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Uro/Nephro Flashcards

1
Q

Tamm-Horsfall protein

A

Inhibits attachment of type 1 fimbriae E.coli to uroepithelial cells –> mitigates against infection

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2
Q

Staghorn calculi

A 
Struvite calculi 
Phosphate + ammonium + magnesium 
Very large and branched 
Pts often asymptomatic 
Infection and hematuria 
Most a/w infections w/ Proteus, Klebsiella, ureaplasma 
Formed in alkalotic environment
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3
Q

Most common type of renal stone

A

Calcium oxalate or calcium phosphate

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4
Q

Preferred imaging method to detect renal stones

A

NCCT KUB

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5
Q

2 stones that are not radio-opaque

A

Uric acid

Indinavir

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6
Q

Irritative urinary symptoms

A 
FUND 
Frequency
Urgency 
Nocturia 
Dysuria
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7
Q

Voiding urinary symptoms

A 
Weak stream 
Intermittency 
Splitting, spraying, straining 
Hesitancy 
Terminal dribble
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8
Q

Drugs often a/w urinary incontinence

A 
Alpha adrenergic agonists 
Alpha adrenergic antagonists 
Anticholinergics
Antipsychotics 
Bromocriptine 
CCB 
CLonazepam
Diuretics 
Ethanol
Lithium 
Metoclopramide 
Misoprostol 
Phenytoin
Sedatives
Skeletal muscle relaxants
Sympatholytics (ie. methyldopa)
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9
Q

Treatment for stress incontinence

A 
In postmenopausal women where intrinsic sphincter deficiency is suspected cause, try estrogen replacement therapy +/- alpha agonists (ie.pseudoephedrine) 
Pelvic floor physio 
Weight loss
Pessaries
Retropubic suspensions/slings
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10
Q

Treatment for urge incontinence

A

Anti-cholinergic to inhibit bladder contraction (Oxybutynin, solifenacin)
Beta-3 adrenergic receptor agonists to cause bladder relaxation (Mirabegron)
Botox, percutaneous tibial nerve stimulation, sacral neuromodulation

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11
Q

Main cause of nephrotic syndrome in peds

A

Minimal change disease

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12
Q

Goodpasture syndrome

A

AKA anti-GBM disease
Formation of antiglomular basement membrane antibodies –> renopulmonary disease –> hematuria, hemoptysis
Tx: PLEX, steroids, cyclophosphamide

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13
Q

Most common cause of primary nephrotic syndrome in adults

A

Membranous glomerulonephritis (recently more FSGS)

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14
Q

Wegener’s granolomatosis

A

AKA granulomatosis with polyangiitis

Vasculitis affecting small vessels –> hematuria, hemoptysis

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15
Q

Minimal change disease etiology

A

Often idiopathic

Can be a/w lithium, NSAIDs, hypersensitive rxn to bee sting, viral URTI in children , heme malignancies

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16
Q

Cockcroft-Gault formula

A

Estimates CrCl
Considers age, gender, serum creatinine, weight but does not include race
Overestimates GFR when renal function severely impaired

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17
Q

MDRD formula

A

Esimates GFR
Considers age, gender, serum Cr, and race but not weight
Underestimates GFR at near norma values

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18
Q

Hypokalemia seen in metabolic acidosis or alkalosis?

A

Metabolic alkalosis

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19
Q

Hypokalemia ECG

A

Initially: U waves, St depression, inverted/flattened T waves, QT prolongation, sinus brady
Severe: PR prolongation, wide QRS, increased risk of digitalis toxicity
VFib, VTach

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20
Q

HypoMg, HypoCa, HypoK which to correct first?

A

HypoMg

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21
Q

Hyperkalemia ECG

A 
Peaked T waves
Eventual loss of P wave 
Prolonged PR interval
WIdening QRS 
AV block 
Vfib, asystolice
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22
Q

K+ level at which you start treatment with insulin

A

6.5

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23
Q

1st line treatment when K>7 and ECG changes

A

Calcium gluconate to protect heart

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24
Q

Fludrocortisone

A

Synthetic mineralocorticoid

Use if suspect adrenal insufficiency

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25
Q

Phosphate and calcium

A

Phosphate binds to calcium

Hyperphosphatemia –> hypocalcemia –> secondary hyperPTH with advanced CKD on dialysis

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26
Q

Tx for acute hyperphosphatemia

A

Hemodialysis if symptomatic
Aluminum hydroxide (careful in renal failure)
Chronic: low po4 diet (initial), then calcium carbonate binder if not resolves with PO4 diet

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27
Q

Hypercalcemia treatment

A

IV NS

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28
Q

AG value

A

AG < 12 is normal

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29
Q

AG and albumin

A

For each 10g/L fall in albumin, AG lowered by 3

30
Q

Osmolar gap

A

Calcualte if AG is elevated
Measured osmolality - calculated osmolality
Calculated = 2xNa + urea + glucose
Normal <10

31
Q

Causes of increased osmolar gap

A

Poisonous alcohols

32
Q

Common causes of AGMA

A 
MUDPILES CAT
Methanol 
Uremia 
DKA 
Paraldehyde
Iron/Ibuprofen/Indomethacin/Isopropyl alcohol
Lactic acid 
Ethylene glycol 
Salicylates 
Cyanide/Carbon monoxide 
Alcoholic ketoacidosis 
Toluene
33
Q

2 most common causes of NAGMA

A

Diarrhea
RTA
involves increased bicarb excretion that is replaced with Cl

34
Q

Renal tubular acidosis

A 
I = Distal; inability to secrete H+ in collecting duct --> impaired excretion of ammonium into urine 
II = Proximal; impaired HCO3- reabsorption
III = Combo Type I and II (Rare) 
IV = Defective ammoniagenesis due to decreased aldo, hyporesponsiveness to aldo or hyperkalemia (most common)
35
Q

Urine AG formula

A

(Na + K) - Cl
<0 = adequate NH4 excretion in urine (likely nonrenal cause)
>0 = lack of NH4 in urine (ie. distal RTA)

36
Q

Most common tx for metabolic alkalosis

A

Volume repeltion +/- carbonic anyhydrase inhibitor (acetazolamide) to facilitate loss of HCO3 in urine

37
Q

Hyperphosphatemia

38
Q

Hypophosphatemia

39
Q

HyperMg

40
Q

HypoMg

41
Q

Gold standard for proteinuria screen

A

24h urine protein

42
Q

Fanconi’s Syndrome

A

Inadequate reabsorption of proximal renal tubules of kidney
Albumin not affected
Edema secondary to salt and water retention
Leads to proteinuria

43
Q

Glomerular disease edema secondary to

A

Hypoalbuminemia
(plus Na/H2O reabsorption)
Ie. Minimal change, Membranous, FSGS

44
Q

Most common type of primary glomerular disease

A

IgA Nephropathy (Berger’s disease)
Most commonly after viral URTI in 2nd/3rd decade of life
A/W cirrhosis, HIV, celiac
Tx: RAAS Blocker if proteinuria, steroids, or steroid sparing agents (azathioprine, cyclophosphamide, mycophenolate mofetil, rituximab)

45
Q

Alport Syndrome

A 
Hereditary nephritis 
X-linked 
Leads to Type IV collagen mutation 
A/w sensorineural hearing loss, misshapen lens 
More severe in males
46
Q

Membranoproliferative glomerulonephritis vs membranous glomerulonephropathy

A

Membranoproliferative GN = thickening of GBM and mesangium

Membranous GN = thickening of GBM only

47
Q

Nephrotic syndromes

A

FSGS
Membranous glomerulopathy
Minimal change

48
Q

Nephrotic/nephritic syndromes

A

Membranoproliferative GN

Focal proliferative GN (IgA, hep B, hep C, SLE)

49
Q

Nephritic syndromes

A

Diffuse proliferative GN

Crescentic GN

50
Q

Granulomatosis with polyangiitis

A

AKA Wegener’s granulomatosis
c-ANCA+
RF+
Inflammation of blood vessels in kidneys, lungs, nose, throat, sinuses

51
Q

Eosinophilic granulomatosis with polyangiitis

A

AKA Churg Strauss
p-ANCA+
Systemic necrotizing vasculitis affecting small and medium sized vessels
Asthma, eosinophilia, pulmonary infiltrates
Tx: steroids mostly

52
Q

Most common renal complication a/w SLE

A

Nephrotic syndrome

53
Q

Cyclophosphamide

A

Immunosuppressant

54
Q

Acute tubulointerstitial nephritis

A

Acute decline in renal function, typically due to drugs, infections, AI or idiopathic (5Is)
Tx: tx underlying cause, steroids
Good prognosis

55
Q

Acute tubular necrosis

A

Abrupt and sustained decline in GFR within minutes to days after ischemic/nephrotoxic insult
Typically toxins or ischemia
Most common cause of non-prerenal AKI
Muddy browncasts/pigmented granular casts

56
Q

CKD duration

57
Q

Calcitriol, hypocalcemia and hyperphosphatemia in CKD

A

Calcitriol can be used to tx hypocalcemia BUT if pt has hyperphosphatemia don’t use it b/c it causes increased absorption of Ca and PO4

58
Q

Tx of hypercalcemia and hyperphosphatemia in CKD pts

A

Sevelamer (phosphate binder)

59
Q

Electrolyte abnormalities in ESRD

A

Hyper: K+, PO4, uric acid
Hypo: Na, Ca, HCO3

60
Q

Indications for dialysis

A 
AEIOU 
Acidosis 
Electrolyte imbalance (K) 
Intoxication (AKI) 
Overload (fluid)
Uremia (encephalopathy, percariditis, urea)
61
Q

GFR at which to initiate dialysis

62
Q

Prostate CA risk factors

A 
>50yo 
African descent 
High dietary fat (2x) 
Fam hx (1st degree relative 2x; 1st and 2nd degree relative 9x) 
\+ve BRCA mutation
63
Q

Most common type of prostate CA

A

Adenocarcinoma

64
Q

PSA values

A

<4 = normal
4-10 = equivocal
>20 = likely CA
Half life of 2.2d

65
Q

Type of GN that cannot present as RPGN

A

Minimal change disease

66
Q

Prostate CA treatment - very low risk, localized

A

Active surveillance with serial monitoring

67
Q

Prostate CA treatment - clinically localized, low - intermediate risk, >10yr life expectancy

A

Definitive therapy with radical prostatectomy, brachytherapy or external beam RT OR active surveillance

68
Q

Prostate CA treatment - high -very high risk, clinically localized

A

RT with external beam combined with brachytherapy and androgen deprivation therapy OR radical prostatectomy +/- lymph node diessection

69
Q

Prostate CA treatment - disseminated disease

A

ADT +/- chemotherapy

70
Q

Prostatitis tx

A

Empiric abx: Septra OR
Cipro or Levo x 6wks
Change abx based on urine C&S
SEPTRA IS A SULFONAMIDE

LMCC (22 decks)

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