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3rd Year (Step 2) > Renal > Flashcards

Renal Flashcards

1
Q

What do Nitrites indicate on Urinalysis?

A

Gram-negative bacteria on dipstick

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2
Q

What are the 2 parts of the Urinalysis?

A
  1. Dipstick if positive (leukocyte esterase, nitrites, etc.)
  2. Microscopic analysis (RBCs, WBCs, bacteria, casts, crystals)
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3
Q

What does moderate vs. proteinuria mean?

A

Moderate = Tubular or Glomerular disease

Severe = Glomerular disease

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4
Q

What can increase urine protein excretion in normal individuals?

A

Standing & physical activity

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5
Q

If proteinuria persists & is not related to prolonged standing, what should be the next step?

A

Kidney biopsy

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6
Q

What type of protein does urine dipstick test?

A

Albumin ONLY

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7
Q

Method used to assess total amount of protein excreted in a day?

A

Protein : Creatinine ratio

also 24-hr urine collection, but less rarely performed b/c takes longer

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8
Q

Normal protein excretion per 24-hr?

A

< 300mg

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9
Q

What do you do for a diabetic patient w/ Microalbuminuria (30-300 mg/24hrs)?

A

Start them on ACE-inhibitor

L-T microalbuminuria in diabetic patients worsens renal function

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10
Q

Eosinophils present on urinalysis indicate what?

A

Allergic interstitial nephritis

specific

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11
Q

Does NSAID-induced renal disease show eosinophils?

A

No

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12
Q

Possible etiologies of hematuria?

A
  • Stones in bladder, ureter, or kidney
  • Coagulopathy (causing bleeding)
  • Infection (cystitis, pyelonephritis)
  • Cancer of bladder, ureters, or kidney
  • Tx (cyclophosphamide – hemorrhagic cystitis)
  • Trauma
  • Glomerulonephritis
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13
Q

What to do next if urine dipstick is markedly positive for blood?

A

Microscopic examination of the urine

- to rule out hemoglobin & myoglobin w/out red cells (false positive)

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14
Q

Most accurate test of the bladder?

A

Cystoscopy

obtain when bladder sonography shows a mass

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15
Q

When to obtain cystoscopy w/ hematuria?

A
  1. Renal U/S or CT doesn’t show an etiology
    or
  2. Bladder sonography shows a mass
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16
Q

Significance of a red cell cast?

A

Glomerulonephritis

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17
Q

Significance of a white cell cast?

A

Pyelonephritis

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18
Q

Significance of an eosinophilic cast?

A

Acute (allergic) interstitial nephritis

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19
Q

Significance of a hyaline cast?

A

Dehydration concentrates the urine & normal Tamm-Horsfall protein precipitates or concentrates into a cast

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20
Q

Significance of a broad, waxy cast?

A

Chronic renal disease

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21
Q

Significance of a granular “muddy-brown” cast?

A

Acute tubular necrosis; they are collections of dead tubular cells

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22
Q

T or F?

You must obstruct both kidneys for the Cr to rise.

A

True

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23
Q

AKI symptoms?

A
  • Nausea & vomiting
  • Tired/malaise
  • Weakness
  • SOB & edema from fluid overload

VERY severe disease p/w: Confusion, arrhythmia from hyperkalemia & acidosis, sharp pleuritic CP from pericarditis

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24
Q

Electrolyte imbalance typically caused by AKI?

A

Hyperkalemia & Acidosis

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25
Q

ATN – urine osmolality?

A

< 300 mOsm/kg

low b/c kidney cells cannot reabsorb water

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26
Q

Prerenal azotemia – urine osmolality?

A

> 500 mOsm/kg

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27
Q

ATN – FeNa?

A

> 1%

high b/c kidney cells cannot reabsorb Na

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28
Q

Prerenal azotemia – FeNa?

A

< 1%

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29
Q

What should be given prior to chemotherapy to prevent renal failure from tumor lysis syndrome?

A

Allopurinol, Hydration, & Rasburicase

b/c TLS causes hyperuricemia, which damages kidneys

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30
Q

How does Tumor Lysis Syndrome cause renal failure?

A

Hyperuricemia

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31
Q

What type of kidney damage do injection opiates cause?

A

Focal Segmental Glomerulonephritis

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32
Q

How does Ethylene Glycol cause ATN?

A

Precipitation of Calcium Oxalate in the renal cortex

thus look for suicidal pt ingesting something w/ kidney damage & hypocalcemia

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33
Q

3 major causes of hypERvolemic hypOnatremia?

A

CHF
Nephrotic Syndrome
Cirrhosis

**pressure receptors in atria & carotids sense decrease in volume & stimulate ADH production/release

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34
Q

4 most common causes of Euvolemic hypOnatremia?

A
  • Hyperglycemia (pseudo-hyponatremia – glucose pulls H2O out of cells, diluting Na)
  • Psychogenic polydipsia (massive ingestion of H2O)
  • Hypothyroidism
  • SIADH
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35
Q

Common causes of HypOvolemic HypOnatremia?

A
  • Sweating
  • Burns
  • Fever
  • Pneumonia (insensible losses 2/2 hyperventilation)
  • Diarrhea
  • Diuretics
  • *all are causes of hypernatremia, but w/ chronic H2O replacement, eventually cause hypOnatremia
  • Addison Disease
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36
Q

Glomerulonephritis: describe the urine sodium & FeNa

A

Both low

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37
Q

Goodpasture Syndrome involves what organs?

A

Lung & Kidney

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38
Q

How to differentiate Goodpasture Syndrome vs. Wegener Granulomatosis?

A
  • WG has upper respiratory tract involvement

- GS is limited to lung & kidney

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39
Q

Goodpasture Syndrome: best initial & most accurate test(s)?

A

Best initial = Antiglomerular basment membrane antibody

Most accurate = Lung or Kidney biopsy w/ “linear deposits”

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40
Q

Most common cause of acute glomerulonephritis in the USA?

A

IgA Nephropathy (Berger Disease)

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41
Q

Dx?

Asian patient w/ recurrent episodes of gross hematuria 1-2 days after URI.

A

IgA Nephropathy (Berger Disease)

  • Poststreptococcal Glomerulonephritis follows pharyngitis by 1-3 wks
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42
Q

Poststreptococcus Glomerulonephritis presentation?

A
  • Dark (cola-colored) urine
  • Edema (often periorbital)
  • Hypertension
  • Oliguria
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43
Q

Alport Syndrome - what is it?

A

Congenital defect of Type 4 Collagen

Presentation = Glomerular disease, Sensorineural hearing loss, & Visual disturbance (lens dislocation)

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44
Q

Polyarteritis Nodosa - what is it?

A

Systemic vasculitis of small & medium-sized vessels

  • almost always affects kidneys & spares lungs
  • can affect virtually all other organs of the body
  • ass’d w/ Hep B
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45
Q

Stroke or MI in a young person suggests what pathology?

A

Polyarteritis Nodosa (vasculitis)

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46
Q

Pathology of nephrotic syndrome?

A

Any damage to the kidney that causes such high proteinuria that the liver cannot keep up its production of albumin
> 3.5 grams of protein / 24hrs

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47
Q

Nephrotic Syndrome – presentation?

A
  • Edema (Periorbital)
  • Hyperlipidemia (lipoprotein signals that turn off production of circulating lipids are lost in urine)
  • Thrombosis (urinary loss of Protein C, Protein S, & antithrombin)
  • Infections frequent (loss of Igs & complement)
48
Q

Nephrotic Syndrome - best initial & most accurate test(s)?

A

Best initial = Urinalysis (Maltese crosses)

Most accurate = Renal biopsy

49
Q

What are Maltese Crosses?

A

Lipid deposits in sloughed-off tubular cells, seen on UA in Nephrotic Syndrome

50
Q

Nephrotic Syndrome - Tx?

A

Glucocorticoids (then other IMs like Cyclophosphamide, if necessary)

  • ACE-inhibitors or ARBs (proteinuria)
  • Salt restriction & diuretics (edema)
  • Statins (hyperlipidemia)
51
Q

Dialysis indications?

A
  • Metabolic acidosis
  • Fluid overload
  • Encephalopathy
  • Hyperkalemia
  • Pericarditis

(any life-threatening condition that can NOT be corrected another way)

52
Q

Uremia definition?

A

Presence of any of these:

  • Metabolic acidosis
  • Fluid overload
  • Encephalopathy
  • Hyperkalemia
  • Pericarditis

(Uremia = conditions for which dialysis is answer as therapy)

53
Q

Manifestations of ESRD?

A
  • Anemia (loss of erythropoietin)
  • Hypocalcemia (no conversion of 25, vit D to 1,25)
  • Hyperparathyroidism (2o) & Osteodystrophy (low calcium)
  • Bleeding (platelets don’t degranulate in uremic environment)
  • Infection (neutrophils don’t work w/out degranulation)
  • Pruritis (uremia)
  • Hyperphosphatemia (hyperparathyroidism + cannot excrete)
  • Hypermagnesemia (cannot excrete)
  • Accelerated Atherosclerosis & HTN (immune system usually clears arteries of lipid accumulation)
  • Endocrinopathy: women are anovulatory & men have low testosterone & impotence. Insulin levels increase as does resistance
54
Q

How to treat Hypocalcemia in ESRD?

A

Give vitamin D & oral Phosphate binders

  • b/c vit D will increase phosphate absorption from GI & secondary hyperparathyroidism causes hyperphosphatemia in ESRD
55
Q

How to treat hyperphosphatemia?

A
  • Calcium acetate
  • Calcium carbonate

if hypercalcemia, use:

  • Sevelamer
  • Lanthanum
56
Q

5 manifestations of TTP?

A
  • Intravascular hemolysis (schistocytes, helmet cells, & fragmented red cells on smear)
  • Renal insufficiency
  • Thrombocytopenia
  • Neurological symptoms
  • Fever
57
Q

TTP & HUS Tx?

A 
TTP = urgen plasmapheresis
HUS = usually resolve spontaneously.  If severe, needs urgent plasmapheresis
  • if no Plasmapheresis available, infusion of Fresh Frozen Plasma
  • steroids do NOT help
58
Q

Causes of Nephrogenic DI?

A

Lithium, Demeclocycline, CKD, hypOkalemia, hypERcalcemia

  • they make ADH ineffective @ the tubule
59
Q

Dx? inc’d urine volume despite dehydration & hyperosmolality of the blood.

A

Diabetes Insipidus

60
Q

How to diagnose Diabetes Insipidus?

A

Water deprivation test

  • “positive” = urine volume stays high = NDI
  • “negative” = CDI
61
Q

CDI – Tx?

A

DDAVP (Vasopressin to replace ADH)

62
Q

NDI – Tx?

A
  • Correct potassium & calcium
  • Stop lithium or demeclocycline
  • Give Hydrochlorothiazide or NSAIDs for those still having NDI despite these interventions
63
Q

Hypo- & Hyper-natremia cause what type of symptoms?

A

CNS — lethargy, confusion, disorientation, seizures, coma

  • Sx are more dependent on the RATE @ which Na levels change
64
Q

SIADH – describe the uric acid & BUN levels?

A

Both low

65
Q

Mild Hyponatremia - Sx & Tx?

A

No symptoms

Tx = restrict fluids

66
Q

Moderate Hyponatremia – Sx & Tx?

A

Sx = Minimal confusion

Tx = Saline & loop diuretics
saline w/out diuretics makes SIADH worse

67
Q

Severe Hyponatremia - Sx & Tx?

A

Sx = Lethargy, Seizures, Coma

Tx = Hypertonic saline, Conivaptan, Tolvaptan (ADH-antagonists)

68
Q

When to use Conivaptan/Tolvaptan vs. Demeclocycline in SIADH?

A

Conivaptan/Tolvaptan are part of urgent inpatient therapy for severe, symptomatic SIADH (no oral versions available)

Demeclocycline treats chronic SIADH, blocking ADH action @ the collecting duct

69
Q

Rate @ which Na can be safely corrected?

A
  1. 5-1 mEq/hr (12-24 mEq/day)

- to avoid Central Pontine Myelinolysis

70
Q

Causes of Pseudohyperkalemia?

A
  • Hemolysis
  • Repeated fist clenching w/ tourniquet in place
  • Thrombocytosis or Leukocytosis
71
Q

Causes of Hyperkalemia?

A
  • Renal failure
  • Aldosterone decrease (ACE-inhibitors/ARBs, RTA type 4, Spironolactone/Eplerenone, Triamterene/Amiloride, Addison disease)
  • Tissue destruction (hemolysis, rhabdomyolysis, tumor lysis syndrome)
  • Decreased insulin (insulin drives K into cells)
  • Acidosis (cells take in H in exchange for K)
  • β-blockers & Digoxin (inhibit Na/K ATPase that brings K into cells)
  • Heparin
72
Q

Hyperkalemia Sx?

A

Interferes w/ muscle contraction & cardiac conductance:

  • Weakness
  • Paralysis (when severe)
  • Ileus (paralyzes gut muscles)
  • Cardiac rhythm disorders
73
Q

EKG in severe hyperkalemia?

A
  • Peaked T waves
  • Wide QRS
  • PR interval prolongation
74
Q

Severe Hyperkalemia w/ EKG changes - Tx?

A
  • Calcium chloride or gluconate (protects heart, doesn’t affect K levels)
  • Insulin & glucose (drives K back into cells)
75
Q

Hyperkalemia - non-urgent Tx?

A
  • Kayexalate (removes K from body via gut)
  • Insulin & bicarbonate (esp. if acidosis)

Other methods: Inhaled β-agonists, Loop diuretics, Dialysis

76
Q

Hypokalemia - causes?

A
  • Shift into cells (Alkalosis, inc’d insulin, β-adrenergic stimulation – accelerates Na/K ATPase)

Renal loss: Loop diuretics, inc’d Aldosterone, Hypomagnesemia, RTA types 1 & 2

GI loss: Vomiting, Diarrhea, Laxative abuse

77
Q

Hypokalemia - Sx?

A
  • Weakness
  • Paralysis
  • Loss of reflexes
78
Q

Hypokalemia – EKG findings?

A
  • U waves (most characteristic)

Other findings: PVCs, flattened T waves, ST depression

79
Q

2 most important causes of normal AG acidosis?

A

RTA & Diarrhea

“Hyperchloremic Acidoses” – these have a normal AG b/c Chloride levels rise

80
Q

RTA type 1 – pathology?

A

“Distal RTA”

  • DT cannot produce Bicarbonate (normally should under influence of Aldosterone)
  • 2/2 damage of DT by drugs such as Amphotericin or autoimmune diseases like SLE or Sjogren syndrome
81
Q

RTA type 1 – Tx?

A

Give Bicarbonate (prox tubule will absorb it & correct acidosis)

82
Q

Which RTA has urine pH > 5.5?

A

RTA type 1

type 2 has basic urine @ first, then turns acidic

83
Q

RTA type 2 – pathology?

A

Proximal tubule damage = cannot reabsorb Bicarbonate

  • distal tubule starts to reabsorb if left untreated, causing urine pH < 5.5
  • Chronic metabolic acidosis leaches Ca out of bones — causes osteomalacia
84
Q

RTA type 2 – Tx?

A

Thiazide diuretics – cause volume depletion, which enhances bicarbonate reabsorption

85
Q

RTA type 4 – pathology?

A

Hyoaldosteronism or lack of response to aldosterone

  • Na loss in urine despite low intake
  • Causes hyperkalemia, which impairs ammonia genesis in the PT, leading to dec’d buffering capacity & dec’d urine pH
86
Q

RTA type 4 – pathology?

A

Fludrocortisone

glucocorticoid w/ most mineralocorticoid effects

87
Q

How to distinguish Diarrhea vs. RTA?

A

Urine Anion Gap (= Na - Cl)

  • Normal in Diarrhea
  • Positive in RTA (acid excreted as NH4Cl, ammonium chloride, except in RTA there’s a prob w/ acid excretion, thus less Cl excretion)
88
Q

Lactic Acidosis – Tx?

A

Correct hypoperfusion (since this is cause of LA)

89
Q

Ketoacidosis – test?

A

Acetone level

90
Q

Oxalic acid acidosis – test? Tx?

A

Test = Crystals on UA

Tx = Fomepizole, dialysis

91
Q

Formic acid acidosis (methanol O/D) – Test? Tx?

A

Test = Inflamed retina

Tx = Fomepizole, dialysis

92
Q

Aspirin overdose causing metabolic acidosis – Tx?

A

Alkalinize urine

93
Q

Acetazolamide effects?

A

Alkalinizes urine, causes “ACIDosis”

  • Carbonic Anhydrase inhibitor, causes self-limited NaHCO3 diuresis & reduction in total body bicarbonate stores
94
Q

Furosemide – AEs?

A

Ototoxicity, Hypokalemia, Allergy (sulfa), Nephritis (interstitial), Gout

“OH DANG!”

95
Q

Hydrochlorothiazide – AEs?

A

HypOkalemic metabolic alkalosis, hypOnatremia, sulfa allergy
- hyperGlycemia, hyperLipidemia, hyperUricemia, & hyperCalcemia
“hyperGLUC”

96
Q

Metabolic Alkalosis – causes?

A
  • GI loss (vomiting or nasogastric suction)
  • Inc’d Aldosterone
  • Diuretics
  • Milk-alkali syndrome: high-volume liquid antacids
  • Hypokalemia (hydrogen ions move into cells so K can be released)
97
Q

What is “Minute Ventilation”?

A

= Resp. Rate x Tidal Volume

98
Q

NSAID that provides analgesia similar to opioids?

A

Ketorolac

99
Q

Nephrolithiasis – most appropriate 1st step?

A

Ketorolac – can stop excruciating pain before Dx tests

+ Hydration

100
Q

Nephrolithiasis – most accurate diagnostic test?

A

CT scan (does not need contrast)

101
Q

Most common cause of nephrolithiasis?

A

Calcium oxalate (inc’d urine pH, >5.5)

102
Q

How can Crohn’s Disease cause nephrolithiasis?

A

Increased Oxalate absorption

103
Q

Type of stones that aren’t visible on x-ray but are on CT?

A

Uric acid stones

104
Q

Tx of stones 5-7mm?

A

Nifedipine & Tamsulosin

  • < 5mm stones will pass on their own
105
Q

Which diuretic prevents kidney stones & how?

A

Hydrochlorothiazide – removes Ca from urine by increasing distal reabsorption

(Furosemide increases Ca excretion into urine & can make it worse)

106
Q

How does Metabolic Acidosis cause stones?

A

removes Calcium from bones
&
decreases Citrate levels
(citrate normally binds calcium, making it unavailable for stone formation)

107
Q

HTN – best initial drug Tx?

A

Thiazide diuretics

108
Q

Pregnancy safe HTN drugs?

A

β-blockers (use first)

  • CCB
  • Hydralazine
  • α-methyldopa
109
Q

HTN & CAD – best initial Tx?

A

BB, ACE, ARB

110
Q

HTN & BPH – best initial Tx?

A

α-blockers

111
Q

HTN & Depression – best initial Tx?

A

avoid BBs

112
Q

HTN & Asthma – best initial Tx?

A

avoid BBs

113
Q

HTN & Hyperthyroidism – best initial Tx?

A

β-blockers first

114
Q

HTN & Osteoporosis – best initial Tx?

A

Thiazides

115
Q

Hypertensive Crisis – best initial Tx?

A

Labetolol or Nitroprusside

(Nitroprusside needs monitoring w/ arterial line, so usually not 1st choice)

  • can really go w/ anything IV that works: Enalapril, CCBs (Diltiazem & Verapamil), Esmolol

3rd Year (Step 2) (44 decks)

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