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PANCE REVIEW > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Buzz word: RBC casts

A

Glomerulonephritis or vasculitis

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2
Q

Buzz word: WBC casts

A

Pyelonephritis, AIN

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3
Q

Hypokalemia findings

A

K<3.5
Muscle weakness, rhabdo, decreased DTR, nephrogenic diabetes insipidus

Flattened T waves/U waves

  • INCREASED RISK OF DIGOXIN TOXICITY
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4
Q

Causes of hyperkalemia

A

***psuedohyperkalemia: MC cause… this is a lab error where vile was shaken… not true hyperK

1) AKI or CKD: decreased excretion
2) Meds: k sparing diuretics, ACE, BB, NSAID
3) decreased aldosterone: adrenal insufficiency
4) Cell lysis
5) metabolic acidosis

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5
Q

Hyperkalemia findings

A

K>5
Ascending weakness, paresthesias, flaccid paralysis
Peaked T waves

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6
Q

MC type of acute kidney injury

A

Prerenal: hypocolemia/hypotension

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7
Q

MC intrinsic cause of acute kidney injury

A

Acute tubular necrosis (ATN)

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8
Q

Causes of Acute Tubular Necrosis

A

Ischemic: prolonged hypovolemia

Nephrotoxic: aminoglucosides, contrast (exogenous) or myoglobin, gout crystals, bence-Jones proteins of MM

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9
Q

Lab findings of ATN

A

On UA: epithelial casts and muddy brown waxy casts

HyperK
Increased phosphate
Low specific gravity : unable to concentrate urine ***

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10
Q

Drugs causing Acute tubuliinterstitial nephritis (AIN)

A
  • PCN
  • NSAID
  • Sulfas
  • allopurinol
  • rifampin
  • cipro
  • cephalosporins
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11
Q

Clinical manifestations of AIN

A

Fever, rash, WBC CASTS, eosinophilia, arthralgias

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12
Q

Azotemia

A

High BUN

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13
Q

Presentation of Acute Glomerulonephritis

A

RBC casts/hematuria, HTN, azotemia, proteinuria

*treat with steroids

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14
Q

Intrinsic causes of Acute Kidney Injury

A

1) Acute Tubular necrosis (ATN)
- MC
2) Acute tubulointerstitial nephritis (AIN)
- hypersensitivity rxn
3) Acute Glomerulonephritis (AGN)
4) vascular causes

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15
Q

Lab values for prerenal AKI

A
  • slow increase in Cr
  • BUN:Cr ratio >20:1 (urea is reabsorbed to pull more water into the vasculature)
  • urine Na LOW, FeNa <1% (Na is retained to pull more water into the vasculature)
  • HIGH specific gravity (highly concentrated urine since there is little water)
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16
Q

Lab findings in intrinsic AKI, specifically ATN

A
  • rapid Cr increase
  • HIGH urine Na, FeNa >2% (inability to reabsorb Na)
  • LOW specific gravity (can’t concentrate urine)
  • epithelial muddy brown granular casts *the more waxy, the more chronic)
  • BUN:Cr ratio of 10:1 (even failure to excrete either substance)
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17
Q

MC cause of ESRD

A

DM!!!!
2nd is HTN
3rd is glomerulonephritis

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18
Q

Best diagnostic test for proteinuria

A
  • spot UAlbumin/ UCreatinine ratio (ACR)
  • albuminuria= ACR 30mg/g

*24 hr urine collection could also work

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19
Q

To of uncomplicated UTI

A
  • Nitrofurantoin (macrobid) *used in pregnancy
  • fluoroquinolone *DOC in pyelo
  • Bactrim
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20
Q

BPH management

A

1) 5-A reductive inhibitors (finasteride): size reduction

2) alpha-1 blockers (tamulosin): symptomatic relief

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21
Q

What will the patients volume statue and osmolality be in SIADH?

A

euvolemic, hyponatremic

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22
Q

Where is ADH secreted from?

A

posterior pituitary

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23
Q

What are common causes of SIADH?

A

1) CNS causes: SAH, tumor, meningitis, head trauma
2) Small Cell Lung Cancer (secretes ADH)
3) MEDS

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24
Q

What medications and cause SIADH?

A

narcotics, SSRI, TCA, HTZD, ecstacy, AED, carbamezapine, IV cyclophophamide

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25
Q

What will the urine osmolarity and serum osmoarity be in a patient with SIADH

A

Serum osmolarity LOW

Urine osmolarity HIGH

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26
Q

Do not exceed this rate of sodium replacement for a patient with hyponatrimia

A

no faster than 0.5 mEq/L per hour to prevent central pontine myelinolysis

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27
Q

what is the mainstay of treatment for SIADH?

A

Water restriction

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28
Q

What is the quick way to roughly determine a patient’s osmolality?

A

serium sodium x2

NML osmoloality is 285-295

29
Q

What is the normal serum osmolality?

A

285-295

30
Q

What are the steps in your work up of a patient with hyponatremia ?

A

1) Check the serum osmolality

2) Check the patient’s volume status (fluid overload, deydrated, or normal)

31
Q

If a patient presents with hyponatremia that is hypotonic and hypovolemic, what are the causes/treatment?

A

The patient is loosing sodium AND water. This could be due to TZD, ACEi, bleeding, burns, N/V

Treatment is by replenishing fluids with .9%NS

32
Q

If a patient presents with hyponatremia that is hypotonic and hypervolemic, what are the causes/treatment?

A

This from third spacing and EXCESS WATER. Common causes are CHF, cirrhosis, nephrosis.

**Treat the underlying cause and restrict H20 and salt

33
Q

If a patient presents with hyponatremia that is hypotonic and isovolemic, what are the causes/treatment?

A

SIADH, hypothyroid, adrenal insufficiency, reset osmostat, polydipsia

Treatment is with water restriction

34
Q

What type of hypoglycemia is TRUE hypoglycemia

A

hypotonic hypoglycemia

35
Q

What is the cause of a hypertonic hypoglycemia ?

A

hyperglycemia or mannitol infusion

36
Q

Clinical symptoms of hyponatremia

A

faitgue, headache, n/v, cramps, seizures, coma, respiratory arrest

37
Q

Nephrotic disease is characterized by what lab findings

A
  1. proteinuria
  2. hypoalbuminemia; loss of albumin in urine
  3. hyperlipidemia
  4. Edema; from loss of oncotic pressure
38
Q

Acute Glomerulonephritis is characterized by what lab findings?

A
  1. HTN
  2. RBC casts
  3. Proteinuria
  4. Azotemia
39
Q

Presentation of patients with acute glomerulonephritis

A

HTN, cola colored urine, possible oligouria, flank pain, fever, edema

40
Q

5 types of acute glomerulonephritis

A
  1. IGA nephropathy (Bergers)
  2. Post infectious
  3. Membranoproliferative
  4. Goodpasture’s
  5. Vasculitis ( microscopic polyangitis & granulomatosis with polyangitis)
41
Q

Hallmarks of IGA nephropathy (berger’s)

A

MOST COMMON. glomerulonephritis following URI or GI infection. IGA deposits on biopsy. Tx. with ACEi and corticosteroids

42
Q

Hallmarks of post infectious glomerulonephritis

A

post GABHS infection. (impetigo commonly) often in young boys, supportive treatment

43
Q

Hallmarks of membranoprolifferative glomerulonephritis

A

mixed nephritic/nephrotic picture ; caused by lupus or hep C

44
Q

Hallmarks of good pasture’s

A

hemoptysis, RAPIDLY PROGRESSIVE (crecents on bx) , anti-GBM antibodies, IgG deposits on bx

*treat with steroids and cyclophosphamide

45
Q

Hallmarks of vasculitic glomerulonephritis

A

1) microscopic polyangitis P-ANCA
2) glomerulonephritis with polyangitis (wegener’s) C-ANCA

*both RAPIDLY PROGRESSIVE (crescent on bx, treat with steroids and cyclophosphamide )

46
Q

Central diabetes insipidus

A

inability of the body to produce ADH.

  • shows response to desmopressin stimulation test
  • treat with synthetic ADH
47
Q

Nephrogenic diabetes insipidus

A

insensitivity of the kidneys to ADH

  • shows no response to desmopressin stimulation test
  • hypercalcemia and lithium can cause it
  • treatment is with hypotonic fluids, salt restriction, and hydrochlorothazide
48
Q

Testicular torsion; PE and tx

A

n/v, negative Prehn’s sign: (no pain relief with scrotal elevation)

-dx with testicular u/s and tx with detorsion

49
Q

Sudden onset of left-sided varicocele in older men indicates what?

A

renal cell carcinoma

50
Q

right-sided varicocele in children under 10 indicates what?

A

retroperitoneal malignancy

51
Q

what is the difference between a varicocele and a hydrocele ?

A

varicocele=varicose veins, “bag of worms” above testicle

hydrocele= cystic testicular fluid collection, PAINLESS, should go away before 1 yr old or else surgery

52
Q

Epididymitis causative organisms

A

if less than 35, Chlamydia (tx with ceftriaxone and doxycycline)

if older than 35, E.coli/enteric organism (tx with floroquinolones)

53
Q

PE in epididymitis

A

postitive perhn’s sign: pain is relieved with testicular elevation, cremasteric reflex in tact

54
Q

Prostatitis causative organisms

A
  • if greater than 35, E.coli (treat with fluoroquinolone or bacterium)
  • if less than 35 , chlamydia/ gonorrhea (treat with doxy & ceftriaxone)
55
Q

Acute vs. chronic prostatitis presentation and treatment

A

ACUTE= boggy and tender, NO rectal exam, tx with abx

CHRONIC= boggy and non-tender, TURP(transurethral resection of the prostate) if refractory

56
Q

Patients with prostate cancer often present with pain where?

A

BACK PAIN

57
Q

A rubbery prostate is consistent with what diagnosis?

A

BPH

58
Q

Tumor marker for prostate cancer

A

PSA (prostate specific antigen) , also elevated in BPH

59
Q

Presentation of renal cell carcinoma

A
  1. hematuria
  2. flank pain
  3. palpable mass

-left sided varicocele, HTN, hypercalcemia

60
Q

4 types of kidney stones

A
  1. calcium (MC)
  2. uric acid (from high protein intake)
  3. struvite (mg ammonium phosphate), from urea-splitting organisms such as PROTEASE, klebsiella, pseudomonas **staghorn calculi may form
  4. Cystine; genetic condition
61
Q

an alkaline ph of >7.2 on UA indicated which type of stone

A

struvite stones

62
Q

management of erectile dysfunction and CI to medications

A

PDE-5 inhibitors

  • Sildenafil (viagra)
  • Tadalafil (Cialis)

**CI in patients taking nitrates and with cardiovascular dz

63
Q

Causes of renovascular hypertension (renal artery stenosis)

A
  • in elderly=atherosclerosis

- in females under 50=fibromuscular dysplasia

64
Q

Treatment of renal artery stenosis

A
  1. stent placement

2. ACEi ; if patient has bilateral stenosis ACEI ARE CONTRAINDICATED

65
Q

Indications that a glomerulonephritis is rapidly progressive

A
  1. There is crescent formation on biopsy
  2. worse prognosis of turning to ESRD in weeks/months
  3. Treat with corticosteroids and cyclophosphamide
  4. Goodpastures and vasculitis are the two different types
66
Q

What is pyurea?

A

WBC in the urine

67
Q

What does it mean in you see epithelial cells on U/A?

A

This was not a clean catch specimen and it needs to be redrawn

68
Q

What is the normal growth of the prostate as men age dependent on?

A

Increased Dihydrotestosterone (DHT) production

PANCE REVIEW (15 decks)

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