Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
131 Cards in this Set
- Front
- Back
|
What is normal 24 hour urine protein?
What signifies significant glomerular pathology? Interstitial renal disease? |
< 150 mg protein
> 3.5 gm/day is probably glomerular. <1 gm/day is probably interstial |
|
|
Are light chains always seen in urine dipsticks in myeloma?
|
No
|
|
|
What are causes of benign proteinuria?
|
In stress/fever/exercise can see transient proteinuria. Also can see benign orthostatic proteinuria in which proteinuria reverts to near-normal values when patient is supine.
|
|
|
Spot protein:creatinine ratio tells us what?
|
It approximates the amount of protein in 24 hour urine.
|
|
|
What acid base disturbance can cause diffuse paresthesias/numbness?
|
Significant alkalemia (high pH increases fraction of bound calcium -> causing hypocalcemia)
|
|
|
What causes a high osmolal gap, normal anion gap in obtunded patient?
Normal osm and normal anion gap in obtunded patient? |
Isopropyl alcohol or acetone ingestion (vs methanol and ethylene glycol)
both gaps normal -- think CO poisoning |
|
|
What urine abnormality is sometimes noted in patients who have ingested ethylene glycol?
|
Calcium oxalate crystals
|
|
|
How do you treat ethylene glycol ingestion? How do you treat methanol ingestion?
|
Treat both with fomepizole + dialysis
|
|
|
How can you confirm that metabolic alkalosis is caused by volume contraction? What are other causes?
|
Urinary Cl- < 10 (bc of avid NaCl absorption)
If urinary Cl- > 10 other causes are Cushing syndrome, primary hyperaldosteronism |
|
|
How do you treat metabolic alkalosis?
|
Restore volume (or underlying problem). If they cannot tolerate extra volume then can use acetazolamide which increases excretion of bicarb.
|
|
|
What is proximal RTA (type 2) caused by? What do you see with this?
What about with distal RTA (type 4)? |
MM and monoclonal gammopathy -- see hypokalemia.
Type 4 RTA caused by aldosterone resistance, see hyperkalemia. |
|
|
What is the adjustment for sodium in setting of hyperglycemia?
|
For each increase of 100 over 100, sodium should be decreased by 1.6. (hypertonic hyponatremia)
|
|
|
What regulates ADH?
|
Osmoreceptors in hypothalamus and stretch receptors in left atrium
|
|
|
How do you treat siADH? In refractory cases? Things to watch for with treatment?
|
fluid restriction, if refractory can use ADH receptor antagonist like tolvaptan.
Demeclocycline has renal toxicity and is associated with photsensitive skin rash - avoid using it. |
|
|
How do you treat severe hyponatremia?
|
hypertonic saline and loop directics
|
|
|
What is the presentation of osmotic demyelineation syndrome?
|
Symptoms start about 1 week later and are irreversible -- speech and swallowing difficulties, paralysis, cognitive deficits.
|
|
|
How do you treat severe hypernatremia?
|
Normal saline first to correct the volume deficit and then with hypotonic fluids to further replace the free water deficit. Multiply TBW (which is 60% of weight) by fractional difference between patient's Na and normal Na
|
|
|
What is the risk of treating hypernatremia too quickly?
|
cellular swelling --> cerebral edema
|
|
|
Normal volume hypernatremia is seen in what?
|
Diabetes insipidus
|
|
|
What two conditions is nephrogenic DI assocaited with?
|
chronic lithium use and Sjogren syndrome
|
|
|
How do you treat central DI? Nephrogenic DI?
|
Central DI- treat with desmopressin (intranasal most potent)
Nephrogenic DI- treat with HCTZ +/- NSAIDs |
|
|
What happens when proximal tubule not working?
|
Failure to reabsorb water (this is where most water and Na is reabsorbed), and failure to reabsorb bicarb and secrete acid (Type 2 proximal RTA), also failure to reabsorb solutes (Na, Cl, K, glucose, a.a.'s = Fanconi syndrome)
|
|
|
How does the loop of Henle work?
|
2 halves - descending and ascending. The descending loop reabsorbs mostly water (20% of total) and the ascending loop reabsorbs solutes.
The ascending loop's actions drives the descending loop's actions. Ascending loops builds up the medullary hypertonicity (by having Na absorbed and active transport of solutes) for water to be reabsorbed in descending loop. |
|
|
What is the use of ethacrynic acid?
|
It is a loop diuretic that is not sulfa based.
|
|
|
Where do thiazide diuretics work? Are they effect if low GFR?
|
Mostly in the early (not late) distal tubule, but also in proximal tubule.
Not effective if low GFR because they have to be secreted to be effective. |
|
|
What controls the late distal tubule? What makes up the late distal tubule?
|
aldosterone and ADH control.
Late distal tubule made up by principal cells and intercalated cells (acid base regulation) |
|
|
What causes type 1 RTA and what is the pathophysiology?
|
Caused by Sjogrens/SLE/RA, ampho B, lithium.
Distal RTA, problem with H+/ATP-ase in intercalated cells in distal urine -- fail to acidify urine, so will see alkaline urine. |
|
|
How does type 1 RTA present?
|
Presents with hypokalemia, hypercalciuria and kidney stones. Urine is alkaline.
|
|
|
What causes type 2 RTA? How does it present?
How do you treat it? |
MM, CA inhibitors, amyloidosis. Proximal tubule disruption.
Presents with hypoK and as Fanconi syndrome (glucose, amino acid, Mg, Phos wasting). Treat with bicarb, vit D, K+ replacement. |
|
|
What causes type 4 RTA?
How do you treat it? |
aldosterone resistance in distal tubule. Common causes: decreased renin (DM nephropathy, ACEi, NSAIDs, chronic interstitial nephritis), aldactone.
Not with florinef bc it is too potent. Treat with dietary restriction of sodium, or with bicarb. Can use lasix. |
|
|
What is the underlying acid base disturbance common to all RTA's? When to suspect RTA specifically when looking at BMP?
|
Non-gap metabolic acidosis
Suspect this when Cl- values are high (disproportionate to Na) |
|
|
What does heparin do to potassium?
|
Heparin will inhibit aldosterone, thus increasing potassium level.
|
|
|
What do NSAIDs do to potassium?
|
NSAID's inhibit prostaglandins --> decrease GFR --> increase renin production --> hypokalemia, especially in patients with CHF (reduced circulating volume).
Also inhibit prostaglandin-mediated renin release from JGA --> hyperkalemia, especially in diseased kidneys. |
|
|
What does bactrim do to K+?
Cisplatin? Pcn's? Liddle's, Barrter's, and Gitelman's disease? |
Bactrim- hyperK+
Cisplatin and Pcn- hypoK+ Liddle, Barter, Gitelman's- hypoK+ |
|
|
When is IV calcium given in hyperK treatment?
|
Only if EKG changes (except if on digoxin, treat only if there is a wide QRS bc of potential for dig toxicity)
|
|
|
What is something to be wary of with kayexalate? What about with bicarb infusions?
|
It has been associated with colon necrosis, especially post-op and in ileus.
Bicarb infusions can cause edema and may precipitate cardiac abnormalities. |
|
|
When working up hypoK, what is the first step?
|
non-anion gap MA or metabolic alkalosis/htn?
if the first, then either diarrhea or Type 1/2 RTA. if metabolic alkalosis/htn then hyperaldosteronism, diuretics (then Urine Na not helpful), Cushing syndrome |
|
|
How do you screen for primary vs secondary hyperaldo?
What can interfere with this screen? |
PAC (plasma aldosterone) : PRA (plasma renin).. PAC:PRA ratio.
BB and ACEi interfere with the test. |
|
|
What is the next step if primary hyperaldo is suspected? If secondary?
|
Primary- confirm dx by giving NS infusion or salt load and seeing that PAC is not suppressed.
Secondary- go straight to renal angiography or CT angio |
|
|
What are differentiating features of Liddle, Bartter, and Gitelman's syndromes?
|
All have hypokalemia and metabolic alkalosis (also on ddx for this is hyperaldo and diuretics and Cushing)
Liddle- will have htn Bartter- no htn, childhood, deafness Gitelman's- no htn, later presentation, significant low Mg |
|
|
What electrolyte disturbance to watch for in patients getting massive whole blood transfusions or plasma exchange?
|
Hypocalcemia - ionized fxn is reduced but plasma concentration normal
|
|
|
What condition is secondary hyperPTH seen in and why?
|
CKD, because decreased renal conversion of 25 to 1,25 vit D
|
|
|
What should prompt workup for secondary htn besides malignant, refractory, abnormal labs?
|
Continuous bruits (not just systolic), age < 30 or > 55
|
|
|
What are the 4 types of diuretics and where do they work?
|
CA inhibitors- proximal tubule (Na/H transport)
Loop diuretics- ascending loop of Henle Thiazides- early distal tubule (Na/Cl) K-sparing- Na/K in principal cells of late distal tubule |
|
|
What are the 3 actions of angiotensin II?
|
Direct vasoconstriction, aldosterone release, and sympathetic activation
|
|
|
What trial studied effects of ACEi+ARB for hypertension? What did it show?
|
ONTARGET trial showed increased adverse effects
|
|
|
How should ACEi/ARB be used in bilateral renal artery stenosis? What increase in Cr is tolerable with ACEi?
What are side effects of renin inhibitors (aliskiren)? |
Avoid in patients with this.
Tolerate 30% Cr increase in 6 weeks. Aliskiren side effects- teratogen, diarrhea, angioedema. |
|
|
Which CCBs are non-dihidropyridines and what is the difference?
Which CCB should not be used in diabetes/CKD? |
Verapamil and dilt -- these also depress cardiac contractility and reduce HR
Dihydropyridines (amlodipine etc) should not be used bc it will worsen proteinuria. |
|
|
What are effects of monotherapy w/BB without post-MI, CHF, afib, angina?
|
Should not be used-- increased risk of stroke and CVD in patients older than 60.
|
|
|
When are 2 drugs as initial treatment recommended for htn?
|
In patients with BP > 160/100
|
|
|
What drugs are used to treat LVH?
|
ACEi/ARB, CCB
not BB or hydralazine |
|
|
What is goal BP for essential htn w/o DM/CAD/CKD? What if with DM/CAD/CKD? How about if proteinuria?
|
If htn w/o comorbidities-- 140/90
If htn w/comorbidities- 130/80 If htn w/proteinuria- 130/85 |
|
|
What is the Rx goal of malignant htn or hypertensive encephalopathy?
|
Rapid decrease of DBP to 100-105 mmHg w/in a few hours, but not reducing presenting BP by > 25%.
|
|
|
What does fibromuscular dysplasia look like on renal angiogram?
|
String of beads with multiple, little aneurysmal dilatations
|
|
|
How do you treat scleroderma renal crisis?
|
ACE inhibitor
|
|
|
What are the causes of primary hyperaldosteronism? How do you manage them?
|
idiopathic b/l adrenal hyperplasia (25%) and Conn syndrome (70%)
bilateral hyperplasia- K sparing diurietics alone (bc b/l adrenalectomy resolves htn in only 1/3 of the patients) Conn syndrome- surgery |
|
|
What tissue do pheo's arise from?
What percent are bilateral? Malignant? Familial? |
Chromaffin tissue, mostly in adrenal medulla.
10% of pheo's are bilateral, 10% are malignant, and 10% are familial. |
|
|
How do you screen for pheo?
|
24h urine for fractionated metanephrine and catecholamines.
|
|
|
What is the definition of preeclampisa? Gestational htn?
|
Htn + proteinuria after the 20th week of gestation.
Gestational htn- just htn (no proteinuria) after 20th week of pregnancy |
|
|
What is the goal of treating elevated BP in pregnancy?
|
Goal is to prevent stroke (BP treatment does not affect the outcome of preeclampsia).
|
|
|
Women who have chronic htn and are pregnant -- how to manage their htn?
When to treat htn in pregnancy? What should the goal be? |
If htn is controlled (less than 120/80), they should be taken off BP meds (bc too low BP will cause IUGR).
Only if SBP > 150 or DBZP > 95 Goal should be 130/80 at the lowest |
|
|
What are 2 important causes of htn that should be excluded in a young patient that does not have renovascular htn, pheo, Cushing syndrome?
|
OCP's and coarctation
|
|
|
What should you suspect in a patient who had recent coronary angiogram and now stepwise progression of renal failure, abdominal pain, livedo reticularis? What can you see in the eyes? On labs? Is biopsy helpful? Treatment of this condition?
|
Cholesterol emboli.
Hollenhorst plaques. Labs- eosinophils Biopsy can confirm the dx Treatment of this condition is supportive only - do not anticoagulate |
|
|
What is seen on u/a in hepatorenal syndrome? FeNa?
How do you treat HRS? |
u/a is normal. FeNa is low.
Treat HRS with midodrine and octreotide until liver tx. |
|
|
In what situations do you see papillary necrosis?
|
Pyogenic kidneys with postrenal obstruction, chronic NSAID abuse, sickle cell disease
|
|
|
What are renal side effects of cisplatin? Aminoglycosides? AmphoB?
|
ATN and hypomagnesemia.
Aminoglycosides also cause ATN and hypomagnesemia. Ampho B causes ATN, Type 1 or 2 RTA |
|
|
How does the presentation of NSAID-induced AIN differ from other drug causes of AIN?
|
-requires months of NSAID ingestion
-rash, fever, eos are frequently absent -nephrotic range proteinuria and histo looks like minimal change disease |
|
|
What does combining tylenol with ASA put you at risk for?
|
Papillary necrosis (can have AIN or chronic interstitial nephritis).
Nephrotic range proteinuria 2/2 NSAIDs is a hint that it is acute |
|
|
What drugs can cause intratubular obstruction?
|
Acyclovir, ganciclovir, bactrim, sulfa, MTX, indinavir
(these drugs crystallize in urine) |
|
|
Besides NSAIDs, what else can cause chronic interstital nephritis?
What else can this culprit cause? |
Lead toxicity (check urine lead level).
Nephrogenic DI |
|
|
How is infection risk affected by having nephrotic syndrome? What about thyroid and iron? Risk for clots?
|
Infection risk is increased because of hypogammaglobulinemia
-also low thyroid and iron levels. Clots: Loss of antithrombin so they are hypercoagulable - risk for PE and renal vein thrombosis. |
|
|
How to approach classification of glomerular diseases?
|
1)Nephritic or Nephrotic?
2)If nephritic, is complement low or normal? 3)If nephrotic, does patient have systemic disorder or primarily kidney? |
|
|
When is complement level normal in nephritic syndrome?
When is complement level low in nephritic syndrome? |
complement level is normal in (5): IgA nephropathy, Alport, vasculitides, Anti-GBM, and TTP/HUS
Complement level is low in nephritic syndrome (2) in Post-infectious GN, MPGN (idiopathic, endocarditis, cryo) |
|
|
If nephrotic syndrome, which disease are systemic and which are mainly kidney?
|
Systemic (3)- DM, AL Amyloidosis and AM amyloidosis
Kidney (3)- MInimal change, FSGS, MGN |
|
|
What are causes of MPGN?
|
idiopathic, SLE, endocarditis, cryoglobulinemia
|
|
|
What is tram tracking associated with? What is subendothelial humps associated with?
|
tram tracking- MPGN
subendothelial humps- PIGN |
|
|
How does MPGN differentiate itself from post-infectious GN (w/o biopsy)?
|
In MPGN, the low C3 level stays low indefinitely.
In PIGN, the low C3 level returns to normal after 2-3 months. |
|
|
What should you do if you suspect MPGN? Why?
|
Get a renal biopsy. It frequently causes renal failure.
|
|
|
What is the most common cause of glomerulonephritis? What demograhic?
|
IgA nephropathy - more common in male Asians
|
|
|
When does hematuria with IgA nephropathy occur?
|
During a viral illness or just after exercise.
|
|
|
What is seen on histology with IgA nephropathy?
|
IgA and C3 deposition (however serum C3 is normal)
|
|
|
What is the management of IgA nephropathy?
What is the prognosis of IgA nephropathy? |
Management is ACEi for proteinuria, steroids if severe.
It is relatively benign, but can get worse if proteinuria is existent. Renal biopsy confirms diagnosis, use this in severe presentation. |
|
|
What is the inheritance of Alport syndrome?
|
Alport syndrome is X-linked
|
|
|
What is the difference between anti-GBM disease and Goodpasture's?
|
Anti-GBM disease refers to only renal disease.
|
|
|
How do you treat Goodpasture's?
|
Plasma exchange, steroids, cytoxan
|
|
|
How do you treat RPGN?
|
high dose steroids, cytoxan, plasma exchange (if pulmonary hemorrhage)
|
|
|
What drugs are associated with minimal change disease? What diseases?
|
Drugs- NSAIDs, lithium, sulfa
Diseases- Lymphoma, contact allergies |
|
|
What does urine sediment show in MCD?
|
Oval fat bodies that appear as Maltese crosses under polarized light
|
|
|
How do you treat MCD?
|
steroids +/- cytoxan or cyclosporine
|
|
|
What is the most common cause of idiopathic nephrotic syndrome in blacks? Nephrotic syndrome in general?
|
FSGS
Diabetes |
|
|
What are risk factors for FSGS?
|
HIV, Heroin, obesity, sickle cell, leukemia, chronic VUR; or just idiopathic
|
|
|
Why is it important to differentiate idiopathic FSGS from other causes of it?
|
Primary disease often responds to steroids unlike secondary disease.
|
|
|
What are causes of membranous nephropathy? Who gets idiopathic MN most frequently?
|
Causes are idiopathic (white men > 40yo), chronic HBV, Drugs (NSAIDs, pcn, gold), solid tumors, autoimmune thyroiditis and SLE
|
|
|
What type of nephrotic syndrome is associated with htn?
|
FSGS
|
|
|
What is the treatment for membranous nephropathy?
|
Steroids +/- cytoxan
|
|
|
Which nephrotic disease is associated with type 4 RTA?
|
Diabetic nephropathy
|
|
|
Which diabetics who develop nephropathy should get a renal biopsy?
|
The ones without preceding retinopathy
|
|
|
What kind of nephropathy does amyloid cause and what does it resemble? What is characteristic about amyloid nephropathy?
|
Light chain nephropathy, resembles diabetic nephropathy (kimmelstiel wilson nodules)
Light chain nephropathy - Congro red stain causes apple-green birefringence |
|
|
What is AL amyloidosis associated with?
AA amyloidosis? |
Multiple myeloma (but this is different from light chain disease associated with MM)
AA amyloidosis is seen in chronic inflammation (rheumatoid arthritis, recurrent skin infections in IV drug users who 'skin pop') |
|
|
How do you treat nephrotic syndromes? (except which two)?
What about nephritic syndromes? |
steroids, except for DM and AA, AL amyloid.
-steroids for - FSGS, MGN, MCD Nephritic syndrome steroids+cytoxan (esp RPGN) |
|
|
What is the number one cause of death in patients with CKD?
|
heart disease
|
|
|
What is stage 2 CKD?
|
Minimally depressed GFR (60-90) + proteinuria
|
|
|
At what point in renal disease is calcium-based PO4 binder good (e.g. phoslo/calcium acetate)? At what point is it better to have renagel/sevelamer?
|
Phoslo is better earlier on because it supplements calcium so that PTH doesn't get very high -- over time PTH will start to drop though and then it is useful to have renagel to prevent adynamic bone (low bone turnover).
|
|
|
What are the three types of bone disorders patients with CKD can get secondary to hyperphosphatemia? Which is most common in dialysis patients?
|
Renal osteodystrophy (PTH high aka secondary hyperPTH)
Adynamic bone disease (PTH low) Osteomalacia (uncommon - 2/2 Vit D deficiency from aluminum toxicity from aluminum containing phos binders) Adynamic bone disease is most common in HD patients (sequale of treating renal osteodystrophy) |
|
|
What is management of renal osteodystrophy?
|
Vit D, phos binder (phoslo initially), +/- cinacalcet (increases PTH receptor sensitivity to calcium)
|
|
|
What is goal hgb when treating patient with CKD anemia?
|
Hgb target should be 11-12
|
|
|
What is the difference in mechanism and contraindications for gout treatment with allopurinol vs with probenecid?
|
Allopurinol decreases uric acid production
Probenecid increases renal excretion or uric acid -- contraindicated in CKD |
|
|
What are biggest concerns to monitor for in intraperitoneal dialysis?
|
Infection (Gram positive first, then Gram negative), and protein deficiency (need high protein diet)
|
|
|
What is the triple therapy most renal transplant patients are on?
|
calcineurin inhibitor (either cyclosporine or prograf)/rapamune, cellcept (or azathioprine), and steroid
|
|
|
What is the interaction between allopurinol and azathioprine? Between allopurinol and cellcept?
|
Allopurinol and imuran - allopurinol will increase levels of imuran
Allopurinol and cellcept- none |
|
|
What are side effects of cyclosporine?
|
tremors/CNS, liver toxicitiy, gum hypertrophy. nephrotoxicity.
|
|
|
What are side effects of prograf?
What are side effects of rapamune? What are side effects of cellcept? |
prograf- diabetogenic and nephrotoxic.
rapamune- wound dehiscence, lymphoma, and hyperlipidemia, nephrotoxic. cellcept- GI with some BM suppression, nephrotoxic. |
|
|
What diseases should be considered in differential for any patient with persistent microscopic hematuria that worsens after an infection?
|
Alport syndrome, post-infectious, IgA nephropathy.
|
|
|
What is seen on pathology of renal biopsy in Alport syndrome?
|
basement membrane - type IV collagen defect
|
|
|
ADPKD presents at what age? Also what other organs are affected? Screen?
|
Presents at age 20. Patients get cysts of the kidneys, liver, pancreas, berry aneurysms in brain (but only screen if symptomatic or high risk)
|
|
|
What do you do with an asymptomatic patient who presents for routine visit and has a FH of PCKD?
|
Renal ultrasound to screen
|
|
|
What is medullary cystic disease - risk factors and presentation?
|
Risk factor- genetic
Presentation- CKD/renal failure with normal urinalysis |
|
|
What are the types and prevalences of renal stones?
|
2/3 of renal stones are either calcium phosphate or calcium oxalate.
1/3 of renal stones are either struvite or uric acid |
|
|
What type of stones do patients with HIV/AIDS on indinavir get?
|
indinavir stones
|
|
|
What is the imaging modality of choice for kidney stone?
|
Helical CT
|
|
|
How much urine should be targeted to be made after first stone?
|
2 liters/day
|
|
|
What further workup should be done after 2nd stone occurs?
|
Urine studies:
-high = stone inducers in: oxalate, uric acid, calcium -low = stone inducer in: citrate |
|
|
What are risk factors for calcium phosphate stones?
|
primary hyperPTH, acetazolamide, Type 1 RTA
|
|
|
What is a risk factor for calcium oxalate stones?
|
Steatorrhea (FFA binds calcium so that oxalate is urinated) like in Crohn's disease.
High uric acid levels in urine, too |
|
|
How do you treat calcium stones?
|
fluids, HCTZ, potassium citrate, treat high uric acid.
do not decrease calcium intake (this will increase oxaluria). |
|
|
How do you treat struvite stones?
|
remove stones, acidify the urine, and abx for proteus mirabilis and klebsiella
|
|
|
What do calcium oxalate crystals look like in urine? struvite crystals? cystine crystals?
|
Calcium oxalate- squares in urine
Struvite crystals- coffin lids Cystine crystals- clear, hexagonal crystals |
|
|
How do you treat cystine stones?
|
Fluids and alkalnize urine (as opposed to struvite stones)
|
|
|
What are RF's for and how do you treat uric acid stones?
|
RF's- myeloproliferative syndromes, chemotherapy
Treat with allopurinol +/- urinary alkalinization |
|
|
What types of stones require urinary acidification instead of alkalinization?
|
struvite and calcium phosphate stones require urinary acidification.
|
|
|
What are features of a simple renal cyst? What if it is not simple?
|
well-defined margin, dense surrounding tissues, no echoes.
if not simple -- surgical exploration is indicated to r/o cancer |
