Nephrology Flashcards
Patient presentation of kidney stone
o Colicky flank pain
o Radiates to groin
o Nausia / vomiting
• How to tell pyelonephritis from a kidney stone and Renal cell carcinoma
o Pyelonephritis will have fever and WBC casts*
o RCC will have palpable mass
o All could have hematuria
Tests to order if kidney stone is suspected
o UA
o Noncon CT is gold standard. IF PREG: use US
o NO KUB
• UA of kidney stone
o Blood (even microscopic hematuria) (Note: in the absence of blood, probability of symptomatic stone is low) o Absence of casts
• Treatment of stone and Difinitive Management based on size of kidney stone
o IVF and analgesia
o < 0.5mm : Pass spontaniously: Hydration and pain control
o 0.7 – 1.5 mm : Medical Exulsive therapy: CCB (amlodipine) and/or Alpha blockers (terazosin
o > 1.5mm : Resection (laproscopic (proximal) / lithotripsy (distal)
o Strain and analyze stone, 24 hr urinalysis in 6 weeks
Radio opaque vs radio leucent stones with causes
o Opaque: Calcium oxalate / Magnesium Ammonium Phosphate
o Leucent: Uric acid / cystine
• What happens in hyponatremia and hyper
o Hyponatrimia – less in blood, fluid extravisates into body
o Hypernatrimia – more in blood, fluid extravisates into blood
- Hypernatrimia
- What is it
- How do you fix it
o Always a deficiency of water
o Fix is with PO water if possible. Consider hypotonic sulutions such as D5W or 1/2ns.
Before replacing the free water deficite, fix volume with NS
• Hyponatrimia AND hypernatremia –sxs in Mild vs Moderate vs Severe state
o Mild – asymptomatic
o Moderate – Nausia, vomiting, headache
o Acute / Severe – Coma, Seizure
• Tx for severe state hyponatremia
o Coma / Seizure
o Hypertonic Saline (3%)
• How fast can you correct hyponatremia?
o No faster than 0.25 mmol / hr OR 6 in a day
o Usually symptoms will go away after a day of treatment
o Correction Too fast will lead to osmotic demyelination syndrome
• General rules of thumb when looking at Urine osms and Na in a patient with hyponatremia
o If urine Na is low – kidneys are working, low perfusion is cause
o If urine has high osms [ ] then ADH is high.
• Euvolemic Hyponatremia
o RATS o Renal Tubular acidosis (UA) o Addisions ( urine cortisol) o Thyroid disease (TSH) o SIADH (dx of exclusion)
SXS of volume up
o JVD
o Edema
o CHF
o Anasarca
• Sxs of volume down
o Dry mucous membranes
o Tachypnia, Hypotension
o Fevers
o Burns
• SIADH tx
o Volume restriction
o Possible gentle diuresis
o If refractory – demeclocycline
• Steps to make DX of cause with Na <135
1) Determine serum osmoles – for every 100 glucose over 100, subtract 1.6 Na
2) Volume status?
Overload (hypervolemic)
— Determine cause and diurese
Normal (Euvolemic)
—- RATS – UA, Cortisol, TSH
Down
IVF – see if it corrects
Urine Na
Intrarenal – High urine Na: ATN AIN
Extranrenal - low urine Na
• Calculation fo Serum Osmoles
o 2xNa + gluc/18 + BUN/2.8
o Normal is 275-295
K normal
o 3.5-5.5
o >4 is normal in cardiac patatients
- Sxs of hyperkalemia
* Exam Findings of hyperkalemia
Usually its asymptomatic. If severe pt will report o Decreased motor, dec sensation o Flaccid paralysis o Parestheisea o Chest pain / palpitations
EXAM may show o ECG changes o Areflexia o Numbness `
• First thing to do when there is a high K level?
o Repeat lab
o ECG
• DDX of hyperkalemia
o Artifact o K-sparing diuretics (Ace, Arb, Spironilactone ) o Hypoaldosterone o CKD / RTA o Ingestion o Hemolysis o Iatrogenic (over administered)
• Findings of High K on ECG
o PR prolongs
o QRS widens
o T waves Peak
• 3 stages of treatment of hyperkalemia
o I : Stabalize myocardium with calcium gluconate
o II: Dec serum K : Insulin + glucose or Bicarbonate
o III: Dec total body K with Kayexalate or diuretics
o If Renal failure or extreme ECG changes, dialysis
o NOTE: if stable – just give kayexelate
• Causes of Hypokalemia
GI loss
♣ Vomiting
♣ Diarhea
♣ Laxatives
Renal Losses
♣ Hyperaldosterone (primary or secondary)
♣ Loop diuretics
♣ Thiazide Diuretics
• Replacement of K
o Oral preferred
o IV: <10meq/hr peripheral or <20 central
What are the regulators of calcium?
What is it bound to?
How to adjust for Alb?
o Clacitonin o PTH ♣ Activates osteoclasts ♣ Kidneys: Ca in, P out ♣ Inc Vit D 1,25absorb Ca and P from gut
o Mostly bound to albumin. Very little is ionized
♣ Alb adjust: every point below 4, add 0.8 Ca
Symptoms of hypercalcemia
Bones – fracture, osteopenia
Psychic Moans – AMS only if severe – 13-15
Stones
Abdominal Groans – (Nausia, Vomiting, abdominal pain)
TX of hypercalcemia
o IVF – always first line
o Furosimide – inc naturesis and Ca exc but ONLY when volume status is corrected
o Calcitonin – acts / fades fast
o Bisphosphonates – long term
DDX of Hypercalcemia
o Primary, secondary, tertiary hyperparathyroid o Familial hypocalciuric hypercalcemia o Malignancy o Immobilization o Vit D excess
Primary Hyperparathyroidism. Cause labs an interesting sequellae, dx tx FU
Cause: Single autonomous gland PTH
Labs: High Ca, Low P
Seq: Could get Brown tumor (fibrosa cystica) – osteoclast stimulation
DX – radionucliotide scan. (sestamibi)
TX – resection
FU – watch for hypocalcemia on FU (Hungry bone syndrome)
Secondary hyperparathyroid
- cause
- labs
Cause: Erly renal failure – vit D not made – causes low Ca, so inc PTH and parathyroid hypertrophy
Labs: High Ca, Low P
Tertiary hyperparathyroid: Cause labs tx a note
o Continued renal failure causes PTH glands to become autonomous (just like primary)
o Labs: High Ca, Low P
o TX –resction
o Note: no risk of cancer
Familial Hypocacciuric Hypercalcemia:
Cause Labs Sxs tx sequellae
o Cause – abnormal calcium sensing receptor, so new set point.
o Labs: inc Ca, low P (inc PTH)
o SXS, Asymptomatic
o TX – none
o Sequellae: inc risk of stenotic aortic disease in old age
Malignancy - two ways it can cause increased Ca
PTH-rp – looks like primary hyperPTH but low PTH
♣ High Ca, Low P
Mets – way high Ca
♣ High Ca, High P
Immobilization as cause of inc in Ca.
Cause
labs
sxs
tx
o Cause – dec impact stress
o Labs- low PTH , Inc Ca, Inc P,
o Sxs – asx
o Tx – inc movement
Vit D excess as a cause of inc Ca
Cause
labs
tx
o Cause: granulomatous dz: TB, sarcoid
o Labs –low PTH, Inc P, Inc Ca
o Tx – steroids to treat dz
Hypocalcemia DDX – extensive
Hypoalbuminemia (adjuct fo alb and ca will normally correct)
♣ Cirrhosis, Nephrosis, poor nutrition
Hypoparathyridism
♣ Iatrogenic (postsurgical “hungry bone” which means atrphyied glands)
Vit D deficiency
♣ Renal failure
♣ Sunlight / diet deprivation
♣ These lead to secondary hyperparathyroidism – initially though there will be decreased Ca
CRF
Calcium Sequestration
♣ PANCREATITS
Pseudohypoprarthytroidism
Sxs of Hypocalcemia
tx
SXS
Perioral tingling
Tetany (chovstek = chvozTAP , trassaue = arm)
TX
replace Ca:
PO Ca and Vit D If non emergent.
IV if emergent
Pseudohypoprarthytroidism – what it is and why the name is bad, labs
o High PTH due to end organ resistance
o High Ca, high P but everything is functioning normally. ignore it.
Hypoparathyridism, cause and labs
o Iatrogenic (postsurgical “hungry bone” which means atrphyied glands) o Labs – dec PTH, Dec Ca, Dec P
Presentation of AKI
o Elevate Cr
o Decreased urine output
Note: Kidneys are redundant, so electrolytes will not be out of wack until GFR is severely reduced. Patient will likely be asx and it will be noted on routine labs
Prerenal AKI
Cause
Labs
TX.
Note on most common cause in outpatient
Cause: Low perfusion
Make sure to check volume status! (ask about this in the future)
Labs:
Low Urine Na, Low Fe Na (Make sure patient not on diuretic)
BUN/CR >20
TX
Volume Down - fluids (this is prerenal azotemia
(gentle diuresis if vol up?)
Note: prerenal azotemia is most common cause in outpatient setting.
Postrenal AKI: Cause, DDX, DX, TX depending on location
Cause: obstruction
DDX
Distal: BPH, Neurogenic bladder, Kinked cath
Proximal: stones and cancer
DX – US preferred, CT can be used.
TX –
Distal – cath.
Poximal – stent, nephrostomy tubes, surg
• Intrarenal AKI ddx and qyick notes about each
ATN
♣ Ischemia
♣ Toxin exposure
♣ Muddy brown casts – phases of recovery
AIN
♣ Drugs, infection, deposition dz
♣ RBCS, WBCS , eosinophils
Glomerularnephritis
♣ RBC casts. TONS of causes. Lupus, IgA neph, goodpast, HSP, etc
♣ Rule out nephrotic synd with with UA spot test / 24 hr urine
AEIOU
reasons for dialysis A - acidosis E -electrolytes (K) I - intoxicants / toxins (methanol ethylene glycol, Li, ASA) O - overload U - uremia
You have ARF, how do you work it up?
Order
U-Na, FEna
BMP for Bun / Cr levels (will rule out Pre renal)
US – R/o post renal
Then get a UA
• Goals of CKD Treatment
Prevent progression
♣ If HTN or Protinuria – Ace / Arb
♣ If DM – Annual UA with goal A1C <7
Manage Complications
♣ Anemia – from dec EPO. Give Iron / EPO. Goal Hg >10. Transfusions w/ dialysis if refractory.
♣ Secondary hyperparathyroidism – A product of phosphate retention (inc PTH!) and Vit D def (no conversion to 1,25). Give binders (sevelamir – causes excretion of P in gut) and calcimimetics (Cinacalcet – acts like Ca, lowers PTH needs). Osteoporosis from long term high PTH – dexa >-2.5 – prev with Calcium and Vit D supplementation.
♣ Volume Overload – due to loss of urinary output. Stilulate nephroms that are working with Furosimide intially, can add metolazone. Ultimately dialysis
Acidosis – will cause bicarb between
• General Pathology of CKD
o Over three months of reduced GFR (60ml/hr), this will cause the Cr to rise (above 2 generally)
Stages of CKD
♣ 1 Above 90 ♣ 2 60-90 mild ♣ 3 30-59 Moderate ♣ 4 15-30 Severe kidney disease - Prep dialysis / xplant ♣ 5 <15 Kidney falure - Dialysis
How to determine if acid base disturbance is resp vs metabolic
♣ pH above or below 7.4?
♣ Is the Co2 above or below 40
What would indicate metabolic acidosis, and what would you do next.
What would DDX be
Labs: pH < 7.4, CO2 < 40
Next: Calculate Anion Gap: Na – Cl – Bicarb
♣ Gap above 12: MUDPILES.
gap below 12: do urine anion gap Na + K – Cl
♣ If positive – RTA
♣ If negative – Diarhea
MUDPILES
Acronym for high anion gap metabolic acidosis M methanol U uremia D KA P paradehyde - ignore I iron - izoniazid L lactiac acidosis E thalyne glycol (antifreeze) S salicylates
What labs indicate resp acidosis, and what is the DDX
Labs pH < 7.4, CO2 >40
DDX: Hypoventilation • Opiates • COPD • Asthma • OSA
What labs would indicate Resp Alkalosis and what is the DDX
♣ pH > 7.4, CO2 < 40
♣ Hyperventialation
• Pain
• Anxiety
• Hypoxia
What labs would indicate Metabolic Alkalosis
what do you do next
If it is volume responsive, general treatment for each.
♣ pH > 7.4, CO2 < 40
♣ Get a urine Cl to rule out weird stuff:
if >10 then consider Hyper aldosterone (RAS, Conns* will also have htn!) or genetics (Bartter, gitelman)
♣ If <10, then it is volume responsive:
DDX inc Diuretics, dehydration
emesis
NG suction
Diuretics - Red dose. Can add K sparing diuretics (spironilactone, amiloride, eplerinone, triamterine) / acetazolamide can be added
dehydration - Fluids
emesis - anti emet.
NG suction - if has to continue, use PPI or H2blockers to lower secretion
• Triad for RCC, risk factors, workup, worried about
o Flank pain, flank manss, hematuria (almost garuntees cancer)
o RF – VHL gene, smoking, ESRD.
o Workup: UA, US or CT, then BX /resect
o Worry about renal vein thrombosis, anemia, polycythemia
