetes mellitus and chronic kidney disease. His only medication is metformin. Serum studies show:
Na 134 mEq/L
K 4.6 mEq/L
Cl 110 mEq/L
HCO3 10 mEg/dL
Glucose 135 mg/dL
Creatinine 1.6 mg/dL
Urine pH is 5.1. Which of the following is the most likely underlying cause of this patient's symptoms?
A:Ethylene glycol intoxication
C: Decreased serum aldosterone levels
Decreased serum cortisol levels
C: Decreased serum aldosterone levels
This patient presents with polyuria, polydipsia, a normal serum anion gap, hyperkalemia, and decreased urine pH. Together with a history of diabetes mellitus and chronic kidney disease, these features suggest type 4 renal tubular acidosis (RTA)