AKI and Male Reproductive Disorders Flashcards
Chronic Kidney Disease (CKD)
○ Progressive, irreversible loss of kidney function
○ Hypertension - chronically uncontrolled
Acute Kidney Injury (AKI):
A potentially reversible, abrupt decline in kidney function leading to increased creatinine, decreased urine output, or both.
Usually associated with other life-threatening conditions
***Follows severe, prolonged hypotension, hypovolemia, or exposure to a nephrotoxic agent (gentamycin, CT contrast - flush with fluids)
Develops over hours - days
High mortality rate
Most common people with AKI
■ Sepsis patients
■ Hypovolemic shock
■ Burn patients
■ Fractures - blood loss
■ Athletes - diaphoresis, not replacing fluids
Manifestations of AKI
Mildly elevated serum creatinine –> anuric renal failure
Prerenal and postrenal AKI correctible – ADDRESS THE CAUSE
Untreated prerenal and postrenal causes +/ or intrarenal causes ATN
Causes leading to AKI
Prerenal
- External to the kidneys (ie hypovolemia or meds)
- Usually, reversible
Infrarenal
- Conditions that cause direct damage to renal tissue (parenchyma) impaired nephron function (ie ATN due to ischemia, nephrotoxins, or sepsis)
- Due to prolonged ischemia OR the presence of nephrotoxins (ie gentamycin or CT contrast dye), Hgb from hemolyzed RBC’s (ie sickle cell disease) or myoglobin released from necrotic muscle cells
Postrenal
- Mechanical obstruction of urine outflow (ie BPH, Prostate Ca, renal calculi, tumors).
- Usually reversible if identified before permanent kidney damage occurs
What are the three phases of AKI
Initiation
Maintenance
Recovery
what happens if people do not recover from AKI?
CKD develops
Initiation phase of AKI
Characterized by:
serum creatinine + BUN
urine output
Maintenance phase of AKI
Days to weeks
May be anuric, oliguric, or nonoliguric
Nonoliguric
dilute urine but uremic toxins present (low specific gravity)
Oliguric
lasts 10-14 days usually. The longer it is prolonged, the poorer the outcome
Oliguric means the patient produces LESS THAN 400mL/day or 20mL/ hr
Manifestations include:
- Changes in urinary output
- Fluid and electrolyte abnormalities
- Uremia
Anuric
Anuric means the patient produces NO URINE
Oliguric changes in maintenance phase
Urinary Changes: U/O decreased to <400mL/24h
Fluid volume excess: JVD, edema, hypertension - pulmonary edema, pericardial and/ or pleural effusions
Metabolic acidosis: Kussmaul’s resps (deep rapid) to increase blowing off CO2 - lethargy/ stupor (if prolonged)
Sodium Balance: Hyponatremia
Potassium Excess: Hyperkalemia - tall, peaked T waves (ECG)
Hematological Disorders: Anemia, increased bleeding,, decreased WBCs.
Calcium and Phosphate: Hypocalemia + hyperphosphatemia
Waste Product Accumulation: increased creatinine, increased BUN, decreased eGFR
Neurological Disorders: Fatigue/ difficulty concentrating - seizures, stupor, coma
Metabolic acidosis
Kidneys can’t synthesize ammonia, which is needed for hydrogen ion excretion or to excrete acid products of metabolism. Serum bicarb level decreases b/c bicarb is used up buffering H+ ions.
Sodium Balance
Damaged tubules cannot conserve sodium, therefore, the urinary excretion of sodium may increase resulting in hyponatremia.
Hematological Conditions
Anemia r/t impaired erythropoietin production. Uremia reduces platelet adhesiveness, leading to bleeding. WBC’s are altered leading to immune deficiency. Infection in association with AKI is associated with double the mortality rate.
Potassium Excess
Occurs b/c the normal ability of the kidneys to regulate an dexcrete potassium is impaired. May be precipitated by a number of causes: massive tissue trauma; bleeding and blood transfusions may cause cellular destruction; acidosis worsens hyperkalemia a hydrogen ions enter the cells and potassium is driven out of the cells into the extracellular fluid. Prompt treatment is essential
Calcium and PO4
Activated Vit D must be present for GI absorption of calcium. Only functioning kidneys can activate Vitamin D, therefore, in damaged kidneys, serum calcium decreases. In response, the parathyroid gland releases PTH, stimulating bone demineralization. Phosphate is released as well, leading to hyperphosphatemia, worsened by the reduced excretion of PO4 by the kidneys. Metabolic acidosis also causes more calcium to be in its ionized state (vs bound to protein). An ionized calcium level that decreases significantly can lead to tetany
Waste Product Accumulation
Kidneys are the primary excretors for urea, the end product of protein metabolism and creatinine, and end product of endogenous muscle metabolism. BUN results have to be interpreted with caution b/c dehydration, corticosteroid use, catabolism d/t infection, severe injury, and GI bleeding can also increase BUN. creatinine and BUN. BUN non-specific. Clinically, the recommended method to evaluate kidney function is with an eGFR.
Neurological Disorders
related to accumulation of nitrogenous waste products in the brain and nervous tissue.
Recovery phase
Marked by return of BUN, Creatinine and GFR towards normal states
Diuresis –> fluid & electrolyte abnormalities
- Begins 1-3 L/ 24h –> 3-5 L/ 24h
- Pts must be monitored for hyponatremia, hypokalemia and dehydration
- May last 1-3 weeks
Patient’s acid-base, electrolyte and waste product values begin to normalize
Renal function may take up to 12 mos to stabilize.
Diuresis
The high urine output occurs d/t osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. In this phase, the kidneys have recovered their ability to excrete wastes but not to concentrate the urine.
AKI dx studies
Urinalysis
- Sediment WITH casts, cells or proteins - intrarenal disorders
Urine specific gravity, sodium content, osmolality - helps differentiate different types of AKI
Renal ultrasound: anatomy and function
Renal CT: can identify causes of obstruction, but exposure to radiation and nephrotoxic contrast is greater risk
MRI and MRA are NOT recommended
Care of AKI
GOALS of CARE:
Eliminate the cause(s)
Manage signs and symptoms
Prevent complications
Care of AKI
Is there sufficient Intravascular volume and cardiac output to perfuse the kidneys?
Diuretic Therapy
- Loop diuretics (ie Lasix)
- Osmotic diuretic (ie mannitol)
Fluid Restriction: 600mL (insensible losses) + previous 24h losses
Treatment of Electrolyte imbalances
Renal Replacement Therapy (RRT) – Usually, hemodialysis (HD)
If AKI is already established, fluids and diuretics will not be effective and may be harmful. Generally, begin early RRT to minimize symptoms and prevent complications.
Nutrition therapy of AKI
Main challenge - Balancing adequate calories to prevent catabolism despite restrictions required to prevent electrolyte and fluid disorders
Energy from fat and carb sources prioritized to prevent ketosis
25-35kCal/kg
Electrolyte replacement in accordance with serum levels
- Sodium is restricted
- Hyperphosphatemia, hypermagnesemia and hypocalcemia
Enteral or parenteral feeding may be required (though parenteral would be done ++ cautiously if pt on RRT)
Health promotion of AKI
ID high-risk populations for AKI
Control nephrotoxic drugs (ie IV contrast)
Prevent prolonged episodes of hypovolemia or hypotension
AKI prevention
essential d/t high mortality rates associated with AKI
For patients with ANY level of renal insufficiency (esp those with diabetes or older adults), special attention must be given to prevent nephrotoxic events secondary to contrast dye. ADEQUATE HYDRATION before and after the test is critical.
Preventing prolonged episodes of hypovolemia INCLUDES monitoring output (esp when pts receiving ++ diuretic therapy, or in with excessive diarrhea/ NG/ vomiting.
Acute intervention of AKI
Managing fluid and electrolyte balance
Monitoring AND recording accurate intake and output
Daily weights (at the same time, same scale)
- 1 kg = 1L of fluid
Reducing risk of infection
- Blunted febrile response
Correct dosing of antibiotics for renal impairment
Skin care and mouth care
Rhabdomyolysis
“..characterized by skeletal muscle injury and release of intracellular contents into the systemic circulation – namely, potassium, phosphate, myoglobin, creatinine kinase (CK) and lactate dehydrogenase (LDH).”
Can cause intrarenal AKI secondary to myoglobin obstruction of the renal tubules due to muscle breakdown
Rhabdomyolysis dx based on…
History – crush injury, fall followed by prolonged immobility, concomitant drug use, status epilepticus
Physical exam
Elevated serum Creatine Kinase (CK) >1000
Urinalysis +’ve for blood (but microscopy NOT), suggesting myoglobin as cause for urinalysis result.
Rhabdomyolysis Manifestations
Aching muscles
Tea-coloured urine
Reduced urine output
Tachycardia secondary to pain, dehydration, or fluid shifts
? Muscle swelling (usu post- fluid resuscitation)
?Bruising/ pressure sores - compression injury
Rhabdomyolysis – Care
Aggressive IV Isotonic Fluid Resuscitation w/ crystalloid (non-anuric patient)
Accurate recording of intake + output
Monitoring pt for signs of fluid overload
RRT as needed to treat AKI
Trending CK and renal function tests (BUN, Creatinine, eGFR), along with electrolyte panel
Benign Prostatic Hyperplasia
Non-inflammatory enlargement of prostate gland resulting from increase in # of epithelial cells and amount of stromal tissue
Most common urological problem in male adults
Research is unclear whether BPH predisposes men to the development of prostate cancer
Prostate
Prostate = gland that surrounds neck of bladder & urethra in males; secretes fluid that forms part of seminal fluid
Benign prostatic enlargement
= prostate growth sufficient to obstruct (block) urethral outlet resulting in lower urinary tract symptoms or UTI
Patho of BPH
Hormonal changes with aging
Develops in inner part of prostate
Cancer more likely to develop in outer part
Enlargement compresses urethra - eventual partial or complete obstruction
Leads to development of clinical symptoms
Risk factors of BPH
Aging
Physical inactivity
Diabetes
Obesity (large waist circumference)
Familial history in first-degree relative
Protective factors of BPH
Diet of fruit & veggies; lycopene
Physical activity
BPH clinical manifestations
Bothersome “LUTS” – lower urinary tract symptoms
Gradual onset
Obstructive symptoms
Decrease in calibre & force of urinary stream, hesitancy, intermittency, dribbling
Irritative symptoms (associated with inflammation or infection)
Urinary frequency, urgency, dysuria, bladder pain, nocturia, incontinence
Complications
Urinary retention, UTI & possible sepsis, calculi, renal failure (hydronephrosis)
Dx of BPH
History and physical
DRE – digital rectal exam
PSA levels (trend) -Prostate specific antigen - a glycoprotein - elevated levels indicate a pathological condition of the prostate, though not necessarily prostate cancer. PSA levels can be slightly elevated in BPH, but more in prostatitis.
Urinalysis with culture
Postvoid residual
Ultrasound
Cysto -Urethroscopy
BPH care
Goals: Restore bladder drainage, relieve symptoms and prevent/ treat complications.
Treatment is generally based on the degree to which the symptoms bother the patient or the degree to which complications are present vs the size of the prostate.
BPH care - active surveillance
“Watchful waiting” (mild luts)
- dietary changes (decreasing caffeine & artificial sweeteners, limiting spicy or acidic foods)
- avoiding decongestants & anticholinergic medications (prevent bladder contraction)
- restricting evening fluid intake
- timed voiding schedule
BPH care - drug therapy
5α-Reductase inhibitors (reduce the growth of prostate tissue, takes time) – 6 mos to see change
α-Adrenergic receptor blockers (smooth muscle relaxants, lowers BP) – 2-3 wks to see change – risk for ortho hypotension
BPH care - invasive therapy
Transurethral resection of the prostate (TURP): GOLD STANDARD
Transurethral incision of the prostate (TUIP): local anesthetic; as effective as TURP
Prostatectomy: surgery of choice for larger prostates
BPH care - minimally invasive therapy
TUMT, TUNA, Laser prostatectomy
TURP
GOLD STANDARD
Done under spinal or general anesthetic
Associated with good outcomes in 90% of patients
HOLD ASA or anticoagulants preop
Pain and UTI most common preop problems necessitating TURP
TURP preop care
Urinary drainage must be restored before surgery
Use of lidocaine jelly ++ helpful
May require coude (curved tip) catheter
Antibiotics usually given before invasive procedures
Patient education on common alterations in sexual function is important – retrograde ejaculation not harmful but orgasms might be less pleasurable
TURP postop care
Main complications:
- Hemorrhage (CBC)
- Bladder spasms (smooth muscle relaxants)
- Urinary incontinence
- Infection
Manage CBI – rate determined by colour of drainage. Goal is light pink with no clots. Small clots are expected for 24-36h, but bright red blood can indicate hemorrhage.
Avoid activities that increase abdominal pressure (ie straining)
Remove CBI 2-4 days postop; trial of void 6h after cath removal
Urinary dribbling/ incontinence common initially; can usu improve with Kegel exercises over first 2 months postop
Dietary interventions / bowel protocol to avoid straining; adequate fluid intake
Prostate cancer
Malignant tumour of prostate gland
Androgen-dependent adenocarcinoma (overgrowth of cells in a gland)
- So after the age of 50 most men have a decrease in testosterone, but have an increase in dihydrotestosterone (a potent form of testosterone)
Majority of tumours in outer aspect of prostate
Usually slow growing but progressive if left untreated
Can metastasize through direct extension, lymph system, or bloodstream
Direct extension
seminal vesicles, urethral mucosa, bladder wall, & external sphincter
Lymphatic system
regional lymph nodes
Bloodstream
pelvic bones, head of femur, lower lumbar spine, liver, lungs
Causes of prostate cancer
Age - Incidence rises markedly after 50 yrs of age (when screening starts); median age is 67 yrs of diagnosis
Ethnicity
Family history
Diet: tomatoes and tomato-based products are protective. Diet high in fat, dairy products, red meat and processed meat and being obese are risk factors.
Prostate cancer risk factors
> 50 years of age
Ethnicity: Black > White > Asian
Family history
High levels of testosterone
Diet high in fats & low in vegetables & fruits
Occupational exposure to cadmium
Genetic link -mutations in luminal and basal cells of the prostate. Also links to BRCA1 and BRCA2 (genetic mutations causing breast cancer)
Prostate cancer prevention
1) Eat a wide variety of fruits & vegetables each day
Consumption of tomatoes, tomato-based products, & garlic may protect against prostate cancer
2) Be physically active
3) Maintain a healthy weight
Clinical manifestations of prostate cancer
Generally asymptomatic during early stages
Urinary symptoms may occur (similar to BPH):
- Difficulty starting or stopping urination
- Slow stream
- Painful urination or ejaculation
- Dribbling
- Frequent urination
- Loss of urinary control
- Blood in urine or ejaculate
- Night-time voiding
Advanced prostate cancer:
- Weight loss
- Fatigue
- Backache or sciatica-like pain, or swelling of legs that doesn’t go away
Dx of prostate cancer
DRE:GOLD STANDARD
PSA screening: NOT RECOMMENDED
- Not specific to prostate cancer!
- Prostate biopsy required for diagnosis
Transluminal ultrasound if suspected
Biopsy to confirm (based on cell type)
Prostate Cancer Associated 3 (PCA3) – gene in urine specific to prostate ca.
AFTER DIAGNOSIS:
- Bone scan
- CT
- MRI
PSA
prostate-specific antigen; glycoprotein produced by prostate gland; elevated in prostate cancer, BPH or prostatitis; not specific to cancer but when cancer exists, is useful marker of tumour volume (i.e. higher the PSA, greater the tumour mass)
Once a diagnosis is made, bone scan, CT and/ or MRI will determine extent of spread.
No provincial screening program in BC
- If screening is going to be done, men between the ages of 55 and 69 most benefit from it. Routine screening not recommended over the age of 70. (CDC)
PSA (prostate specific antigen) used for:
- Monitoring established prostate cancer & metastatic disease or detection of early recurrence, where prostate cancer is already known
- Diagnostic adjunct in combination with other tests in symptomatic men
- Screening tool
Prostate cancer staging and grading
Whitmore-Jewett
TNM Classification System
Tumor
Characteristics of the primary tumor (grading)
Nodes
Involvement of lymph nodes
Metastasis
Evidence of spread
Gleason scale (2-10)
Grading of tumour based on histology
Provides an indication of the risk for spread
Care of prostate cancer
Watchful waiting
Chemotherapy
Hormone therapy
Radical prostatectomy
Cryotherapy
Radical prostatectomy for prostate cancer
removal of entire prostate, seminal vesicles, part of bladder - entire prostate removed b/c cancer tends to be in many different locations within the gland
- catheter in place for 1-2 weeks postop
- risk for erectile dysfunction & incontinence
- may be possible to do nerve-sparing procedure to spare nerves responsible for erection
Cryotherapy for prostate cancer
destroys cancer cells by freezing tissue
Chemo for prostate cancer
limited to treatment for those with hormone-resistant cancer in late-stage disease
Hormone therapy for prostate cancer
block androgen (testosterone) production to reduce tumour growth; may be used as adjunct therapy before surgery or radiation
Treatment of prostate cancer
Most treatments have very undesirable side effects including:
Hormonal side effects
- Hot flashes, muscle atrophy, loss of libido
Specific surgical side effects
- Risk for incontinence or “dribbling”
- Risk for impotence
Chemotherapy and radiation therapy side effect
- Depends on type of therapy.
- Common side-effects may include:
Nausea, vomiting, fatigue, hair loss …
Testicular cancer
Most common type of cancer in males ages 15-29 years
More common:
- In right testicle
- In males with hx of undescended testes
- In males with a family hx of testicular anomalies or cancer
Predisposing factors: HIV, orchitis, maternal exposure to diethylstilbestrol, testicular ca in contralateral testis
Testicular cancer manifestations
Slow or rapid onset depending on type of tumor
Painless lump, scrotal swelling, and/ or feeling of heaviness
Scrotal mass usually nontender and very firm
Sometimes concurrent lower abd/ scrotal/ perianal dull ache or heavy sensation
Testicular cancer dx
Palpation of firm mas
Ultrasound
Serum alpha-fetoprotein, LDH, and hCG; CBC/ LFT’s
CXR and/ or CT abdo/pelvis to detect metastases
Care of testicular cancer
Early recognition: TSE (see Table 57-9) from the age of 15 yrs
Fertility and sperm banking should be discussed preop. Tx can affect both erections and fertility
Surgery
Orchiectomy or radical orchiectomy (removal of affected testis, spermatic cord, and regional lymph nodes)
Postop Care:
- Surveillance
- Chemotherapy/ radiation
Treatment-related toxicity significant
Vasectomy
Def’n: Bilateral surgical ligation of the vas deferens for the purpose of sterilization
15-30 minutes in duration
Outpatient procedure under local anaesthesia
Usually irreversible
Does NOT affect production of hormones nor ejaculation
Not “reliable” until 6 month postop; alternate forms of contraception should be used until verification occurs
