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Nephrology Flashcards

1
Q

What is Pre-renal Azotemia?

A

Decrease in renal blood flow and/ or decrease in Glomerular hydrostatic pressure

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2
Q

Causes of Pre-renal Azotemia?

A
  • Hypovolemia
  • Hypotension
  • Renal artery stenosis/fibromuscular dysplasia
  • Decreased cardiac output
  • Medications that interfere with glomerular filtration (ACEIs, NSAIDs)
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3
Q

What is Intrinsic Renal Disease?

A

Damage to the renal parenchyma

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4
Q

Causes of Intrinsic Renal Disease?

A
  • Glomerular Disease
  • Tubular-interstitial Disease
  • Vascular Disease
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5
Q

Causes of Glomerular Disease?

A

Rapidly Progressive Glomerulonephritis:

  • Type I: GoodPasture
  • Type 2: Post-streptococcal Glomerulonephritis, Lupus nephritis, IgA nephropathy
  • Type 3: Small vessel vasculitides (Wegner’s)
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6
Q

Causes of Tubular-Interstitial Disease?

A
  • Acute Tubular Necrosis: Muddy Brown Casts
    (From Ischemic or Nephrotoxic Insults)
  • Acute Interstitial Nephritis
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7
Q

Causes of Vascular Disease of the kidney?

A
  • Intrarenal Vascular Occlusion: Renal artery thrombosis, HUS/TTP
  • Intrarenal Vasculitis: Small vessel vasculitis (Wegener’s)
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8
Q

What is Post-Renal Azotemia?

A

Renal failure due to urine obstruction

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9
Q

Causes of Urine Obstruction?

A
  • Urethral obstruction by BPH
  • Nephrolithiasis (kidney stones in urethra or impacted at bladder neck)
  • Obstruction due to neoplastic invasion/extension (e.g. neoplasia of cervix, prostate, bladder)
  • Bilateral obstruction of ureters (e.g.retroperitoneal fibrosis—ureters are retroperitoneal structures)
  • Bilateral obstruction of kidneys (e.g.bilateral staghorn stones)
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10
Q

Most Common Clinical Manifestions of Acute Kidney Injury?

A
  • Weight Gain
  • Edema
  • Oliguria
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11
Q

What type of acute renal injury has the following urine findings:

  • Minimal/no Proteinemia
  • Possible Hyaline Casts
  • Osmolarity >500
  • BUN/Cr: > 20
  • Fractional Execretion of Sodium < 1%
A

Prerenal Azotemia

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12
Q

What type of acute renal injury has the following urine findings:

  • Mild Proteinemia
  • Pigmented Granular Casts
  • Osmolarity < 350
  • BUN/Cr: < 20
  • Fractional Execretion of Sodium > 1%
A

Tubular Intrinsic Renal Disease

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13
Q

What type of acute renal injury has the following urine findings:

  • Mild Proteinemia AND Leukocytes
  • WBCs, WBC casts, RBCs, Eosinophils
  • Osmolarity < 350
  • BUN/Cr: < 20
  • Fractional Excretion of Sodium > 1%
A

Acute Interstitial Nephritis

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14
Q

What type of acute renal injury has the following urine findings:

  • Severe Proteinemia
  • RBCs AND RBC casts
  • Osmolarity > 500
  • Fractional Excretion of Sodium < 1%
A

Acute Glomerulonephritis

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15
Q

What type of acute renal injury has the following urine findings:

  • Minimal/No Proteinemia
  • Crystals, RBCs, WBCs
  • Osmolarlity < 350
  • Fractional Excretion of Sodium > 1%
A

Postrenal Azotemia

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16
Q

Treatment for Acute Kidney Injury?

A
  • Treat underlying cause
  • Treat fluid imbalances
  • Treat electrolyte imbalances
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17
Q

Definition of Chronic Kidney Disease?

A
  • GFR < 60

- Urinary Albumin Excretion > 30

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18
Q

Causes of Chronic Kidney Disease?

A
  • Type II Diabetes Mellitus
  • Hypertension
  • Chronic Glomerulonephritis
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19
Q

Lab Findings in Chronic Kidney Disease?

A
  • Elevated BUN & Cr
  • Increased K+& phosphate
  • Decreased Na+& Ca2+
  • Normochromic, normocytic anemia
  • Metabolic acidosis
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20
Q

Therapy to reduce Proteinuria in Chronic Kidney Disease?

A

ACE- Inhibitors or ARBs

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21
Q

Therapy to treat Anemia in Chronic Kidney Disease?

A

Erythropoietin Stimulating Agents

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22
Q

Dietary Modifications in Chronic Kidney Disease?

A
  • Low Phosphorous Diet/ Phosphorous Binders
  • Vitamin D analogs-> Decrease PTH levels
  • Low Potassium Diet-> Treat Hyperkalemia
  • Protein Restriction (Advanced CKD)
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23
Q

Therapy to treat Metabolic Acidosis in CKD?

A

Sodium Bicarbonate

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24
Q

Indications of emergent dialysis?

A

AEIOU

  • Acidosis
  • Electrolyte abnormalities
  • Ingestion of toxins
  • Overload of fluid
  • Uremia
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25
Q

Medications that cause Acute Interstitial Nephritis?

A
  • Penicillin derivatives (methicillin, ampicillin)
  • NSAIDs
  • Allopurinol
  • Sulfa-derivedDiuretics (thiazides, furosemide)
  • Cephalosporins
  • Proton pump inhibitors
  • Sulfonamide antibiotics (sulfamethoxazole)
  • Sulfasalazine (used to treat Crohn disease, UC, RA)
  • Rifampin
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26
Q

Other toxins that cause Acute Interstitial Nephritis?

A
  • Cadmium
  • Lead
  • Copper
  • Mercury
  • Toxins from some mushroom
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27
Q

Diseases/Conditions that cause Acute Interstitial Nephritis?

A
  • Infections (Strep. Legionella)
  • Sarcoidosis
  • Amyloidosis
  • SLE
  • Myoglobinuria
  • High uric acid levels
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28
Q

Kidney biopsy in Acute Interstitial Nephritis will show?

A

Infiltration of Inflammatory Cells and Tubular Cell Necrosis

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29
Q

Complications of Acute Interstitial Nephritis?

A
  • Acute tubular necrosis
  • Acute or chronic renal failure
  • Renal papillary necrosis
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30
Q

Clinical Presentation of Minimal Change Disease?

A

Young Child w/ massive proteinuria. May have recent respiratory infection

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31
Q

Treatment of Minimal Change Disease?

A
  • Oral Prednisone
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32
Q

Indications for a kidney biopsy to diagnose Minimal Change Disease?

A
  • In Adults

- In Children refractory to steriods

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33
Q

Light and Electron Microscopy Findings in Minimal Change Disease?

A
  • Light Microscopy: Normal

- Electron Microscopy: Effacement of Podocytes

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34
Q

Lab Findings in the Minimal Change Disease?

A
  • Hyperlipidemia
  • Hypoalbuminemia
  • Heavy proteinuria
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35
Q

Risk Factors for Focal Segmental Glomerulosclerosis?

A
  • Minority (African Americans)
  • Obesity
  • Sickle cell disease
  • AIDS (HIV)
  • IV drug abuse (heroin) andInterferon treatment
  • Chronic kidney disease(secondary to congenital absence or surgical removal)
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36
Q

Symptoms of Nephrotic Syndrome?

A
  • Edema
  • Foamy urine
  • Hypertension
  • Dyspnea
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37
Q

Treatment for FSGS?

A
  • Corticosteriods (Prednisone)

- Calcineurin Inhibitors (Cyclosporine, Tacrolimus)

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38
Q

Clinical Presentation of FSGS?

A
  • Hyperlipidemia
  • Hypoalbuminemia
  • Hematuria
  • High levels of proteinuria
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39
Q

What type of nephritic/nephrotic syndrome is associated with the following conditions?

    Henoch Schönlein purpura
Cirrhosis
Celiac disease
Inflammatory disorders (e.g. sarcoidosis and IBD)
A

IgA Nephropathy

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40
Q

Clinical Presentation of IgA Nephropathy?

A
  • Hemoturia
  • Flank Pain
  • Low Grade Fever
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41
Q

Diagnostic test for IgA Nephropathy?

A

Kidney Biopsy

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42
Q

Light and Electron Microscopy Findings?

A
  • Light Microscopy: Mesangial widening

- Electron Microscopy: Mesangial proliferation and Immune complexes

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43
Q

Urine analysis findings in IgA nephropathy?

A
  • Hemoturia (RBCs and RBC casts)

- Proteinuria

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44
Q

Treatment for IgA Nephropathy?

A
  • ACE- Inhibitors/ ARBs

- Glucocorticoids (Severe)

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45
Q

Causes of secondary Membranous Nephropathy?

A
  • Hepatitis B,syphilis
  • Systemic lupus erythematosus
  • Solid tumors(esp.carcinomas)
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46
Q

Medications that cause Membranous Nephropathy?

A
  • Penicillamine
  • High-dose captopril
  • NSAIDs(eg, diclofenac)
  • Parenteral gold salts(eg, gold sodium thiomalate)​
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47
Q

Urinalysis in Membranous Nephropathy?

A
  • Nephrotic-range proteinuria
  • Oval fat bodies, lipid droplets, fatty casts
  • Microscopic hematuria
  • Glucosuria despite normal blood glucose levels*
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48
Q

Clinical Presentation of Membranous Nephropathy?

A
  • Anorexia
  • Fatigue
  • Malaise
  • Edema w/o HTN
49
Q

Complication of Membranous Nephropathy?

A
  • DVT in extremities

- Renal Vein Thrombosis

50
Q

Light and Electron Microscopy Findings in Membranous Nephropathy?

A

Light Microscopy:
- Basement Membrane and Capillary wall thickening

Electron Microscopy:

  • Spike and dome appearance from Subepithelial deposits of IgG and C3
  • Podocyte Effacement
51
Q

Treatment for Membranous Nephropathy?

A
  • ACE-Inhibitors/ ARBs

- Anticoagulation (Patients w/ Serum Albumin < 3)

52
Q

Membranproliferative Glomerulonephritis is associated with which conditions?

A
  • Autoimmune disease
  • Hepatitis B &C
  • Lupus
  • Bacterial endocarditis
53
Q

Lab Findings of Membroproliferative Glomerulonephritis?

A
  • Hematuria

- Hypocomplementemia

54
Q

Electron Microscopy findings in Membroproliferative Glomerulonephritis?

A
  • Type I: Tram-track appearance due to basement membrane splitting
  • Type II: Dense intramembranous deposits
55
Q

Treatment of Membroproliferative Glomerulonephritis?

A
  • Corticosteroids w/ Aspirin, Dipyridamole

* Treatment slows progression but will progress to renal failure*

56
Q

Cause of Post-Streptococcal Glomerulonephritis?

A

Strep pharyngitis or impetigo infection 2-4 weeks prior

57
Q

Clinical Presentation of Post-Strep GN?

A
  • Gross Hematuria (Tea colored urine)
  • Hypertension
  • Edema (Periorbital)
58
Q

Urine Findings in Post-Strep GN?

A
  • Hematuriawithdysmorphic red cells
  • ± Red blood cell casts
  • Pyuria
  • Proteinuria(nephritic range, <3.5 g/day)
59
Q

Lab Findings in PSGN?

A
  • Transient Decrease in GFR
  • Increased BUN and Creatinine
  • Hypocomplementemia (C3)
60
Q

Electron microscope findings of PSGN?

A
  • Starry sky, Lumpy bumpy
  • Subepithelial dome shaped deposits of C3, IgG, IgM
  • In a diffuse, finely granular pattern
61
Q

Treatment of PSGN?

A

Supportive Care

  • Fluid & sodium restriction
  • Loop diuretics for HTN, edema
  • K+, PO43-restriction as necessary
62
Q

Treatment for Rapidly Progressive Glomerulonephritis?

A
  • Steriods
  • Plasmapheresis
  • Cytotoxic Agents
63
Q

Clinical Presentation of RPGN?

A
  • Nephritic Syndrome
  • Sudden Renal Failure
  • Olgiuria
64
Q

Characteristics of the 3 types of RPGN?

A
  • Type 1: Anti-GBM antibodies
  • Type 2: Immune Complex Deposition
  • Type 3: Absence of Immune Complexes
65
Q

Definite Diagnostic test for RPGN?

A

Kidney Biopsy

66
Q

Lights Microscopy Findings in RPGN?

A

Crescents in Glomeruli

67
Q

Clinical Triad of Goodpasture Syndrome?

A
  • Pulmonary Hemorrhage (Hemoptysis)
  • Anti-GBM antibodies
  • RPGN (Hematuria, edema)
68
Q

Treatment for Goodpasture Syndrome?

A
  • Steriods
  • Plasmapheresis
  • Cyclophosphamide
69
Q

Kidney Biopsy findings in Goodpasture Syndrome?

A

Linear Pattern with immunofluorescence

70
Q

Stones that occur when a patient develops an upper urinary tract infection with a urease-producing organism such as Klebsiella or Proteus?

A

Struvite stones

71
Q

Uric acid stones occur in patients with which conditions?

A
  • Gout
  • Diabetes Mellitus
  • Chronic Diarrhea
  • Increased Uric Acid Production
72
Q

Signs and Symptoms of renal stones?

A
  • Renal Colic
  • Hydronephrosis
  • Infection
  • Gross Hematuria
73
Q

Abdominal X-ray will show most renal stones except?

A
  • Uric acid Stones

- Very small stones

74
Q

Urinary pH of > 6 indicates which type of kidney stone?

A

Struvite Stones

75
Q

Urinary pH of < 5 indicates which type of kidney stone?

A

Uric Acid Stones

76
Q

Best diagnostic imaging for kidney stones?

A

Noncontrast Abdominal/Pelvic CT

77
Q

Treatment for Nephrolithiasis with small stones (<5mm)?

A

Analgesics (NSAIDs) and Hydration until stones passes

78
Q

Treatment for Nephrolithiasis with large stones (>8mm)?

A
  • Extracorporeal shockwave lithotripsy

- Percutaneous nephrolithotomy.

79
Q

Best diagnostic tests for diabetic nephropathy?

A

Albumin to creatinine ratio on spot urine test (>300 mg/day)

80
Q

Characteristics of Diabetic Nephropathy?

A
  • Persistent Albuminuria

- Progressive GFR decline

81
Q

Kidney Biopsy Findings in Diabetic Nephropathy?

A
  • Nodular Sclerosis (Kimmelstiel-Wilson nodules)
82
Q

Treatment for Diabetic Nephropathy?

A
  • Maintain Glucose Control

- ACE- Inhibitors/ ARBs to slow progression

83
Q

What is Diabetes Insipidus?

A

The body’s inability to reabsorb water from the urine

84
Q

What is Central Diabetes Insipidus?

A

Decreased ADH synthesis from the hypothalamus or Decreased ADH release from the posterior pituitary

85
Q

Causes of Central Diabetes Insipidus?

A
  • Idiopathic: destruction of the ADH-secreting cells in the hypothalamus
  • Trauma
  • Tumors
  • Anorexia nervosa
86
Q

What is Nephrogenic Diabetes Insipidus?

A

The kidneys are resistant to ADH

87
Q

Conditions that cause Nephrogenic Diabetes Insipidus?

A
  • Hereditary renal diseases
  • Drugs
  • Hypokalemia
  • Hypercalcemia
88
Q

Drugs that cause Nephrogenic Diabetes Insipidus?

A
  • Lithium
  • Demeclocycline (tetracycline antibiotic)
  • Cidofovir (antiviral)
  • Foscarnet (antiviral)
  • Amphotericin (antifungal)
89
Q

Urinalysis Findings in Diabetes Insipidus?

A
  • Urine osmolality will be < Serum osmolality
  • Urine specific gravity <1.006
  • Urine osmolality < 200 osmol/kg
  • Serum osmolality >290 osmol/kg
90
Q

Low urine specificity and low serum osmolarity indicates?

A

Psychogenic Polydypsia

91
Q

Water deprivation test findings of Diabetes Insipidus?

A

No change in urine osmolality after water deprivation

92
Q

Results of DDVAP for Central and Nephrogenic Diabetes Insipidus?

A

Central: Increased Urine Osmolality

Nephrogenic: No change in Urine Osmolality

93
Q

Treatment for Central Diabetes Insipidus?

A

Desmopressin (Synthetic ADH)

94
Q

Treatment for Nephrogenic Insipidus?

A
  • Treat Underlying Condition
  • Hydrochlorothiazide
  • Indomethacin
  • Amiloride (Lithium induced DI)
95
Q

Diagnostic Criteria for Diabetes Mellitus?

A
  • Fasting Serum Glucose > 126
  • HbA1C > 6.5%
  • Random Blood Glucose > 200 w/ symptoms
96
Q

Lab Findings in Type 1 DM?

A
  • Autoantibodies against Pancreatic islets

- Low or inappropriate normal C-Peptide

97
Q

Complications of Hyperglycemia?

A
  • Nephropathy
  • Neuropathy
  • Vascular Damage
  • Diabetic Ketoacidosis
98
Q

Treatment for Type I DM?

A

Insulins

  • Long acting insulin (Lantus)
  • Rapid acting (Lispro) at meals
99
Q

Clinical Presentation of Diabetes Mellitus?

A
  • Polyphagia
  • Polydipsia
  • Polyuria
100
Q

Screening Recommendations for patients with Diabetes Mellitus (Type 1 &2)?

A
  • Albumin/creatinine ratio minimum yearly
  • Hemoglobin A1c every 3 months
  • Annual eye and foot exams
101
Q

Risk Factors for Type II DM?

A
  • Obesity
  • Sedentary lifestyle and physical inactivity
  • History of gestational diabetes
  • Family history of diabetes
  • Coexisting hypertension and dyslipidemia
  • Increasing age
  • Certain ethnic groups (African-Americans, Native Americans, Asian Americans, Pacific Islanders)
102
Q

Adverse effects of Metformin?

A
  • GI upset
  • Vitamin B12 Deficiency
  • Lactic Acidosis
103
Q

Contraindications of Metformin?

A

Renal insufficiency (leads to lactic acidosis)

104
Q

Adverse effects of Sulfonylureas (Glipizide) and Meglitinides (Repaglinide)?

A
  • Hypoglycemia

- Weight Gain

105
Q

Adverse effects of Chlorpropramide (sulfonylurea)?

A
  • Disulfiram-like reaction

- Hyponatremia

106
Q

How do GLP-1 agonists (Exenatide, Lixisenatide) treat diabetes?

A
  • ↓Inappropriateglucagon release
  • ↑ Glucose-dependent insulin release
  • ↓ Gastric emptying→↑ satiety→↓ food intake→weight loss
107
Q

Adverse effects of GLP-1 agonists?

108
Q

Contraindications of GLP-1 agonists?

A
  • Gastroparesis
  • History of Pancreatitis
  • MEN 2A or 2B
  • Medullary thyroid cancer history
109
Q

Complications of DPP-4 Inhibitors (Linagliptin, Saxagliptin)?

A
  • Upper Respiratory Infection

- UTI

110
Q

Contraindications of Thiazolidinediones (Pioglitazone, Rosiglitazone)?

A
  • Bladder Cancer
  • CHF
  • Active Liver Disease
  • Fractures
111
Q

Adverse effects of Alpha Glucosidase Inhibitors?

A
  • Flatulence

- Diarrhea

112
Q

Screening recommendations for Diabetes Mellitus?

A

Every 3 years for Adults (40-70 yrs old) who are overweight or obese.

113
Q

Diagnostic Criteria for Pre-Diabetes?

A
  • A1C of5.7% to 6.4%
  • FPG between 100 mg/dL to 125 mg/dL
  • 2-hour plasma glucose of140 to 199 mg/dL via OGTT
114
Q

Clinical Presentation of Diabetic Ketoacidosis?

A
  • Abdominal Pain
  • Vomiting
  • Fruity odor breath
  • Profound Dehydration
115
Q

Respiratory compensation for the metabolic acidosis in DKA?

A

Kussmaul Respirations (deep, rapid breathing)

116
Q

Diagnostic Criteria of DKA?

A
  • Elevated glucose (>250mg/dL)
  • Anion gap metabolic acidosis (bicarbonate < 15mEq/L, pH < 7.30, AG > 17)
  • Urine strongly positive for glucose and ketones
117
Q

Treatment for DKA?

A
  • Normal saline
  • Potassium
  • Insulin and glucose
  • Treatment of the precipitating event as appropriate (infection, intoxication, etc)
118
Q

Why should fluid resuscitation be done slowly in DKA?

A

To prevent cerebral and pulmonary edema

Internal Medicine (15 decks)

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