Nephrology Flashcards
Buzz word: RBC casts
Glomerulonephritis or vasculitis
Buzz word: WBC casts
Pyelonephritis, AIN
Hypokalemia findings
K<3.5
Muscle weakness, rhabdo, decreased DTR, nephrogenic diabetes insipidus
Flattened T waves/U waves
- INCREASED RISK OF DIGOXIN TOXICITY
Causes of hyperkalemia
***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
Hyperkalemia findings
K>5
Ascending weakness, paresthesias, flaccid paralysis
Peaked T waves
MC type of acute kidney injury
Prerenal: hypocolemia/hypotension
MC intrinsic cause of acute kidney injury
Acute tubular necrosis (ATN)
Causes of Acute Tubular Necrosis
Ischemic: prolonged hypovolemia
Nephrotoxic: aminoglucosides, contrast (exogenous) or myoglobin, gout crystals, bence-Jones proteins of MM
Lab findings of ATN
On UA: epithelial casts and muddy brown waxy casts
HyperK
Increased phosphate
Low specific gravity : unable to concentrate urine ***
Drugs causing Acute tubuliinterstitial nephritis (AIN)
- PCN
- NSAID
- Sulfas
- allopurinol
- rifampin
- cipro
- cephalosporins
Clinical manifestations of AIN
Fever, rash, WBC CASTS, eosinophilia, arthralgias
Azotemia
High BUN
Presentation of Acute Glomerulonephritis
RBC casts/hematuria, HTN, azotemia, proteinuria
*treat with steroids
Intrinsic causes of Acute Kidney Injury
1) Acute Tubular necrosis (ATN)
- MC
2) Acute tubulointerstitial nephritis (AIN)
- hypersensitivity rxn
3) Acute Glomerulonephritis (AGN)
4) vascular causes
Lab values for prerenal AKI
- 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)
Lab findings in intrinsic AKI, specifically ATN
- 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)
MC cause of ESRD
DM!!!!
2nd is HTN
3rd is glomerulonephritis
Best diagnostic test for proteinuria
- spot UAlbumin/ UCreatinine ratio (ACR)
- albuminuria= ACR 30mg/g
*24 hr urine collection could also work
To of uncomplicated UTI
- Nitrofurantoin (macrobid) *used in pregnancy
- fluoroquinolone *DOC in pyelo
- Bactrim
BPH management
1) 5-A reductive inhibitors (finasteride): size reduction
2) alpha-1 blockers (tamulosin): symptomatic relief
What will the patients volume statue and osmolality be in SIADH?
euvolemic, hyponatremic
Where is ADH secreted from?
posterior pituitary
What are common causes of SIADH?
1) CNS causes: SAH, tumor, meningitis, head trauma
2) Small Cell Lung Cancer (secretes ADH)
3) MEDS
What medications and cause SIADH?
narcotics, SSRI, TCA, HTZD, ecstacy, AED, carbamezapine, IV cyclophophamide
What will the urine osmolarity and serum osmoarity be in a patient with SIADH
Serum osmolarity LOW
Urine osmolarity HIGH
Do not exceed this rate of sodium replacement for a patient with hyponatrimia
no faster than 0.5 mEq/L per hour to prevent central pontine myelinolysis
what is the mainstay of treatment for SIADH?
Water restriction
What is the quick way to roughly determine a patient’s osmolality?
serium sodium x2
NML osmoloality is 285-295
What is the normal serum osmolality?
285-295
What are the steps in your work up of a patient with hyponatremia ?
1) Check the serum osmolality
2) Check the patient’s volume status (fluid overload, deydrated, or normal)
If a patient presents with hyponatremia that is hypotonic and hypovolemic, what are the causes/treatment?
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
If a patient presents with hyponatremia that is hypotonic and hypervolemic, what are the causes/treatment?
This from third spacing and EXCESS WATER. Common causes are CHF, cirrhosis, nephrosis.
**Treat the underlying cause and restrict H20 and salt
If a patient presents with hyponatremia that is hypotonic and isovolemic, what are the causes/treatment?
SIADH, hypothyroid, adrenal insufficiency, reset osmostat, polydipsia
Treatment is with water restriction
What type of hypoglycemia is TRUE hypoglycemia
hypotonic hypoglycemia
What is the cause of a hypertonic hypoglycemia ?
hyperglycemia or mannitol infusion
Clinical symptoms of hyponatremia
faitgue, headache, n/v, cramps, seizures, coma, respiratory arrest
Nephrotic disease is characterized by what lab findings
- proteinuria
- hypoalbuminemia; loss of albumin in urine
- hyperlipidemia
- Edema; from loss of oncotic pressure
Acute Glomerulonephritis is characterized by what lab findings?
- HTN
- RBC casts
- Proteinuria
- Azotemia
Presentation of patients with acute glomerulonephritis
HTN, cola colored urine, possible oligouria, flank pain, fever, edema
5 types of acute glomerulonephritis
- IGA nephropathy (Bergers)
- Post infectious
- Membranoproliferative
- Goodpasture’s
- Vasculitis ( microscopic polyangitis & granulomatosis with polyangitis)
Hallmarks of IGA nephropathy (berger’s)
MOST COMMON. glomerulonephritis following URI or GI infection. IGA deposits on biopsy. Tx. with ACEi and corticosteroids
Hallmarks of post infectious glomerulonephritis
post GABHS infection. (impetigo commonly) often in young boys, supportive treatment
Hallmarks of membranoprolifferative glomerulonephritis
mixed nephritic/nephrotic picture ; caused by lupus or hep C
Hallmarks of good pasture’s
hemoptysis, RAPIDLY PROGRESSIVE (crecents on bx) , anti-GBM antibodies, IgG deposits on bx
*treat with steroids and cyclophosphamide
Hallmarks of vasculitic glomerulonephritis
1) microscopic polyangitis P-ANCA
2) glomerulonephritis with polyangitis (wegener’s) C-ANCA
*both RAPIDLY PROGRESSIVE (crescent on bx, treat with steroids and cyclophosphamide )
Central diabetes insipidus
inability of the body to produce ADH.
- shows response to desmopressin stimulation test
- treat with synthetic ADH
Nephrogenic diabetes insipidus
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
Testicular torsion; PE and tx
n/v, negative Prehn’s sign: (no pain relief with scrotal elevation)
-dx with testicular u/s and tx with detorsion
Sudden onset of left-sided varicocele in older men indicates what?
renal cell carcinoma
right-sided varicocele in children under 10 indicates what?
retroperitoneal malignancy
what is the difference between a varicocele and a hydrocele ?
varicocele=varicose veins, “bag of worms” above testicle
hydrocele= cystic testicular fluid collection, PAINLESS, should go away before 1 yr old or else surgery
Epididymitis causative organisms
if less than 35, Chlamydia (tx with ceftriaxone and doxycycline)
if older than 35, E.coli/enteric organism (tx with floroquinolones)
PE in epididymitis
postitive perhn’s sign: pain is relieved with testicular elevation, cremasteric reflex in tact
Prostatitis causative organisms
- if greater than 35, E.coli (treat with fluoroquinolone or bacterium)
- if less than 35 , chlamydia/ gonorrhea (treat with doxy & ceftriaxone)
Acute vs. chronic prostatitis presentation and treatment
ACUTE= boggy and tender, NO rectal exam, tx with abx
CHRONIC= boggy and non-tender, TURP(transurethral resection of the prostate) if refractory
Patients with prostate cancer often present with pain where?
BACK PAIN
A rubbery prostate is consistent with what diagnosis?
BPH
Tumor marker for prostate cancer
PSA (prostate specific antigen) , also elevated in BPH
Presentation of renal cell carcinoma
- hematuria
- flank pain
- palpable mass
-left sided varicocele, HTN, hypercalcemia
4 types of kidney stones
- calcium (MC)
- uric acid (from high protein intake)
- struvite (mg ammonium phosphate), from urea-splitting organisms such as PROTEASE, klebsiella, pseudomonas **staghorn calculi may form
- Cystine; genetic condition
an alkaline ph of >7.2 on UA indicated which type of stone
struvite stones
management of erectile dysfunction and CI to medications
PDE-5 inhibitors
- Sildenafil (viagra)
- Tadalafil (Cialis)
**CI in patients taking nitrates and with cardiovascular dz
Causes of renovascular hypertension (renal artery stenosis)
- in elderly=atherosclerosis
- in females under 50=fibromuscular dysplasia
Treatment of renal artery stenosis
- stent placement
2. ACEi ; if patient has bilateral stenosis ACEI ARE CONTRAINDICATED
Indications that a glomerulonephritis is rapidly progressive
- There is crescent formation on biopsy
- worse prognosis of turning to ESRD in weeks/months
- Treat with corticosteroids and cyclophosphamide
- Goodpastures and vasculitis are the two different types
What is pyurea?
WBC in the urine
What does it mean in you see epithelial cells on U/A?
This was not a clean catch specimen and it needs to be redrawn
What is the normal growth of the prostate as men age dependent on?
Increased Dihydrotestosterone (DHT) production
