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226 Cards in this Set
- Front
- Back
when is coronary artery calcium score indicated? |
asymptomatic patients with intermediate risk of CAD (10%-20% 10-year risk) --> high score (>400) is an indication for more intensive preventive treatment |
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what is Fanconi syndrome?
|
disease of proximal renal tubules; where BAGUP (bicarbonate, amino acids, glucose, uric acid, phosphate) are passed into the urine, instead of being reabsorbed |
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findings in minimal change disease
|
normal light and immunofluorescence microscopies; effacement of podocyte foot processes on electron microscopy.
|
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biopsy findings in primary membranous glomerulopathy
|
diffuse glomerular membrane thickening without cellular infiltration, and coarsely granular deposits of IgG and C3 along the capillary loops by immunofluorescence microscopy. Electron microscopy shows moderate podocyte foot process effacement
|
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clinical clue to diagnosis of multiple myeloma
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elevated total urine protein, (quantifies both albumin and non-albumin protein (paraprotein)) with small amounts of protein on urine dipstick (measures only albumin)
|
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when to change HCTZ to furosemide
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GFR <30, HCTZ becomes ineffective as a diuretic
|
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kidney biopsy, what is an acceptable BP?
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<160/95
|
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contraindications to kidney biopsy (7)
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uncontrolled HTN, coagulopathy, thrombocytopenia, hydronephrosis, atrophic kidney, numerous kidney cysts, and acute pyelonephritis
|
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describe FENA in urinary obstruction
|
in early obstruction, urine sodium and FENa may be low; in late obstruction, urine sodium and FENa may be high (tubular damage)
|
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lab findings in gentamicin toxicity
|
hypokalemic metabolic alkalosis
|
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describe pathophysiology of gentamicin nephrotoxicity
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Aminoglycosides are divalent cations that activate calcium-sensing receptor in TALOH; this inhibits Na-K-Cl cotransporter, mimicking effect of loop diuretics and leading to hypokalemic metabolic alkalosis
|
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fibrosing skin disease caused by an inflammatory reaction to gadolinium that accumulates in the body due to kidney failure
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nephrogenic systemic fibrosis
|
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in DM, when to test for microalbuminuria?
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annual testing to assess urine albumin excretion in patients with type 1 diabetes of 5 years' duration and in all patients with type 2 diabetes starting at the time of diagnosis by measuring the albumin–creatinine ratio
|
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how is microalbuminuria diagnosed?
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albumin–creatinine ratio of 30 to 300 mg/g; diagnosis requires an elevated albumin–creatinine ratio on two of three random samples obtained over 6 months |
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how do NSAIDs cause hyperkalemia?
|
inhibit renin synthesis, resulting in hyporeninemic hypoaldosteronism, decreased potassium excretion, and hyperkalemia
|
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formula for TTKG
|
TTKG = [Urine Potassium ÷ (Urine Osmolality/Plasma Osmolality)] ÷ Serum Potassium OR Uffine K / serum K all div by Uosm/Posm
|
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how to interpret TTKG?
|
TTKG in patient on normal diet is 8 to 9; >10 in hyperkalemic states, reflecting excretion of excess potassium; if not then prob hypoaldosterone state |
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fevers and leukopenia post kidney transplant
|
CMV infection |
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mechanism of kidney injury due to tenofovir (Viread)
|
drug-related damage to mitochondrial DNA (most significantly in renal tubules causing tubular dysfunction)
|
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mechanism of kidney injury due to Bactrim?
|
Trimethoprim, particularly in acid urine, blocks the epithelial sodium channel in the cortical collecting duct, leading to increased lumen positive potential, impaired potassium and proton secretion, hyperkalemia, and metabolic acidosis |
|
X-linked disease affecting basement membranes due to a collagen protein synthesis defect. Clinical disease is characterized by sensorineural hearing loss, ocular abnormalities, and a family history of kidney disease and deafness
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Alport syndrome
|
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differential diagnosis of combined increased anion gap metabolic acidosis and respiratory alkalosis
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salicylate toxicity, liver disease, and sepsis |
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ferritin levels that exclude or diagnose iron deficiency
|
>100ng/mL excludes and <15 diagnoses iron def |
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formula for urine potassium–creatinine ratio
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Urine Potassium (meq/L) × 100 [(mg × L)/(dL × g)] ÷ Urine Creatinine (mg/dL)
|
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interpretation of urine K-crea ratio
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> 20 meq/g c/w kidney potassium wasting, << 15 meq/g suggests extrarenal potassium loss, cellular redistribution, or decreased intake
|
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metabolic alkalosis, urine cl levels low, differentials?
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vomiting or decreased effective arterial blood volume (prior diuretics)
|
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metabolic alkalosis, urine Cl levels high, differentials?
|
on diuretics, Bartter or Gitelman syndrome
|
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define hypercalciuria
|
urine calcium >300 |
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treatment of calcium stones with hypercalciuria
|
thiazide diuretic, promotes distal reabsorption of calcium
|
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kidney injury which results when a patient with vascular risk factors and hypertension attains a blood pressure lower than usual measurements
|
normotensive ischemic AKI
|
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time frame for AIN to occur
|
1 week after exposure
|
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JNC 7 definition of prehypertension
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average blood pressure reading of 120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic. Remember goal blood-pressure for people with diabetes regardless of age is a BP less than 130/80.
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blood pressure that is higher at home than in the office setting
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Masked hypertension
|
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White coat hypertension
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3 office BP >140/90 mm Hg, 2 home BP <140/90 mm Hg and no target organ damage.
|
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Resistant hypertension
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BP above goal despitee 3 antihypertensives, including 1 diuretic
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pathophysiology of Gitelman syndrome
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defect is due to inactivating mutations in the gene for the thiazide-sensitive sodium chloride cotransporter in the distal convoluted tubule, and the electrolyte profile is analogous to that induced by thiazide diuretics (hypokalemia, hypochloremic metabolic alkalosis) |
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electrolyte and acid base abnormality in diuretic abuse and surreptitious vomiting
|
hypokalemic metabolic alkalosis |
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define gestational hypertension
|
refers to hypertension that develops after 20 weeks' gestation in the absence of proteinuria or other maternal end-organ damage
|
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what is preeclampsia?
|
new-onset hypertension accompanied by the development of proteinuria, develops any time after 20 weeks of pregnancy but usually occurs close to term.
|
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classic presentation of AIN
|
fever, rash, and eosinophilia with elevated crea (only in 10%)
|
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how to interpret fractional excretion of urea
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<35% prerenal (less influenced by diuretics)
|
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propofol-related infusion syndrome is characterized by
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type B lactic acidosis, hypertriglyceridemia, rhabdomyolysis, and J-point elevation or a Brugada-like pattern on EKG
|
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treatment of primary membranous glomerulopathy
|
control risk factors - ACEi for HTN and statin if HL
|
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differentiate type A and type B lactic acidosis
|
Type A due to tissue hypoperfusion / hypoxia. Type B due to medication / toxin; or in advanced malignancy, liver disease, or G6PD def
|
|
drugs that cause type B lactic acidosis
|
linezolid, acetaminophen overdose, metformin, the NRTis stavudine and didanosine, propofol, and salicylates
|
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kidney stones that will pass and will not pass?
|
5mm or less will pass, 10mm or more will not
|
|
at what levels of creatine kinase should one suspect rhabdo?
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>5000
|
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abnormal ARR
|
>25 considered abnormal
|
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when to start bicarbonate therapy in CKD?
|
Stage 4-5 with bicarb 15-20 (delays progression of CKD)
|
|
treatment of hyperoxaluria
|
calcium carbonate supplements
|
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When to consider evaluating for secondary causes of HTN? (6)
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young age, no family history, no risk factors, rapid onset, abrupt change, endocrine abnormality
|
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Indications for rasburicase (being that it is more expensive) (2)
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high risk for tumor lysis syndrome or very high UA levels in chemo
|
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NOTE: Plain AXR has no role in
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the acute diagnosis of kidney stones.
|
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NOTE: There is no role for the routine measurement of
|
EPO in CKD.
|
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How does GFR relate to creatinine?
|
inversely proportional; 50% reduction in GFR = doubling of serum crea
|
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medications that block tubular secretion of creatinine (resulting in higher crea without change in GFR)
|
TMP, cimetidine
|
|
alternative marker of GFR that is less influenced by age, gender, muscle mass, and body weight compared with serum creatinine
|
cystatin C
|
|
high urinalysis pH
|
strict vegetarians, distal RTA (Type 1), urease–splitting organisms (Proteus and Pseudomonas)
|
|
urine dipstick reads negative or trace for protein but shows increased positivity for protein by the SSA test
|
consider multiple myeloma – presence of urine light chains or Ig not detected by urine dipstick
|
|
at what serum glucose does glucosuria occur?
|
180–200 mg/dL
|
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differential diagnosis for (+) ketones
|
DKA, starvation / alcoholic ketoacidosis; salicylate toxicity, isopropyl alcohol poisoning
|
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ketones detected by urinalysis
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acetoacetate, not B–OH
|
|
when is nitrites (+)?
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GN UTI (Kleb, E. coli, Proteus, Pseudomonas)
|
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differentials for (+) urobilinogen in urinalysis |
hemolytic anemia or hepatic necrosis (NOT obstructive causes)
|
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differentials for (+) bilirubin in urinalysis
|
severe liver disease or obstructive jaundice |
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sterile pyuria differentials
|
M. tuberculosis, AIN, kidney stones, kidney transplant rejection
|
|
common causes of AIN
|
antibiotics, NSAIDs, PPI
|
|
differentials for urine eosinophil (+) in urinalysis
|
allergic reaction, atheroembolic disease, RPGN, small vessel vasculitis, UTI, prostatic disease, parasitic infections
|
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blood in urine: isomorphic RBCs
|
tumor, stone or infection. The fact that the RBCs are isometric by definition determines their origins not at the glomeruli level.
|
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blood inurine: acanthocytes and RBC casts
|
GN, severe interstitial nephritis, ATN
|
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casts in urinalysis
|
hyaline casts – hypovolemia; pigmented granular (muddy brown) casts – tubular injury; RBC casts – GN; WBC casts – tubulointersitial inflammation of kidney, pyelonephritis
|
|
urine crystal shapes |
-Calcium oxalate: envelope / dumbell / needle
-Calcium phos: prism, needle, star–like clump
-Uric acid: rhomboid / needle / rosette
-Struvite or Mag ammonium phos: coffin
-Cystine: Hexagonal |
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Nephrotic–range proteinuria
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protein–creatinine ratio greater than 3.5 mg/mg
|
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ADA recommendation: when to check urine albumin–crea ratio in DM?
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typ1DM x 5 years; all type 2 DM at time of diagnosis |
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ADA definition of microalbuminuria
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urine albumin–creatinine ratio of 30 to 300 mg/g; two of three random samples over 6 months
|
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transient proteinuria differentials
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fever, rigorous exercise
|
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proteinuria increases during the day and decreases at night when the patient is recumbent
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orthostatic proteinuria
|
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diagnostic test for orthostatic proteinuria
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split urine collection
|
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imaging used in the evaluation of hematuria
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CT urography, MR urography, US, IVP
|
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which urinary tract imaging to choose in hematuria
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CT uro for high–risk patients with preserved GFR; MR uro when GFR 30–60; US in <40y/o with no RF for urologic malignancy; noncontrast abd CT if stones suspected; IVP no longer recommended
|
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hematuria ffd by negative evaluation of upper urinary tract, next step
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cystoscopy; assess for lower ureteral, bladder or urethral causes |
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gold standard for quantifying the glomerular filtration rate and renal plasma flow
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radionuclide kidney clearance scanning
|
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when to order MRI of kidneys |
mass lesions and cysts
|
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test of choice for the evaluation of urologic bleeding in patients at high risk for bladder cancer with an estimated GFR above 60 mL/min/1.73 m2 |
CT urography
|
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can identify non–uric acid–containing kidney stones
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KUB xray
|
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Indications for kidney biopsy
|
suspected glomerular pathology such as glomerulonephritis and the nephrotic syndrome, acute kidney injury of unclear cause, and kidney transplant dysfunction
|
|
Contraindications to kidney biopsy |
bleeding diatheses, active infection of the genitourinary system, hydronephrosis, atrophic kidneys, and uncontrolled hypertension; relative C/I: solitary kidney, severe anemia, and chronic anticoagulation
|
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abnormal serum osmolal gap
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>10 mosm/kg H20; reflects the presence of unmeasured solutes
|
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Formula: plasma Osmolality (mosm/kg H2O)
|
2 × Sodium (meq/L) + Glucose (mg/dL)/18 + BUN (mg/dL)/2.8
|
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normal effective osmolality
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275–295 mosm/kg H204 to 6 meq/L (4–6 mmol/L) over the first 24 hours is sufficient
|
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goal rise in sodium in patients with symptomatic hyponatremia
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4–6 meq/L over 1st 24 hours
|
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conditions causing pseudohyponatremia |
Hyperglobulinemia or severe hyperlipidemia
|
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most common form of hyponatremia
|
hypotonic hyponatrmeia
|
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causes of hypertonic hyponatremia
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marked hyperglycemia or exogenously administered solutes such as mannitol or sucrose
|
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first step in the evaluation of hyponatremia
|
check plasma osmolality – normal in pseudohyponatremia (check chol, TG, serum total Pr)
|
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how is cause of hypotonic hyponatremia established
|
history, vol status, urine osmolality, urine sodium level
|
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Uosm for primary polydipsia and hyponatremia
|
<100
|
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mechanism of hyponatremia in beer potomania |
water excretion is in part solute dependent, chronic ETOH + low solute intake = decrease free water excretion; hyponatremia develops in setting of modest increases in fluid intake
|
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when does reset osmostat occur?
|
quadriplegia, TB, advanced age, pregnancy, psych disorders
|
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how to distinguish reset osmostat from SIADH
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document excretion of dilute urine following a water load
|
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What is cerebral salt wasting?
|
syndrome of hypotonic hyponatremia that may complicate subarachnoid hemorrhage or neurosurgery
|
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risk factors for acute hyponatremia |
pos–op hypotonic fluids; use of thiazides, use of ecstacy, overhydration with extreme exercise, primary polydipsia
|
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treatment of symptomatic hyponatremia
|
hypertonic saline in symptomatic SIADH; NS for hypovolemic hyponatremia; seizure or coma – 100ml or 2ml/kg bolus infusions of 3% NS, repeated up to 2x as needed
|
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maximum rate of correction of hyponatremia
|
not >10 meq/l within 24 hours or 18 within 48 hours
|
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clinical features of osmotic demyelination syndrome
|
progressive quadriparesis, speech and swallowing disorders, coma, locked–in syndrome (IRREVERSIBLE)
|
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treatment of asymptomatic hyponatremia
|
fluid restriction in SIADH or hypervolemic hyponatremia
|
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causes of diabetes insipidus
|
decreased release of ADH (central diabetes insipidus); ADH resistance (nephrogenic diabetes insipidus); and metabolism of ADH by circulating vasopressinase (gestational diabetes insipidus)
|
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define polyuria |
urine volume >3L/24h
|
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diff Dx of polyuria
|
DI, primary polydipsia, osmotic diuresis
|
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urine osmolality in osmotic diuresis, primary polydipsia and DI
|
>300 in osmotic diuresis; <200 in Di and primary polydipsia
|
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effect of water deprivation testing in primary polydipsia and DI
|
increases urine osmolality to ~600mosm/kg H20; <200 in DI
|
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effect of desmopressin in central DI / gestational DI / nephrogenic DI
|
rise to 600 mosm/kg H20 except in nephrogenic DI
|
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treatment of hypernatremia
|
in shock, NS – avoid boluses; estimate water deficit, D5 water
|
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rate of correction of hypernatremia
|
no more than 10 meq/L to avoid cerebral edema
|
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estimated water deficit formula
|
Total Body Water [0.6 in Men and 0.5 in Women × Body Weight (kg)] × [(Serum Sodium/140 [or target serum sodium]) – 1]
|
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treatment of central and gestational DI
|
intranasal desmopressin
|
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treatment of nephrogenic DI
|
thiazide diuretics (increase prox Na and water reabsorption); d/c lithium if possible or add amiloride |
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DDx of hypokalemia
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cellular redistribution, kidney (diuretics) or GI losses, decreased intake
|
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conditions that result in increased intracellular uptake of serum K
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marked leukocytosis (myeloprolif disorders), B2 agonists, epinephrine, insulin, Vit B12 repletion, systemic alkalosis; toxicity to barium, chloroquine, quetiapine, risperidone
|
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rare syndrome that presents with acute episodic muscle weakness, often following a high carbohydrate meal or strenuous exercise
|
hypokalemia periodic paralysis
|
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this amount of 24 hour urine K excretion suggests ongoing urinary potassium losses
|
>30meq/L
|
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formula for urine potassium–crea ratio
|
(meq/g) = Urine Potassium (meq/L) × 100 [(mg × L)/(dL × g)] ÷ Urine Creatinine (mg/dL)
|
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interpretation of urine K–crea ratio
|
>20 in kidney potassium wasting, <15 suggests cellular reditribution, decreased intake or extrarenal K loss
|
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used for patients with concomitant metabolic acidosis due to renal tubular acidosis and hypokalemia
|
potassium citrate
|
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the most efficient intervention that enhances intracellular potassium uptake
|
IV insulin +/– glucose
|
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evolution of EKG changes in hyperkalemia
|
peaked T waves with a shortened QT interval initially, followed by an increased PR interval and QRS duration, decreased P wave amplitude, and eventually a sinoventricular pattern heralding ventricular standstill
|
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NOTE: Severe leukocytosis (leukocyte count >120,000/microliters [120 × 109/L]) and thrombocytosis (platelet count >600,000/microliters [600 × 109/L]) |
can result in the release of intracellular potassium in serum specimens.
|
|
how to diagnose pseudo–hyperkalemia related to leukocytosis
|
by repeating a serum potassium measurement in a sample carefully transported to the laboratory without agitation immediately following phlebotomy or measurement of whole blood potassium in uncentrifuged specimens using ion–specific electrodes also confirms the diagnosis
|
|
what does TTKG estimate?
|
the ratio of the potassium level in the CCD to that in the peritubular capillary; capacity of kidney to excrete K in the setting of hyperK
|
|
formula for TTKG
|
[Urine Potassium ÷ (Urine Osmolality/Plasma Osmolality)] ÷ Serum Potassium
|
|
how to interpret TTKG
|
>10 under normal conditions; < 10 indicates kidney defect in K excretion
|
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how is IV calcium given in hyperkalemia?
|
every 5 minutes until ECG changes resolve
|
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When is IV calcium contraindicated in hyperkalemia?
|
digoxin toxicity
|
|
onset and duration of effect of glucose insulin solution in hyperkalemia
|
within 10 minutes and is sustained for 4 to 6 hours
|
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Caveat with using sodium polystyrene sulfate in hyperkalemia
|
use sorbitol–free preparation – sorbitol implicated in GI necrosis and bleeding
|
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treatment of mild–moderate hyperkalemia
|
dietary potassium restriction to less than 2500 mg/d
|
|
DDx of hypophosphatemia
|
chronic alcohol use, critical illness, malnutrition
|
|
presentation of hypophosphatemia |
<2 symptomatic weakness, <1 resp muscle weakness, hemolysis, rhabdomyolysis
|
|
when to correct low phos with IV? |
<1
|
|
NOTE: When hypophosphatemia is due to increased cellular uptake or extrarenal phosphate loss, |
the 24–hour urine phosphate excretion is less than 100 mg/dL (32.3 mmol/L) and the fractional excretion of phosphate is less than 5%
|
|
risks of IV phosphate treatment
|
hypocalcemia and AKI. Because serum phosphate and calcium have an inverse relationship.
|
|
maximum dose of intravenous phosphate
|
doses of phosphate should be restricted to 80 mmol over 12 hours
|
|
DDx of hyperphosphatemia
|
advanced CKD, increased cell turnover, cell injury, or exogenous phosphate administration
|
|
normal reference range for the anion gap
|
8 to 10 meq/L ± 2 meq/L
|
|
correction of anion gap in hypoalbuminemia
|
For every 1 g/dL (10 g/L) decrease in serum albumin, for example, the expected or “normal” anion gap falls by approximately 2.3 meq/L (2.3 mmol/L).
|
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define lactic acidosis
|
serum lactate level greater than 4 mg/dL
|
|
MOA fomepizole
|
inhibitor of alcohol dehydrogenase that prevents the formation of toxic acid metabolites
|
|
formula for corrected bicarbonate
|
24– change in AG
|
|
interpretation of delta delta
|
if measured HCO3 > corrected bicarb – concomitant MAlk in addition to HAGMA; if measured HCO3 < corrected – concomitant NAGMA + HAGMA |
|
What is the goal blood pressure for person younger than 80 years?
|
Less than 140/90
|
|
And what hemoglobin should erythropoietin stimulants be started in CKD?
|
Less than 10. With a target hemoglobin level of 10 to 11.
|
|
Acetazolamide causes kidney excretion of what:
|
Bicarb and sodium
|
|
When to start dual antihypertensive therapy?
|
When blood pressure more than 20 points above goal blood pressure based on age.
|
|
How long to treat UTI and patience with autosomal dominant polycystic kidney disease?
|
Cipro for 2 to 4 weeks
|
|
Most important thing to do to prevent tumor lysis syndrome?
|
Intravenous fluids at 250 mL per hour if possible
|
|
What is the most common primary nephrotic syndrome?
|
Focal segmental glomerulosclerosis. This condition as a predilection for African-Americans. Typically these patients at minimal edema.
|
|
Type of kidney disease seen with lupus?
|
Proliferative lupus nephritis
|
|
What is the most common primary nephrotic syndrome?
|
Focal segmental glomerulosclerosis. This condition as a predilection for African-Americans.
|
|
How soon to follow up on blood pressure in pre-hypertension?
|
Recheck in 1 year
|
|
What type of alcohol poisoning should Fomepizole be used?
|
Methanol and Ethylene glycol
|
|
I what pH is sodium HCO3 generally indicated in?
|
Persistent severe acidemia with pH less than 7.15
|
|
What test is done in the patient's home to confirm resistant hypertension?
|
Ambulatory blood-pressure monitoring
|
|
Conditions associated with lead toxicity:
|
-CKD
-Hypertension -Gout |
|
Best test for lead toxicity:
|
Chelation mobilization testing
|
|
NOTE: beta blockers are no longer universally recommended as first-line agents to treat hypertension in the absence of compelling indication such as history of MI or heart failure.
|
X
|
|
When to add Allopurinol in patients with recurrent uric acid stones?
|
After recurrent stones despite alkalinization (treatment with potassium citrate) of the urine.
|
|
Type of kidney injury caused by amyloidosis?
|
Nephrotic syndrome. Amyloidosis also affects the heart typically causing a restrictive cardiomyopathy and subsequent heart failure.
|
|
Describe liddle syndrome:
|
-Early onset hypertension
-Metabolic alkalosis -Hypokalemia in this condition renin and aldosterone are suppressed. Treated with amiloride or triamterene. |
|
When his GFR calculation using chronic disease epidemiology collaboration equation best?
|
When GFR thought to be greater than 60. Use
|
|
How does dysmorphic RBCs look in glomerular hematuria:
|
Round in shape but with blebs protruding from their membranes.
|
|
Urine cast seen in acute interstitial nephritis (AIN)
|
Leukocyte casts
|
|
You're in cast seen in acute tubular necrosis (ATN)?
|
Muddy brown casts |
|
Type of acute kidney injury seen with Intravenous bisphosphonate therapy?
|
Acute tubular necrosis
|
|
Characteristics of type 1 renal tubular acidosis:
|
-Normal anion gap metabolic acidosis |
|
Lab values seen a laxative abuse:
|
-Normal anion gap metabolic acidosis
-Hypokalemia |
|
Characteristics of proximal (type 2) renal tubular acidosis:
|
A defect in the regeneration of bicarbonate in the proximal tubule's.
-Normal anion gap metabolic acidosis -Hypokalemia -Glucosuria in setting of normal plasma glucose -Renal phosphate wasting -Acidic urine pH unlike that scene and type 1 RTA |
|
When his GFR calculation using chronic disease epidemiology collaboration equation best?
|
When GFR thought to be greater than 60. Use modification of diet in renal disease study equation at lower GFRs.
|
|
Target blood pressure for people with diabetes regardless of age:
|
Less than 130/80
|
|
How does dysmorphic RBCs look in glomerular hematuria:
|
Round in shape but with blebs protruding from their membranes.
|
|
What is the normal urine albumin to creatinine ratio?
|
Less than 30
|
|
What is the normal urine protein to creatinine ratio?
|
Less than 0.2
|
|
Laboratory evidence of hemolytic anemia:
|
-Elevated reticulocyte count
-Elevated lactate dehydrogenase |
|
What diseases associated with a classic triad of: microangiopathic hemolytic anemia, low haptoglobin level, and schistocytes?
|
Hemolytic uremic syndrome. Caused by some strains of E. coli including 0157-h7 that produces Shiga-like toxins.
|
|
Next test for sustained, isolated proteinuria?
|
Split urine collection: Protein urine collection during the day and collection during the night. to a valve for the benign condition of orthostatic pastoral proteinuria.
|
|
What is the normal urine protein loss over 24 hours?
|
Less than 150 mg/24 hours
|
|
Which chemotherapeutic agent is well known for causing type 2 RTA and or Fanconi syndrome?
|
Ifosfamide
|
|
Lab values associated with postinfectious glomerulonephritis secondary to strep or staph:
|
-Low complement levels
-Elevated antistreptolysin O antibodies when associated with streptococcal infection Note in this condition there should be a latency period between infection and the onset of kidney disease. |
|
What two conditions should be thought of in the presence of resistant hypertension?
|
1. Primary hyperaldosteronism
2. Renovascular hypertensio |
|
What is the treatment for primary membranous glomerulopathy?
|
Ace inhibitor and Statin
|
|
What condition is associated with: type B lactic acidosis, hypertriglyceridemia, rhabdomyolysis, myocardial abnormalities seen as J point elevation or Brugada like pattern on EKG
|
Propofol-related infusion syndrome
|
|
Treatment of mild to moderate salicylate toxicity:
|
Sodium bicarb infusion. Alkalinizing the arterial blood to a pH 7.5 to 6.6 is indicated to decrease intracellular uptake and toxicity of salicylic acid. additionally with hydration and urine alkalinization to a pH of 7.5 to 8.0 will promote salicylate excretion. Blood salicylate levels and other electrolyte should be done q2 hours while treating. Any hypokalemia should be corrected to prevent increased salicylate absorption in the distal tubule. Impaired mentation should be treated with intravenous glucose to attenuate salicylate induced neuroglycopenia.
|
|
When is hemodialysis indicated in salicylate toxicity?
|
-Serum salicylate levels that exceed 80 mg/dL are
-Altered mentation -Pulmonary edema -Advanced kidney disease -When clinical status worsens despite optimal medical therapy |
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Expected lab values in syndrome of inappropriate ADH secretion:
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-Low plasma osmolality
-Urine sodium level exceeding 40 |
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Definition of hyperkalemia:
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Potassium over 5
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Definition of abdominal compartment syndrome:
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Defined by new organ dysfunction in the setting of sustained, abnormal increase in the intra-abdominal pressure. Things that increase pressure include: massive ascites, volume overload, intra abdominal or retroperitoneal bleed.
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Medication to increase the likelihood of expulsion of ureteral stone if less than 10 mm in diameter?
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Tamsulosin (Flomax)
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What two conditions should be thought of in the presence of resistant hypertension?
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1. Primary hyperaldosteronism
2. Renovascular hypertension. |
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Describe biopsy characteristics of primary membranous glomerulopathy:
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-Diffuse glomerular membrane thickening
-No cellular infiltration -Coarsely granular deposits of IgG and C-3 along capillary loops -moderate podocyte foot process effacement seen on electron microscopy |
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Describe characteristic biopsy results of minimal change glomerulopathy:
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This condition is common in children and is not an immune complex disease process.
-Normal light and immunofluorescent microscopy but effacement of podocyte foot processes on electron microscopy. |
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How to treat lithium induced partial nephrogenic diabetes insipidus if patient must continue on lithium?
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Start Amiloride. This agent directly blocks the epithelial sodium channel and decreases lithium uptake, resulting in less long-term damage.
Tolvaptan is not used in this case because the diabetes insipidus caused by lithium is only partial," not complete. |
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When is Hemodialysis of the ofindicated in salicylate toxicity?
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-Serum salicylate levels that exceed 80 mg/dL are
-Altered mentation -Pulmonary edema -Advanced kidney disease -When clinical status worsens despite optimal medical therapy |
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The primary temporizing measures for hyperkalemia?
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-Intravenous calcium
-Insulin-dextrose solution |
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Differential diagnoses of combined increased anion gap metabolic acidosis + respiratory alkalosis:
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-Salicylate toxicity which can be found in oils of wintergreen, aspirin
-Liver disease -Sepsis |
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What is the best diagnostic test to diagnose fibromuscular dysplasia?
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Catheter-based kidney angiography
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Treatment of choice for ESKD and setting of Alport syndrome?
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Kidney transplantation. There are no specific therapies were Alport syndrome.
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Types of kidney stones seen post gastric bypass surgery?
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Calcium oxalate stones secondary to enteric hyper oxaluria. Oxalate absorption is increased because calcium, which normally buns to oxalate in the gut and limits oxalate absorption, binds to fatty acids. Treatment is calcium carbonate supplements, low-fat diet, good hydration.
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Over-the-counter medications and other nonprescription drugs that can cause hypertension:
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-Decongestants with pseudoephedrine or phenylephrin
-NSAIDs -Recent caffeine intake -Cigarette smoking |
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Best treatment to reduce risk of preeclampsia in patients with high risk?
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Low-dose aspirin 75 to 150 mg/day
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Definition of preeclampsia:
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-Systolic blood pressure greater than or equal to 140 or diastolic BP greater than or equal to 90
-24 hour urine protein greater than 300 mg -After 20th we could just station in a woman who did not have hypertension or proteinuria early in pregnancy |
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The most common disease associated with rapidly progressive glomerulonephritis?
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ANCA vasculitis. If severe, patient may require induction therapy with plasmapheresis and then cyclophosphamide and steroids. Followed with maintenance therapy with Azathioprine and steroids
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If suspecting kidney disease confirmed by laboratory data what is the next test to get?
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Kidney ultrasound. Do this prior to biopsy to rule out obstruction, determine kidney size, or evaluate for kidney cysts. And remember kidney biopsy is predominately used for patients with glomerular disease.
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Test to check in cases of metabolic alkalosis?
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-Blood pressure
-dehydration status -urine chloride level |
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What is the goal LDL level in CKD?
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Less than 100 and preferably less than 70.
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What is the first line medication for management of hypertension during pregnancy?
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Labetalol. Methyldopa works but may cause sedation and has to be given TID to be effective.
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What brain conditions should be screened for an autosomal dominant polycystic kidney disease?
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Cerebral aneurysms with MR angiography.
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Method of PTH suppression in CKD:
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Vitamin D treatment. Use vitamin D3 or cholecalciferol if actually vitamin D deficient. If intact PTH level elevated but 25 hydroxy vitamin D be more than 30, use active or vitamin D such as calcitriol.
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Normotension definition:
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BP less than 120/80
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Define chronic hypertension during pregnancy versus hypertensive disorder of pregnancy:
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Normally during pregnancy BP levels typically decrease early in the first trimester and may remain lower then nun pregnant levels until term. Therefore when hypertension is present before 20 weeks just station, this represents chronic hypertension.
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What are the lab values associated with gentamicin toxicity:
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Hypokalemic, metabolic alkalosis
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What test order for iron deficiency anemia:
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1. Serum iron level -Typically low
2. Ferritin level -Typically low 3. TIBC -Typically high Because ferritin is an acute phase reaction it can be normal or elevated in the presence of our deficiency anemia. But generally if ferritin greater than 100 it excludes iron deficiency and is less than 15 confirms iron deficiency. |
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Describe electrolytes and acid base seen in Bartter's syndrome: |
- Hypokalemia, hypochloremic metabolic alkalosis, spot urinary Cl: greater than 20
Due to abnormal chloride transporters in the ascending loop of Henle. Onset during childhood or adoles. |
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Describe electrolytes and acid base seen in Gitelman's syndrome: |
- Hypokalemia, hypochloremic metabolic alkalosis, spot urinary Cl: greater than 20
Due to abnormal chloride transporters in the distal tubules. This condition is also associated with hypocalciuria. |
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GFR in stage 2 CKD: |
60-89 |
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GFR in stage 3 CKD: |
30-59 |
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GFR in stage 4 CKD: |
15-29 |
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GFR in stage 5 CKD: |
Less than 15 |