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Surgery > Urology/Renal from PANCE Pearls > Flashcards

Urology/Renal from PANCE Pearls Flashcards

1
Q

What is Incontinence

A

Involuntary loss of urine

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2
Q

What is Stress Incontinence

A

Increased intraabdominal pressure leads to urinary leakage

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3
Q

How does Stress Incontinence occur

A

Increased intrabdominal pressure is greater than the urethral resistance to blood flow
Laxity of pelvic floor muscles caused by childbirth, obesity, estorgen

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4
Q

Sx of Stress Incontinence

A

Sneezing, Coughing, Laughing all lead to increased intrabdominal pressure which leads to leakage

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5
Q

Tx of Stress Incontinence

A

Pelvic Floor Exercises: Kegel, Biofeedback
Alpha Agonists: Midodrine, Pseudoephedrine (increase urethral sphincter tone)
Surgery: Increase urethral outlet resistance

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6
Q

What is Urge Incontinence

A

Urine leakage accompanied by or preceding urge

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7
Q

What causes Urge Incontinence

A

Detrusor muscle overactivity
Remember, detrusor muscle is stimulated by muscarinic Ach receptors
Contraction of detrusor causes release of urine

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8
Q

Sx of Urge Incontinence

A

Urgency, frequency, small volume voids, nocturia

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9
Q

Tx of Urge Incontinence

A

Bladder training (timed, frequent voids)
Anticholinergics are 1st line (Tolterodine, Propantheine, Oxybutynin)
TCA’s (Imipramine)

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10
Q

What is Overflow Incontinence

A

Urinary Retention

Incomplete bladder emptying

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11
Q

What leads to Overflow Incontinence

A

Decreased Detrusor Muscle activity
“Underactive bladder”
Bladder outlet obstruction: BPH

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12
Q

Sx of Overflow Incontinence

A

Small volume voids, frequency, dribbling

Increased Post void residual >200mL

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13
Q

Tx of Overflow Incontinence

A

Intermittent or indweling catheter 1st line
Cholinergics (Bethanacol)
BPH: Alpha-1 Blockers (Tamsulosin)

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14
Q

What is Chronic Kidney Disease

A 
Chronic Kidney damage for > 3 months evidence by:
Proteinuria
Abnormal Urine Sediment
Abnormal Serum/Urine Chemistries
Abnormal Imaging Studies
Inability to buffer pH
Inability to make urine
Inability to excrete nitrogenous waste
Decreased Synthesis of Vitamin D/Erythropoietin
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15
Q

What are the different stages of Chronic Kidney Disease

A 
Stage 0: At risk patients (DM, HTN, Chronic NSAID)
State 1: Normal GFR with kidney damage
Stage 2: GFR 60-89
Stage 3: GFR 30-59
Stage 4: 15-29
Stage 5: GRF
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16
Q

What interventions occurs with end stage renal disease

A

Uremia requiring dialysis and/or transplant

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17
Q

What is a normal GFR

A

120-130

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18
Q

What is common causes of end stage renal disease

A

DM #1
HTN
Glomerulonephritis

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19
Q

Dx of Chronic Kidney Disease

A 
Proteinuria: Can test with spot Microalbumin/Microcreatine Ratio or 24 hour urine collection
Urinalysis: See broad waxy casts
GFR
BUN/Cr ratio
Renal Ultrasound: Small Kidney
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20
Q

What are dietary modifications for Chronic Kidney Disease

A

Protein Restriction
Water Restriction
Potassium and phosphate restriction

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21
Q

What are the two most important modifications to prevent Chronic Kidney Disease

A

Reduce blood pressure to

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22
Q

What is the gold standard for Dialysis access

A

AV fistula which connects an artery to a vein

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23
Q

What is the primary regulator of water secretion and what does it do

A

ADH

It conserves water by concentrating urine

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24
Q

What are 4 ways to regulate water

A

ADH
Thirst
Aldosterone
Sympathetics

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25
Q

What happens in the environment of high ADH

A

The kidney excretes small volumes of concentrated urine

ADH makes aquaporins to preserve water

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26
Q

What stimulates ADH

A

Hyperosmolarity

Decreased Arterial Volume (Hypovolemia) which reduces blood pressure

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27
Q

What happens in the environment of low ADH

A

Kidney generates large volumes of dilute urine

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28
Q

What inhibits ADH

A

Hypoosmlarity, which increases free water

Note that hypovolemia always takes precedence over hypoosmalarity (so ADH will be stimulated)

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29
Q

What stimulates thirst

A

Dehydration = Decreased free water

Hyerosmolarity which increases serum osmolarity

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30
Q

What does Aldosterone do

A

Causes sodium to be reabsorbed which in turn, water follows

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31
Q

What role does the sympathetic nervous system have in water regulation

A

Alpha-1 activation causes arteriole constriction

Afferent Arteriole constriction decreases renal perfusion (decreases GFR) which leads to less urine formation

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32
Q

How is sodium regulated in the body

A

Aldosterone

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33
Q

How is Aldosterone stimulated

A

Hypovolemia = low blood pressure = decreased intravascular volume (sodium + water)
Hyperkalemia

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34
Q

Water homeostasis is determined by ____

Sodium homeostasis is determined by ___

A 
Water = ADH
Sodium = Aldosterone
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35
Q

What is Hyponatremia

A

Increased free water = Decreased serum sodium

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36
Q

What is Hypernatremia

A

Decreased free water = Increased serum sodium

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37
Q

What makes up extracellular volume

A

Sodium and Water

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38
Q

What is hypovolemia
Hypervolemia
Euvolemia

A

Total body sodium is decreased
Total body sodium is increased
Normal total body sodium

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39
Q

Sx of Hypervolemia

A

Peripheral edema
Pulmonary edema
Jugular venous distension
HTN

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40
Q

Sx of Hypovolemia

A 
Poor skin turgor
Dry mucous membranes
Flat neck veins
Hypotension
Increased BUN:Cr ratio
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41
Q

What is True Hyponatremia

A

Kidney unable to excrete free water to match oral free water intake
Associated with increased free water

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42
Q

What is Hypovolemic Hyponatremia

A 
Decreased volume (water and sodium) AND increased free water
Usually due to impaired free water excretion, leads to increased ADH
43
Q

Sx of Hyponatremia

A

CNS dysfunction due to cerebral edema

44
Q

Tx of Hyponatremia

A

Isovolemic: Water restriction
Hypervolmeic: Sodium and water restriction
Hypovolemic: Normal saline

45
Q

What is Hypernatremia

A

Due to net water loss

Sustained hypernatremia is seen when appropriate water intake is not possible

46
Q

Sx of Hypernatremia

A

CNS dysfunction due to shrinkage of brain cells

Confusion, lethargy, coma, muscle weakness, seizures

47
Q

Tx of Hypernatremia

A

Hypotonic fluids to replace water deficit
Oral route is best (pure water)
D5W, 0.45%NS, o.2% saline

48
Q

What is Magnesium essential for

A

DNA and protein synthesis
Parathyroid hormone production
Cardiovascular and neurologic function

49
Q

What is Hypomagnesemia and what causes it

A

GI Loss: Malabsorption, Alcoholics, Celiac

Renal Loss: Diuretics, PPI, DM

50
Q

Sx of Hypomagnesemia

A

Neurovascular: AMS, lethargy, weakness, Increased DTR
Hypocalcemia: Increasd DTR, Trousseau’s and Chvostek’s sign
Cardiovascular: Arrhythmias, Palpitations

51
Q

What do you see on EKG with Hypomagnesemia

A

Prolonged PR and QT intervals

52
Q

Tx of Hypomagnesemia

A

IV Magnesium Sulfate if Torsades de pointes or severe

Oral Magnesium

53
Q

What causes Hypermagnesemia

A

Renal insufficiency or Increased Mg intake

54
Q

Sx of Hypermagnesemia

A

N/V
Skin flushing
Weakness
Decreased DTR, Muscle Weakness

55
Q

What do you see on EKG with Hypermagnesemia

A

Bradyarrhythmias, Prolonged PR or QT intervals

56
Q

Tx of Hypermagnesemia

A

Mild to Moderate: IV fluids + Furosemide

Severe: Calcium Gluconate (antagonizes toxic effects and stabilizes cardiac membranes)

57
Q

What is Hypokalemia

A

Increased urinary/GI losses usually due to vomiting, diarrhea, diuretic therapy

58
Q

Sx of Hypokalemia

A

Neuromuscular: Severe muscle weakness, Rhabdomyolysis
Cardiovascular: Palpitations, Arrhythmias

59
Q

What do you see on EKG with Hypokalemia

A

T wave flattening, prominent U waves

60
Q

Tx of Hypokalemia

A

Potassium replacement

Potassium sparing diuretics

61
Q

What leads to Hyperkalemia

A

Decreased renal excretion usually due to acute or chronic renal failure
Potassium supplements, Potassium sparking Diuretics
Cell Lysis: Rhabdomyolysis, burns, hypovolemia

62
Q

Sx of Hyperkalemia

A

Neuromuscular: Weakness, fatigue, parasthesias
Cardiovascular: Palpitations, Cardiac Arrhythmias
GI: Abdominal distention, diarrhea

63
Q

What do you see on EKG with Hyperkalemia

A

Tall Peaked T waves with eventual QR interval shortening, Wide QRS

64
Q

Tx of Hyperkalemia

A

IV Calcium Gluconate
Insulin with glucose
Beta-2 Agonist
Kayexalte (enhances GI potassium excretion, lowers total body potassium)

65
Q

What is Metabolic Alkalosis and what causes it

A 
Increased pH
Increased Bicarbonate
Loss of protons from GI/Kidneys: Vomiting/N Tube
Exogenous: Diuresis
Post Hypercapnia: Mechanical Ventilation
66
Q

What is Respiratory Acidosis and what causes it

A

Decreased pH
Increased CO2
Anything that decreases respiration
CNS Depression: Opiates, Sedatives, Trauma
Chronic Diseases: COPD, Obesity, Neuromuscular Disorders

67
Q

What is Respiratory Alkalosis and what causes it

A

Increased pH
Decreased CO2
Due to Hyperventiation

68
Q

What is Testicular Cancer

A

Most common solid tumor in young men 15-40yrs

69
Q

What are risk factors for Testicular Cancer

A

Cryptochidism, usually right sided

70
Q

What are the different forms of Testicular Cancer

A

Germinal Cell Tumor (most common)
Nongerminal Cell Tumors

Germinal Cell

  • Seminoma: Most common type
  • Nonseminoma: Embryonal cell, tratoma, choriocarcinoma (bad prognosis)

Non-Germinal
-Leydig, Sertoli, Gonadoblastoma

71
Q

Sx of Testicular Cancer

A

Painless testicular nodule, solid mass or enlargement
Hydrocele is sometimes present
Gynecomastia

72
Q

Dx of Testicular Cancer

A

Scrotal Ultarsound and Serum Studies (alpha-fetoprotein, HCG, LDH)
Seminomas are radiosensitive and lack tumor markers
Nonseminomas are radioresistant and tumor markers are noted (increased apha-fetoprotein and HCG)

73
Q

Tx of Testicular Cancer

A

Low rade Nonseminoma: Orchiectomy with retroperitoneal lymph nodes
Low grade seminoma: Orchiectomy followed by radiation
High Grade Seminoma: Debulking chemo followed by orchiectomy and radiation

74
Q

What are the pathogens involved in Cystitis and Pyelonephritis

A

E.Coli is most common in complicated and uncomplicated
Staph. Saprophyticus in sexually active women
Enterococci with indwelling catheter

75
Q

Sx of Acute Cystitis

A

Dysuria, Frequency, Urgency, hematuria, Suprapubic Discomfort

76
Q

Sx of Pyelonephritis

A

Fever, Tachycardia, Back/Flank Pain, CVA tenderness, N/V

77
Q

Dx of Acute Cystitis

What is the definitive dx

A

Urinalysis: Pyuria and Leukocyte Esterase, Nitrites, Hematuria
Dipstick: Leukocyte Esterase, Nitrites, Hematuria, WBC
Cultures: Definitive

78
Q

Dx of Pyelonephritis

What is the definitive dx

A

Urinalysis: Pyuria, Leukocyte Esterase, WBC Casts, Nitrites, Hematuria
Dipstick: Leukocyte Esterase, Nitrites, Hematuria, WBC
Cultures: Definitive

79
Q

Tx of Uncomplicated Cystitis

A

Increased fluid itake
Fluoroquinolones are tx of choice (Cipro)
Nitrofurantoin (Macrobid)
TMP-SMX (Bactrim)

80
Q

Tx of Complicated Cystitis

Pregnancy

A

Fluoroquinolone
Aminoglycoside
Pregnancy: Amoxicillin, Nitrofurantoin

81
Q

Tx for Pyelonephritis

A

Fluoroquinolones

82
Q

What is Bladder Cancer

A

Most are Transitional Cell or Uroepithelial Cell

Most present early and respond to treatment

83
Q

What are risk factors for Bladder Cancer

A

Smoking

Occupational Exposures such as dyes, rubber, leather, white males

84
Q

Sx of Bladder Cancer

A

Painless microscopic or gross hematuria

Dysuria, Urgency, frequency, Hesitancy if locally advanced

85
Q

Dx of Bladder Cancer

A

Cytoscopy with Biopsy

86
Q

Tx of Bladder Cancer

A

If Localized or Superficial: Transurethral Resection with cautery
If Invasive (involves muscular layer): Cystectomy, Chemi
Recurrent: BCG Immune Therapy

87
Q

What is Renal Cell Carcinoma

A

Tumors originating in the kidney
Tumor of proximal convoluted renal tubule cells
Usually no warning signs

88
Q

Risk factors for Renal Cell Carcinoma

A

Smoking, Dialysis, HTN, Obesity, Men

89
Q

Sx of Renal Cell Carcinoma

A

Hematuria
Flank/Abdominal Pain
Palpable Mass
Malaise, Weight Loss, Left sided varicocele, HTN and Hypercalcemia

90
Q

Dx of Renal Cell Carcinoma

A

CT scan

91
Q

Tx of Renal Cell Carcinoma

A

Localized: Radical Nephrectomy

Bilateral Involvement or patient with solitary kidney: Partial Nephrectomy

92
Q

What is Wilms Tumor

A

Nephroblastoma
See in kids within first 5 yrs of life
Usually associated with other GU abnormality (cryptochidism, hypospadias)

93
Q

Sx of Wilms Tumor

A

Painless, Palpable abdominl mass

Hematuria, HTN, Anemia

94
Q

Tx of Wilms Tumor

A

Nephrectomy followed by Chemo

If beyond Renal Capsule, Pulmonary METS or large tumor, radiation post surgery

95
Q

What is the most common site for METS for Wilms Tumor

A

Lungs

96
Q

What is Renovascular Hypertension

A

HTN due to renal artery stenosis

Due to increased RAAS activation

97
Q

What can cause Renovascular HTN

A

Atherosclerosis in eldery

Fibromuscular dysplasia in women less than 50

98
Q

Sx of Renovascular HTN

A

Severe/Refractory HTN

Adominal Bruit

99
Q

Dx of Renovascular HTN

What is the gold standard

A

Renal Angiogram: Gold Standard

Renogram (best non-invasive): Captopril Test

100
Q

Tx of Renovascular HTN

A

Angioplasty with stent is definitive
Ace-I, however contraindicated in patients with bilateral stenosis or solitary kidney because Ace-I reduces renal blood flow and GFR in these patients

101
Q

What is Nephrolithiasis and what is their composition

A 
Stones
Calcium is most common
Uric Acid (high protein foods)
Struvite Stones (Mg Ammonium Phosphate)
Cystine
102
Q

Sx of Nephrolithiasis

A

Renal Colic: Sudden onset of constant upper/lateral back pain over CVA, radiating to groin
+ CVA tenderness

103
Q

Dx of Nephrolithiasis
What is most common 1st line
What is gold standard

A

Urinalysis: Microscopic hematuria
pH7.2=Struvite stones
Noncontrast CT: Only will see Calcium and Struvite stones (most common 1st line)
IV Pyelography is gold standard

104
Q

Tx of Nephrolithiasis

A

If 7mm: Shock wave lithotripsy, Uretoscopy with stent, Percutaneous Nephrolithotomy (used for large stones or struvite)

Surgery (12 decks)

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