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First AId 2CK > Renal/GU > Flashcards

Renal/GU Flashcards

1
Q

Hypernatremia

A

Na > 145

- usually due to free water loss than sodium gain

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2
Q

Hypernatremia: PE/History

A
  • presents with THIRST due to hypertonicity
  • neuro sx: mental status changes, weakness, focal neuro deficits
  • “doughy:” skin
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3
Q

Hypernatremic causes “6 D’s”

A
  • Diuresis
  • Dehydration
  • Diabetes insipidus
  • Docs (iatrogenic)
  • Diarrhea
  • Disease ( sickle cell, kidney,)
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4
Q

Tx: euvolemic hypernatremia

A
  • use hypotonic fluids (e.g. D5W or .45% NaCl)
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5
Q

Tx: hypovolemia hypernatremia

A
  • D5W

- if vital signs unstable, use 0.9% NaCL before correcting free water deficit

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6
Q

Tx: hypervolemia hypernatremia

A

Use diuretics and D5W to remove excess sodium

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7
Q

Important key facts to keep in mind during correction of hypernatremia

A
  • Chronic hypernatremia (> 36 - 48 hrs) should occur over 48- 72 hrs (<0.5mEq/L/hr to prevent cerebral edema
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8
Q

Hyponatremia

A

Na < 135mEq/L

- almost due to increased ADH

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9
Q

Hx/PE: hyponatremia

A
  • may be asymptomatic or may present with confusion, lethargy, muscle cramps, hyporeflexia, and nausea
  • can progress to seizures coma, or brainstem herniation
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10
Q

Dx: high osmolality hypernatremia

A

> 295mEq/L

- due to hyperglycemia, hypertonic infusion (e.g mannitol)

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11
Q

Dx: normal osmality hyponatremia

A

280-295mEq/L

- caused by hypertriglyceridemia, paraproteinemia (pseudohyponatremia)

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12
Q

Dx: low osmolality hyponatremia

A

< 280 mEq/L

- majoriity of cases

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13
Q

Tx: hypervolemia hyponatremia

A
  • Water resitriction
  • consider diuretics
  • cortisol replacement w/ adrenal insufficiency
  • thyroid replacement w/ hypothyroidism
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14
Q

Tx: euvolemia hyponatremia

A

water restriction

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15
Q

Tx: hypovolemia hyponatremia

A

replete volume w/ normal saline

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16
Q

Complication of correcting hyponatremia too quickly?

A

Central pontine myelinosis

– hyponatremia > 7 hrs should be corrected more than 0.5mEq/L/hr

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17
Q

Hyperkalemia

A

> 5mEq/L

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18
Q

Spurious hyperkalemia

A
  • hemolysis of blood sample
  • delays in sample analysis
  • extreme leukocytosis or thrombocytosis
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19
Q

Hyperkalemia 2/2 to decreased excretion

A
  • Renal insufficiency

- Drugs (e.g. spironolactone, triamterene, acodisos, calcineurin)

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20
Q

Hyperkalemia 2/2 to cellular shifts

A
  • Cell lysis
  • Tissue injury (rhabdo)
  • Insulin deficiency
    Drugs (e.g. succinylcholine, digitalis, B-blockers)
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21
Q

Hx/PE: hyperkalemia

A
  • may be asymptomatic

- may present w/ nausea, vomiting, intestinal colic, areflexia, weakness

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22
Q

Dx: hyperkalemia

A
  • confirm w/ repeat blood draw esp in setting of extreme leukocytosia or thrombocytosis
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23
Q
  • ECG findings: hyperkalemia
A

tall peaked T waves, wide QRS,
PR prolongation
loss of P waves

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24
Q

Tx: hyperkalemia

A

C BIG K DROP

  1. Give calcium gluconate for cardiac cell membrane stabilization
  2. Give bicarb and/or insulin + glucose to temp shift K into cells
  3. B-agonists (e.g. albuterol) to promote cellular reuptake of K
  4. Kayexalate to remove K from body
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25
Q

Contraindications to kayexylate (esp for tx of hyperkalemia)

A
  • Ileus
  • Bowel obstruction
  • Ischemic gut
  • Pancreatic transpants
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26
Q

Hypokalemia

A

< 3.5 mEq/L

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27
Q

Etiologies of hypokalemia

A
  1. Transcellular shifts (e.g. insulin, B-agonists)
  2. GI losses (e.g. diarrhea, laxatives, vomiting)
  3. Renal losses (e.g diuretics, hypomagnesemia)
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28
Q

ECG findings: hypokalemia

A

T wave flattening, U waves (additional wave after T wave)

ST segment depression leading ot AV block and cardiac arrest

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29
Q

Tx: hypokalemia

A
  • treat underlying disorder
  • Oral and/ IVpotassium repletion
  • Don’t excess 20mEq/hr
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30
Q

Carbonic anhydrase inhibitors: site of action

e.g acetazolamide

A

proximal convoluted tubule

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31
Q

Carbonic anhydrase inhibitors (e.g acetazolamide): mechanism of action

A

inhibit carbonic anhydrase

  • increase H+ reabsorption
  • block Na+/H+ exchange
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32
Q

Carbonic anhydrase inhibitors (e.g acetazolamide): side effects

A

Hyperchloremic metabolic acidosis

Sulfa allergy

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33
Q

Osmotic agents (e.g. mannitol, urea): site of action

A

entire tubule

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34
Q

Osmotic agents: (e.g. mannitol, urea): mechanism of action

A

increase tubular fluid osmolarit

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35
Q

osmotic agents (e.g mannitol, urea): side effects

A

pulmonary edema due to CHF and anuria

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36
Q

Furosemide

A
  • loop diuretic
  • inhibits Na/K/2Cl in thick ascending limb loop of Henle
  • abolishes hypertonicity of medulla preventing concentration of urine
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37
Q

Furosemide: Clinical Use

A

edematous states (CHF cirrhosis, nephrotic syndrome, pulmonary edema)

  • HTN
  • Hypercalcemia
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38
Q

Furosemide: Side effecs

A

OH DANG

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstinal)
  • Gout
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39
Q

Ethacrynic acid

A
  • loop diuretic
  • inhibits Na/K/2Cl in thick ascending limb loop of Henle
  • abolishes hypertonicity in medulla
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40
Q

Ethacrynic acid: clinical use

A
  • diuresis in patients allergic to sulfa drugs
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41
Q

Ethacrynic acid: toxicity

A
  • can cause hyperuricemia

* * never use to treat gout

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42
Q

Hydrochlorothiazide

A
  • thiazide diuretic
  • inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of neuron
  • decreases Ca excretion
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43
Q

Hypothiazide: clinical use

A
  • HTN
  • CHF
  • idiopathic hypercalciuria
  • nephrogenic insipidus
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44
Q

Hydrochlorothiazide: toxicity

A

Hyper GLUC

  • hypokalemic metabolic alkalosis
  • hyponatremia
  • hyperglycemia
  • hyperlipidemia
  • hyperuricemmia
  • hypercalcemia
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45
Q

K sparing diuretics

A
  • spironolactone
  • triamterene
  • amiloride
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46
Q

K sparing diuretics: mechanism

A
  • sprironolactone and epelerone are aldosterone receptor antagonists in the cortical collecting tubules
  • triamterene and amiloride block Na channels in CCT
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47
Q

K sparing diuretics: clinical use

A

Hyperaldosteronism
K depletion
CHF

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48
Q

K sparing toxicity

A

Hyperkalemia (can lead to arrhythmias)

Endocrine effects w/ spironolactone (e.g. gyncecomastia, antiandrogen effects)

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49
Q

ACE inhibitors

A
  • captopril, enalapril, lisinopril
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50
Q

ACE inhibitors: mechanism

A

inhibit ACE –> decr. angiotensin II –> decr. GFR by preventing constriction of efferent arterioles
- levels of renin incr due to feedback inhibitor

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51
Q

ACE inhibitors: clinical use

A 
HTN
CHF
proteinuria
diabetic renal disease
- prevent heart remodeling due to chronic hypertension
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52
Q

ACE inhibitor toxicity

A

CATCHH

  • Cough
  • Angioedema
  • Teratogen (fetal renal malformations)
  • Creatinine increase (decr. GFR)
  • Hyperkalemia
  • Hypotension
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53
Q

Renal Tubular Acidosis I

A
  • found in distal tubules
  • defect in H+ secretion
  • hypokalemia
  • pH > 5.3
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54
Q

Etiology of RTA

A
  • hereditary
  • cirrhosis
  • autoimmune disorders (e.g. SLE, Sjorgen’s syndrome, sickle cells disease)
  • Drugs (lithium, amphotericinB
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55
Q

RTA I: Treatment

A

Replace bicarbonaate

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56
Q

RTA I: Complications

A

Nephrolithiasis

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57
Q

RTA II

A

defect in bicarb reabsorption
- low K
initially urine pH is 5.4 , then < 5.3 once serum becomes more acidotic

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58
Q

RTA II: Etiologies

A 
Hereditary (Fanconi's syndrome or cystinosis)
Drugs (carbonic anhydrase inhibitor)
Multiple myeloma
Amyloidosis
Heavy metal poisoning
Vitamin D deficiency
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59
Q

RTA II: Treatment

A

Thiazide

Volume depletion to increase absorption

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60
Q

Complications of RTA: II

A

Rickets, osteomalacia

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61
Q

RTA IV

A
  • in distal tubules
  • aldosterone deficiency
  • high K
    urine pH > 5.3
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62
Q

RTA IV: Etiologies

A

1st aldosterone deficiency
hyporeninemic hypoaldosteronims
(e.g. kidney disease, ACEis, NSAIDS(
Drugs (e.g amilorde

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63
Q

Treatment of RTA IV

A
  • Furosemide

- Mineralcorticoids +/- glucocorticoid replacement

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64
Q

Acid Base Disorder: pH < 7.4, pCO2 > 40 mmHG

A

respiratory acidosis

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65
Q

Causes of Respiratory Acidosis

A

Hypoventilation (retaining CO2)

  • Airway obstruction
  • Acute lung disease
  • Chronic lung disease
  • Opioids, narcotics
  • Weakening of respiratory muscles
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66
Q

Acid Base Disorder: pH < 7.4, pCO2 < 40 mmHg

A

Metabolic acidosis

**check anion gap (Na - [K + Cl])

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67
Q

Anion gap metabolic acidosis

A

MUDPILES

  • Methanol
  • Uremia
  • Diabetic ketoacidosis
  • Paraldehyde or pheniform
  • Iron tablets or INH
  • Lactic acidosis
  • Ethylene glycol –> kidney stons
  • Salicylates
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68
Q

Normal anion gap acidosis

A 
HARDUP
Hyperalimentation
Acetazolamide use
Renal tubular acidosis
Diarrhea
Uretocolonic fistula
Pancreatic fistula
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69
Q

Acid Base Disorder: pH >7.4, pCO2 < 40 mm Hg

A

respiratory alkalosis

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70
Q

Causes of respiratory alkalosis

A 
Hyperventilation (e.g. high altitude exposure)
Aspiration ingestion (early)
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71
Q

Acid base disorder: pCO2 > 40 mm Hg

A

Metabolic alkalosis with compensation (hypoventilation)

  • Diuretic use
  • Vomiting
  • Antacid use
  • Hyperaldosteronism
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72
Q

Acute Kidney Injury

A
  • defined as abrupt decline in renal fxn
  • retention of BUN and Cr
  • decreased urine output ( < 500 cc/day)
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73
Q

Prerenal AKI

A
  • cause by hypoperfusion
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74
Q

Common causes of prerenal AKI

A
  • Hypovolemia
  • Sepsis
  • Drugs (ACEis, NSAIDS)
  • Renal artery stenosis
  • De
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75
Q

Intrinsic AKI

A
  • injury within nephron unit
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76
Q

Common causes of instrinscicAKI

A

ischemic or nephrotoxic ATN
Allergic interstitial nephritis
Glomerulonephritis

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77
Q

Post renal AKI

A
  • urinary outflow obstruciton
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78
Q

Common causes of post renal AKI

A
  • prostatic disease
  • pelvic tumors
  • intratubular causing obstruction
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79
Q

Ddx scrotal swelling

A
  • Hydrocele
  • Varicocele
  • Epididymitis
  • Testicular torsion
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80
Q

Painless causes of scrotal swelling

A
  • Hydrocele

- Varicocele

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81
Q

Hydrocele

A
  • remnant of processus vaginalis

- usually asymptomatic, transilluminates

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82
Q

Varicocele

A
  • dilation of pampiniform venous plexus (“bag of worms”)
  • asymptomatic or presents with vague scrotal pain
  • affects left testicle more than right
  • may disappear in supine position
  • DOES NOT TRANSILLUMINATE
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83
Q

Hydrocele: Dx

A

Lab and radiologic workups rarely indicated

- obtain U/S if concern for inguinal hernia or testicular cancer

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84
Q

Epididymitis

A
  • infection of epididymitis, usually for STDs, prostatitis and/or reflux
  • affects > 30 y/o
  • presents w/ epididymal tenderness
  • enlarged testicles, fever, scrotal thickening, erythema, and pyuria
  • pain may decrease with elvevation
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85
Q

Epididymitis: Dx

A
  • UA, culture (pyuria)
  • Culture often shows N. gonorrhoeae, E.coli, or Chlamydia
  • Doppler ultrasound shows normal to increased flow to testes
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86
Q

Hydrocele: Tx

A

Typically none unless hernia is present beyond 12-18 mths age
- indicates patent processus vaginalis, which leads to increased risk for inguinal hernia

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87
Q

Varicocele: Dx

A

Ultrasound

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88
Q

Varicocele: Tx

A
  • if symptomatic or if testes makes < 40% of total volume, maybe treated surgically w/ a varicocelectomy or ligation or through embolization via IR
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89
Q

EpididymitisL Tx

A

Abx (tetracyclines, fluoroquinolone)
NSAIDS
Scrotal support

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90
Q

Testicular torsion

A
  • twisting of spermatic cord, leading to ischemia and possible testicular torsion
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91
Q

Testicular torsion:

A

Typically affects those < 30 y.o

  • presents with intense, acute-onset scrotal pain that increases or remains the same w/ scrotal elevation
  • pain accompanied by N/V and/or dizxiness
  • loss of cremestaric reflex
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92
Q

Testicular torsion: dx

A

Doppler ultrasound shows DECREASED blood flow to testes

- SURGICAL EMERGENCY

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93
Q

Testicular torsion: tx

A

attempt manual detorsion

  • immediate surgery to salvage testis (testis is often unsalvageable after 6 hrs of ischemia)
  • orchiopexy of both testes to prevent future torsion
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94
Q

BPH

A
  • enlargement of prostate that is normal part of aginge
    > 80% of men by 80
  • can result in urinary retension, recurrent UTIs, bladder and renal calculi, hydronephrosis and kidney damange
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95
Q

BPH: Hx

A

Obstructive sx: hesitancy, weak stream, urinary retenton
Irritative sx: nocturi, daytime frequency, urge incontinence
- DRE shows uniformly enlarged with rubbery texture

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96
Q

BPH: Dx

A

DRE to screen for masses, if findings are suspicious
Obtain UA and urine culture to r/o infection and hematuria
Measure creatinine levels to r/o obstructive uropathy and renal insufficiency

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97
Q

BPH : Treatment

A

Alpha-blockers (e.g. terasozin) - relax smooth muscles in prostate and bladder neck
5-alpha reductase inhibitors (e.g. finasteride) - inhibit production of DHT
- TURP or open prostatectomy is appropriate for patients

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98
Q

Renal Cell Carcinoma

A
  • adenocarcinoma from tubular epithelial cells ( 80-90% malignant tumors of kidney)
  • tumors can spread along renal vein to IVC
  • can metastasize to lung and bone
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99
Q

Risk factors for RCC

A
  • Male gender
  • Smoking
  • Obesity
  • Acquired cystic kidney disease in ESRD
  • von Hippel Lindau disease
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100
Q

RCC: Hx

A
  • presenting signs: hematuria, flank pain, and palpable mass
  • left sided varicocele often seen due to blockage of gonadal vein into left renal vein then into IVC
  • anemia is common but may see polycythemia
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101
Q

DDx for hematuria

A 
I PEE RBCS
Infection (UTI)
Polycystic kidney disease
Exercise
External trauma
Renal glomerular disease
Benign prostatic hyperplasia
Cancer
Stones
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102
Q

RCC: Dx

A

Ultrasound and/or CT to characterie renal mass as complex cysts or solid tumor

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103
Q

RCC: Treatment

A

Surgical resection may be curative in localized disease

Response rate from radiation or chemotherapy are only 15-30%

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104
Q

Sx of ARF

A
  • fatigue, nausea and vomiting, anorexia, SOB, menal status changes
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105
Q

Signs of ARF

A
  • increased BUN and Cr
  • metabolic acidosis
  • hyperkalemia
  • tachypnea (due to acidosis and hypervolemia)
  • hypervolemia (b/l rales on exam, JVD, and dilutional hyponatremia)
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106
Q

Three broad categories of renal failure

A
  • Prerenal
  • Renal/intrarenal
  • Post renal
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107
Q

Prerenal failure

A
  • inadequate perfusion to kidney (which is normal)
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108
Q

Common cause of prerenal failure

A
  • HYPOTENSION - (SBP < 90 mm Hg) from sepsis, anaphylaxis, bleeding
  • HYPOVOLEMIA - diuretics, burns, pancreatitis
  • Renal artery stenosis
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109
Q

Dx for prerenal failure

A
  • Urinanalysis
  • Urine sodium
  • Fractional excretion of Na
  • Urine osmolality
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110
Q

Prerenal failure (in terms of Una and FeNa)

A

low Una < 20

low FeNa < 1%

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111
Q

Sx of hypovolemia

A
  • tachycardia, weak pulse, decreased fontanelle
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112
Q

Postrenal failure

A
  • urine is blocked from excreting at some point beyond the kidneys (ureters, prostate, urethra)
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113
Q

Low urine osmolality in healthy persion (no renal issues)

A
  • can be sign of hypervolemia (fluid overload0
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114
Q

Urine osmolality in patient with ATN

A
  • inappropriate LOW urine osmolality

* * patient cannot absorb water b/c of damaged tubule cells**

115
Q

High urine osmolality in healthy person

A

Signs of dehydration

116
Q

Why should pts with sickle cell trait avoid dehydration?

A
  • Sickle cell patients have defect in concentrating urine due to defect in renal concentrating ability
117
Q

Lab testing for prerenal failure

A

BUN:Cr > 20
UNa < 20mEq/L
FeNa < 1%
UOsm > 500 mOsm/kg

118
Q

Acute Tubular Necrosis

A
  • injury to kidneys from ischemia and/or toxins resulting in sloughing of tubulr cells in urne
119
Q

Discuss IV contrast and renal failure

A
  • IV contrast can precipitate renal failure esp in diabetics and pts w. renal sdsase
  • if must do so, give saline hydration
  • may use acetylcysteine before and day of administration
120
Q

Causes of toxin-induced ATN

A
  • Aminoglycoside abx
  • Amphotericin
  • Cisplatin
  • Vancomycin
  • Acyclovir
  • Cyclosporine
  • ** occurs within 5 - 10 days
121
Q

Causes of ATN

A
  • Toxins (e.g. aminoglycosides)
  • Contrast media
  • Hemoglobin and myoglobin (rhabdomyolysis)
  • Hyperuricemia
  • Ethylene glycol
  • Bence-Jones protein
  • NSAIDS
122
Q

Ethylene glycol induced ATN

A
  • caused by precipitation of calcium oxalate in renal cortex
  • appears as envelope-shaped crystals
  • associated with hypocalcemia
123
Q

Rhabdomyolysis

A
  • caused by trauma
  • prolonged immobility
  • snake bites, seizures
  • crush injuries
124
Q

Best test to diagnosis rhabdomyolysis

A

URINANALYSIS

125
Q

Lab values associated with rhabdomyolysis

A
  • Urine test positive for myoglobin
  • Creatinine phosphokinase (CPK) are elevated
  • Hyperkalemia occurs with release K from damaged cells
  • Hypocalcemia due to calcium binding to muscle
  • Hyperuricemia due to damaged cells releasing nucleaic acids
126
Q

Treatment of rhabdomyolysis

A
  • saline hydration
  • mannitol (as osmotic diuretic)
  • bicarbonate (to drive potassium back into cells and prevent precipitation from tubtules
127
Q

Prevention of tumor lysis syndrome

A

Before chemotherapy, give:

  • allopurinol
  • hydration
  • rasburicase
128
Q

Treatment of ATN

A
    • no therapy proven to benefit ATN
  • patients should be managed w/ hydration and correction of electrolyte abnormalities
  • *DIURETICS HAVE NO ADDED BENEFIT**
129
Q

Indications for dialysis

A

AEIOU

  • Acidosis
  • Electrolyte abnormalities
  • Intoxicants
  • Overload (volume)
  • Uricemia
130
Q

How does furosemide cause ototoxicity?

A

Furosemide damages hair cells of cochlea resulting in sensoneurial hearing loss
- caused by how fast it is injected

131
Q

Hepatorenal syndrome

A

renal failure developed secondary to liver disease

- kidneys are intrinsically normal

132
Q

Sx of hepatorenal syndrome

A
  • severe liver disease (cirrhosis)
  • new-onset renal failure w/ no other explanation
  • very low urine sodium (< 1%
  • elevated BUN:Cr (> 20:1)
133
Q

Tx of hepatorenal syndrome

A

Midodrine
Octeotride
Albumin

134
Q

Atheroemboli

A
  • cholesterol plaques in aorta or near coronary arteries that are fragile enough that they can be “broken off” when vessels are manipuated during catheter procedures
135
Q

How can atheroemboli cause AKI?

A

Emboli lodge in kidney

136
Q

PE signs of atheroemboli

A
  • Purplish skin lesions in fingers and toes
  • Livedo reticularis
  • normal peripheral pulses (artheroemboli too small to occlude radial or brachial artery)
137
Q

Diagnostic tests for atheroemboli

A
  • Eosinophilia
  • Low complement levels
  • Eosinophiluria
  • Elevated ESR
138
Q

Most accurate test for atheroemboli

A

Biopsy of purplish skin lesions

139
Q

Acute (Allergic) Interstitial Nephritis

A
  • form of ARF that damages tubules on idiopathic basis

- antibodies and eosinophis attack tubule linings as reaction to drugs

140
Q

Common meds associated with AIN

A
  • Penicillins
  • Sulfa drugs (e.g. thiazides and furosemide)
  • Phenytoin
  • Rifampin
  • Quinolones
  • PPIs
  • Allopurinol
141
Q

Important note about AIN

A
  • Same meds that cause AIN are the same that cause:
  • Drug allergy and rash
  • Steven-Johnson syndrome
  • Toxic epidermal necrolysis
  • Hemolysis
142
Q

Common presentation of AIN

A
  • Fever
  • Rash
  • Arthralgias
  • Eosinophilia and eosinophiluria
143
Q

Diagnostic tests for AIN

A
  • Elevated BUN and Cr with ratio < 20
  • White and red cells in urine
  • Hansel or Wright stain which determines whether eosinophils are present
    • UA can’t detect eosinophils
144
Q

Treatment of AIN

A

Usually resolves spontaneously with stopping the drug or controlling the infection

  • Severe is managed with dialysis
  • If Cr continues to rise after drug has been stopped, give glucosteroids
145
Q

Analgesic nephropathy presents with?

A
  • ATN from direct toxicity
  • AIN
  • Membranous glomerulonephritis
  • NSAID use
  • Papillary necrosis
146
Q

How do NSAIDs cause analgesic nepropathy?

A

Vascular insufficiency inhibit prostaglandins

  • prostaglandins dilate afferent arteriole
  • NSAIDS constrict afferent arteriole and decrease renal perfusion
  • important in elderly or pts with renal insufficiency
147
Q

Papillary necrosis

A
  • sloughing of renal pappilae
  • caused by NSAIDS or sudden vascular insufficiency leading to cell death in papillae
  • pts usually have baseline renal damage
  • usually see 60 - 70% renal fxn loss before Cr begin to rise
148
Q

History of patients with papillary necrosis

A 
- - Look for NSAID use with hx of:
Sickle cell dz OR
Diabetes
Urinary obstruction
Chronic pyelonephritis
149
Q

Papillary necrosis: classic presentation

A

Sudden onset of flank pain
Fever
Hematuria

150
Q

Diagnostic tests for papillary necrosis

A
  • CT scan
  • UA that shows red and white cells – may show necrotic kidney tissue
  • Urine cx wlll be normal
151
Q

Best test for papillary necrosis

A

CT SCAN

- can show abnormal internal structures of kidney due to loss of papillaw

152
Q

Pyelonephritis

A
  • onset: few days
  • symptoms: dysuria
  • Positive urine cx
  • Swollen kidney on CT
153
Q

Tx of pyelonephritis

A

Abx such as ampicillin/gentamicin or fluoroquinolones

154
Q

Papillary necrosis

A
  • onset: few hrs
  • sx: necrotic material in urine
  • Negative urine cs
  • Bumpy contour of interior where papillae were loss
155
Q

Tx of papillary necrosis

A

None

156
Q

Tubular Disease

A
  • usually acute
  • caused by toxins (drugs, myoglobin, Hgb)
  • none cause nephrotic syndrome
  • not treated with steroids
  • add’l immunosuppressants are not used
  • correct hypoperfusion and remove toxin
157
Q

Glomerular Diseases

A
  • chronic
  • not from toxins/drugs
  • can cause nephrotic syndrome
  • biopsy sample
  • often treated with steroids
158
Q

Glomerulonephritis

A
  • UA w/ hematuria
  • Dysmorphic red cells (deformed as they squeeze through glomerulus)
  • Red cell casts
  • Urine sodium and FeNa are low
  • Proteinuria
159
Q

Goodpasture Syndrome

A
  • present wit lung and kidney involvement
  • NO UPPER RESPIRATORY INVOLVEMENT
  • no systemic vasculitis
  • no skin, joint, GI, or neuro involvement
160
Q

Diagnostic Test of Goodpasture Syndrome

A
  • antiglomerular basement membrane antibodies
  • linear deposits
  • most accurate test is kidney or lung biopsy
  • anemia is often present due to hemoptysis
161
Q

Tx of Goodpasture’s Syndrome

A
  • Plasmapheresis and steroids

* * cyclophosphamide can be helpful

162
Q

IgA Nephropathy (Berger disease)

A
  • most common cause of glomerulonephritis in US

- usually Asian pt with recurrent episodes of gross hematuria 1-2 days after URI

163
Q

Diagnosis of IgA Nephropathy

A
  • Kidney biopsy

- may see increase in IgA levels by 50%

164
Q

IgA Nephropathy

A
  • no treatment proven to reverse disease
  • 40 - 50% slowly progress to ESRD
  • severe proteinuria treated wtih ACEi’s and steroids
165
Q

Postinfectious glomerulonephritis

A
  • commonly caused by Streptococcus but can be caused by any organism
  • occurs 1-3 WEEKS after throat infection
166
Q

Postinfectious glomerulonephritis

A
  • Dark (coca cola) urine
  • Edema that is periorbital
  • Hypertensin
  • Oliguria
167
Q

Dx of postinfectious glomerulonephritis

A
  • UA with proteinuria, red cells, and recd cells cases
  • ASO titers and anti-DNAse Ab tters
  • Biopsy is most accurate but blood tests are sufficiently accurate
168
Q

Tx of postinfectious glomerulonephritis

A
  • antibiotics

- diuretics to control fluid overload

169
Q

Alport Syndrome

A
  • congenital defect of collagen that results in glomerular disease combined with:
  • senorineural hearing loss
  • visual disturbance from loss of the collagen fibers that hold the lens of the eye in place
170
Q

Tx of Alport Syndrome

A
  • No specific therapy to reverse defect of type IV collagen
171
Q

Polyarteritis Nodosa

A
  • systemic vasculitis of small/medium sized arteries that affect kidney
  • ## affects nearly every organ except lung
172
Q

Polyarteritis Nodosa associated with which diseases

A
  • Hepatitis B

- PAN should be tested for Hep B

173
Q

Presentation of Polyarteritis Nodisa

A
  • glomerulonephritis

- nonspecific sx of fever, malaise, weight loss, myalgias, and arthralgia developing over months and weeks

174
Q

GI sx associated with PAN

A

Abdominal pain, bleeding

Pain worsened by eating

175
Q

Neuro symptoms associated with PAN

A

vasculitis damages surrounding peripheral nerves (peroneal, ulnar, radial, and brachial nerve)

  • mononeuritis multiplex
  • stroke in young person
176
Q

Skin symptoms associated with PAN

A
  • Can cause purpura and petechia

- can give ulcers, digital gangrene, and livedo reticularis

177
Q

Diagnostic tests associated with PAn

A
  • anemia and leukocytosis
  • Elevated ESR and C-reactive protein
  • ANCA _ NEGATIVE
  • angiography showing aneurysms of renal, mesenteric, or hepatic arter
178
Q

Most accurate test for PAN

A

Biopsy of symptomatic site such as skin, nerves, or muscles

179
Q

Tx for PAN

A

Prednisone and cyclophosphamide

- treat hepatitis when found

180
Q

Lupus nephritis

A
  • SLE can show mild, ansymptomatic proteinuria

- severe disease presents with membranous glomerulonephritis

181
Q

Most accurate test for lupus nephritis

A

Biopsy

- more important to guide therapy for lupus nephritis

182
Q

Tx for lupus nephritis

A

Severe nephropathy is treated with glucocorticoids combined with cyclophosphamide or mycophenolate

183
Q

Amyloidosis

A

abnormal protein produced in association w/

  • myeloma
  • chronic inflammatory disease
  • rheumatoid arthritis
184
Q

Renal amyloidosis

A

primary (plasma cell dyscrasia)

secondary (infectious or inflammatory) are most common

185
Q

Renal amyloidosis (Hx and PE)

A
  • patients may have multiple myelomaa or chronic inflammatory disease (e.g. rheumatoid arthritis)
186
Q

Renal amyloidosis (Labs/ Histo)

A

Nodular glomerulosclerosis

  • EM reveals amyloid fibrils
  • apple green birefringence with Congo red stain
187
Q

Tx of renal amyloidosis

A

Prednisone and melphalan

- bone marrow transplant may used for multiple myeloma

188
Q

Membranoproliferative nephropathy

A
  • can also be nephritic

- Type I : associated with HCV, cryoglobulinemia, SLE, and subacute bacterial endocarditis

189
Q

Membranoproliferative nephropathy: Hx and PE

A

idiopathic form is present at 8-30 years of age

- slow progression to renal failure

190
Q

Membranoproliferative nephropathy: Labs and Histo

A

TRAM TRACK - double layered basement membrane

  • Type I: subENDOthelial depositis and mesangial depositis
  • all 3 types have low serum C3
  • Type II occurs by way of nephritic factor
  • IgG leads to constant activation of extrinsic clotting pathway
191
Q

Membranoproliferative nephropathy: Tx

A

Corticosteroids and cytotoxic agens may help

192
Q

Minimal change disease

A
  • most comon cause of nephrotic syndrome in children

- idopathic etiology: secondary causes include NSAIDS and hematologic malignancies (e.g. Hodgkins disease)

193
Q

Minimal change disease: Hx and PE

A

tendency towards infections and thrombotic events

- sudden onset of edema

194
Q

Minimal change disease: Labs and Histo

A

light micropscopy appears normal

- EM shows fusion of epithelial foot processes with lipid containing renal cortices

195
Q

Minimal change disease: Tx

A

Steroids

- excellent prognosis

196
Q

Focal Segmental Glomerulosclerosis

A

-idiopathic, IV drug use, HIV, obesity

197
Q

FSGS: History and PE

A

typical patient is young African American male with uncontrolled hypertension

198
Q

FSGS: Labs and Histo

A

microscopic hematuria;

biopsy shows sclerosis in capillary tufts

199
Q

FSGS: Tx

A

Prednisone, cytotoxic therapy, ACEis/ ARBs to decrease proteinuria

200
Q

Membranous nephropathy:

A

most common nephropathy in Caucasian adults

- secondary causes are solid tumor malignancies, esp in pts > 60 and immune complex disease

201
Q

Membranous nephropathy: History and PE

A

associated with HBV, syphillis, malaria, and gold

202
Q

Membranous nephropathy: Labs and History

A

“Spike and dome” appearance due to granular deposits of IgG and C3 at basement membrane

203
Q

Membranous nephropathy: Tx

A

Prednisone and cytotoxic therapy for severe disease

204
Q

Diabetic nephropathy

A

has 2 characteristic forms:

diffuse hyalinization and nodular glomerulosclerosis (Kimmlstiel-Wilson lesions)

205
Q

Diabetic nephropathy: History and PE

A

Patients generally have long-standing, poorly controlled DM with evidence of retinopathy or neuropathy
- increased GFR is pathological mechanism

206
Q

Diabetic nephropathy: Labs and Histo

A

Thickened GM

- increased mesangial matrix –> nodular sclerosis

207
Q

Diabetic nephropathy:

A

Tight control of sugar

- ACEis

208
Q

Nephrotic syndrome

A
  • > 3.5 g/dam
  • generalized edema
  • hypoalbunemia
  • hyperlipidemia
  • hypercoagulable state
  • increased atherosclerosis
209
Q

Nephritic Syndrome Findings

A 
"PHAROAH"
P-roteinuria
H- ematuria
A - zotemia
R -BC casts
O - liguria
H - ypertension
210
Q

Immune Complex nephritic syndromes

A
  • Postinfectious glomerulosclerosis

- IgA Nephropathy

211
Q

Post-infectious glomerulonephritis

A
  • classically associaed with recent Group A B- hemolytic streptococcal infection, but can be seen in any infection (usually 2-6 weeks prior)
212
Q

Postinfectious glomerulonephritis: Hx and PE

A
  • oliguria
  • edema
  • hypertension
  • coca-cola urine
213
Q

Postinfectous glomerulonephritis: Labs and Histo

A

Low serum C3 that normalizes 6-8 weeks after presentation

- increased ASO titer, lumpy-bumpy immunoflourescence

214
Q

Postinfectous glomerulonephritis: Tx

A

supportive with diuretics to prevent fluid overload

- most patients have complete recovery

215
Q

IgA nephropathy

A
  • most common type: typically follows upper respiratory or GI infections
  • commonly seen in young males, may be seen in Henoch Schonlein purpura
216
Q

IgA nephropathy: Hx and PE

A

episodic gross hematuria or persistent microscopic hematuria

217
Q

IgA nephropathy: Labs and Histo

A

Normal C3

218
Q

IgA nephropathy: Treatment

A

Glucocorticoids for select patients
ACEis in patients with proteinuria
Some 20% of cases progress to ESRD

219
Q

Pauci-immune nephritic disease

A
  • Wegener’s granulomatosis
  • Goodpasture’s syndrome
  • Alport Syndrome
220
Q

Wegener’s granulomatosis

A
  • granulomatous infection of the respiratory tract and kidney with necrotizing vasculitis
221
Q

Wegener’s granulomatosis: Hx and PE

A
  • Fever, weight loss, hematuria,
  • Hearing disturbances
  • Repiratory and sinus symptoms
  • Cavitary pulmonary lesions bleed and lead to hemoptysis
222
Q

Wegener’s granulomatoisis: labs and histo

A

ANCA positive

Renal biopy shows segmental necrotizing glomerulonephritis with few immunoglobulin deposits on immunoflourescence

223
Q

Wegener’s granulomatosis: Tx

A

High dose corticosteroids and cytotoxic agents

Patients tend to have frequent relapses

224
Q

Goodpasture’s syndrome

A

rapidly progressing glomerulonephritis with pulmonary hemorrhage
-peak incidence is in males in their mid 20s

225
Q

Goodpasture’s syndrome: hx and pe

A

hemoptysis, dyspnea, possible respiratory failure

No upper respiratory tract involvement

226
Q

Goodpasture’s syndrome: labs and histo

A

Linear anti-GBM deposits on immunofluorescence
Iron deficiency anemia
Hemosiderein filled macrophages in sputum
Pulmonary infiltrates on CXR

227
Q

Goodpasture’s syndrome: Tx

A

Plasma exchange therapy
Pulsed steroids
May progress to ESRD

228
Q

Alport’s Syndrome

A
  • hereditary glomerulonephritis

- presents in boys 5-20 years of age

229
Q

Alport’s syndrome: Hx and PE

A

asymptomatic hematuria

associated with sensoneurial hearring loss and eye disorders

230
Q

Alport’s syndrome: Labs and histo

A

GBM splitting on EM

231
Q

Alport’s syndrome: tx

A

Progresses to renal failure

anti-GBM nephritis may recur after transplant

232
Q

Drug induced interstitial nephritis

A 
Bactrum
Sulfonamides
PCNs
Rifampin
Phenytoin
233
Q

Drug induced interstitial nephritis

A

Arthralgia

Diffuse maculopapular rash

234
Q

Drug induced interstial nephritis

A

Eosinophils on UA

WBC casts

235
Q

Sx of uremia

A
  • Pericardial rub
  • Asterixis
  • hHypertension
  • Decreased urinary output
  • Increased respiratory rate
236
Q

Hyaline casts in urine sediment

A

normal finding

  • increased amt suggests volume depletion
  • assoc w/ prerenal AKI
237
Q

Red cell casts, dysmorphic red cells in urine sediment

A

Glomerulonephritis

- sign of intrinsic AKI

238
Q

White cells, eosinophils in urine sediment

A

Allergic interstitial nephritis

  • atherembolic disease
  • sign of intrinsic AKI
239
Q

Granular casts, renal tubular cells, “muddy brown casts” in urine sediment

A

ATN

- sign of intrinsic AKI

240
Q

White cells, white cell casts in urine sediment

A

Pyelonephritis

- sign of postrenal AKI

241
Q

Hypercalcemia

A

> 10.2 mg/DL

  • most common causes are hyperparathyroidism and malignancy
  • use mneumonic CHIMPANZEE
242
Q

Causes of hypercalcemia

A

CHIMPANZEE

  • Calcium supplementation
  • Hyperparathyroidism/Hyperthyoridism
  • Iatrogenic (e.g. thiazides, parental nutrition)/ Immobility (esp in ICU setting)
  • Milk-alkali syndrome
  • Paget’s disease
  • Adrenal insufficiency/Acromegaly
  • Neoplasm
  • Zollinger-Ellison (e.g. MEN I)
  • Excess Vitamin A
  • Escess Vitamin D
  • Sarcoidosis adn other granulomatous disease
243
Q

Hypercalcemia: PE and Hx

A 
Asymptomatic but may present with:
Bones (osteopenia, fractures)
Stones (kidney stones)
Groans (anorexia, constipation)
Psychiatric overtones (weakness, fatigue, altered mental status)
244
Q

Hypercalcemia: Diagnosis

A
  • Order Ca
  • ## Order Albumin, phosphate, PTH, PTHrP, Vit D, and ECG
245
Q

Hypercalcemia finding on ECG

A

short QT interval

246
Q

Hypercalcemia: Tx

A

IV hydration followed by furosemide to increase calcium excretion
- AVOID THIAZIDES which can increase absorption of Ca

247
Q

Discuss digitalis and hypokalemia

A
  • digitialis and K fight for same site on Na/K pump so hypokalemia sensitizes patient to digitalis
248
Q

Monosymptomatic enuresis

A

urinary incontinence in children > 5

249
Q

Management of monosymptomatic enuresis

A

FIRST LINE: BEHAVIOR MODIFICATION

  • avoid sugary drinks
  • void regularly during day and immediately before bedtime
  • drink ample fluid in morning & early afternoon

Pharm therapy
1st line: desmopression
2nd line: TCA

250
Q

1st line pharm therapy in monosymptomatic enuresis

A

Desmopression

251
Q

Best test for suspected BPH

A

Abdominal U/S to check for obstruction

252
Q

Calcium oxalate/calcium phosphate

A
  • most common type of renal stone

- MCCs: idiopathic hypercalcuria and hyperparathyroidsm

253
Q

Tx of calcium oxalate/calcium phosphate

A

Hydration, Dietary sodium and protein restriction, Thiazide diuretics

  • DO NOT DECREASE CA INTAKE
  • alkaline urine
  • radiopaque
254
Q

Struvite renal stones

A 
associated w/ urease producing organisms (e.g Proteus)
form STAGHORN CALCULI
alkaline urine
radiopaque
- alkaline urine
255
Q

Tx of struvite renal stones

A

Hydration
treat UT if present
surgical removal of staghorn stone

256
Q

Uric acid stones

A 
associated with gout, xanthine oxidase deficiency and high purine turnover rate (e.g. chemotherapy)
acidic urine (pH < 5.5)
RADIOLUCENT on plain film but detectable on CT
257
Q

Tx of uric acid stones

A

Hydration

Alkalinize urine w/ citrate with is converted to HCO in liver

258
Q

Cystine renal stone

A

due to defect in renal transport of certain amino acids (COLA - cysteine, ornithine, lysine, and argine)

259
Q

Dx of cystine renal stone

A
  • HEXAGONAL CRYSTALS

- POSITIVE CYANIDE NITROPRUSSIDE TEST

260
Q

Tx of cystine renal stone

A

Hydration
Dietary sodium restriction
Alkalinization of urine
Penicillamine

261
Q

Nephrolithiasis: Hx and PE

A

acute onset of severe, colicky flank pain that may radiate to testes or vulva

  • associated w/ nausea and vomtng
  • patient unable toget comfortable and shifts position frequently
262
Q

Best test for nephrolithiasis

A

Non contrast CT for diagnosis of kidney stones

263
Q

U/A for kidney stones

A

Microhematuria and altered urine PH

264
Q

Best diagnostic modality for suspected kidney stones in children and pregnant women

A

Ultrasound

265
Q

Tx for renal stones

A

Hydration and analgesia are intiail streatment
Stones < 5mm can pass spontaneously
Stones > 5mm but < 3cm can be treatmed with ESWL

266
Q

AD Polycystic kidney disease

A
  • usually asymptomatic until > 30 years

- associated with increased risk of cerebral aneurtyrm esp in patients w/ positive family hx

267
Q

Polycystic kidney disease: History and PE

A
  • Pain and hematuria are most common symmptoms

- Large palpable kidneys

268
Q

Dx of Polycystic kidney disease

A

CT scan

-wlll show multiple bilateral cysts through renal parenchy

269
Q

Tx of polycystic kidney disease

A

prevent complications and decrease rate of progression of ESRD

  • early mgmt of UTIs
  • BP control (ACEis and ARBs)
270
Q

Hydronephrosis

A

dilation of renal calcyces

- usually secondary to obstruction of urinary tract

271
Q

Hx and PE: Hydronephrosis

A
  • may be asymptomatic
  • may present w/ flank/back pain
  • decreased urine output
  • abdominal pain and UTiS
272
Q

Dx of Hydronephrotis

A
  • ULTRASOUND (first line) to detect dilitation of renal calyces or ureter
  • can use CT scan
273
Q

Tx of hydronephrosis

A

surgically tx anatomic obstruction

274
Q

Complications of untreated hydronephrosis

A
  • Urinary obstruction leading to HTN, acute or chronic renal failure
    Sepsis
275
Q

Vesiculoureteral reflux

A
  • retrograde projection of urine from bladdder to ureteres and kidney
  • may be due to posterior urethral valves, urethral or meatal stenosi
276
Q

Hx and PE: of vesiculouretal reflux

A

patient present with recurrent UTIs, typically in childhood

277
Q

Dx: of vesiculourethral reflux

A

Voiding cystogram (VCUG) to detect abnormalities at ureteral insert sites and identify grade of reflx

278
Q

Tx of vesiculourethral reflux

A
  • Treat infxns aggressively. Mild reflux with prophylactiv abx (amoxicillin < 2 mths or bactrim or nitrofurantoin)
  • Surgery (urereteral reimplantation) reserved for children with high grade reflux
279
Q

Complication of vesiculourethral reflux

A
  • Progressive renal scarring and ESRD
280
Q

Cryptochordism

A
  • failure of 1 or both testes to descent into scrotum

- LOW BIRTH WEIGHT IS A RISK FACTOR

281
Q

History and PE: cryptochordism

A

Bilateral cryptochordism associated w prematurity, oligospermia, congenital malformation syndromes (Prader-Willi, Noonan) and infertility)
- associated w increased risk of testicular malignancy

282
Q

Dx: cryptochordism

A

testes can’t be manipuated into scrotal sac with gentle pressure
- may be palpable anywhere along inguinal canal or in abdomen

283
Q

Tx: cryptochordism

A

Orchiopexy by 6-12 months of age (most testes will spontaneously descend by 3 months)
- treat w/ orchiectomy to avoid testicular cancer

First AId 2CK (22 decks)

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