Nephrology Flashcards
what is the mnemonic for IgA vasculitis?
what is the tx?
Palpable purpura Abdominal Pain Arthritis**** Hematuria >>> IgA nephritis
tx: supportive (bc its usually in children; baby wants his PAPAH)
intusseption is associated with which nephritis?
IgA vasculitis» IgA complex deposits in kidney> nephritis
Purpura Abdominal Pain (intusseption) Arthritis He matures
Priapism is a urologic emergency due to blood clotting/getting stuck in the penis>necrosis.
What is the 1st line in management?
What is injected after?
aspiration of blood from the corpus cavernous
THEN
injection of alpha agonists (vasoconstriction)
how do multiple blood transfusions»_space; hypocalcemia?
too many blood transfusions» citrate toxicity
citrate is an anticoagulant used in transfused blood products
Citrate binds to calcium & depletes it!!
1st line for prevention of diabetic nephropathy is either ACEi or ARB (NOT both>AKI)
what additional med can be added to enhance the effects of ACEi or ARB and therefore decrease risk of diabetic nephropathy?
CCBssssss
what does Intravenous pyelography evaluate for?
RENAL injury only.
what examine finding and visual dx tool is used to evaluate for urethral injury?
foley catheter placement (if successful = NO urethral injury)
retrograde urethrography (shows fluid extravasation at urethral injury)
protocol for evaluating GU injury
look at
urethra, bladder, ureters, kidney (in this exact order)
what are the 3 main criteria for dx of Potter sequence
combination of oligohydramnios, bilateral hydronephrosis, and respiratory distress
what dx test is used for evaluation of Potter sequence & why?
Voiding cystourethrogram
the most common cause of bilateral hydronephrosis in potter sequence (or period) = posterior urethral valve.
A voiding cystourethrogram allows us to see that there’s a obvious blockage when fetus tries to void/urinate
in RTA, what is the function of the distal tubule ?
the DISTAL tubule MAKES BICARB.
what is the electrolyte abnormality in all RTA ?
NON-AG HYPERCHLOREMIC metabolic acidosis
no anion gap bc Chloride rises
in RTA, what is the function of the Proximal tubule?
the proximal tubule RE-ABSORBS BICARB into the serum :)
Which RTA presents with an inability to secrete H+ from the serum & why?
RTA 1 (gun) @ distal tubule.
distal tubule can not make enough bicarb> no H+ secreted into the urine == all H+ stays in serum == metabolic acidosis
which RTA has a urine pH >5.5? Why?
RTA 1 (gun) @ distal tubule.
no H+ is secreted in the urine (bc no Bicarb is made at the distal tubule)
== alkalotic urine
Which RTA presents with urine pH <5.5
RTA 2 (shoe) @ proximal tubule.
proximal tubule is NOT reabsorbing Bicarb> serum acidosis
»> DCT decides to increase H+ secretion in attempt to correct serum metabolic acidosis == more H+ secreted into urine = acidic urine
which RTA does Nephrocalcinosis (calcified kidney) occur in & why?
RTA 1 (gun).
alkalized urine allows Calcium Oxalate & Phosphate stones to form in kidneys> nephrocalcinosis
how do you tx RTA 1 ?
give Bicarb!
in RTA 1 (gun); the DCT is not making any Bicarb = no acid is being excreted in to urine
- if yo uadmin Bicarb, the body will secrete H+ into urine & there will no longer be nonAG hyperchloremic metabolic acidosis
Fanconi syndrome is RTA 2 on steroids/beast mode.
what electrolytes are lost in regular RTA 2 vs Fanconi syndrome?
RTA = low bicarb & hypokalemia
Fanconi:
increased excretion of glucose, phosphate, amino acids, bicarbonate, uric acid, sodium, potassium, and water
why does Fanconi syndrome cause osteomalacia?
decreased reabs of phosphate> hypophosphatemia»_space;
Vitamin D-resistant hypophosphatemic rickets/osteomalacia
aka: no matter how much Vit D you give, the pt will have rickets/osteomalacia bc PTH is pullling calcium out of bones while tring to increase serum Phos + cal
what are the electrolyte findings in RTA 4
@ collecting tubule; RTA4 = hypoaldosteronism = HYPERkalemic metabolic acidosis
what drug is used to treat RTA 2 and why?
what form of therapy is used in RTA 2?
Thiazides; they cause reabsorption of Bicarb
alkali therapy + potassium citrate
what is the mnemonic for SLE?
Rash (malar/discoid)
Arthritis
Serositis
Hematologic probs (anemia, cytopenia)
Oral ulcers
Renal failure
Photosensitivity
Anti nuclear ABs
Immunoglobulins decreased C3/C4
Neuro (seizure, personality, depression, psychosis)
what shape are uric acid stones?
rhomboid shape
which stones are radiolucent akadont show on Xray?
uric acid stones
how do you tx uric acid stones?
give potassium citrate to alkalinize urine> stone will desolve
what are the only stones that LOVE/LAUGH/LIVE for alkaline urine?
Calciyum alkaline urine
- calcium phosphate
- calcium oxalate
what do Hyaline & Waxy renal casts represent?
Hyaline = dehydrated
Waxy = Chronic RF
what kind of AKI does Tacrolimus cause?
why?
Pre-Renal AKI (dec blood flow)
Tacrolimus is a vasoconstrictor> dec blod flow to kidneys = Pre-renal nephrotoxicity
how do NSAIDs and ACEi/ARBs cause Pre-renal AKI?
NSAIDs (constrict afferent arteriole= no blood in)
ACEI/ARB (efferent arteriole vasodilation= blood flies out before it is reasborbed)
Contrast is the fastest cause of interstitial AKI.
What is the UA findings?
& why is it different than the traditional interstitial AKI UA findings?
Contrast» afferent arteriole spasm> HIGH reabsorption of H20 & Na:
- low Urine FeNa, low Urine Na
- high Urine Osm (bc water stays in body> hyperconcentrated urine)
Tumor lysis syndrome (TLS) = hyperuricemia, hyperphosphatemia, & hypocalcemia.
why is the calcium low in TLS? *its the same reason for why its low in rhabdo ;) *
Phosphate loves Calcium (the same why Oxalate loves Calcium).
When either phosphate or oxalate is high, calcium is low bc they both bind to it»_space; secondary hypocalcemia +++ precipitates in kidney as stones
What is ethylene glycol used for?
Ethylene glycol precipitates as what kind of stones in the kidney?
= a sweet-tasting fluid used in radiators to stop engines from freezing! (aka ingestion of ANTI-freeze)
ethylene glycol metabolizes to oxalate» calcium oxalate stones & hypocalcemia
what shape are Calcium OXALATE stones?
Envelope shape
why do you never replinish the calcium in pts w/ hypocalcemia from rhabdo?
In rhabdo, calcium binds to damaged muscles = dec in calcium circulation
when muscles revive, the calcium detaches from them & goes back into circulation
renal papillary necrosis only occurs in patients predisposed to….
pts w/ have vascular insufficiency:
- on chronic NSAIDs
- chronic dehydration (SCD/SCT)
- DM, CAD
what is the MAIN drive of hypernatremia?
a hyperosmolar state! (serum is very cooncentrated)
The causes of Hyper-natremia are broken into 2 categories:
Intrarenal (Urine osm <600; happens @ level of kidneys)
Extrarenal (urine osm >600= functioning kidney)
how does Hyper-natremia» intracranial hemorrhage?
high serum solute in hypernatremia drives fluid out of brain tissue> brain shrinkage & vessel rupture
Give examples of intra-renal Hypernatremia (Urine Osm <600)
Hypovolemia
- drug diuresis (lithium, demeoclocycline)
- osmotic diuresis (HHS, DM, manitol/urea)
Euvolemia
- DI (central, nephrogenic)
Hypervolemia
- Hyperaldosteronism (Conn syn or Cushing syn)
Give examples of extra-renal Hypernatremia (Urine Osm >600)
hypovolemia:
- GI loss (V/D/NG tube)
- dehydration (PNA, skin burns, excessive sweating)
Hypervolemia
- excess salt intake (IV saline fluids, soy sauce)
Euvolemia
- low water intake (immobility, dementia)
what is the 2 step treatment protocol for hypovolemic hypernatremia?
- REPLINISH volume with 0.9% = NORMAL SALINE = isotonic (will not effect solute conc/inc serum sodium levels).
* we do this first to prevent shock from hypovolemia> MI/cerebral ischemia* - lower sodium w/ 5% dextrose IN 0.45% saline = hypotonic solution (will dilute the serum to lower the serum sodium level)
How do you approach dx the cause of Hyponatremia?
1) Volume status. Is the pt hypervolemic (edema), euvolemic, or hypovolemic (dec skin turgor, dry MM)
2) Osmolality volumes (serum, urine, urine sodium excretion)
what is the urine sodium level in a pt with SIADH? what is the pathophys?
patients with SIADH are EUVOLEMIC === NO RAAS ACTIVATION== NO serum sodium retention
there will be nl to HIGH urine sodium excretion (> 20 mEq/L).
what is the protocol for increasing serum sodium in hyponatremic pts to prevent central pontine myelin-o-lysis?
maximum increase of 10–12 mmol/L of sodium within 24 hours
or
0.5 mmol/L/hour
why is SIADH inappropriate?
the ADH is high> low serum osm & high urine osm == makes sense
BUT
the urine sodium is HIGH (despite high levels of ADH, pt is still euvolemic= NO RAAS telling body not to let go of H20/sodium)
what is the classic symptoms that hyperkalemia AND hypokalemia share?
cardiac arrhythmias (VFib) Muscle weakness Decreased deep tendon reflexes
what are the differences in GI symptoms between hyperkalemia & hypokalemia?
hyperkalemia = paralytic ILEUS
hypokalemia = constipation
what are the cause of secondary hypertension using the mnemonic R.E.C.E.N.T
R= renal (RAS, ) E= endocrine (conn syndrome, cushing syndrome, pheochromocytoma, hypokalemia) C= coartaction of the aorta E= estrogen (OCPs) N= neuro for IIH T= tx (NSAIDs, exogenous steroids)
what is always the lab & imaging workup for secondary hypertension?
check renin-aldosterone levels
check cortisol levels
check serum metanephrine
renal ULSTRASOUND!!!!!!
what is a vesicostomy?
when is a vesicostomy indicated?
its a suprapubic catheter!
when a pt CANT PEE (posterior urethra valve or neurogenic bladder)
what is the more common cause of UTIs in infant males?
what is the best way to prevent morbidity of UTIs in these pts?
urinary tract malformations
daily AB therapy!!!
explain the pathophys of the renin-angiotensin-aldosterone system.
the juxtaglomerular cells in kidney sense dec Na/blood flow & increased sympathetic tone.
kidneys secrete RENIN. renin converts angiotensinogen (from liver) to angiotensin 1.
ACE (from lungs) converts angiotensin 1> angiotensin 2
Angiotensin 2 tells the adrenals to ~WERK~ by producing aldosterone
explain the following labs in primary hyperaldosteronism :
aldosterone renin sodium potassium bicarb serum state (alkalosis or acidosis)
HIGH aldosterone
LOW renin (high aldo has negative FBL on renin> increased renin to aldosterone ration)
high sodium
low potassium
HIGH bicarb (aldo excreted K+ and H+ from body to preserve Na= metabolic alkalosis )
what etiology causes a HIGH renin and aldosterone @ the same time (ie Negative FBL doesnt occur)?
when theres a DEC renal bood flow. this will increase renin> inc in aldosterone. But since RBF does not improve, Renin will remain high
firstline management for urethral strictures?
2nd line/when first line fails?
internal urethrotomy = non-invasive, outpt procedure to cut (-OTOMY) the stricture
urethroplasty= invasive surgical procedure to reconstruct (-PLASTY) the entire urethra
a plateau curve on uroflowmetry suggests?
a widened, bell shaped curve on uroflowmetry suggests?
an irregular/wavy curve on uroflowmetry suggests?
urethral sphincter
BPH
detrussor-sphincter dyssynergia
what 2 ABs are used in tx of acute prostatitis ?
ciprofloxacin & TMP/SMX (bactrim/)
what clinical symptoms/PE findings differentiate acute and chronic bacterial prostatitis?
acute= high spiking fevers, UTI sym, & painfully tender prostate exam
chronic= \+/- B symptoms normal prostate exam \++ UTI signs blood in semen erectile dysfunction
clinical presentation & tx of Chronic Pelvic Pain syndrome
MALES only.
- months of PAIN in lower abd, back, thighs, perineum/penis/scrotum
- pain w/ ejaculation & bloody semen
tx:
Alpha blockers (e.g., tamsulosin, doxazosin) relax muscles
5-alpha-reductase inhibitors (e.g., finasteride) reduces prostate size
what AB causes RTA IV & how?
Trimethoprim in LARGE doses»_space; Hyperkalemia == RTA 4
what are the normal age related effects on erection?
As males get older:
- takes longer to get erected
- orgasms aren’t as intense
difficulty maintaining an erection = ABNORMAL
Pts should only be on an indwelling catheter for ~3 days before switching to what safer (less CAUTIs) form of bladder management ?
CLEAN intermittent catheterization (CIC) 4-6 times daily with HAND WASHING
what drugs tx ethylene glycol poisoning ?
1 Fomepizole: inhibits alcohol dehydrogenase = no conversion of formaldehyde to formic acid (the TOXIN that causes death in eythlene glycol poisoning)
2nd line: Ethanol= BINDS with high affinity to alcohol dehydrogenase so no conversion activity
all tetracyclines are eliminated renally (& therefore should be avoided in RF) except for what drug?
Doxycycline= GI elimination (doxycycline is the only tetracycline that is SAFE IN RENAL FAILURE)
