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Urology > Week 2 > Flashcards

Week 2 Flashcards

1
Q

underlying etiology of glomerulonephropathies?

A

damage to GBM

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2
Q

findings in nephritic syndrome?

A 
PHAROH
proteinuria (mild, <3.5 g/d)
hematuria
azotemia (abn high levels of nitrogen containing compounds such as BUN, Cr)
red blood cell casts
oliguria
HTN
ssxs: edema, possible rash and/or heart murmur
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3
Q

causes of nephritic syndrome?

A

post-infectious: GABHS –> PSGN
autoimmune: goodpasture’s, SLE, Henoch-schonlein purpura, Guillain-Barre, amyloidosis, Wegener’s
primary KD dz: IgA nephropathy, Berger’s dz

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4
Q

ddx of nephritis syndrome?

A

cirrhosis/liver failure, severe HTN, AIN, RCHF, DM, hemolytic-uremic syndrome

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5
Q

how to differentiate glomerular from urologic bleeding? urine color, RBC morphology, renal fxn

A

glomerular urine color will be dark red, brown, cola-colored, RBCs will be dysmorphic, renal fxn is reduced
urologic urine color will be bright red, RBCs will be isomorphic, renal fxn will be normal

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6
Q

general w/u for nephritis?

A

retinal exam for HTN changes, hearing test (Alport’s), skin rash (SLE, Fabry dz, vasculitis, Henoch-Schonlein), jt changes (collagen vascular dz)
labs: 24 hr urine protein, serum Cr, serum complement, anti-DNA, ANCA, c-ANCA, p-ANCA, anti-GBM, HBV, HCV, CXR, echo, renal U/S

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7
Q

post infectious GN is what type of hypersensitivity reaction?

A

type III
ag-ab complexes lodged in GBM podocytes leads to complement acitvation
prior ssxs of GABHS infxn followed by rash, fever, confusion, HTN, periorbital edema, hematuria, HA, N/V, malaise

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8
Q

dx of post infectious GN?

A

UA: cola-colored urine, RBCs, WBCs, RBC casts (PATHOGNOMONIC!) present, proteinuria <3.5
CMP: increase in BUN & Cr, mild decrease in GFR
streptozyme test fro anti-streptolysin, anti-hyaluronidase, anti-streptokinase, anti-nicotinamide-adenine dinucleotidase, anti-DNAse B and complement
light microscopy shows thickened GBM

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9
Q

tx for post infectious GN?

A 
tx infxn if present
treat edema or HTN
limit protein and sodium
bed rest
anti-inflammatories: curcumin, boswellia, quercetin, bromelain
antimicrobials: echinacea
antioxidants: vit C, Vit E, taraxacum
constitutional hydro or wet sheet wrap
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10
Q

complication with untreated post infectious GN?

A

MAY LEAD TO NEPHROTIC SYNDROME, AKI, HTN ENCEPHALOPATHY

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11
Q

when do you need to refer a post infectious GN pt?

A

fluid overload present or unresponsive to therapy, refractory HTN, worsening renal fxn via Cr levels

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12
Q

main DDX of post infectious GN?

A

rapidly progressing GN - cresenteric GN, most commonly caused by drugs

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13
Q

auto immune causes of GN?

A

ANCA associated

anti-GBM GN and Goodpasture’s syndrome

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14
Q

subtypes of ANCA associated GN

A

ANCA = necrotizing GN with GU sxs (hematuria and proteinuria) as well as either
Wegener’s granulomatosis - bleeding respiratory tract nodules, hemoptysis, crackles, skin, eye, sinuses affected
OR
Churg-Strauss syndrome - asthma w/eosinophilia which can lead to RPGN

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15
Q

asthma with eosinophilia
Can lead to RPGN. Considered “pauci-immune” since vasculitis shows little sign of hypersensitivity on immunofluorescence. Work-up includes: CBC (eosinophilia) ANCA titer, IgE levels—inc, Chest CT, PFTs, bronchoaveolar lavage
is what condition?

A

autoimmune GN specifically Churg-Strauss syndrome

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16
Q

bleeding respiratory tract nodules—hemoptysis, crackles– skin, eye, sinuses. Work-up includes: ANCA titers, Chest CT, bronchoaveolar lavage is what condition?

A

Wegener’s granulomatosis

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17
Q

anti-GBM GN and Goodpasture’s syndrome is associated with what? presents w/what? need to run what titers to differentiate from Wegener’s?

A

influenza A infxn, hydrocarbon exposure or HLA-DR2 ag
presents w/pulmonary hemorrhage, dyspnea, hemoptysis, crackles, edema, HTN
have to run ANCA to differentiate from Wegener’s

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18
Q

assoc with influenza A infection, hydrocarbon solvent exposure or HLA-DR2 antigen. Concomitant pulmonary hemorrhage—dyspnea, hemoptysis, crackles—and renal symptoms (edema, HTN). Type II hypersensitivity reaction. Often idiopathic. Possible death by aspiration of blood.
Work-up includes: Anti-GBM titers, Renal biopsy
May have Wegener’s as well, thus ANCA titers run
TX with steroids, chemo, plasma exchange.
is what condition?

A

anti-GBM GN and Goodpasture’s syndrome

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19
Q

what is the MC nephritic syndrome worldwide?

A

primary KD dz - IgA nephropathy (Berger’s dz)

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20
Q

what is IgA nephropathy (Berger’s dz)?

A

IgA deposition in the glomerular mesangium w/mesangial proliferation
unk etiology, can be assoc w/ celiac, HBV, alcoholic cirrhosis, sarcoidosis, HIV, SLE, RA, Sjogren’s

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21
Q

ssxs of IgA nephropathy?

A

1 or recurrent episodes of gross hematuria < 5 d after viral or bacterial URI or gastroenteritis, flank pn, mild fever, HTN

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22
Q

how to dx IgA nephropathy?

A

UA: proteinuria, RBC and casts, WBCs
serum Cr mb elevated
serum IgA increased (only in 50% of cases)
KD bxs: if persistent proteinuria >1g/d - see IgA deposits on mesangium

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23
Q

progressive IgA nephropathy seen when?

A

increased serum Cr
HTN > 140/90
persistent proteinuria >1 g/d

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24
Q

Tx for IgA nephropathy?

A 
if mild, monitor
GF diet
artemesia
fish oil
saccharomyces boulardii
cordyceps sinesis
perilla frutescens
rheum palmatum
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25
Q 
ages and sex: All ages,  2:1 male
nephrotic syndrome in 10-20%
HTN in 70%
ARF in 50% (transient)
latent period 1-3 wk
labs: ASO titers
immunogenetics: HLA-B12
light microscopy: Diffuse proliferation
prognosis: 95% resolve spont
tx: Supportive
A

PSGN

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26
Q 
ages and sex: 15-35 yo, 2:1 male
nephrotic syndrome Rare
HTN 30-50% 
ARF is rare
follows viral syndromes
labs: Serum IgA (50% cases)
immunogenetics: HLA-Bw
light microscopy: Focal proliferation
prognosis: Slow progression in 25-50%
tx: ACEi, ARB, steroids if resistant
A

IgA nephropathy

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27
Q 
age and sex: 15-30 yo, 6:1 male
nephrotic syndrome: Rare
HTN: Rare
ARF: 50%
pulmonary hemorrhage
labs: Positive anti GBM ab
immunogenetics: HLA-DR2
light microscopy: focal diffuse c crescents
prognosis: 75% stabilize or improve with tx early
tx: Plasma exchange, steroids
A

Goodpasture’s

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28
Q 
age and sex: Mean 58 yr, 2:1 male
nephrotic syndrome: 10-20%
HTN: 25%
ARF: 60%
fast progression, drug hx?
labs: Positive ANCA
immunogenetics: None
light microscopy: Cresentic GN
progression: 75% stabilize or improve with tx early
tx: steroids
A

RPGN

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29
Q

general 10 tx ideas for nephritic syndrome?

A
  1. avoid high sodium, high potassium foods; low protein in diet, low antigen diet
  2. incorporate immune amphoterics (ganoderma, grifola, tinospora, artemesia)
  3. diuretics with edema
  4. fish oil
  5. treat HTN
  6. probiotics
  7. remove allergens
  8. quit smoking, limit/no EtOH
  9. maintain healthy wt
  10. conventional approach (drugs)
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30
Q

5 tx options specifically for IgA nephropathy?

A
  1. fish oil
  2. saccharomyces boulardii
  3. cordyceps
  4. perilla
  5. rheum palmatum
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31
Q

worst prognosis with nephritis syndrome?

A

many forms of acute GN can progress to chronic glomerulonephritis which is IRREVERSIBLE which can lead to CKD and ESRD

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32
Q

nephrotic syndrome is result of what?

A

end result of variety of diseases that damage the glomerular filtration barrier leading to protein wasting, increased permeability of glomerular capillaries and lipids can pass through as well

33
Q

key findings of nephrotic syndrome?

A 
severe proteinuria >3.5 g/d on 24 hr urine collection which leads to decreased oncotic P and ultimately edema 
HTN
oliguria
edema
foamy urine 
cough, exertional dyspnea
34
Q

RFs and secondary causes of nephrotic syndrome?

A

poorly controlled DM, IgA nephropathy, nephritic conditions in general, SLE, amyloidosis, HIV, pre-eclampsia, drugs, snake bite, CA, FHx of congenital KD dz

35
Q

ddx nephrotic syndrome?

A

CHF, liver failure, ATN, PN, malignant HTN, multiple myeloma

36
Q

pneumonic for ssxs associated with multiple myeloma?

A 
CRAB
calcium (elevated)
renal failure
anemia
bone lesions
37
Q

5 nephrotic syndromes?

A

minimal change dz (lipoid nephrosis)
focal semental glomerulosclerosis
membranous nephropathy
membranoproliferative glomerulonephritis

38
Q

MC nephrotic syndrome present in kids <10 yo?

A

minimal change dz

39
Q

MC nephrotic syndrome in young adults, African Americans?

A

focal segmental glomerulosclerosis

40
Q

MC nephrotic syndrome in white adult pts?

A

membranous nephropathy

41
Q

not specifically MC for any subpopulation

A

membranoproliferative glomerulonephritis

42
Q

etiology: Unclear in most cases. Can occur after URI or immunization
In adults may be assoc with drugs (NSAID, antibiotics, lithium) Hodgkin’s dz, Syphilis, TB, Allergy
symptoms: No to mild HTN, edema
signs/history: Hematuria,
proteinuria
Light microscopy: mild mesangial prolif and few deposits
Electron microscopy:
epithelial foot process flattened

A

minimal change dz

43
Q

etiology: 1°: Idiopathic :can be rapid onset
2°: Heroin, lithium, NSAIDs HIV, Parvovirus B19, obesity, vesicoureteral reflux, sickle cell symptoms: HTN, edema
signs/history: Hematuria,
proteinuria
Light microscopy: segments of mesangial collapse sclerosis, hyaline deposits
prognosis: Poor outcome

A

focal segmental glomerulosclerosis

44
Q

etiology: Idiopathic
Hodgkin’s, SLE, malignancy, HBV, HCV, syphilis, malaria, penicillamine, Captopril, NSAIDs mercury and gold symptoms: HTN, edema,
Complications:
Renal vein thrombosis
signs/history: Elec microscopy: immune complex deposits (IgG or IgM) on thickened capillary loops
Spike and Dome appearance

A

membranous nephropathy

45
Q

etiology: SLE, RA, HCV, HBV
Variant: C3 GN—C3 deposits: hematuria after URI symptoms: Insidious, mild HTN, may progress to RPGN
signs/history: Hematuria, hypocomplementemia
Diffuse thickening (hypercellularity) of glomerular capillary wall with Ig deposits

A

membranoproliferative glomerulonephritis

46
Q

secondary diseases that can cause nephrotic dz?

A 
lupus
diabetic nephropathy
amyloidosis
infective endocarditis associated GN
HBV, HCV
HIV-associated nephropathy
multiple myeloma related KD dz
47
Q

is a rare, x-linked deficiency of alpha-galactosidase A (a-Gal A) leading to accumulation of glycolipids in blood vessels. In kidney, causes proteinuria, renal insufficiency, and renal failure. SSx also in joints, skin, eyes, heart, and GI. IV enzyme replacement given.

A

Fabry dz - DDX of nephrotic syndrome

48
Q

is an inherited collagen (Type IV) synthesis defect leading to GBM thinness and dysfunction, as well as sensorineural hearing loss and ocular lesions (eg cataracts). Presents with hematuria possibly after a URI, then can progress with worsening proteinuria/edema/HTN/oliguria to ESKD
Rare, more severe and persistent in males

A

Alport syndrome - is a DDX of nephrotic syndrome

49
Q

is an immune-mediated (IgA deposits) systemic vasculitis common in children 3-8 yrs. Purpura, arthralgias, abdominal pain and renal disease (hematuria, proteinuria, inc creatinine). Skin biopsy reveals vasculitis. Resolvable

A

Henoch-Schonlein purpura - is a DDX of nephrotic syndrome

50
Q

treatment considerations for nephrotic syndrome?

A 
immunosuppressive for primary dz: steroids, abx, immunologics 
anti-HTN
anti-hyperlipidemic
anti-coagulants 
limit dietary protein and sodium
remove allergens
fish oil
anti-inflammatory, anti-oxidant, immune amphoteric, renal protective herbs
constitutional hydro
control DM
51
Q

specific tx options for FSGS?

A

CoQ10 and ganoderma

52
Q

specific tx options for MPGN?

A

ALA, Vit E, rosmarinic acid

53
Q

specific tx for membranous nephropathy?

A

astragalus

54
Q

Inflammation of the renal interstitium, from cell-mediated immune response binding to interstitial proteins, leading to a decrease in renal function. Interstitial compartment infiltrated by T-cells, monocytes, and plasma cells

A

acute interstitial nephritis

55
Q

categories of AIN?

A 
drug hypersensitivity
infections 
tubulointerstitial nephritis-uveitis syndrome
related to systemic AI dz
idiopathic
56
Q

general presentation of AIN?

A

acute onset of dec in renal fxn days to 2 wks post-administration of infection or drugs

symptoms: rash, fever, hematuria, oliguria, N/V, malaise, flank pain, arthralgai (uveitis in TINU)
signs: decreased urine concentration, decreased GFR

57
Q

dx of AIN?

A 
UA: hematuria, mild to mod proteinuria, high WBCs, WBC casts, eosinophiluria may be present
CBC: eosinophilia
inc serum BUN and Cr
FENa >1% indicating tubular damage 
bx if persistent sxs
58
Q

AIN management and tx considerations?

A

normal renal fxn usu returns w/discont of suspected causative agent
low protein, low K, low Na diet
anti-inflammatories, antioxidants
Renafood
alternative natural tx for conditions treated w/offending agentes
pharmacologic (short dose of prednisone)
some pts may require dialysis

59
Q

Patchy focal necrosis of tubule. Lumens fill with casts, cellular debris (Tamm-Horsfall mucoprotein)

A

acute tubular necrosis - can be due to toxins (drugs - nephrotoxins) or ischemia

60
Q

3 forms of ATN?

A

contrast induced nephropathy
cisplatin induced nephropathy
lithium nephropathy

61
Q

possible presentation of ATN?

A

uremic pruritus, pericardial friction rub, asterixis, HTN, edema, oliguria

62
Q

ATN tx considerations?

A

correct ischemic cause or remove drugs, manage ARF
chelation tx may be needed once sxs managed if dt heavy metals
NAC to prevent radiation nephropathy
general protectives: silybum, gingko, cordyceps, urtica, CoQ10, selenium, vit C
green tea to protect

63
Q

specific tx options for cisplatin induced ATN?

A

lipoic acid, NAC, selenium, quercetin

64
Q

Symptoms and signs: nocturia, uremia sx, small kidneys, hyperkalemia, reduced SG,
Hyperchloremic metabolic acidosis from:
1. Reduced ammonia production
2. Inability to acidify the distal tubules
3. Proximal tubule bicarbonate wasting

A

chronic tubulointerstitial disease

65
Q

5 forms of acute tubulointerstitial disease?

A 
prolonged obstructive uropathy
reflux neuropathy
analgesic nephropathy
lead nephropathy
cadmium nephropathy
66
Q

Causes: renal stone, prostate dz, carcinoma of cervix, colon, bladder
SSX: in partial obstruction urine output alternates from polyuria (vasopressin insensitivity) and oliguria (dec GFR)
Azotemia and HTN
Hematuria or pyuria, but often benign UA

A

obstructive uropathy - chronic tubulointerstitial dz

67
Q

“Vesicoureteral reflux” VUR
congenital incompetent vesicoutereral sphincter allows retrograde flow during voiding leads to inflam
SSX: HTN, polyuria, nocturia, renal insufficiency, hx of recurrent UTI
Renal scarring can lead to proteinuria, Na wasting, metabolic acidosis and CKD.
Pelvic ultrasound
Voiding cystourethrography VCUG can visualize ureteral dilatation
Prophylactic Ab and surgery

A

reflux neuropathy - chronic tubulointerstitial dz

68
Q

Acetaminophen—reactive metabolites bind to interstitial cells causing necrosis
NSAIDs decrease medullary blood flow and decrease glutathione
Aspirin—unknown mechanism
SSX: many are asx, found incidentally
polyuria, HTN, flank pain, malaise, dyspepsia
Lab: hematuria, non-nephrotic proteinuria, anemia, inc creatinine, low SG
Sloughed papillae can be found in the urine late in the disease
CT: small kidneys, papillary calcifications

A

analgesic neuropathy - chronic tubulointerstitial dz

69
Q

Pb: filtered by glomerulus and transported across the proximal convoluted tubules and accumulated. Progressive tubular atrophy and interstitial fibrosis
See hyperuricemia, HTN
Multisystem involvement—GI, Neuro, hemo
X-ray fluorescence shows bone accumulation

A

Lead nephropathy - chronic tubulointerstitial dz

70
Q

Deposits cause tubular dysfunction leading to proteinuria, glucosuria, increase in urinary cadmium

A

cadmium nephropathy - chronic tubulointerstitial dz

71
Q

management and tx of chronic tubulointerstitial dz?

A

prevent renal scarring if early stages - treat the cause
tubular dysfxn may require K and Ph restriction, Na, Ca and bicarb supplementation
chelation therapy for heavy metals
natural analgesics, HP and physical medicines for chronic pain syndromes
anti-inflammatories (turmeric, boswellia, bromelain)
renal protectives: nettle seed, salvia miltiorrhiza
renal anti-oxidants: ginseng, coptis, vaccininum, quercetin, Vit C, ALA
fish oil

72
Q

Damaged proximal tubule leads to wasting of those products normally reabsorbed there—thus phosphaturia, glucosuria, albuminuria, uricosuria, bicarbonate wasting.
The condition may be familial or acquired (eg. assoc w multiple myeloma, lead or cadmium intoxication, antiretroviral drugs, tetracycline).
SSx: Presents as osteomalacia in adults, hypophosphatemic rickets in kids, polyuria, polydipsia.
Tx: Phosphate supplementation, vit D

A

Faconi syndrome - type of RTA

73
Q

results in hyperchloremic metabolic acidosis
Causes include heredity, autoimmune disease (Sjogren’s, Lupus, RA), drugs/toxins (toluene, lithium, ibuprofen, amphotericin B, lead), heavy metals, chronic obstruction.
SSX: urinary stone formation (calcium oxalate, uric acid), bone demineralization, hypokalemia, poor growth in kids
Tx: sodium bicarb or sodium citrate, potassium citrate, thiazide diuretic may be needed

A

renal tubular acidosis

74
Q

Granulomatous deposits caseate and can rupture into the tubular lumen, can lead to calcifications and progressive medullary injury. Scarring, abscess, fibrosis occurs
Complications: urinary obstruction, hydronephrosis, recurrent UTI
Early signs are pyuria without positive culture on routine media, hematuria, mild proteinuria
X-ray show calcifications
CT show caseous masses

A

renal tuberculosis

75
Q

Inherited (autosomal recessive) defect in thick ascending loop:
Low SG, hypercalciuria, hypokalemia, metabolic alkalosis, normal BP
In kids, presents as polyuria, polydipsia, dehydration, growth and mental retardation.
Treated with dietary Na, K, ACE inhibitors, Anti-inflammatories

A

bartter syndrome

76
Q

Inherited (autosomal recessive) defect in the distal convoluted tubule leading to excess excretion of sodium, magnesium, chloride and potassium.
Presents with fatigue, ms cramps, polyuria, HTN
Labs: hypochloremic metabolic acidosis, hypokalemia, hypocalciuria, hypomagnesmia

A

Gitelman syndrome

77
Q

Very rare. Autosomal dominant defect in tubules. Presents as severe and/or refractory HTN, metabolic alkalosis from hypokalemia, hypoaldosteronism

A

Liddle syndrome - pseudoaldosteronism

78
Q

Nephropathy induced by consuming aristocholic acid containing herbs. Nephrotoxin produces interstitial fibrosis with atrophy and loss of tubules in renal cortex, and renal insufficiency. Most cases in Eastern Europe and China

A

AA nephropathy

79
Q

Congenital (x-linked) or Acquired (eg chronic lithium use, amphotercin-B, PN, PKD) defect to renal tubular responsiveness to ADH.
SSx—polyuria, polydipsia, failure to thrive, hypernatremia, dehydration, urine concentration <200 Osm/kg, SG<1.005.
TX with hydration, low sodium, low protein diet, chlorothiazide

A

nephrogenic diabetes insipidus

Urology (9 decks)

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