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
Q

NEUROGENIC BLADDER

FLACID (HYPERTONIC)

A
  • 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
Q

DETRUSOR

(BLADDER WALL)

HYPERTROPHY

A

Obstructions

27
Q

OVERACTIVE BLADDER

(OA)

A

4 symptoms:

  • Urinary urgency
  • Urinary frequency
  • Nocturia
  • Urge incontinence

***Usually the result of involuntary contraction of the bladder***

28
Q

TREATMENT OF

OVERACTIVE BLADDER

A

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
Q

UTI

URINARY TRACT INFECTIONS

A

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
Q

ORGANISMS THAT

CAUSE UTI

A

Factors:Community associated

E.coli (80%)

Hospital associated

Klebsiella, Enterobacter, Proteus

Catheter-associated urinary tract infection (CAUTI)

31
Q

TREATMENT OF

UTI’s

A
  • Sulfonamides
  • Trimethoprim
  • Penicillins
  • Aminoglycosides
  • Cephalosporins
  • Fluoroquinolones
  • Nitrofurantoin
32
Q

ACUTE

CYSTITIS

A
  • 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
Q

TREATMENT OF

ACUTE

CYSTITIS

A

Oral antibiotics

  • Treatment ranges from 1 day to 7 days
  • Drugs of choice:
  • Trimethoprim/Sulfamethoxazole (Bactrim)
  • Nitrofuratoin
  • Ciprofloxacin
34
Q

ACUTE UNCOMPLICATED

PYELONEPHRITIS

A
  • 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
Q

TREATMENT OF

ACUTE UNCOMPLICATED

PYELONEPHRITIS

A

oral antibiotics

36
Q

COMPLICATED UTI

A
  • 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
Q

RECURRENT UTI’s

A

Relapse or reinfection

If more than 3 infections a year, prophylaxis may be indicated:

  • Nitrofurantoin
  • Trimethoprim/sulfamethoxazole (Bactrim)
38
Q

ACUTE BACTERIAL PROSTATITIS

A
  • 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
Q

NITROFURANTOIN

A
  • 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
Q

GLOMERULAR DISEASE

A

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
Q

ACUTE

GLOMERULONEPHRITIS

A
  • 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
Q

NEPHROTIC SYNDROME

(Proteins in Urine)

A

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
Q

ACUTE KIDNEY INJURY

(AKI)

A

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
Q

PATHO OF

AKI

A

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
Q

PRERENAL AKI

A
  • 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
Q

INTRARENAL (INTRINSIC)

AKI

A
  • 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
Q

POSTRENAL

AKI

A
  • Rare
  • Caused by urinary tract obstruction, enlarged prostate, neurogenic bladder
48
Q

TREATMENT OF AKI

A
  • Prevention and early diagnosis
  • Correct fluid & electrolyte disturbances, special diet
  • Correcting cause, like low BP, etc.
  • Treat infections (if any)
  • Avoid nephrotoxic medications
49
Q

CHRONIC KIDNEY DISEASE

(CKD)

A
  • 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
Q

METABOLIC CHANGES

WITH CKD

A
  • Na+/H2O is lost in the urine
  • K+ is retained
  • Metabolic acidosis develops
  • Ca & phosphorus metabolism are altered
  • Erythropoietin production is diminished
  • Proteinuria
51
Q

CLINICAL MANIFESTATIONS OF

CKD

A
  • 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
Q

CARDIOVASCULAR

COMPLICATIONS

A

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
Q

TREATMENT OF

CKD

A
  • Ultrasound, CT scan to visualize kidney
  • Obtain UA and serum electrolytes
  • Dialysis
  • Supportive therapy
    • Restrict phosphate, K+
    • Supplement vitamin D
  • Renal transplant