3312 Adult Health Exam 4 Study Guide

Chapter 53 Assessment of Kidney and Urinary Function

Kidneys = collect urine and puts it down ureters

o Glomerulus (renal tubules) = ball of blood vessels in nephron; receives unfiltered blood then it filters the blood,
contains loop of Henley. Filtered blood goes out through veins, contents that were filtered out of the blood (i.e.
water, Na+, K+, Urea) go out through tubes
 If we need to retain Na+, K+, water, it will happen in the renal tubules
o As waste products come through, it makes urine
o Each kidney has 1 million nephrons
o Kidneys are extremely vascular, cannot withhold pressure, will damage arteries & veins – this is why we see
renal damage w/ HTN

Ureters = (2) connects kidney to bladder; lined w/ smooth muscles - see spasm of ureters w/ irritation or kidney stones

Bladder = normal & healthy holds 400 – 500 mL

 Normal & healthy less than 60 years old should expel all urine when voiding (its ok if 5 – 10 mL is left though
 At 60 years old, it’s acceptable to have 100 mL left in bladder after urination

Urethra = male urethra is longer than women – women are more prone to UTI; men urethra goes through prostate

Functions of the kidney

o Main component for electrolyte balance – regulates sodium, potassium, chloride
o Regulate hydrogen (acid-base); if too much hydrogen, they’ll excrete hydrogen; make more bicarb if there’s too
much acid; reabsorbs bicarb
o Fluid volume balance = RAA system – aldosterone release which retains Na+ & water starts in kidneys with renin,
antidiuretic hormone works in kidney by retaining water
o Medication metabolism/renal clearance/excretion of waste = liver takes ammonia (which is toxic to the body) turns
it into urea and kidneys excrete urea
o Blood pressure = kidneys release renin we hold on to fluid and then we have vasoconstriction increases BP –
back to RAA system
o Kidneys do not produce RBC, but it does release erythropoietin that helps produce RBC
** Someone in renal failure has electrolyte imbalances, fluid imbalances, acid-base imbalances, hard time secreting meds,
abnormal BPs, and anemic

Gerontological considerations: renal function (GFR) how quickly is the glomerulus filtering
 GFR is not best indicator for elderly
 Normal & healthy middle age adults you would look at GFR level

Assessment
 What can be a potential cause of kidney disease?
 Any recent trauma, major surgeries, infections, drop in BP, nephrotoxic antibiotics, uncontrolled DM or HTN for yrs?
 Other symptoms: does it burn when they urine (dysuria), is there blood in their urine (hematuria), do they have
hesitancy, do they pee more at night (nocturia), do they not pee at all, do they have no urine at all (anuria) or low
urine (oliguria)
 Physical assessment = looking at fluid volume, looking at electrolyte imbalances, looking at buildup of waste
products, looking at actual urine – what does it look like, are they anemic, do they have edema, do they have HTN

Labs
o Creatinine = 0.7 – 1.3 mg/dL (better for renal function. Creatinine is a byproduct, kidney filter it out; kidney failure -
creatinine level rises if not filtered out)
o BUN = 7 – 20 mg/dL (more volume related; filter of urea and nitrogen)
o BUN/Creatinine ratio = 10-20:1 – is it more of a fluid problem or kidney problem itself
o GFR = 60 – 100 mL/min = how quickly the glomerulus is filtering; < 60 = kidney disease < 15 = kidney failure
o Creatinine clearance = 24hr urine collection – tells you how well the kidneys are at secreting the creatinine
o Equation = volume of urine x urine creatinine
serum creatine
o BMP = what is the patients potassium level; kidney damage/failure have higher potassium level and lower sodium
level b/c of dilution; gives creatinine and BUN; gives chloride
o CBC = HGB & HCT = chronic renal are more anemic b/c of low erythropoietin; low hct = too much fluid – hemodilution
o ABG = need to take bicarb supplement – not producing enough bicarbs (usually see metabolic acidosis)
Urinalysis
 Cultures = to make sure we are treating the right bacteria w/ right antibiotic
 Glucose = should not have any glucose in the urine, if we do – glucose level in the body is too high. It is damaging
the tubules
 Proteins = should not have proteins in urine; when we see protein in urine, indicative for kidney damage and related
to diabetes
 RBC = Should not have any RBC in urine; indicative for kidney stone and damaging ureter, bladder irritation from
infection; important to ask if they are on their menstrual cycle (not an actual result for RBC in the urine because it is
contaminated by menstrual blood)
 Leukocytes = WBC; should not have leukocytes in urine, usually associated w/ UTI
 Specific gravity = normal 1.01 - 1.03; how concentrated the urine; if low = too dilute, if high = too concentrated
 Renal injuries making plenty of urine but not filtering particles = low specific gravity b/c just producing water

Diagnostics
 KUB = abdominal x-ray; position it to bottom of the rub, down to pelvis to see kidney, ureter, and bladder
 Pyelography = KUB w/ injected dye: catheter in, inject dye higher to see ureters and kidneys
 Cystography = KUB w/ injected dye in bladder
 Renal arteriogram = inject dye to look at vasculature in kidneys
 Cystoscopy = go in the bladder and look with a camera; can do biopsy while we are there
 Biopsy
 Bladder scan = < 200 mL in bladder leave alone; > 200 mL and cannot pee, we need to get it out w/ catheter

Chapter 54 Management of Patients with Kidney Disorders

Acute Kidney Injury (AKI) aka Acute Renal Failure (ARF)

Risk factors
o Age: Elders
o Race: African American
o Genetic factors
o HTN, diabetes, metabolic syndrome
Depending of the severity of the kidney injury and the risk factors, it can lead to end stage renal disease (ESRD), chronic
kidney disease (CKD), cardiac death etc.

Causes of AKI / ARF

1. Prerenal = happens before kidney; related to perfusion to the kidney; pt has had severe drop in kidney
perfusion, BP could drop and be in shock, hypovolemic and BP low
2. Intrarenal = happens inside the kidney. Things that can damage inside the kidneys: infections, toxins,
BIG CAUSE = medications (like high doses of antibiotics)
3. Postrenal = happens after kidney due to obstruction of urine flow. Massive kidney stones, bladder injury,
tumor, large prostate in men, something that obstructed urine flow and causes back up of urine

Initial Phase = initial injury or when the injury is occurring

o An injury occurs and secondary injury to the kidneys; don’t see symptoms related to kidneys injury yet
o BP is 60/20 = they’re in shock
o Couple days later after fixing the initial injury, now we start seeing symptoms from the kidneys:

1. Oliguria Phase
o Oliguria = less than 400 mL/day (low urine output)
o Can still produce urine but kidneys aren’t working so low specific gravity of urine – not
filtering out like they need to; urine is diluted
o Might see WBC, RBC, casts (seen on microscope – breakdown and part of RBC)
o A lot of time in metabolic acidosis – not excreting hydrogen or reabsorbing bicarb
o You’ll see hyperkalemia; S&S – cardiac arrhythmias, tall T waves
See hyponatremia (high potassium, low sodium)
 o Elevated BUN and creatinine
o Fatigue and malaise
o Whatever the cause is for oliguria phase we correct it. We hydrate the kidneys. May take
week or so. Kidneys kind of repair self like having a cold and recovering
2. Diuretic Phase
o See gradual increase in urine output. Went from oliguric < 400 mL or anuric < 50 mL and
all of a sudden, the kidneys are working really well. Put out massive amounts of fluid = 3
– 5 L of fluid/day, just a part of kidney recovery process
o This amount of output can cause kidneys to become dehydrated, hypovolemic, kidney
perfusion to go down, and kidney injury to go up. If you don’t watch pt closely, damage
can get wrost and go back to Oliguria Phase
o Hydration is huge key. Watch BP and fluid status
o Should see BUN and creatinine level status return to normal

3. Recovery Phase
o Begins when GFR starts to go up as well
o BUN and creatinine are normal at this point
o Can take up to 6 months for recovery

Treat the cause: if medication – take away meds, if volume issue tx volume. If post renal issues tx that.
o From there it is symptomatic treatment for AKI:
 Metabolic acidosis = give bicarb
 Hyperkalemia = kayexalate best way, quickest is insulin and D50
 Hyponatremia will correct itself as we correct the fluid imbalance
 If potassium is really high, creatinine really high, really sick and not making any urine = put them on
dialysis to take off toxins, normalize electrolyte and pull off fluid

Chronic Kidney Injury (CKD) / Chronic Renal Failure CRF)

 < 60 = kidney disease
 < 15 = kidney failure/end-stage kidney/renal disease (ESRD)
 CKD is symptom management
 Monitor and manage symptoms until pt hits kidney failure
 Kidney failure looking at dialysis, kidney transplant or hospice
 As GFR declines, CKD worsens
 ESRD S/S: weakness, fatigue, headache, sleep disturbances
o Usually HTN b/c increase fluids
o Swelling, pitting edema of legs, orbital edema
o HF, pericarditis
o Fatigue
o High incidence of depression (more increased than other chronic disease)
o Usually anemic (no erythropoietin)
o Hyperkalemic
o Metabolic acidic
o Dry flaky skin, pruritus (itch)
o Ecchymosis (bleeding related to anemia)
o Yellowish gray skin color b/c kidney is not getting rid of bilirubin
o Musculoskeletal cramps
o Bone pain and osteoporosis b/c high phosphorus levels inversely to low calcium levels making them steal
calcium from the bone
o Ammonia odor to breath b/c the urea is a byproduct and is not coming out through kidney
o Renal osteodystrophy
o Anorexia, N/V
o GI bleeds b/c increase risk for bleeds

Complications of CKD
 Manage sodium balance = restrict sodium intake (water follows sodium) and put them on diuretics, it will help
the electrolyte side of kidney failure (gently use diuretics)
 Manage potassium = limit potassium intake, restrict through their diet, and avoid NSAIDs. Take kayexalate (it’s
a liquid) PO at home
  Acid excretion = Fix metabolic acidosis - give sodium bicarb (Tums) to replace bicarbs they are not reabsorbing
 Calcium/phosphate balance = Give phosphate binders - take w/ every meal so it binds to phosphate in their
food and secrete it; or give Calcimimetics (inverse w/ phosphate – high calcium causes low phosphate)
 Erythropoiesis (Anemia) = can give them EPO/erythropoiesis injection (very expensive), make sure they are on
iron supplement that helps increase RBC; if on dialysis, give blood transfusion at the same time b/c they are too
anemic
Renal Diet
 Limit amount of high-quality proteins
 Limit dairy – sodium is high in dairy
 Low sodium
 Low potassium
 Low phosphorus
Food you can eat: Red grapes, cherries, cranberries, raspberries, strawberries, red bell peppers, garlic, onions, cabbage,
cauliflower, olive oil, wild salmon

End Stage Renal Disease (ESRD)/Chronic Kidney Failure (CKF) Managements

Peritoneal Dialysis (PD)

 Only done with CKD
 Can be done at home, overnight, while sleeping
 Have a solution bag. Put the solution (2,000 mL sometimes 3,000 mL
depending on size of pt) in pt’s abdomen. The abdomen is surrounded by the
peritoneal sac that acts as semipermeable membrane and pulls solutes
(things the kidneys would usually filter out K+, Na+, urea, excess fluid) into
this fluid. Then we drain the fluid after it has dwelled in the sac, dwelling can
take 4 hrs. This is one exchange. Some can be on a machine and have this
done 2-3 times a night in 8 hrs.
o It is a sterile technique. You and pt wear masks. At home pt wear a
mask and hand sanitize before touching anything
o While not receiving PD there is a cap on end of catheter with iodine
solution to prevent bacteria (frequent complication – can get infected)
 Complications: putting a lot of fluid in their abdomen and not draining all out, they can have anorexia, nausea,
heartburn, reflux, hernias, peritonitis, weight gain, exit site infection, dyspnea

Hemodialysis
 Done with AKD/AKI or CRF
 For AKI: Vascathe can be in for a couple month (like central line but larger). Only for Dialysis
 You do not touch it for anything for if you’re coding the pt
 Fistula/Graft:
 Fistula is putting artery and vein together (anastomosis = putting 2 things together)
 Graft is where they take a synthetic material and bridge an artery and vein together
 Two needle pokes – one for drawing blood out and other one is putting clean blood back in after
going through dialysis machine
o Chronic renal failure pts gets hemodialysis 3x a week
o A lot of pt will go on this if they are waiting for kidney transplant
o Normal to see massive bulging veins in their arms in dialysis pts, makes it easier for dialysis
o You should be feeling and hearing access. Should feel thrill/turbulence and hear bruit
o Synthetic grafts do not last as long as fistulas
o Complications of hemodialysis:
 Hypotension = need to slow down or stop short of dialysis
 Muscle cramps = b/c drop potassium
 Infection = anytime piercing skin can cause risk of infection – is a sterile procedure to prevent this
 Hemorrhage = needle is in vein and artery. Can get dislodged if knocked. Or if clot get dislodged. Teach
how to hold pressure if they start bleeding

Continuous Renal Replacement Therapy (CRRT)

 Similar to hemodialysis
 Usually used in ICU with really, really sick pts
 Not stable enough for hemodialysis, put them on CRRT – done through vascathe central line
 If pt come in in septic shock and meds are toxic to kidneys, plus fluid overload, we’d use this method
 Works better than hemodialysis b/c we can use it with unstable pts
Glomerular Disease
 Nephritic Syndrome = glomerulonephritis, usually an autoimmune disease, usually related to Berger’s disease
 You’ll see hematuria (biggest thing), some casts, some protein in urine
 Glomerulonephritis = inflammation of glomerulus. Hematuria, protein in urine, RBC casts
o Type of Nephritic syndrome. Over time can lead to scarring if happens recurrently and lead to CRF/CKF
 Nephrotic Syndrome = most common major diabetes complications – large glucose molecule causing damage.
Leads to CKF/CRF
 Increase permeability. Losing large glucose molecules and protein
 See massive proteinuria causing low protein in blood level (hypoalbuminemia – low albumin level)
 hypoalbuminemia causes water to shift from vascular space to tissues which leads to peripheral edema
 Polycystic Kidney Disease = is a genetic disease; pt gets multiple cysts in kidneys – cysts damages and prevents
nephrons from working = leads to CRF/CKF

Special considerations
 Renal surgery (biopsy, tumor, etc.) the kidney vasculature makes hemorrhage post procedure a big deal
o Monitor closely for S&S of hemorrhage = blood in urine, blood in abdominal space via signs of tachycardia,
hypotensive, pain
o Replace blood, make sure pt doesn’t become hypovolemic
o High incidence of problems w/ bowels = paralytic ileus (part of the bowel went to sleep causing back up) - N/V
and abdominal distention. Often need an NG tube. Listen to bowel sounds and get pt up and mobile to prevent
 Renal Transplantation: kidney transplant – usually don’t take out old kidney – so three kidneys unless necrotic or
cancerous. If ESRD don’t take out. New kidney in pelvis, want it protected by bones and leave old kidneys
o Anti-rejection meds that cause immunosuppression – get flu shots, avoid crowds – wear mask, no live vaccines,
avoid infection strict hand hygiene
o S&S of rejection = pain at transplant site, decrease in kidney function
 Renal Trauma: admit pt to unit and watch them closely. Any hemodynamic change (ex. BP drop, or HR goes up)
they will need immediate surgery b/c of how vascular the kidney is

Chapter 55 Management of Patients with Urinary Disorders

Urine sample
 Clarity = Cannot see words through it – cloudy. Can be so cloudy its purulent like it came out of a wound (UTI)
 Color = amber, yellow, orange, tea color (tea or brown = hypovolemia/dehydration) pink or red (RBC in urine),
blue or green = genetic issue, bright orange or bright blue = meds (orange = Pyridium, AZO blue then urine blue)

Urinalysis
 To get specimen – antiseptic wipe clean around urethra for men, women front to back. Clean catch specimen =
start urinating first, then midstream put in the cup
 In and out catheter = sterile procedure
 Self-cath is a clean technique at home
 Indwelling catheter = cannot get the urine out of the bag because it’s been sitting and bacteria can grow;
drain everything out of the tube; kink off the tube to the bag, wait a little bit and go back. Scrub the small
port and pull the urine out with 10 mL syringe
Results:
o Specific gravity = 1.01-1.025: tells me concentration. Particle to water ratio
 Low 1.003 = less concentration, too diluted (hypervolemia/overhydration/kidneys not working to filter particles
but producing water)
 High 1.3 too concentrated (hypovolemia)
o Protein in urine = indicative for kidney/renal damaged
o RBC = should not see in urine = infection, kidney stones, menstrual cycle for females
o Nitrite = should be none. Nitrite positive indicative for UTI
o Leukocytes = WBC fights infection
o Cast (break down of RBC) = not normal to see in urine

Urine Culture and Sensitivity

 Tells you what antibiotic works for patient and bacterial infection; test results take about 3 days to come in
 R = resistant (bacteria is resistant to that antibiotic, does not work)
  S = susceptible (kills the bacteria)
 Call pt and let them know if their antibiotic is resistant or susceptible
o If resistant, they’ll need to come in and change antibiotics (call MD to change)
o If susceptible, make sure they finish the entire course of antibiotic
 MD do not follow up on this, it is the nurse’s job. Want most common susceptible drug and less harsh
 If pt has 3 different bacteria (E. faecalis, E. coli, K. pneumoniae), pt need an antibiotic that is susceptible to all or
be on multiple antibiotics for each one
UTI aka Cystitis = bladder infection, UTI; more common in women b/c of shorter urethra and closer to bladder
 Symptoms of UTI = burning w/ urination (dysuria), foul smelling urine, cloudy urine, urgency, frequency, can have
lower abdominal pain, elderly (causes confusion and anorexia, do not want to eat)
 Treatment = antibiotics, analgesics for frequency and urgency (Pyridium-rx and AZO blue–over the counter)
 Teach women = void after intercourse, loose cotton undergarments, stay hydrated, wipe front to back
 Boys under ten getting UTI – sign of abuse, should not be getting it

CAUTIs: Catheter Associated Urinary Tract Infections

o Indications for catheter (if it is really necessary to have a catheter):
 Recurrent urinary retention
 Surgery
 when they get epidural
 Unresponsive (really sick patient and kidney issues)
 Really bad sacral ulcers (stage 4, tunneling, nasty, really bad that need to stay dry)
 If they need I&O monitoring
o Sterile technique to prevent contamination and infections
o Proper care is necessary = Clean at least once a shift; aseptic towels from tip and away from the urethra, need
really good perineal care
o Use bladder scan before catheter to determine issue
o Alternatives = Condom catheters for men
o Absorbent products and moisture barriers to help with wound care
o Mobility is NOT a reason to add a Foley

Pyelonephritis = Kidney infection. If cystitis (UTI) is not treated, it can move north to kidney(s) – can be one or both
 Symptoms = flank pain (percuss over the kidney and have pain = costovertebral tenderness), high fevers,
malaise, WBCs and bacteria in urine, urinary symptoms similar to UTI
 Elevated WBC count in blood draw
 If not treated = pt will turn septic. Bacteria will travel up tubules to blood stream

Incontinence = 3 main kinds

1. Overflow Incontinence = bladder unable to empty normally, more urinary retention. Bladder stays distended
o Common in males with Prostate issues. Prostate inflamed and blocks urethra – not peeing out all urine
o See trickles of urine b/c bladder is so distend
o Treatment = Flomax (alpha blockers) to relax sphincter and prostate; Cholinergic to increase force of
contraction of bladder

2. Stress Incontinence = common in women during pregnancy and pot-pregnancy

o Pelvic muscles relax. Any time increase abdominal pressure there is leakage
o Increase abdomen pressure causes leakage (baby causes pressure, coughing, laughing, sneezing)
o Help prevent by Kegels (go pee, stop the pee for a sec – movement of stopping the pee is Kegel)
o If they do it early in pregnancy, they can prevent stress incontinence

3. Urge Incontinence = oversensitivity of the bladder; contracting too much, “gotta go gotta go right now”
o Overactive bladder leads to urge incontinence
o Treatment = Anticholinergics to decrease contraction
o Also associated w/ neurological disorders and spastic bladder

Urinary Retention = seen with overflow incontinence

 Surgery (because of general anesthesia) is a big one, especially abdomen surgery
 Abdomen does not want to work after surgery. Need in & out catheter, usually 6 – 8 hrs sometimes start Flomax
 Same day surgery patients have to pee before they can leave
 A normal healthy adult should be able to fully empty bladder
  > 60 years old, it is normal to have 50-100 mL of urine in bladder after peeing
 Med treatment = Cholinergic for contractions and Flomax
 Anticholinergics can cause urinary retention. Watch out for these

Neurogenic Bladder
 Caused by neuro injury (stroke, trauma, lesion, something interfering w/ the brain talking to the bladder)
o Flaccid bladder = lower paralysis – sacral injuries; muscles don’t contract like they need to
 Retain large amount of urine but no pressure to get it out
 Causes overflow incontinence
 Treatment = cholinergic or indwelling catheter
 For long-term to prevent infection switch to suprapubic catheter
o Spastic bladder = related to upper T12 and higher spinal injuries (cervical fractures)
 Contracting all the time – do not have a lot of volume in their bladder. No retention
 Treatment = anticholinergics to decrease contraction

Suprapubic Catheter = meant for long-term

 Decrease infections associated with urethral catheter
 Goes through the abdominal wall. Hooked to drainage bag
 Urine should be clear; Should be closed system; Position below the bladder
 Need really good care around stoma (site) – clean close to the site and work your way out

Urinary Diversions = having to bypass the bladder due to trauma

 Conduit = take part of the bowels and make a pouch (an artificial bladder)
 Will need a drainage bag. Urostomy bag to collect the urine
 Sometimes we get bowel sloth b/c the intestines make mucous.
 You will see mucous in the urine (mucous inside the bowel to create the pouch)
 Continent = Smaller stoma, a tube that connects ureters to the outside
 B/c of the opening on the outside is smaller, patient will self-cath through the stoma (stoma is smaller and
stay close, do not need a drainage bag)
** Ureterosigmoidostomy = connecting the ureters to the sigmoid through an ostomy. Allowing the patients to empty the
ureters through the bowels. Not done often for risk of infection

Urolithiasis aka Kidney Stones aka Renal Calculi

 Some say it’s worse than childbirth
 Biggest sign = flank pain that can radiate to the front
 Increase incidence in male over 40
 Other S&S = severe pain, hematuria, N/V; if one gets stuck, they can have pyelo symptoms
 Diagnosed with KUB (Kidney, ureter, bladder X-ray), can do a CT w/o contrast
 Made up of calcium stones or oxalate stones
o Calcium stone = avoid calcium-containing food (dairy)
o Oxalate stone = avoid raspberries, tomatoes, beans, beets, soy, chocolate, rhubarb, spinach, seeds and nuts,
wheat bran, potatoes
 Can have broccoli, peppers, bananas, coffee, cantaloupes, low fat dairy, papaya, iceberg lettuce, bok choy,
water w/ lemon
o Need to stay hydrated. Need fluids to get these stones moving through
 Treatment for pain = Hydrocodone or codeine (narcotics), can add NSAIDs w/ narcotics to help w/ inflammation
 Treatment for smooth muscle spasm = Calcium channel blockers (CCB)
 Treatment to help dilate = alpha blockers (doxazosin/Cardura)

When patient cannot pass kidney stones, there are procedures:

 Ureteroscopy = go through urethra, bladder and ureter w/ camera. Go in and retrieve the stone and put in stent
so ureter doesn’t collapse
 Lithotripsy: more common
o Extracorporeal shockwaves = external noninvasive
 Use shock waves directed at kidney. Break up stones into tiny pieces to urinate out
o Percutaneous lithotomy: invasive
 o Go in through skin into the kidney, break up the stone or remove the stone, depending on the size
o Risk = infection and bleeding due to vasculature of kidney
** Patients need to strain urine, even at home. Bring stone back in to see if oxalate or calcium so we can better manage
them, especially when they are recurrent in a pt

Bladder Cancer = mimics UTI but when symptoms are treated, it doesn’t go away and no bacteria is growing in culture
despite symptoms
o Risk factors = smoking, frequent UTI, exposed to chemicals, frequent stones, family hx, age (elderly), AA
o Treatment = remove the bladder, chemo, radiation
Chapter 59 Assessment and Management of Patients with Male Reproductive Disorders

Health History = very important to look at health hx

 Medical hx = are they taking beta blockers causing ED, mumps as a kid, hx of std’s and now infertility issues
 Sexual hx = homo/hetero/mixed, high risk behaviors, multiple partners
 GU hx = frequent UTI, hard time starting urinary stream, cannot fully empty bladder
 Social hx = smoking, alcohol use, drugs use
 Psychosocial = stress can lead to ED, what’s there support system like?
 Self-exams = are they doing monthly self-exams

Assessment
o Digital Rectal Exam = palpate prostate, should be smooth, uniform free of lumps/bumps, should not be tender
o Testicular Exam = turn head and cough, palpate their spermatic cord and testes, should not be tender or feel
lumps/bumps, should be smooth
 Self-exams = should be monthly, smooth, uniform
 Testicular cancer more common in young males; prostate cancer more common in elderly
 Need to teach young males to check monthly and report testicular pain immediately
Diagnostics:
 PSA level (prostate specific antigen)
o Not indicative of prostate cancer or BPH, all it tells us is inflammation in prostate
o Normal level = < 2
o Start PSA checks at age of 50, do it annually until about age of 70
o Elevated PSA don’t mean prostate cancer, it can mean they have BPH, prostatitis (inflammation of prostate)
1. Assess the pt further (digital rectal exam)
2. Look at the trend on how rapid it is elevating in how much time (BPH tend to go a lot slower,
prostate cancer PSA will elevate a lot further)
 Ultrasound = look at spermatic cord
 Tissue biopsy
 Semen evaluation = to check for motility, low sperm counts, infertility disorders

Erectile Dysfunction
 For erectile = need blood flow going to the penis, penis swells, and tissue stretches
 Can be tissue issue = decreased elasticity – doesn’t stretch
 Can be sensory issue = lack/unable to feel sensation (diabetics have sensory issues)
 Can be hormonal issue = low testosterone levels
 Biggest cause = decrease in blood flow (related to diabetes and build-up of plaque in the artery that supplies the
penis (atherosclerotic disease)
 Tons of meds that causes erectile dysfunction – need to educate about meds side effects b/c pt will stop meds
 Antihypertensives is a big one
Treatments:
o Med = PDE5 inhibitors (inhibits vascular constriction so it dilates) = increase blood flow to the penis
 Viagra = use to be given for hypertension but now for erectile dysfunction (side effect = hypotension)
 If they have dizziness when they stand up or their BP is low, might need to change meds
 Contraindicated:
 Pt who has heart attack in last 6 months
 Pt who had aortic stenosis (they have softer BP)
 Pt w/ unstable angina b/c they take nitroglycerin – combo w/ PDE5 causes BP to tank
o Hormone replacement = supplement for testosterone
o Mechanical = vacuum pump, gets blood flow to the area, not permanent
o Prosthetic implants = surgical shaft (rod) implanted into penis (permanent)
1. Pump sits in testicles and has a button – press to inflate rod causing erect penis; can still eject
 2. Bluetooth version – can press on phone to erect penis

Phimosis = narrowing of the foreskin

 Foreskin is unable to be retracted to keep it clean – see frequent infection (most common is yeast infection)
o Treat = can stretch it back out or have adult circumcision

Priapism = sustain erection

 Blood is not flowing back out so ischemia happens b/c blood isn't flowing in or out (lose blood flowing to penis)
 MEDICAL EMERGENCY, have to have it treated
o Treat = vasoconstrict, most common drain blood w/ butterfly needle and 60 cc syringe
Epididymitis = epididymis connects testes to vas deferens (spermatic cord) occasionally gest inflamed and infected
 Most common cause = STDs like gonorrhea or chlamydia
o Treat = antibiotics

Orchitis = inflammation of the testicles (could be one or both)

 Usually bacterial or viral
 Swelling of the testicles, pain, N/V, fever, can’t sit or barely walk, particularly lay on their stomach (very painful)
o Viral = Tylenol/Motrin let run course
o Bacteria = antibiotics. Usually STD related

Testicular Torsion
 Spermatic cord gets twisted. Twisted arteries and veins cut of blood supply to testicles (sudden severe pain)
 MEDICAL EMERGENCY
 Most common in teenage boys (early 20s), need to be educated to report pain immediately
o After 8 hrs, testicles cannot be salvage and will need to be removed
o Can manually untwist, if not able to then it will be surgically untwisted to restore blood flow

Testicular Cancer
 Most common in early adult hood and teenage years
 Testicles should be smooth and round, no lumps and bumps
o Treat = removal of testicle sometimes chemo/radiation. There are implants for aesthetics only

BPH: Benign Prostatic Hypertrophy and/or Hyperplasia = enlarged prostate

 Hyperplasia begins at age 40
 50% of all men older than 60 have BPH
 Related to androgen dihydrotestosterone – tissue starts to replicate in amount of cells and prostate will enlarge

Manifestations
 Prostate surrounds urethra in men so prostate enlarged, causing urethral compression
 S&S = weak urinary stream, overflow incontinent, frequency of urination, frequent UTI

Meds treatment
o Decrease DHT using finasteride (Proscar)
 Pregnant women or trying to get pregnant should not touch these drugs
o Alpha adrenergic antagonists = Doxazosin (Cardura), Flomax (relax smooth muscle and increase ctx)

Treatments
o Transurethral microwave thermotherapy (TUMT) = go in with microwaves and irradiate cells
o Transurethral needle ablation (TUNA) = ablation of area around it
o Laser = (brief) 45 mins and minimal invasive, better than meds, less than surgery
** These txs decreases the size, relieve symptoms but not curative. Good for pts who are not candidates for surgery

Transurethral resection/incision of prostate (TURP) = more common, bigger surgery, work better for severe symptoms
 Go in through urethra and scrap out the prostate tissues
 Post-op care w/ TURP is complicated, the area needs to heal
 When pts need to pee, pt will have a 3-way Foley= extra port for irrigation – continuous irrigation to prevent clots
o Use 3000 mL of fluid bag. Control speed w/ roller clamp. Control speed based on color of urine in tube not bag
 Looking for pink light Kool-Aid cherry color in tube w/ no clots
 If really dark = increase irrigation
 If really light pink = decrease irrigation
  If clots = increase irrigation (do not want clots), might do manual irrigation (use syringe to forcefully break
up clots; sterile technique and usually done by urologist)
o Need to monitor urine output. Pt is on strict I&O. Minimum 30 mL/hr of urine + all irrigation should come back
 3000 mL input, get out 3200 mL over 8 hours = only 200 mL of urine out, not good. Need to be 30 mL/hr
 3000 mL input, what is the amount you’ll see over 12 hours = 3360 mL
 12 hrs x 30 mL = 360 mL + 3000 mL input = 3360 mL
o Patients will go home with leg bag – pt should not sleep in them. It is a smaller triangular bag
o Post-procedure = intake/output, have Foley, no straining or Valsalva maneuvers (give stool softeners), no
intercourse for 6 weeks (risk for infection), leg bag teaching

Prostate Cancer
 27,000 deaths annual
 Most time pts asymptomatic
 Symptomatic is already bone metastasis
 Untreated takes 10 years
 Left untreated b/c it does take longer and later in life to diagnose

Risk factors
o greater than 65
o Increase in African American
o High fat diets
o Genetic hx
o Hx of vasectomy increases prostate cancer

Treatment
o Prostatectomy = goal to remove prostate and leave sphincter in place to avoid incontinence
 Go through retro pubic (abdomen). More complications with bowel and bladder
 Go through perineal area. Less complications b/c prostate is easily accessible
 Post-procedure = intake/output, have Foley, no straining or Valsalva maneuvers (give stool
softeners), no intercourse for 6 weeks (risk for infection), leg bag teaching
o Brachytherapy = implant radioactive palates into tissue and irradiate the area around
 Children and pregnant women should not be exposed to radiation
 Sleep in bed by themselves
o Hormone therapy = put on testosterone blocker
o Sometimes don’t leave sphincter in place and have balloon pump for incontinence.

Chapter 51 Assessment and Management of Patients with Diabetes

Review of the endocrine functions of the pancreas

 What is insulin? What does it do? How is its’ secretion stimulated?
o Secreted by beta cells, decrease blood sugar.
 What is glucagon? What does it do? How is its’ secretion stimulated?
o Secreted by alpha cells, increase blood sugar.

Diabetes = A group of disorders causing inappropriate hyperglycemia d/t a relative or absolute deficiency in insulin

Type I = progressive autoimmune disorder that results in Beta Cell Destruction Theories:
1. Antibodies – purely autoimmune
2. Virus-stimulated autoimmune
3. Genetic-likely component. We are unable to produce insulin

Risk factors = parents or sibling w/ type 1 diabetes

S&S
o Polyuria (increase urination)
o Polydipsia (increase thirst)
o Polyphagia (increase hunger)
 o Weight loss (usually on smaller side)
o Fatigue
o Increase frequency of infections
o Rapid onset
o Insulin dependent (beta cells not producing insulin b/c destroyed)
o Familial tendency
o Peak incidence from 10-15 yrs (usually diagnosed in childhood 3-6 yrs old)

Treatments
 Mainly insulin replacement
 Islet cell transplantation = islet cells produces alpha and beta cells that give us insulin and glucagon
 Diet, exercise and stress management
Type Duration
Brand Name Onset Peak

2 – 4 hours
Lispro (Humalog) 10 - 15 mins 1 hour
2- 4 hours
Aspart (Novolog) 5 – 15 mins 40 – 50 mins
Rapid-acting
2 hours
Glulisine (Apidra) (fastest 2 – 5 mins 30 – 60 mins
acting)

Short-acting
Regular (Humulin R,
(only one that
Novolin R, Iletin II 30 min – 60 min 2 - 3 hours 4 – 6 hours
can be given
Regular)
IV)
2 – 4 hours
NPH (neutral protamine 4 - 12 hours 16 – 20 hours
Hagedom)
Intermediate- 3 – 4 hours
(Humulin N, Iletin II 4- 12 hours 16 – 20 hours
acting
Lente, Iletin II NPH,
Novolin N [NPH])

Glargine (Lantus) 1 hour 24 hours

Long-acting detemir (Levemir) 6 hours Continuous / no peak 24-36 hours
Glargine (Toujeo)

Question: You gave lispro insulin at 8 am. What time will you assess for hypoglycemia? 1 hour is peak so 9 am roughly.
 Peak = most risk for hypoglycemic
 Don’t mix long-acting
 Cloudy to clear, clear to cloudy

Type II = producing insulin but having a problem utilizing it

 Not always progressive
 Some people can reverse it with diet and exercise
 Insulin resistance = insulin receptors are damaged and not working – cannot utilize insulin

Risk factors
 Metabolic syndrome (5 characteristics):
1. Central obesity (apple shape)
2. High BP
3. High triglycerides
4. Low HDL – good cholesterol
5. Insulin resistance
 Increase glycemic carb diet with sedentary lifestyle
 Onset in age 40s – 50s
 Obesity/overweight
  Ethnicity and/or race (African Americans)
 HDL < 35, Triglycerides > 250
 Gestational diabetes or baby > 9lbs
 Polycystic ovary syndrome (PCOS)
 < 6.5 hrs of sleep/night

S&S = symptoms are a lot more vague

o Fatigue
o Weight gain (if you don’t utilize glucose you store it as fat)
o Acanthosis nigricans (neck lines)
o Lesser degree of 3 P’s when glucose high

Treatments
 Mainly anti-hyperglycemic meds
 Oral glucose lowering agents
o Biguanide = Metformin (stops absorption in GI tract. Big side effect = diarrhea)
 Also increase muscle use
 Least likely to cause hypoglycemia
o Sulfonylureas; DDP4 inhibitors
 Increase insulin secretion
 Overload insulin
 Cause hypoglycemia
 Work in beta cells
o SGLT2 inhibitors = work in kidneys
 Insulin
 Lifestyle modifications = very important to manage metabolic syndrome
o Manage stress (stress increases glucose and releases glucose)
o Want low glycemic food (low carb diet) – avoid candy, bread, coke, pasta
o Activity – exercise increase sensitivity of insulin receptors
o Illness

Diagnostics for Diabetes

 Fasting peripheral glucose (FPG), fasting blood sugar (FBS), fasting blood glucose (FBG)
o NPO at midnight
o check sugar at 7am
 Diabetes = > 126
 Prediabetes = > 100 – 126
 Normal = < 100 normal. If this is high than add an A1C

 Hgb A1C = gives you an average over last three months. Most common
o Diabetes = > 6.5
o Prediabetes = > 5.7 – 6.5
o Normal = < 5.7
o Diabetic goal < 7. Means sugar is less than 150

 OGTT: Oral Glucose Tolerance Test. Generally reserved for pregnant woman
o Diabetes = > 200
o Prediabetes > 140 – 200
o Normal < 140

Patient Education
 Insulin administration:
o Ok to keep insulin room temp up to 28 days. Store extra in fridge
o Do not randomly rotate sites, but don’t keep using same spot. Pick quad and work around inside the
quad. When quad is all used, start new quad = body gets used to reacting to insulin in same area
o Make sure alcohol is dried
o Subcut 45 - 90 degrees (no IM, muscles absorb it too quickly)
o Need to have a puncture disposal (needle disposal). If they don’t have it, use a hard-plastic container
(milk carton, trash bin that closes)
  Self-monitoring blood glucose:
o Before meals (ac), finger stick, sticker patch and cellphone app (self-monitor)
o Dipstick – monitor urine, ketones in urine level at least 180 if ketones in urine (DKA)
o Ketone finger stick monitor - more accurate

 Sick Day and other dietary changes: illness stresses body = increase glucose. Not eating, still need to check level
o Will still need some insulin: administer insulin based on current blood sugar reading
o Caution oral meds b/c only one dose
 Especially Sulfonylureas and DDP4 inhibitors that increase insulin secretion. Be very cautious.
Check with provider
o Increase frequent of monitoring glucose and/or ketones
o Hydration
o Keep easily digestible food on hand, simple carb sugar snacks in case sugar drops (sugar free snacks,
jello, soda, popsicle apple juice, sports drinks, etc. – stay hydrated)
Complications – Acute
 Hypoglycemia = most common; < 60 mg/dL (no magic number depend on pts normal)
o Sympathetic adrenergic response when sugar drops
 Caused by increased insulin, increased exercise, or decreased food

S&S = “Cool and Clammy, give them some candy”

o Shakiness/dizziness
o Nervousness, diaphoresis, confusion
o Unarousable
o Headache
o Fast, pounding HR
o Sweating, cold, clammy skin
Treatment = Give sugar
o Give simple carb/sugar first b/c it’s fast acting (but not long acting)
o F/u with complex carb so glucose level won’t drop back down
o Give juice (simple carb) first 15 min check sugar, if doing better than give peanut butter and cracker
(complex carb)
o If unconscious or NPO we can give:
 IV glucose (Dextrose)
 15 mL (amp) of D50 (Dextrose) syrup/sugar water
 Check 15 mins later
 Dextrose can be IV push or drip
 Glucagon injections IM or Subcut

 DKA = complication primarily seen with Type 1. Very rarely with type 2. Diabetic Keto Acidosis
o Missed meds, ran out of insulin
o Sick and didn’t manage well
o New diagnosis usually in children

Manifestations = Glucose rises b/c they are not getting insulin, not managing sugar level
o 300-800mg/dL
o These pts get really sick really quick
o Body has glucose but can’t use it so the body thinks its starving
o When it goes into starvation mode, it breaks down fats and proteins
 Side effect of break down = it releases acids (acetone and ketoacid)
 Drops pH level = metabolic acidosis
o When sugar is high in the kidneys:
 Kidneys will release glucose in the urine (water will excrete, water will follow the large molecule)
 Protein will follow and water = osmotic diuresis (peeing a lot out)
 Damaging kidneys – cannot make or reabsorb bicarb to correct acidosis so acidosis gets worse
b/c we are losing bicarb
o Lose potassium
S&S
o Fruity breath = acetone in body
 o Kussmal’s expiration (fast and long exhale – trying to blow of CO2)
o Hot and dry skin
o Flushed
o Fatigue
o Confuse
o Can be in a coma b/c of acidosis
o Polyuria
Treatment = don’t give insulin first b/c it'll bind with glucose and potassium. Potassium is already low or will get
low very quick. Treatment steps happen in 30 – 60 mins but take a couple of days to fully treat
o First = Potassium (If potassium is normal (3.5 – 5), then great. If not normal, give potassium)
o Second = Fluids for perfusion and to dilute glucose
o Third = Insulin regular – as IV continuous drip and start slow. Recheck potassium after insulin is given
(every 4 hrs) to make sure potassium level doesn’t drop
 NPO – ice chips while on insulin drip and in beginning stages of DKA
 Metabolic acidosis should correct self during treatment

Educate on diet, meds, depending on what got them there

** Can happen in a day. Type 1 who are sick should take blood sugar every couple of hours to prevent DKA
 HHNS / HHNK = hyperglycemic hyperosmolar non-ketotic syndrome
o Body doesn’t think its starving. No acidosis. No Ketones
o Happens gradually over time
o Usually type 2, not as severe in Type 1
o Doesn’t happen as often but is more severe than DKA
o 600 – 1200 mg/dL sugars but pt specific
o Usually seen in response to pt illness or emotional stress for days. It is a gradual thing

Manifestation = massive amounts of urination. Dumps fluid “waterfall” = SEVERELY HYPOVOLEMIC

o Higher mortality rate b/c of hypovolemia

Treatment = Fluid is a priority, don’t lose as much potassium, but check potassium before giving insulin b/c insulin
will cause potassium to drop
o Fluids
o Potassium
o Insulin

Education = Educate on what got them to this point

Chronic Complications
 Vascular changes = glucose molecules are large, change fluid volume all the time and damages endothelial lining
o We have small vessels in eyes, kidneys, hands, fingers, toes
o When we start damaging, vessels don’t have elasticity they need, increase platelets that stick, inflammation
 Leading to MI, peripheral artery disease, strokes, etc.
 Neurological = increase risk Cerebrovascular Disease (Stroke)
o Neuropathies = damage to the nerves – peripheral the biggest one (cannot feel feet)
o Autonomic dysfunction (bladder issues, digestive issues) all related to large glucose molecules
 Sensory = diabetic retinopathy (causes vision lost) = need to have annual exams w/ dilation to see vasculature
 Cardiovascular = MI leading cause of death for diabetics
o 2-3x greater risk for MI than regular population. Not if properly controlled though
o Increase preload, increase afterload, decrease perfusion
 Renal = large glucose molecules damage kidneys
o Proteinuria in nephrotic syndrome which leads to chronic renal failure
 Musculoskeletal = Motor nerve damage, fatigue easier, decrease in activity tolerance
 Integumentary = Diabetic foot ulcers b/c cannot feel feet
o Daily foot exams, check shoes before putting on
o Blisters can lead to bad situations. Fitted for shoes is important
o Monitor for swelling in legs/foot may need to adjust shoes
o Cannot walk around barefoot at home
o Delayed wound healing bc damage to vascular and infection loves to live on glucose
 Immune = vasculature is filled w/ glucose molecules and there is no room for WBC making pt at risk for infections
o Frequent infection
o Bone marrow need perfusions for WBC
o If bone marrow is also decreased, lack of WBC