MKSAP Flashcards
(97 cards)
What are the risk factors for development of cyst in a ESRD patient
Male with long standing ESRD on HD
Why is screening for cysts important in patients with ESRD?
Because of malignant transformation. Screening is based on individual risk vs life expectancy and should be performed using annual renal US.
Medication approved for ADPKD
Tolvaptan
Rx of myeloma kidney
Bortezomib based chemotherapy + high dose dexamethasone
Why does nephrotic syndrome increase the risk of VTE
Increased hepatic production of procoagulants (fibrinogen, 5, 8) and increased loss of renal Anti thrombin 3 and protein S
What is the surrogate marker for increased VTE risk in nephrotic syndrome and what is the cutoff
Albumin <2.8
Define BP goal for severe pre-eclampsia
> 160/110
Rx of severe pre eclampsia and HELLP
BO control and IV magnesium for seizure prophylaxis. Unlike TTP no role for plex and steroids
Preferred Rx for GERD in patients with CKD
H2 blockers - dose and frequency adjusted for kidney function
Electrolyte derangement associated with PPI use and the mechanism
PPI in a patient with genetic TRMP mutations in Mg channels in GI tract —> GI loss of Mg—> hypo Mag—> persistent opening of K channel in distal nephron (Mg Gaurd K channel) —> K wasting
How do you approach white coat HTN (screen for CV risk, progression to HTN, pharmacotherapy, lifestyle interventions)
- No evidence of CV benefit with Rx of white coat HTN
- Can use screening echo —> LVH warrants Rx
- No pharmacotherapy if BP 130-160/80-100
- Lifestyle modifications still recommended
- 1-5% progress to HTN
Which antacid should be avoided in CKD patients
Magnesium based —> increased risk of hyperMg
What are the effects of hyper Mg and above what level are they seen?
Blocks K and Ca channels —> reduced neuronal transmission leading to weakness or paralysis —> bradycardia and hypotension.
Typically above >4.8
What is the immidiate and definitive management of hyper Mg
- Immediate: Iv Calcium gluconate —> rapid reversal of neuronal and CV effects
- Definitive : HD
Causes and Evaluation algorithm for NAGMA
Causes: hyperCl-, HCO3 loss (renal or GI) and H+ retention (inability of kidney to excrete acid)
Next step: asses kidneys ability to excrete acid by measuring urinary NH3. Urinary NH3 difficult to measure due to short half life —> measure Cl instead —> calculate urinary anion gap: (Na+K) - Cl. Negative AG indicated appropriate acid generation.
If kidneys adequately excreting NH3–> look for GI loss
What are the causes of AIN with fever, rash, eosinophils and without and what is the timeline for development of both
- With fever, rash, peripheral eosinophilia —> antibiotics, autoimmune, and systemic illness; develops within days
- Without the above —> NSAID including celebrex (6-18 months) and PPI (3 months)
Rx of AIN
- D/C offending meds
- Steroids to slow progression
- Repeat KFT within 5-10 days after d/c meds —> should improve —> no improvement—> kidney Bx
Proximal RTA losses mnemonic
Bicarbonate GAP (glucose, amino acids, phosphorus >5%)
Proximal RTA also known as Fanconj syndrome drug
Cyclophosphamide and Ifosfamide
Kidney disease in a young to middle aged male who is migratory agricultural worker from Central America/Asia
Chronic interstitial nephritis
Normal osmolarity range
279-295
Normal osmolal gap
<10
Hormone that regulates osmolarity
ADH
Na correction for glucose
1.6-2.2 for every 100 increase in glucose