Exam 3 Renal Flashcards

1
Q

ROLE OF THE KIDNEY

A
  • Balance solute and water
  • Help control blood pressure
  • Cleansing (filtering) of extracellular fluid (ECF) and maintenance
  • of ECF volume and composition
  • Excrete metabolic water-soluble wastes & foreign substances
  • Convert nutrients
  • Regulates acid/base
  • Secretes renin and erythropoietin
  • Help maintain red blood cell levels
  • Converts vitamin D
  • Calcifediol to calcitriol, the active form
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2
Q

NEPHRONS

A
  • Nephrons are the functional unit of the kidney
    • Renal corpuscle (Glomerulus + Bowman capsule)
    • Proximal convoluted tubule
    • Loop of Henle
    • Distal convoluted tubule
    • Collecting duct
  • All the components of the nephrons contribute to URINE formation
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3
Q

GLOMERULAR FILTRATION RATE

(GFR)

A
  • Filtration rate of plasma per unit per time
  • 125 mL/minute
  • Prostaglandins increases GFR
  • Epinephinre and Endothelin decreases GFR
    *
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4
Q

HOW DO KIDNEYS AFFECT

BP

A

Blood Pressure

  • Juxtaglomerular cells measure blood flow in the afferent arteriole and urine flow and composition.
  • Release renin, to Angiotensin II to aldosterone (RAAS)
  • Turns on Na/K ATPase
  • Increases BP
  • Vasoconstriction/thirst
  • Does not change blood osmolarity
  • Na and H2O reabsorbed
  • Lowers K
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5
Q

MICTURITION REFLEX

A

Micturition Reflex Begins when the bladder contains 150 to 250 mL of urine

Can be filled to ~500 ml, but pressure of detrusor muscle will overcome external sphincter

Bladder fills with urine  stretch receptors  sacral spinal cord stimulated  Spinal reflex stimulated

Babies

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6
Q

HYDROURETER

A

Dilation of the ureter

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7
Q

HYDRONEPHROSIS

A

Expansion of the kidney with urine

  • Increased pressure inside the renal capsule
  • Compartment syndrome compresses blood vessels inside kidney; renal ischemia
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8
Q

URINARY STASIS

A

Urinary Retention

  • Risk of infection
  • Stones
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9
Q

POSTOBSTRUCTIVE DIURESIS

A

Polyuric state in which copious amounts of salt and water are eliminated after the relief of a urinary tract obstruction

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10
Q

CAUSES OF

KIDNEY STONES

A
  • Masses of crystals, protein or other substances that are a common cause of urinary tract infections

Saturation theory: Urine is supersaturated with stone components. Influenced by pH and temperature

  • Alkaline urine > chance of Ca+ stone formation
  • Acidic urine > of uric acid stone formation

Matrix theory: Organic materials act as a nidus for stone formation

Inhibitor theory: A deficiency of substances that inhibit stone formation

  • Unilaterally located in the kidneys, ureters, bladder
  • Renal tubules have many surfaces which attract a stone
  • Stones < 5mm have a 50% chance of spontaneous passage

Risk factors:

  • Race
  • Age
  • Gender
  • Geographic location& seasonal factors
  • Fluid intake
  • Occupation
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11
Q

SIGNS & SYMPTOMS OF

KIDNEY STONES

A

Flank pain (moderate to severe), may radiate to groin

If stone is obstructing, pt may experience urgency, frequent voiding

May or may not have hematuria

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12
Q

TREATMENT OF

KIDNEY STONES

A
  • Imaging needed to determine location of stone, severity of obstruction, size of stone
  • Obtain a UA to determine pH of urine
  • STRAIN urine to retrieve stone for further analysis
  • Pain management
  • Dietary modification PRN
  • Nephrolithotomy or lithotripsy to remove stones
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13
Q

Benign Prostatic Hyperplasia

(BPH)

A
  • Non-malignant prostate enlargement due to excessive epithelial cell growth
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14
Q

SIGNS and SYMPTOMS

Benign Prostatic Hyperplasia

(BPH)

A

S&S

  • Urinary hesitancy
  • Dysuria
  • Straining to void
  • Postvoid dribbling
  • Frequent daytime voiding
  • Nocturia
  • Poor force of stream
  • Intermittent stream
  • Feelings of incomplete emptying
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15
Q

TREATMENT

Benign Prostatic Hyperplasia

(BPH)

A
  • Invasive treatment
  • Transurethral resection of the prostate (TURP)

Drug therapy

  • 5-Alpha Reductase Inhibitors
  • Alpha1-Adrenergic Receptors
  • Ie. Finasteride (Proscar)

Reduces prostate size, takes several months

MOA. Inhibits 5-alpha reductase enzyme that converts testosterone to dihydrotestosterone (DHT)

SE. decreased ejaculate, toxic to male fetus

  • Ie. Doxazosin (Cardura), Tamsulosin (Flomax)

MOA. Blockade of alpha1 receptors, relaxes smooth muscle in bladder neck, decreasing obstruction of urethra

SE. Hypotension, fainting, dizziness

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16
Q

URGE INCONTINENCE

(DETRUSOR OVERACTIVITY)

A

Common Causes:

  • Stroke
  • Alzheimer’s disease
  • Parkinson’s disase
  • BPH with overflow

Common Symptoms:

  • Urgency and frequency, day or night

Pharmacological Treatment

  • Anticholingergic drugs
  • Oxybutynin
  • Tolterodine
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17
Q

STRESS INCONTINENCE

(OUTLET INCOMPETENCE)

A

Common Causes:

  • Urologic procedures
  • history of multiple childbirths

Common Symptoms:

  • small volumes of urnie loss with coughing, sneezing

Pharmacological Treatment:

  • Alpha agonists
  • Topical estrogen
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18
Q

MIXED UI and SI

A

Common Causes:

See UI and SI

Common Symptoms:

Pharmacological Treatment:

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19
Q

OVERFLOW INCONTINENCE

A

Common Causes:

  • BPH
  • Fecal impaction

Common Symptoms:

  • Poor stream
  • Incomplete emptying

Pharmacological Treatment:

  • Alpha-adrenergic blockers (e.g., terazosin and tamsulosin)
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20
Q

ATONIC BLADDER

A

Common Causes:

  • Severe diabetic neuropathy, stroke

Common Symptoms:

  • Complete loss of bladder control

Pharmacological Treatment:

  • Intermittent catherizations
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21
Q

FUNCTIONAL INCONTINENCE

A

Common Causes:

  • Inability to get to the bathroom
  • Change in mental status

Common Symptoms:

  • Symptoms will vary

Pharmacological Treatment:

  • Eliminate causes
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22
Q

NOCTURNAL ENURESIS

A
  • involuntary urination that happens at night while sleeping, after the age when a person should be able to control his or her bladder.
23
Q

NEUROGENIC BLADDER

UNINHIBITED BLADDER

A

(loss of bladder sensation)

Uninhibited bladder: reduced awareness of bladder fullness and a low capacity bladder; urinary incontinence

24
Q

NEUROGENIC BLADDER

SPASTIC (HYPERTONIC)

A
  • Spastic (hypertonic): volume is typically small, pressures increase and involuntary contractions occur; increased frequency, urine leakage
  • Lesions between the pontine micturition center and sacral spinal cord
  • Bladder contraction and external urinary sphincter relaxation are typically uncoordinated (detrusor-sphincter dyssynergia)
25
NEUROGENIC BLADDER ## Footnote FLACID (HYPERTONIC)
* Flaccid (hypotonic): volume is large, pressure is low, and contractions are absent; overflow incontinence * Lesions from the sacral cord or sacral nerve root injuries
26
DETRUSOR (BLADDER WALL) HYPERTROPHY
Obstructions
27
OVERACTIVE BLADDER (OA)
4 symptoms: * Urinary urgency * Urinary frequency * Nocturia * Urge incontinence \*\*\*Usually the result of involuntary contraction of the bladder\*\*\*
28
TREATMENT OF ## Footnote OVERACTIVE BLADDER
Behavioral * Schedule voiding, time fluid intake, Kegel exercises, avoid caffeine Drug * Anticholinergic agents which block muscarinic receptors * Ie. Oxybutynin (Ditropan) * These drugs block muscarinic receptors not only in the bladder but elsewhere…a way around this is using drugs that are selective for muscarinic receptors in the bladder (M3 receptors) * Even so they have a high SE profile of anticholinergic activity causing constipation (from reducing bowel motility), blurred vision and photophobia (from preventing contraction of the ciliary muscle)
29
UTI ## Footnote URINARY TRACT INFECTIONS
Bacteria usually enter through the urethra Host defenses include: * Washout phenomenon * Protective mucin layer * Local immune responses and IgA * Phagocytic blood cells * Normal bacterial flora and prostate secretions Inflammation of urinary epithelium from bacteria Can occur in the urethra (urethritis), prostate (prostatitis), bladder (cystitis), ureter, kidney (pyelonephritis) Subtypes: complicated and uncomplicated; upper or lower Risks: * Premature newborns * Sexually active and pregnant women * Spermicide users * Individuals with indwelling catheters * DM patients * Neurogenic bladder patients
30
ORGANISMS THAT CAUSE UTI
Factors:Community associated E.coli (80%) Hospital associated Klebsiella, Enterobacter, Proteus Catheter-associated urinary tract infection (CAUTI)
31
TREATMENT OF UTI's
* Sulfonamides * Trimethoprim * Penicillins * Aminoglycosides * Cephalosporins * Fluoroquinolones * Nitrofurantoin
32
ACUTE CYSTITIS
* Inflammation of the bladder, most common site of UTI in women of childbearing age * Bacteria: E.coli (80%) * S&S: urinary frequency, urgency, dysuria, suprapubic discomfort and LBP * Diagnosis: urinalysis (+ bacteria \> 100k,+leukocyte esterase, + nitrite reductase), urine culture for species
33
TREATMENT OF ## Footnote ACUTE CYSTITIS
Oral antibiotics * Treatment ranges from 1 day to 7 days * Drugs of choice: * Trimethoprim/Sulfamethoxazole (Bactrim) * Nitrofuratoin * Ciprofloxacin
34
ACUTE UNCOMPLICATED PYELONEPHRITIS
* Usually women of childbearing age, kids, elderly * Infection in one or both urinary tracts (ureter, renal pelvis, interstitium) * Shorter course of treatment * Usually symptomatic * Pathogen: E.coli (90%) * Treatment: oral antibiotics
35
TREATMENT OF ACUTE UNCOMPLICATED PYELONEPHRITIS
oral antibiotics
36
COMPLICATED UTI
* Males & females * Associated with a predisposing factor * Renal stones * Enlarged prostate * Indwelling catheter * Impediment to flow of urine * Longer course of treatment 3-7 days, may take as long as 14 days * Pathogen: E. coli
37
RECURRENT UTI's
Relapse or reinfection If more than 3 infections a year, prophylaxis may be indicated: * Nitrofurantoin * Trimethoprim/sulfamethoxazole (Bactrim)
38
ACUTE BACTERIAL PROSTATITIS
* Causes: Indwelling catheter, instrumentation from urethral or prostate surgery * S&S: High fever, chills, myalgias, localized pain as well as UTI symptoms * Responds well to antimicrobial therapy usually a fluoroquinolone
39
NITROFURANTOIN
* Active against a large # of gram+ and gram- bacteria * MOA. Damages DNA; slowing growth rather than killing bacteria * Can treat lower UTIs and prophylax recurrent UTIs * SE. GI disturbances, dyspnea, anemias
40
GLOMERULAR DISEASE
Refers to a group of related diseases * Glomerular capillaries and the Bowman capsule are both made of epithelial cells sitting on a basement membrane. * They are so tightly attached to each other that they share one basement membrane. * The epithelial cells of the Bowman capsule stand up from the basement membrane on foot processes, leaving pores between the feet for filtration. * Causes of injury include: * Immune responses * Toxins or Drugs * Vascular Disorders
41
ACUTE GLOMERULONEPHRITIS
* Inflammatory damage to the glomerulus from a streptococcal infection * S&S. proteinuria, hematuria, significant loss of kidney function * Diagnosis. UA, renal biopsy, electron microscopy * Tx. Antibiotics, steroids, cytotoxic agents to reduce immune response
42
NEPHROTIC SYNDROME ## Footnote (Proteins in Urine)
Albumin "leads to" edema and increased free drug * Immunoglobulins and complement "leads to" immune suppression * Binding proteins "leads to" low ions and hormones * Clotting and anticlotting factors "leads to" thrombosis
43
ACUTE KIDNEY INJURY (AKI)
Sudden decline in kidney function with a decrease in the glomerular filtration and accumulation of nitrogen (Cr, BUN) Stages: * Risk: 1.5-fold increase in the serum creatinine, or GFR decreased by 25%, or UO \<0.5 mL/kg/hr for 6 hrs * Injury: 2-fold increase in the serum creatinine, or GFR decreased by 50%, or UO \<0.5 mL/kg/hr for 12 hrs * Failure: 3-fold increase in the serum creatinine, or GFR decreased by 75%, or UO \<0.3 mL/kg/hr for 24 hrs or no UO for 12 hrs * End-stage renal failure: Complete loss of kidney function \>3 mo (requiring dialysis or transplant)
44
PATHO OF AKI
Extracellular volume depletion, decreased renal blood flow, toxic injury to kidney cells "leads to" alterations in renal function Classifications: * Prerenal (renal hypoperfusion) * Intrarenal (disorders of renal parenchyma; intrinsic) * Postrenal (urinary tract obstructive disorders)
45
PRERENAL AKI
* Most common cause of AKI * Usually due to renal hypoperfusion (hypotension, hypovolemia, hemorrhage, low CO) * Shock, dehydration, vasoconstriction * Failure to restore blood volume (or BP) can cause cell injury and ATN (acute tubular necrosis)
46
INTRARENAL (INTRINSIC) AKI
* Results from ATN, acute glomerularnephritis, vascular disease, use of nephrotoxins, interstitial disease (drug allergy, infection, tumor) * Kidney tubule function decreased * Ischemia, toxins, intratubular obstruction
47
POSTRENAL AKI
* Rare * Caused by urinary tract obstruction, enlarged prostate, neurogenic bladder
48
TREATMENT OF AKI
* Prevention and early diagnosis * Correct fluid & electrolyte disturbances, special diet * Correcting cause, like low BP, etc. * Treat infections (if any) * Avoid nephrotoxic medications
49
CHRONIC KIDNEY DISEASE | (CKD)
* Progressive loss of renal function * Fewer nephrons are functioning. * Remaining nephrons must filter more * Hypertrophy * Defined as: GFR \< 60 for 3 months * Associated with HTN, DM, chronic pyelonephritis, chronic glomerulonephritis
50
METABOLIC CHANGES WITH CKD
* Na+/H2O is lost in the urine * K+ is retained * Metabolic acidosis develops * Ca & phosphorus metabolism are altered * Erythropoietin production is diminished * Proteinuria
51
CLINICAL MANIFESTATIONS OF CKD
* Uremia/Azotemia: increased levels of serum creatinine, urea, and other nitrogenous compounds * CNS, GI, immune disturbances * Cardiovascular complications * Hypertension, heart disease * Mineral metabolism disorders  metastatic calcifications, and bone disease * Hyperphosphatemia  hypocalcemia  increased PTH  calcium resorption from bone  bone loss * Decreased vitamin D activation  increased PTH, impaired osteoblasts * Decreased inflammation and immunity * CNS and PNS alternations * Peripheral neuropathy, restless leg syndrome, uremic encephalopathy * Sexual dysfunction * Impotence, hypofertility, dysmenorrhea * Skin disorders * Dryness, bruising, Terry nails * GI disorders * Anorexia, nausea, vomiting, ulceration
52
CARDIOVASCULAR COMPLICATIONS
Anemia: from hemolysis, bone marrow suppression, decreased erythropoietin and iron * Weakness, fatigue, depression, insomnia, decreased cognitive function * Decreased blood viscosity "leads to" increased heart rate, peripheral vasodilation * Angina pectoris and other ischemia Decreased platelets "leads to" bleeding
53
TREATMENT OF CKD
* Ultrasound, CT scan to visualize kidney * Obtain UA and serum electrolytes * Dialysis * Supportive therapy * Restrict phosphate, K+ * Supplement vitamin D * Renal transplant