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
Causes of HAGMA
Glycols Oxoproline (acetominophen) L-lactic acidosis D-lactic acidosis Methanol Aspirin Renal failure Ketoacidosis
Causes of Increased Serum Osmolality Gap
Methanol Ethanol Diethylene glycol Isopropyl alcohol Ethylene glycol
Discuss the effect of acidosis and alkalosis on serum K+ levels
Acidosis- hyperkalemia
Alkalosis- hypokalemia
Discuss meaning and be able to calculate urine anion gap when appropriate
Used to determine renal vs. non-renal causes
Marker of ammonium chloride excretion (can urine be acidified or not)
UAG= Urine Na + urine K - Urine Cl
+= appropriate acidification
-= inappropriate acidifcation
Causes of NAGMA
Diarrhea
RTA
Discuss clinical presentation and pathophysiology of RTA type 1,2 and 4 and be able to differentiate between them
1: cannot acidify (decrease H+ secretion or gradient defect), caused by glue sniffing or Sjogren’s syndrome, will see nephrolithiasis or nephrocalcinosis; seen in NAGMA, severe hypokalemia, + UAG
2: can acidify (proximal tubule, HCO3- issue), seen in Fanconi syndrome, NAGMA and hypokalemia
4: lack of aldosterone/aldosterone resistant, causes DM, NSAIDs, beta-blockers, ACEi/ARBs, high dose heparin, sickle cell, obstructive nephropathy, SLE, amiodarone, triameterone; see HYPERKALEMIA
Discuss clinical presentation of metabolic alkalosis
Causes: hypokalemia, vomiting, NG tube suctioning, diuretics, volume depletion, mineralocorticoid excess
Discuss clinical presentation of respiratory alkalosis
Anything that increases RR- pneumonia, PE, sepsis, CHF, anxiety, ASA, exercise, trauma
Define nocturia, dysuria, urinary incontinence
Nocturia- getting up more than 2x a night
Dysuria- pain or discomfort when urinating
Urinary incontinence- stress, urge and overflow
Differentiate between nocturia and dysuria
Nocturia- age-related delay, peripheral edema, medications, fluid intake, caffeine, alcohol
Dysuria- infections
Common Causes of urinary incontinence
Delirium Infection Atrophic urethritis and vaginitis Pharmaceuticals Psychological factors Excessive urinary output Restricted mobility Stool impaction
Identify important historical elements of urinary incontinence
Stress- standing w/ a full bladder stress test (few second delay)
Urge- standing full bladder stress test (immediate release)
Overflow- elevated postvoid residual (determines if detrussor is underactive or overactive) urodynamic testing differentiates it from urethral obstruction
Medications
UA
hyperglycemia, hypercalcemia, diabetes insidious
Imaging (US to determine postvoid residual, older men w/ planned surgery)
