UW - Med/Renal Flashcards

1
Q

What is membranous nephropathy and what are its major clinical associations?

A

Nephrotic syndrome (2nd most common)

AdenoCA, NSAIDs, Hep B, SLE

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2
Q

What is focal segmental glomerulosclerosis and its major clinical associations?

A

1 nephrotic syndrome

African Americans, HIspanics, Obesity, HIV, Heroin use

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3
Q

What symptoms are characteristics of mixed cryoglobulinemia?

A

Palpable purpura, proteinuria, hematuria, arthralgias, hepatosplenomegaly, decreased complement

Older patients, most have HCV infection

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4
Q

What are the causes of normal anion gap metabolic acidosis?

A
HARDUP
Hyperalimentation; hyperchloremic acidosis, Hypoaldosteronism
Acetazolamide, Argenine
Renal tubular acidosis
Diarrhea
Ureteral diversion
Pancreatico-duodenal fistula
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5
Q

What are the etiologies of primary adrenal insufficiency?

A

HIMA
Hemorrhagic infarct (meningococcemia, anticoagulants)
Infections (TB, HIV, disseminated fungal)
Metastatic cancer (lung)
Autoimmune

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6
Q

What are the main symptoms in acute and chronic primary adrenal insufficiency?

A

Acute - SHOCK, Ab tenderness w/ deep palp, FEVER, N/V/Wt loss/Anorex, HypoNa, HyperK, HyperCa, Eosinophilia

Chronic - Fatigue, WEAK, anorex, GI (n/v/ab pain), Weight loss, HyperPIGMENT/VITILIGO, LOW BP, same ion imbalance, Eosinophilia, ANEMIA

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7
Q

Where does aldosterone primarily act and what does it do? What can happen if it gets blocked?

A

Distal renal tubules, “saves sodium”, secretes K+ and H+

If blocked, K+ and H+ are saved –> Normal AG Met Acid

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8
Q

What is the treatment for uric acid stone?

A

Hydration, Alkalization of urine (to 6-6.5 w/ potassium citrate), low purine diet,

Add allopurinol for recurrent symptoms

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9
Q

What is the risk of calcium restriction, or decreased Ca in renal tubules for patients with kidney stones (Ca or Uric acid)?

A

Ca restriction in diet –> Negative calcium –> Hyperoxaluria from increased GI absorption of oxalate

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10
Q

What is the effect of Furosemide on urine Ca?

A

Increased excretion (because action of Na/K/Cl transport brings Ca in)

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11
Q

What is the treatment for severe hypernatremic hypovolemia? Less severe?

A

Severe = 0.9% saline which gradually corrects hyperosmolality while normalizing patient’s volume status then switch to 0.45% saline to replace free water deficit

Less = 5% dextrose in .45% saline

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12
Q

What is D5W (5% dextrose in water) used in the treatment of?

A

Euvolemic and hypervolemic hypernatremia (oral free water in stable patients)

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13
Q

What possible medication in diabetics should be removed during acute kidney injury and/or sepsis and why?

A

Metformin -> can cause lactic acidosis, withhold until renal function improves

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14
Q

What is the target blood glucose level in patients who are acutely ill and have hyperglycemia? What treatment can facilitate this?

A

140-180 mg/dL, use short acting insulin

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15
Q

What should always be considered in patients getting CT scan w/ contrast? What alternatives are available?

A

Pts w/ renal insufficiency (Cr >1.5) or history of diabetes are increased risk of contrast induced nephropathy

Use non-ionic contrast agents

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16
Q

What is the most common cause of AA amyloidosis and what can result from this?

A

Rheumatoid arthritis -> amyloidosis can lead to Nephropathy via glomerular amyloid deposits (congo red staining etc.)

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17
Q

What are linear glomerular deposits seen with immunoflorescence staining characteristic of? Granular deposits?

A

Linear = Antiglomerular basement membrane disease (Goodpasture’s)

Granular = immune complex glomerulonephritis (Lupus nephritis, IgA nephropathy, postinfection glomerulonephritis)

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18
Q

What are common causes of nephrogenic DI?

A

HyperCa, severe HypoK+, tubulointerstitial renal disease, and medication (lithium, cidofivir, foscarnet, demeclocycline, amphotericin)

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19
Q

What is detrusor sphincter dyssnergia?

A

Neurological disease where detrusor contracts while urethral spinchter contracts –> difficult voiding/interruption of urine stream

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20
Q

What are the causes of hypervolemic hypernatremia?

A

CHF, cirrhosis, chornic kidney disease or nephrotic syndrome

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21
Q

What are the causes of euvolemic and hypovolemic hypoNa+?

A

Euvol = SIADH, primary psycho polydipsia, Hypothyroid, secondary adrenal insufficiency

Hypovol = Volume loss (hemorrhage), Primary adrenal insufficiency, GI loss (diarrhea, vomit), Renal loss (diuretics)

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22
Q

How do you calculate serum osmolality and osmolar gap?

A

Serum Osm = [2Na + Glu/18 + BUN/2.8]

Osm Gap = Observed Osm - Calculated Osm

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23
Q

What causes omsolar gap met acidosis?

A

Methanol, ehtylene glycol, ethanol poisoning

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24
Q

How do you treat patients with sever hyperK+ with major EKG changes?

A
  1. Emergent administration of IV calcium gluconate to stabilize cardiac membrane
  2. Lower serum K+ by driving into cell w/ insulin and glucose, sodium bicarb, and beta 2 agonists
  3. Lower total body K+ –> loop diuretic
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25
Q

What does hyponatremia in the setting of serum Osm > 290 mOsm/kg suggest?

A

Marked hyperglycemia, Advanced renal failure

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26
Q

When should bicarb be used for the treatment of lactic acidsosis?

A

Only very severe cases where pH

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27
Q

How do you manage severe hypercalcemia?

A

Short term: NS hydration + Calcitonin (avoid loop diuretics, only use in small doses for HF pts)

Long term: bisphosphonates,

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28
Q

What are common meds that can cause hyperkalemia?

A

Nonselective beta blockers, potassium sparing diuretics (esp triamterene), ACE inhibitors, ATII-R blockers, NSAIDs

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29
Q

What are some features of cyanide toxicity?

A

Skin flushing (cherry red), AMS/seizures/coma, Arrhythmias, Tachypnea then resp depression/pulm edema/cyanosis, Ab pain/N/V, Metabolic acidosis (lactic acid) and renal failure

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30
Q

What is the presentation for patients with acute nephritic syndrome + fluid overload?

A

Anasarca, pulmonary + facial edema, HTN, proteinuria and micro hematuria (>50 rbcs, rbc casts)

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31
Q

What acid/base disorder can result with aspirin toxicity (give abg) and how does this occur?

A

Direct stimulation of medullary respiratory centers -> Tachypnea -> Resp alkalosis
Anion gap metabolic acidosis from increased production and decreased renal excretion of organic acids

Normal pH, low PaCO2 and bicarbonate

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32
Q

What is the etiology of Familial Hypocalciuric Hypercalcemia?

A

PT gland and renal tubule cell receptors resistant to Ca –> secrete excess PTH (can be high or high normal)

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33
Q

What is renal tubular acidosis?

A

Normal Anion Gap Met Acidosis w/ preserved renal fxn (usually elderly w/ poorly controlled DM

Resistance to or deficiency of Aldosterone –> K+/H+ retention

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34
Q

What is the cause in 70% of cases of interstitial nephritis?

A

Drugs like cephalosporins, penicillins, sulfonamides, sulfonamide containing diuretic, NSAIDs, rifampin, phenytoin and allopurinol

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35
Q

What two compounds are frequently observed in the urine of pts with UTI and what do they indicate?

A

Leukocyte esterase - significant pyuria

Nitrites - Enterobacteriae convert Nitrates to nitrites

36
Q

Which medications can lead to hyperkalemia?

A

Nonselective beta blockers, ACEI, ARBs, K+ sparing diuretics, Digitalis, Cyclosporine, Heparin, NSAIDs, Succinylcholine, Trimethoprim (HIV pts on high doses)

37
Q

What is the pathophysiology of membranoproliferative glomerulonephritis? Patients sx?

A

Dense intramembranous deposits of C3, caused by IgG antibodies (C3 nephritic factor) that react with C3 convertase leading to persistent activation of the complement pathway

Signs of Nephrotic Syndrome & dense deposits in glomerular basement membrane w/ IF + for C3

38
Q

What are the main clinical features of renal cell carcinoma?

A
  1. Classic Triad = Flank pain, hematuria, and palpable abdominal renal mass
  2. Scrotal vericoceles that don’t improve with lying down (left sided)
  3. Paraneoplastic signs - Anemia/erythrocytosis, Thrombocytosis, fever, hypercalcemia, cachexia
39
Q

What is a major risk factor in using Succinylcholine and what patients should it not be used in?

A

Significant potassium release, and life threatening arrthymias (do not use in patients with high risk for hyperkalemia)

Do not use in Crush or Burn injuries >8 hours old (rhabdomyolysis), demyelinating syndromes (GBS), tumor lysis syndrome

40
Q

What are the features of non-ketotic hyperglycemic coma and most important management?

A

Very elevated glucose, BUN, Cr, K+, Unconscious/AMS

If volume depleted FLUID RESUSCITATE

41
Q

What important complication should you look for in patients with GTC with high Cr, urine ketones, and blood, but low RBCs?

A

Rhabdomyolysis - large amounts of myoglobin released to urine

42
Q

What drug can be very helpful in facilitating stone passage and why?

A

stone impaction causes reflex ureteral spasm causing ureter to constrict leading to renal colic

Alpha-1-adrenergic receptor blockers will decrease the pain by relaxing the ureteral muscles

43
Q

What are the key associations for minimal change disease?

A

NSAID use and Lymphoma (most common nephrotic syndrome in hodgkins)

44
Q

What hematological conditions are associated with Amyloidosis nephrotic syndrome?

A

Multiple myeloma

45
Q

What type of nephropathy is often associated with solid tumor malignancies?

A

Membranous glomerulopathy

46
Q

How do you treat hypovolemic hypernatremia?

A

Volume replete w/ NS (.9%) and hypotonic fluid (D5W + .45% saline) once euvolemic

47
Q

What complication of pneumonia in an elderly patient can result w/ hypotension?

A

HoTN -> Decr Blood flow –> Renin/AT system activates -> glomerular arterioles constriction –> PreRenal Azotemia

48
Q

What is the indication to operate/amputate in diabetic foot ulcers?

A

Grade 4 (localized gangrene) and Grade 5 (Extensive gangrene of whole foot)

49
Q

How may Chronic Kidney Disease affect Calcium metabolism?

A

Decreased renal production of Vit D leading to hypocalcemia, hyperphosphatemia, and compensatory rise in PTH

50
Q

How can malignancy affect Calcium metabolism?

A

Tumor production of 1,25 - dihydroxyvitamin D (lymphoma), increased IL6 (multiple myeloma), increased tumor secretion of PTH related peptide (PTHrP), bony destruction by mets

All would cause Hypercalcemia and compensatory suppression of PTH

51
Q

If a patient presents with waxing and waning abdominal pain and pees out needle-shaped crystals, what may this indicate and how can you confirm?

A

Uric Acid stones

CT abdomen or IV pyelography (if radiolucent)

52
Q

What metabolic ion destabilization can occur following a large high risk surgery (e.g. laparotomy for liver laceration)? Symptoms?

A

Hypocalcemia, which can often occur following large surgeries requiring extensive transfusions (decreased ionized calcium from binding citrate) –> Hyperactive DTRs, muscle cramps, rarely convulsions

53
Q

What may be the cause of urinary retention in someone w/ herniated intravertebral disk and BPH?

A

Pain is limiting patient’s ability to valsalva to overcome intrabdominal pressure required to urinate

54
Q

What is the most common cause of erectile dysfunction in a patient with recent pelvic surgery?

A

Neurogenic - I.E. nerve injury

55
Q

What toxicity should you suspect highly in a patient who recently escaped a house fire? How do you treat?

A

Cyanide (tx w/ hydroxocobalamin or sodium thiosulfate) and CO poisoning (intubation/O2 therapy)

56
Q

What is methemoglobinemia?

A

Oxidation of ferrous (Fe2+) to Ferric (Fe3+) iron in Hb causing left shift of Hb curve

Caused by oxidizing agents (dapsone, nitrates, topical/local anesthetics)

57
Q

What are the reversible causes of urinary incontinence in elderly?

A

DIAPPERS
Delirium, Infection (UTI), Atrophic urethritis/vaginitis, Pharma (alpha blockers, diuretics), Psych (depression), Excessive urine output (diabetes, CHF), Restricted mobility (post surgical), Stool impaction

58
Q

When would you require long term urinary catheter placement?

A

Neurogenic bladder, urinary retention due to anatomic obstruction

59
Q

What are the clinical features of mixed cryoglobulinemia?

A

Moderate-Severe glmoerulonephritis (low complement, blood, prot in urine), arthralgias, palpable purpura, elevated transaminases, associated w/ Hep C (IgM Abs)

60
Q

What is anti-phospholipid syndrome?

A

Elevated anti-cardiolipin Abs, A/V thrombosis, loss of pregnancy, Neuro findings (cog defect), microangiopathic hemolytic anemia

61
Q

What are 2 major risk factors for Rhabdomyolysis? What is the pathophysiology and complications that can result?

A

Immobilization and Cocaine abuse

direct muscle dmg and release of CPK (elevated potassium and CPK) –> acute tubular necrosis from excessive myoglobin filtration

62
Q

How can chronic renal failure affect hemostasis and why does this occur? How can this be corrected?

A

UREMIC COAGULOPATHY

  • Platelet to vessel wall or platelet to platelet binding dysfunction -> hemorrhage, increased bleeding time
  • From Uremic toxins (guanidinosuccinic acid)
  • Tx: DDAVP, Cryoprecipitate, and conjugated estrogens
63
Q

What medications should be avoided in patients w/ severe renal insufficiency requiring anti-coagulation and why?

A

LMWH (enoxaparin), Fondaparinux (injection Factor Xa inhibitor), and Rivaroxaban (oral FXa inhib)

B/c reduced renal clearance increases anti-Xa activity levels, leading to increased bleeding risk

64
Q

An elderly patient presented w/ signs of pyelonephritis w/ a multi-drug resistance organism. What type of bacterial species was it and what tx would have been used? Risks of this treatment?

A

Gram negative rod, tx w/ aminoglycosides like Amikacin

Can lead to acute renal failure, must monitor renal function closely

65
Q

What is the earliest renal abnormality in patients w/ diabetes? later abnormality?

A

Glomerular hyperfiltration -> intraglom HTN -> progressive glomerular damage & renal fxn loss (ACEI decrease HTN)

Thickening of the glomerular basement later

66
Q

When should osmolar gap be calculated?

A

increased AG met acidosis, w/ methanol, ethanol, or ethylene glycol tox (calculate by measured and calculated serum Osm)

67
Q

When should urine anion gap be calculated?

A

When normal AG met acidosis, to determine if acidosis is due to renal (RTA or acetazolamide) vs. intestinal bicarb loss (diarrhea)

68
Q

What is a common Tx for patients w/ ascites/hypervolemia from decompensated cirrhosis? Risks involved and why?

A
  • Loop diuretics (Furosemide) –> Blocking channel causes increased Na+ to DTC –> elevated H+ and K+ secretion in urine
  • Volume contraction and increased aldosterone further promote H+ secretion
  • All this leads to: Hypokalemia, Metabolic Alkalosis, and Prerenal AKI
69
Q

What are signs of proteus mirabilis UTI? How can you differentiate from Candida, E Coli, enterococci causes?

A

-Alkalizatio nof urine (pH >7) which promotes struvite stone formation -> staghorn caliculi
-Urease positive
(normal pH and urease negative for others)

70
Q

What are the symptoms associated w/ hypercalcemia?

A

-Constipation (altered intestinal smooth muscle tone), anorexia, vomit, weakness, polyuria (defect in concentrating ability of urine), and neuro abnormalities (confusion, lethargy)

71
Q

What is the proper management of a solid testicular mass and why?

A

Radical orchiectomy (removal of testes + cord) - examine under microscope to determine cancer type and provide additional surgery, RT, Chemo depending on need

High cure rate w/ aggressive management

72
Q

What type of drug is chlorthalidone?

A

Thiazide diuretics

73
Q

What are the different types of metabolic acidosis and how can you differentiate?

A
  1. Saline-resistant has High urine chloride (excess mineralocorticoid causes H+/K+ loss and Na+ retention -> increased extracell volume -> kidneys excrete NaCl) - Cushing’s, Primary hyperaldost, Severe HypoK+
  2. Saline responsive has Low urine chloride (due to hypovolemia and hypochloremia)
74
Q

What are the dietary measures to take in preventing recurrent nephrolithiasis and why?

A
  1. Increase fluids (>2L urine/day)

2. Reduce sodium (

75
Q

What drug therapies help prevent recurrent kidney stones?

A
  1. Thiazide diuretics -> lead to mild volume depletion -> compensatory rise of Na reabsorption -> increased passive Ca reabsorption
  2. Urine alkalinization (potassium citrate/ bicarbonate salt)
  3. Allopurinol (for hyperuricosuria stones)
76
Q

What does side abdominal pain and positional discomfort that radiates to the groin most likely signify, and what diagnostic study would be most helpful?

A

Obstructive ureterolithiasis -> Abdominal Ultrasound

77
Q

What would urine analysis reveal in patients w/ contrast induced nephropathy?

A

Muddy-brown granular casts, resolves w/in 3-5 days

78
Q

What does the urinary cyanide nitroprusside test help detect?

A

Elevated cystine levels –> think Cystinuria, especially w/ hexagonal crystals in urine

79
Q

What clotting complication often occurs with nephrotic syndrome? What are the symptoms?

A

Renal vein thrombosis and other thromboembolism because of loss of antithrombin 3 (especially w/ membranous glomerulopathy)

Sx = abdominal pain, fever, hematuria

80
Q

What is used to treat SLE w/ renal involvement?

A

Cyclophosphamide

81
Q

What are the main causes of membranous glomerulonephritis?

A

Hep B/C, syphillis, gold, penicillamine, SLE and Rheumatoid arthritis

82
Q

What is the cause of acute kidney injury 2/2 acyclovir?

A

Crystal induced renal tubular obstruction

83
Q

How long does it take for drug induced acute interstitial nephritis to set in? What other findings are associated?

A

7-10 days after drug exposure

-Skin rash, eosinophilia, eosinophiluria, and pyuria

84
Q

What is the most common initial presentation of patients w/ ADPCKD and how can you diagnose?

A

HTN + bilateral upper abd masses, renal ultrasound

85
Q

What are the urine/serum osm and urine/serum Na findings in SIADH?

A

UNa >20, Uosm > 300, Serum Osm

86
Q

What is hyposthenuria? What type of patients are at risk?

A

IMpairment in in kidney’s ability to concentrate urine leading to nocturia
-Pt w/ sickle cell disease/trait may present

87
Q

What are indications for urgent dialysis?

A

AEIOU - Acidosis, Electrolyte abnormalities, Ingestion (toxic alcohols, Li), Overload, Uremia