Renal Flashcards
hemodialysis vs transplant in ESRD
transplant is +++ in all parameters
HTN + hyokalemia
- Decreased renin, increased aldosterone –> primary hyperaldo (tumor, B/L adrenal hyperplasia)
- Increased renin, inc aldo –> 2ndry hyperaldo (renovascular HTN, malignant HTN, renin tumor, diuretics, cirrhosis)
- dec renin, dec aldo –> non-aldo causes (CAH, corticosterone-producing adrenal tumor, Cushing’s, exogenous mineralocorticoids
Renal SEs ACEis
-decreased GFR –> hyperkalemia, elevated creatinine
Renal SEs thiazide diuretics
hypokalemia, hyponatremia, hyperuricemia, elevated glucose
can decrease effective arterial volume to kidney and cause secondary hyperaldosteronism
SIADH
- excess ADH –> water retention and natiuresis –> volume expansion, hyponatremia, w/o edema
- Causes: Neoplasm (esp lung, prostate, bladder), CNS disorder, pneumonia, ventilators, meds, postop
- chronic hyponatremia can be asymptomatic. Acutely –> neuro Sx
- Hypourecemia, low BUN, low/nml Cr
- Tx: fluid restriction, correct underlying cause. Can use hyper tonic saline if refractory, but SLOWLY (myelinolysis)
Winter’s formula and implications
- Expected PaCO2 for metabolic acidosis = 1.5 * [HCO3] +8 +/- 2
- If not as expected, have another primary resp problem.
- If higher than expected, have a primary respiratory acidosis (i.e. respiratory failure)!! NB: asthmatic whose PaCO2 normalizes w/o treatment = BAD SIGN
Salicylate OD
-primary resp alkalosis AND primary met acidosis
Anion gap
Na+ - (Cl + HCO3)
Nml = 5-15
Causes of normal AG met acidosis
HARD ASS: Hyperalimentation Addison's RTA Diarrhea Acetazolamide Spironolactone Saline Infusion
Causes of elevated AG met acidosis
MUDPILES: Methanol (formic acid) Uremia DKA Propylene glycol Iron tablet or INH Lactic acid Ethylene glycol Salicylates (late. Also causes resp alkalosis)
Effects of alkalosis
Decreased cerebral blood flow
Left shift in O2/Hg dissociation decreases O2 delivery
Arrhythmias
Tetany, seizures
Effects of alkalosis
Decreased cerebral blood flow
Left shift in O2/Hg dissociation decreases O2 delivery
Arrhythmias
Tetany, seizures
HTN + hyokalemia
- Decreased renin, increased aldosterone –> primary hyperaldo (tumor, B/L adrenal hyperplasia)
- Increased renin, inc aldo –> 2ndry hyperaldo (renovascular HTN, malignant HTN, renin tumor, diuretics, cirrhosis)
- dec renin, dec aldo –> non-aldo causes (CAH, corticosterone-producing adrenal tumor, Cushing’s, exogenous mineralocorticoids
Renal SEs ACEis
-decreased GFR –> hyperkalemia, elevated creatinine
Renal SEs thiazide diuretics
hypokalemia, hyponatremia, hyperuricemia, elevated glucose
can decrease effective arterial volume to kidney and cause secondary hyperaldosteronism
SIADH
- excess ADH –> water retention and natiuresis –> volume expansion, hyponatremia, w/o edema
- Causes: Neoplasm (esp lung, prostate, bladder), CNS disorder, pneumonia, ventilators, meds, postop
- chronic hyponatremia can be asymptomatic. Acutely –> neuro Sx
- Hypourecemia, low BUN, low/nml Cr
- Tx: fluid restriction, correct underlying cause. Can use hyper tonic saline if refractory, but SLOWLY (myelinolysis)
Winter’s formula and implications
- Expected PaCO2 for metabolic acidosis = 1.5 * [HCO3] +8 +/- 2
- If not as expected, have another primary resp problem.
- If higher than expected, have a primary respiratory acidosis (i.e. respiratory failure)!! NB: asthmatic whose PaCO2 normalizes w/o treatment = BAD SIGN
Salicylate OD
-primary resp alkalosis AND primary met acidosis
Anion gap
Na+ - (Cl + HCO3)
Nml = 5-15
Causes of normal AG met acidosis
HARD ASS: Hyperalimentation Addison's RTA Diarrhea Acetazolamide Spironolactone Saline Infusion
Causes of elevated AG met acidosis
MUDPILES: Methanol (formic acid) Uremia DKA Propylene glycol Iron tablet or INH Lactic acid Ethylene glycol Salicylates (late. Also causes resp alkalosis)
Effects of acidosis
Right shift in O2/Hg dissociation increases O2 delivery CNS depression Dec pulmonary blood flow Arrhythmias Decreased CO Hyperkalemia Kussmaul's breathing (acute)
Effects of alkalosis
Decreased cerebral blood flow
Left shift in O2/Hg dissociation decreases O2 delivery
Arrhythmias
Tetany, seizures
Metabolic alkalosis
- Two events: initial alkalosis (loss of H+ or increased HCO3 (e.g. volume contraction) + maintenance of alkalosis (kidney problem)
- Two types: saline sensitive (urine chloride 20) has ECF expansion
- Tx: Saline + K if ECF contracted. Address cause/give spironolactone if ECF expanded.
ECF contracted (saline sensitive) Met alkalosis
- (Urine Cl <10)
- Vomiting, NG suction
- Diuretics (decreased volume increases bicarb concentration)
- Villous adenoma of colon, diarrhea with high Cl content
- Tx: Saline + K
ECF expanded (Saline-resistant) met alkalosis
- (Urine Cl >20)
- 2/2 adrenal d/os (primary hyperaldo). mineralocorticoids cause volume expansion and Cl wasting
- Others: Cushings, severe K deficiency, Bartters, Diuretic abuse
- Tx: underlying cause/give spironolactone
Compensation formula Respiratory Acidosis
- Acute (takes 12-24 hrs): HCO3 inc by 1 per 10 inc in PCO2
- Chronic (takes days): HCO3 up 4 for every 10 inc in PCO2
Respiratory Acidosis (Clinical, Causes, Tx)
- Somnolence, confusion, myoclonus, asterixis. Acute: Headaches, confusion, papilledema (increased ICP)
- Causes: pulmonary disease, NM diseases (e.g. MG), CNS malfunction, drug-induced hypoventilation, resp muscle fatigue
- Tx: Airway!, CO2 (caution in “CO2 retainers,” Tx resp disease, clear toxins, bronchodilators, intubate if necessary
Compensation formula Respiratory Alkalosis
- Acutely, for each 10 dec in PCO2, HCO3 dec by 2
- Chronically, for each 10 dec in PCO2, HCO3 dec by 5
Respiratory Alkalosis (Clinical, Causes, Tx)
- Decreased Cerebral blood flow: lightheadedness, dizziness, anxiety, paresthesias, perioral numbness, Tetany (can be confused with hypocalcemia), arrhytmias (severe)
- Causes: Anxiety, PE, pneumonia, asthma, sepsis, hypoxia, mechanical ventilation, pregnancy, cirrhosis, salicylate toxicity, hyperventilation
- Tx: treat underlying cause, inhale CO2
Type 1 RTA
- Distal
- Defect in CT H+ excretion
- Urine pH >5.5 –> inc risk of kidney stones, nephrocalcinosis
- hypokalemia, normal AG met acidosis
- Causes: autoimmune (sjogrens, SLE), transporter defects, cirrhosis, nephrocalcinosis, renal transplant, sickle cell, Toxins (toluene, lithium, ampho B), IV bisphosphonates
Type 2 RTA
- Proximal
- Urine pH can be s syndrome, amyloidosis, multiple myeloma, Paroxysmal noceturnal hemoglobinuria, Toxins (HAART, Ifosfamide, lead, cadmium)
Angioedema
- Edema in face, mouth, lips, tongue, glottis, larynx (can compromise airway)
- Most common acquired: ACEis. Lead to buildup of bradykinin –> edema
- Management: check for airway obstruction, use epinephrine if necessary, trach if necessary
Uremic Pericarditis
- Occurs in 6-10% of renal failure pts
- BUN > 60
- Does not usually present with EKG changes of pericarditis (diffuse ST elevation)
- Tx: hemodialysis
AKI (definition, urine output, etiology classes)
- rapid decline in kidney function w increase in Cr (twofold) and 50% decreased GFR
- Can be oliguric, nonoliguric, anuric
- Prerenal: Volume loss/sequestration, decreased CO, hypotension. NSAIDS, ACEi, cyclosporins
- Postrenal: intra (crystals, proteins), extra (pelvis/ureter, bladder/urethra)
- Renal: Glomerulonephritis, vascular (large, small), interstitial, ATN
Prerenal failure
- always oliguric
- BUN/Cr >20:1
- Urine >500 mOsm
- FENA < 1%, UNa <20
- Reversible, but can progress to ischemic AKI if hypoperfusion lasts
