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STEP2 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

what is the mnemonic for IgA vasculitis?

what is the tx?

A 
Palpable purpura
Abdominal 
Pain 
Arthritis****
Hematuria >>> IgA nephritis

tx: supportive (bc its usually in children; baby wants his PAPAH)

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2
Q

intusseption is associated with which nephritis?

A

IgA vasculitis» IgA complex deposits in kidney> nephritis

Purpura
Abdominal 
Pain (intusseption) 
Arthritis 
He matures
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3
Q

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?

A

aspiration of blood from the corpus cavernous

THEN

injection of alpha agonists (vasoconstriction)

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4
Q

how do multiple blood transfusions&raquo_space; hypocalcemia?

A

too many blood transfusions» citrate toxicity

citrate is an anticoagulant used in transfused blood products

Citrate binds to calcium & depletes it!!

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5
Q

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?

A

CCBssssss

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6
Q

what does Intravenous pyelography evaluate for?

A

RENAL injury only.

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7
Q

what examine finding and visual dx tool is used to evaluate for urethral injury?

A

foley catheter placement (if successful = NO urethral injury)

retrograde urethrography (shows fluid extravasation at urethral injury)

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8
Q

protocol for evaluating GU injury

A

look at

urethra, bladder, ureters, kidney (in this exact order)

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9
Q

what are the 3 main criteria for dx of Potter sequence

A

combination of oligohydramnios, bilateral hydronephrosis, and respiratory distress

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10
Q

what dx test is used for evaluation of Potter sequence & why?

A

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

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11
Q

in RTA, what is the function of the distal tubule ?

A

the DISTAL tubule MAKES BICARB.

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12
Q

what is the electrolyte abnormality in all RTA ?

A

NON-AG HYPERCHLOREMIC metabolic acidosis

no anion gap bc Chloride rises

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13
Q

in RTA, what is the function of the Proximal tubule?

A

the proximal tubule RE-ABSORBS BICARB into the serum :)

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14
Q

Which RTA presents with an inability to secrete H+ from the serum & why?

A

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

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15
Q

which RTA has a urine pH >5.5? Why?

A

RTA 1 (gun) @ distal tubule.
no H+ is secreted in the urine (bc no Bicarb is made at the distal tubule)
== alkalotic urine

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16
Q

Which RTA presents with urine pH <5.5

A

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

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17
Q

which RTA does Nephrocalcinosis (calcified kidney) occur in & why?

A

RTA 1 (gun).

alkalized urine allows Calcium Oxalate & Phosphate stones to form in kidneys> nephrocalcinosis

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18
Q

how do you tx RTA 1 ?

A

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

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19
Q

Fanconi syndrome is RTA 2 on steroids/beast mode.

what electrolytes are lost in regular RTA 2 vs Fanconi syndrome?

A

RTA = low bicarb & hypokalemia

Fanconi:
increased excretion of glucose, phosphate, amino acids, bicarbonate, uric acid, sodium, potassium, and water

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20
Q

why does Fanconi syndrome cause osteomalacia?

A

decreased reabs of phosphate> hypophosphatemia&raquo_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

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21
Q

what are the electrolyte findings in RTA 4

A

@ collecting tubule; RTA4 = hypoaldosteronism = HYPERkalemic metabolic acidosis

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22
Q

what drug is used to treat RTA 2 and why?

what form of therapy is used in RTA 2?

A

Thiazides; they cause reabsorption of Bicarb

alkali therapy + potassium citrate

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23
Q

what is the mnemonic for SLE?

A

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)

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24
Q

what shape are uric acid stones?

A

rhomboid shape

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25
Q

which stones are radiolucent akadont show on Xray?

A

uric acid stones

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26
Q

how do you tx uric acid stones?

A

give potassium citrate to alkalinize urine> stone will desolve

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27
Q

what are the only stones that LOVE/LAUGH/LIVE for alkaline urine?

A

Calciyum alkaline urine

  • calcium phosphate
  • calcium oxalate
28
Q

what do Hyaline & Waxy renal casts represent?

A

Hyaline = dehydrated

Waxy = Chronic RF

29
Q

what kind of AKI does Tacrolimus cause?

why?

A

Pre-Renal AKI (dec blood flow)

Tacrolimus is a vasoconstrictor> dec blod flow to kidneys = Pre-renal nephrotoxicity

30
Q

how do NSAIDs and ACEi/ARBs cause Pre-renal AKI?

A

NSAIDs (constrict afferent arteriole= no blood in)

ACEI/ARB (efferent arteriole vasodilation= blood flies out before it is reasborbed)

31
Q

Contrast is the fastest cause of interstitial AKI.

What is the UA findings?

& why is it different than the traditional interstitial AKI UA findings?

A

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)
32
Q

Tumor lysis syndrome (TLS) = hyperuricemia, hyperphosphatemia, & hypocalcemia.

why is the calcium low in TLS? *its the same reason for why its low in rhabdo ;) *

A

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&raquo_space; secondary hypocalcemia +++ precipitates in kidney as stones

33
Q

What is ethylene glycol used for?

Ethylene glycol precipitates as what kind of stones in the kidney?

A

= 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

34
Q

what shape are Calcium OXALATE stones?

A

Envelope shape

35
Q

why do you never replinish the calcium in pts w/ hypocalcemia from rhabdo?

A

In rhabdo, calcium binds to damaged muscles = dec in calcium circulation

when muscles revive, the calcium detaches from them & goes back into circulation

36
Q

renal papillary necrosis only occurs in patients predisposed to….

A

pts w/ have vascular insufficiency:

  • on chronic NSAIDs
  • chronic dehydration (SCD/SCT)
  • DM, CAD
37
Q

what is the MAIN drive of hypernatremia?

A

a hyperosmolar state! (serum is very cooncentrated)

38
Q

The causes of Hyper-natremia are broken into 2 categories:

A

Intrarenal (Urine osm <600; happens @ level of kidneys)

Extrarenal (urine osm >600= functioning kidney)

39
Q

how does Hyper-natremia» intracranial hemorrhage?

A

high serum solute in hypernatremia drives fluid out of brain tissue> brain shrinkage & vessel rupture

40
Q

Give examples of intra-renal Hypernatremia (Urine Osm <600)

A

Hypovolemia
- drug diuresis (lithium, demeoclocycline)
- osmotic diuresis (HHS, DM, manitol/urea)
Euvolemia
- DI (central, nephrogenic)
Hypervolemia
- Hyperaldosteronism (Conn syn or Cushing syn)

41
Q

Give examples of extra-renal Hypernatremia (Urine Osm >600)

A

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)

42
Q

what is the 2 step treatment protocol for hypovolemic hypernatremia?

A
  1. 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*
  2. lower sodium w/ 5% dextrose IN 0.45% saline = hypotonic solution (will dilute the serum to lower the serum sodium level)
43
Q

How do you approach dx the cause of Hyponatremia?

A

1) Volume status. Is the pt hypervolemic (edema), euvolemic, or hypovolemic (dec skin turgor, dry MM)
2) Osmolality volumes (serum, urine, urine sodium excretion)

44
Q

what is the urine sodium level in a pt with SIADH? what is the pathophys?

A

patients with SIADH are EUVOLEMIC === NO RAAS ACTIVATION== NO serum sodium retention

there will be nl to HIGH urine sodium excretion (> 20 mEq/L).

45
Q

what is the protocol for increasing serum sodium in hyponatremic pts to prevent central pontine myelin-o-lysis?

A

maximum increase of 10–12 mmol/L of sodium within 24 hours
or
0.5 mmol/L/hour

46
Q

why is SIADH inappropriate?

A

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)

47
Q

what is the classic symptoms that hyperkalemia AND hypokalemia share?

A 
cardiac arrhythmias (VFib)
Muscle weakness
Decreased deep tendon reflexes
48
Q

what are the differences in GI symptoms between hyperkalemia & hypokalemia?

A

hyperkalemia = paralytic ILEUS

hypokalemia = constipation

49
Q

what are the cause of secondary hypertension using the mnemonic R.E.C.E.N.T

A 
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)
50
Q

what is always the lab & imaging workup for secondary hypertension?

A

check renin-aldosterone levels
check cortisol levels
check serum metanephrine

renal ULSTRASOUND!!!!!!

51
Q

what is a vesicostomy?

when is a vesicostomy indicated?

A

its a suprapubic catheter!

when a pt CANT PEE (posterior urethra valve or neurogenic bladder)

52
Q

what is the more common cause of UTIs in infant males?

what is the best way to prevent morbidity of UTIs in these pts?

A

urinary tract malformations

daily AB therapy!!!

53
Q

explain the pathophys of the renin-angiotensin-aldosterone system.

A

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

54
Q

explain the following labs in primary hyperaldosteronism :

aldosterone
renin
sodium 
potassium
bicarb
serum state (alkalosis or acidosis)
A

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 )

55
Q

what etiology causes a HIGH renin and aldosterone @ the same time (ie Negative FBL doesnt occur)?

A

when theres a DEC renal bood flow. this will increase renin> inc in aldosterone. But since RBF does not improve, Renin will remain high

56
Q

firstline management for urethral strictures?

2nd line/when first line fails?

A

internal urethrotomy = non-invasive, outpt procedure to cut (-OTOMY) the stricture

urethroplasty= invasive surgical procedure to reconstruct (-PLASTY) the entire urethra

57
Q

a plateau curve on uroflowmetry suggests?

a widened, bell shaped curve on uroflowmetry suggests?

an irregular/wavy curve on uroflowmetry suggests?

A

urethral sphincter

BPH

detrussor-sphincter dyssynergia

58
Q

what 2 ABs are used in tx of acute prostatitis ?

A

ciprofloxacin & TMP/SMX (bactrim/)

59
Q

what clinical symptoms/PE findings differentiate acute and chronic bacterial prostatitis?

A

acute= high spiking fevers, UTI sym, & painfully tender prostate exam

chronic= 
\+/- B symptoms
normal prostate exam 
\++ UTI signs
blood in semen
erectile dysfunction
60
Q

clinical presentation & tx of Chronic Pelvic Pain syndrome

A

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

61
Q

what AB causes RTA IV & how?

A

Trimethoprim in LARGE doses&raquo_space; Hyperkalemia == RTA 4

62
Q

what are the normal age related effects on erection?

A

As males get older:

  • takes longer to get erected
  • orgasms aren’t as intense

difficulty maintaining an erection = ABNORMAL

63
Q

Pts should only be on an indwelling catheter for ~3 days before switching to what safer (less CAUTIs) form of bladder management ?

A

CLEAN intermittent catheterization (CIC) 4-6 times daily with HAND WASHING

64
Q

what drugs tx ethylene glycol poisoning ?

A

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

65
Q

all tetracyclines are eliminated renally (& therefore should be avoided in RF) except for what drug?

A

Doxycycline= GI elimination (doxycycline is the only tetracycline that is SAFE IN RENAL FAILURE)

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