Exam 3 Flashcards
Identify and discuss relevant historical and physical exam findings that will aid in evaluating patients presenting with oliguria and/or proteinuria
Volume status- JVD, oral mucosa, capillary refill, skin tenting S3, crackles, ascites, LE pitting edema, sacral edema
HEENT- retinopathy, nasal ulcers, tonsillar exudates, oral ulcer
Cardiac- S3, heart rhythm
Lungs- crackles, pleural effusions
Abdomen- bruits, palpable kidneys, tense abdomen, ascites
Skin- malaria rash, palpable purport, non-blanching purport, buttock/leg purport, lived reticular, emboli, drug rash
MSK- synovitis, myalgia, CVA tenderness
Recommend and interpret common diagnostic tests that will aid in evaluating patients presenting with oliguria and proteinuria (4 diseases)
1: CKD: eGFR, urine albumin-to-creatinine ratio or protein-to-creatinine ratio, UA, Renal US (atrophic kidneys, cortical thinning, increased echogenicity, elevated resistance indices)
2: AKI: UA w/ microscopy, urine albumin/Cr ratio or protein/Cr ratio, Renal US
3: Nephrotic syndrome: Serum Cr w/ GFR, UA w/ microscopy, urine albumin/Cr ratio or protein/Cr ratio, 24 hours protein collection, glomerulonephritis serologic evaluation, Renal Bx
4: Nephritic Syndrome: Same as nephrotic
Discuss common risk factors, causes, clinical presentation, diagnosis and treatment for CKD
Causes/Risk Factors: HTN or diabetes mellitus, glomerulonephritis, chronic interstitial nephritis, urinary obstruction, hereditary/cystic disease, vasculitis, unknown
Clinical presentation: Edema, HTN, decreased UOP, foamy urine, uremia, asterisks, pericardial friction rub, uremic frost
Diagnosis: Need at least 1 for 3 months, marker of kidney damage (albuminuria, urine sediment, electrolyte abnormalities, abnormalities detected by histology or imaging, hx. of renal transplant), GFR under 60 mL/min/1.73m2
Treatment: low salt/bp control for proteinuria/HTN, statins for hyperlipidemia, Ironize and ESA for anemia, bicarb. supplementation for metabolic acidosis, Renal failure diet, diuretics for hyperkalemia, CKD-BMD give renal failure diet, phosphorus binder, Vitamin D supplements, dialysis, Volume overload- diuretics, fluid restriction, dialysis
Indicators for dialysis
A: severe acidosis E: electrolyte disturbance I: ingestion O: volume overload U: uremia
Discuss common risk factors, causes, clinical presentation, diagnosis and treatment for AKI
Causes: prerenal, intrinsic, or post renal
Clinical presentation: edema, HTN, decreased UOP, proteinuria, hematuria, SOB, uremia, pericardial friction rub, asterixis, uremic frost
Treatment: depends on underlying condition, most supportive- avoid hypotension, discontinue nephrotoxins, renal replacement therapy as needed
Stages of AKI
Stage 1: Cr 1.5-1.9 times baseline OR less than 0.3mg/dl increase OR UOP less than 0.5 mL/kg for 6-12 hours
Stage 2: Cr 2-2.9 times baseline OR UOP is less than 0.5 mL/kg for more than 12 hours
Stage 3: Cr 3 times baseline OR serum increase over 4.0mg/dL OR patient on renal replacement therapy OR patient is under 18 w/ an eGFR under 35 mL/min OR UOP less than 0.3 mL/kg for more than 24 hours OR anuria for 12 hours
Discuss common risk factors, causes, clinical presentation, diagnosis and treatment for Nephrotic Syndrome
Clinical presentation: NEW onset of HTN, edema, proteinuria, lipiduria, hyperlipidemia, minimal hematuria
Diagnosis: Proteinuria over 3.5 grams/day, hypoalbuminemia, peripheral edema, hyperlipidemia, lipiduria
Treatment: treat underlying disease, edema (diuretics and dietary sodium restriction) proteinuria (lower BP), hyperlipidemia (statins), thrombosis (anti-coagulation), infection (IVIG supplementation), vitamin D deficiency
Discuss common risk factors, causes, clinical presentation, diagnosis and treatment for Nephritic Syndrome
Causes: many
Clinical presentation: New onset HTN, hematuria, AKI, mild proteinuria
Diagnosis: minimal proteinuria, hematuria, HTN, renal failure is common, Active Urinary Sediment
What is the Henderson-Hasselbach equation
pH= 6.1 + log ([HCO3-]/ (0.03* [PCO2]))
Types of acid-base disturbances
Metabolic acidosis- low HCO3-, respiratory alkalosis compensation
Metabolic alkalosis- high HCO3-, respiratory acidosis compensation
Respiratory acidosis- high PCO2, metabolic alkalosis compensation
Respiratory alkalosis- low PCO2, metabolic acidosis compensation
Be able to accurately interpret an ABG via a systemic process
- Acidosis or Alkalosis
- Metabolic or respiratory
2a. Calculate AG if metabolic acidosis
2b. Calculate Osmolar gap
2c. Calculate delta-delta gap - Calculate compensation pattern
Discuss normal values on an ABG
HCO3-: 24 PCO2: 40 pH: 7.35-7.44 Anion gap: 12 Osmolality gap: 10 mmol/L
Be able to calculate anion gap and osmolar gap when appropriate
Anion gap: AG= Na - (HCO3 +Cl) Determines HAGMA from NAGMA Hypoalbuminemia- for every 1g/dL drop in albumin, the AG drops by 2.5 Osmolar gap: calculated serum osmolality: 2(Na+) + (glucose/18) + (BUN/2.8) Measured - calculated greater than 10- ingestion likely
Compensatory equations
Metabolic acidosis: PCO2= 1.5[HCO3] + 8 +/- 2
Metabolic alkalosis: PCO2 will increased by 0.7 for every 1 mEq/L increase in HCO3-
Respiratory acidosis: acute- increase by 1; chronic increase by 3.5
Respiratory alkalosis: acute- increase by 2, chronic- increase by 5
Delta-Delta gap calculation
Used in patients with HAGMA to see if there is NAGMA or metabolic acidosis Delta gap= calculated AG- measured AG nml HCO3 - Delta gap= calculated HCO3- Compare with measured If low, it is NAGMA If high, it is metabolic acidosis
