urinary Flashcards
Name where in the urologic tract a patient can experience an obstruction and the causes
Renal pelvis- stomach of the kidney; Cause: renal calculi
Ureter- takes urine from kidney to bladder; Cause: renal calculi, pregnancy, tumors
Bladder or pelvis; Cause: bladder cancer, neurogenic bladder, prostatic hyperplasia, prostate cancer, urethral strictures.
Describe the potential complications of urinary stasis and back-up pressure.
o Urinary stasis complications: infection, recurrent UTIs
o Back-up pressure complications: hydroureter, hydronephrosis, postrenal acute kidney injury.
Differentiate between hydronephrosis and hydroureter
Hydroureter: enlarged d/T backup of urine and increased pressure
Hydronephrosis: kidney is holding urine
Discuss why the manifestations of acute urologic obstruction can vary from person to person
Depends on the site, cause, and speed of onset
renal calculi: definition, size, shape
Definition: clumps of crystals in the urinary tract
Size: small (grain of sand) or large (golf ball)
Shape: smooth or jagged
Most common cause of renal obstruction.
Risk factors for nephrolithiasis
Sex: men, age: 20-30s, race: white, family hx, congenital defects, weather, obesity
specific risk factors for the 3 major types of kidney stones.
Calcium oxalate or calcium phosphate (70-80%)-IDIOPATHIC, Family hx, ↑ calcemia, ↑ oxaluria.
Struvite (15%)- UTI
Uric acid (7%) gout
most preventable cause of Calcium oxalate stones is _ and _ _.
dehydration & low UOP
Diet high in _, _ _ &, _ can cause these stones as well.
Na, oxalate intake & protein
patho for nephrolithiasis.
Urine is a solution of solvent (water) & solutes (particles).
Problem: super-saturation with a solute therefore crystals begin forming in the NEPHRON.
Crystal formation is enhanced by: PH changes: UTI, Excessive concentration of insoluble salts in the urine d/t dehydration, bone disease, gout, renal disease, Urinary stasis: immobility/sedentary lifestyle.
CM for nephrolithiasis.
Pain of Acute Renal Colic:
– location – “flank”
– radiation – “lower abd and groin”
– spasms – “colicky” last 20-60 minutes
– intermittent – “ureter spasms”
– sharp - “calculi scrape the ureter wall”
Accompanying symptoms:
– N/V
– Dysuria
– Chills, Fever →ONLY if infection is present
– Hematuria
– Foul smelling urine
– Diaphoresis
where do crystals begin forming
in the nephrons
pharmacotherapy of nephrolithiasis, including acute pain management and preventive management.
Acute pain: morphine or NSAIDS, IV fluids
Preventative meds:
Calcium= thiazide diuretics
Struvite= antibiotics
Urate= allopurinol
PYELONEPHRITIS (other names for this) & definition
UPPER UTI, KIDNEY INFECTION.
inflammation of kidneys
Risk factors for PYELONEPHRITIS
pregnancy, recurrent lower UTIs, abx resistant strain.
Protective factors for UTIs (Pulled from NUR 325.)
PH=acidic, presence of urea, men=prostatic secretions, women=urethral gland secretions, urine flow id unidirectional, immune system
etiology for pyelonephritis
ascending infection (starts at bottom & goes up the tract) or bloodstream infection (Ex. E. coli)
patho for pyelonephritis
Kidneys become inflamed & filled with infectious exudate.
Inflammatory response from untreated or recurrent UTIs can lead to kidney tissue DAMAGE.
Abscesses & necrosis can develop impairing renal function.
CM for pyelonephritis
Sudden onset: fever, chills, CVA tenderness
Lower UTI symptoms: dysuria, frequency, urgency
Hematuria
N/V, anorexia
Define urosepsis and describe the typical patient population who experiences it.
potentially life-threatening condition that occurs when a UTI spreads to the kidneys and causes sepsis, the body’s response to infection.
It’s a severe systemic response and has high mortality rates.
Ex. ELDERLY
Describe the different types of antibiotic therapy that can be used for UTI, and the factors that influence the treatment regimen.
Meds: Trimethoprim/sulfamethoxazole, Ciprofloxacin, nitrofurantoin
Community acquired = short course abx
Recurrent= 7-14 days, may need IV abx
Get UA, culture & sensitivity to determine severity of organism.
Trimethoprim/sulfamethoxazole (Bactim)
Class: Sulfonamides
MOA: don’t destroy bacteria but inhibit their growth= bacteriostatic by preventing the synthesis of folic acid needed for DNA synthesis
Indication: uncomplicated UTIs, respiratory infections, salmonella, shigellosis
SE: photosensivity
NC: ‘Sulfa allergies’
Ciprofloxacin (Cipro)
Class: Fluoroquinolones
MOA: destroy bacteria by altering their DNA. Interfere with the bacterial enzymes DNA gyrase and topoisomerase
Indications: UTIs, some STIs, upper and lower respiratory tract infections, gonorrhea, and other infections. anthrax: infection with Bacillus anthracis
SE: arthropathy (joint disease), often irreversible. Prolonged post-antibiotic effects: concentrated in the neutrophils.
NC: PO, IV, Topical. Minimal penetration of the BBB/CSF. Avoid in patients <18 & >60.
List the top 2 causes of end stage kidney disease (list the other causes as well)
Top 2 causes: DM-50%, HTN-30%, glomerulonephritis-10%, Other-10%
major risk factors for CKD
Family history, Increasing age (>60), Male, Black/African American, HTN, DM, smoking, Overweight and obesity
2 major signs of worsening CKD
Increased angiotensin 2 & proteinuria
CV s/s of CKD
HTN, HF, CAD, PAD, pericarditis
GI s/s of CKD
anorexia, N/V, GI bleeding, gastritis
neuro s/s of CKD
fatigue, headache, sleep disturbances, encephalopathy
pulmonary s/s of CKD
Pulmonary edema
integumentary s/s of CKD
pruritis, ecchymosis, dry, scaly skin.
Describe how the loss of normal kidney function results in the clinical manifestations.
- No longer maintains F & E homeostasis: Edema, hyperkalemia, hyperphosphatemia, hypermagnesemia, metabolic acidosis
- No longer rids the body of wastes via urine: Anorexia, malnutrition, itching, CNS changes
3.Decreased production of erythropoietin: Anemia
4.Decreased activation of Vitamin D: Renal osteodystrophy
Discuss the two different ways drugs are used in chronic kidney disease
Slow the rate of progression of CKD
Treat the complications of CKD
Describe why ACE and ARBs are still used in patients with CKD, even when the drug book says we are supposed to use “caution” in patients with renal insufficiency.
For Blood pressure control.
Reduce BP to less than 140/90.
Other BP meds as needed to maintain SBP (110-130) 140
List the drugs commonly used to treat these complications of CKD:
volume overload- loop diuretics, use w/ low salt diet
hyperkalemia- multiple (ex. = diuretic), Addressed with hemodialysis in ESRD
metabolic acidosis- SODIUM BICARBONATE (an alkaline agent)
hyperphosphatemia- CALCIUM CARBONATE (a phosphate binder)
renal osteodystrophy-CALCITRIOL (activated vitamin D)
anemia- erythropoietin (black box warnings)
sodium bicarbonate
indications: To treat metabolic acidosis
Goals: Slow progression of CKD, Prevent bone loss, Improve nutritional status
Given PO
Initiate when HCO3 is less than 15 mEq/mL (Goal HCO3 18-20)
SE: bloating
calcium carbonate
MOA: Binds to phosphate [phos binder]
Indication: treat hyperphosphatemia
Goals: Keep normal phosphate levels, decrease mortality
SE: hypercalcemia
NC:monitor calcium levels, Take with meals
calcitriol
MOA: activated form of vitamin D; stimulate intestinal absorption of calcium/phosphate and bone mineralization
Adverse effects: Hypercalcemia, hyperphosphatemia
Indication: treat renal osteodystrophy
Describe the clinical manifestations of calcium toxicity that the nurse should be aware of when administering calcium carbonate and calcitriol
HYPERCALCEMIA= Excess calcium acts as a sedative= reduced excitability of muscles & nerves.
Confusion, psychosis, seizures, comas
Nausea, upset stomach
Explain acute kidney injury
Usually, the result of ischemic injury r/t loss of volume -> decreased perfusion (Toxins or sepsis are also common causes)
Kidney function can be mildly affected to severe.
Define the types of AKI and the conditions that can cause them
Pre-renal: volume loss related, ex. Dehydration.
Intrarenal: acute tubular necrosis [chemical, kidney cell death], ex. Chemical/toxin, kidney disease, meds, vascular disease- HTN, DM.
Post-renal: not as common, obstruction causing cell death
Manifestations of AKI
oOliguria (< 400 ml/24 hr)
oBegins 1 day after hypotensive event & lasts 1-3 weeks
oFluid volume excess- d/t kidney not filtering out
oMetabolic acidosis
oHyponatremia
oHyperkalemia
oWaste product accumulation- azotemia or uremia.
oNeurologic disorders
Explain the treatment goals and how physiologic alterations from AKI are managed
address the cause
Hematuria
blood in urine
Azotemia
buildup of waste products
oliguria
low UOP
proteinuria
protein in urine
Define and discuss the important characteristics of glomerulonephritis, including where the damage occurs.
Definition: a variety of conditions that cause inflammation of glomeruli.
Can be focal or diffuse
Focal= specific area of glomerulus.
Diffuse= can affect both kidneys & all areas of glomerulus.
Primarily an immune process
where the damage occurs Glomerulus: delicate network of arterioles within the bowman’s capsule. Tubules: massive consumer of oxygen.
Discuss the layers of the glomerulus
1- endothelial
2-basement membrane- where a lot of the issues occur
3-podocytes (special epithelial cells)- cells produce the start of urine
Describe the 2 main etiologies of glomerulonephritis, including what these 2 etiologies have in common
Two types of injury: 1. Antibodies attach to antigens of the glomerular basement membrane (“anti-GBM antibodies”) - 5% (Type II). 2. Antibodies react with circulating antigens and are deposited as immune complexes in the GBM – 90% (Type III)
BOTH forms have this in common: Accumulation of antigens, antibodies, and complement. Complement activation results in tissue injury.
Discuss the HARP clinical manifestations of glomerulonephritis.
Abrupt sudden onset of acute glomerulonephritis
Hematuria
Azotemia
Retentions: Sodium & water retention, Oliguria- low OUP, Leads to HTN & edema
Proteinuria
Describe the triggers of glomerulonephritis.
Post-Infectious: Poststreptococcal infection, Nonstreptococcal infection (Bacterial, viral, parasitic).
Primary Disease: Berger disease
Multisystem Disease: Goodpasture syndrome, systemic lupus erythematosus (SLE), vasculitis.
pathogenesis of acute glomerulonephritis
Trigger (infection)
Immune complexes form (direct attack or complexes circulating & depositing into basement membrane)
Complement activated (start inflammatory process)
Release of mediators (causes further inflammation)
Tissue Injury!
Hematuria, Proteinuria, Decreased GFR
chronic glomerulonephritis.
Long term inflammation of the glomerulus ->scar tissue
Manifestations: like presentation of acute glomerulonephritis
Prognosis: Slow progressive destruction ->ESRD
define nephrotic syndrome
The glomerulus is too permeable to plasma proteins, Elimination of >3 grams of protein per day.
etiology of nephrotic syndrome
Glomerulonephritis, Diabetes mellitus
patho of nephrotic syndrome
Increased glomerular permeability →Proteinuria→Hypo-albuminemia
CM of nephrotic syndrome
Edema, Hypertension.
Liver Problems: HLD, Hypercoagulation, Loss of antithrombin III and plasminogen
Define & list manifestations of Glomerulopathy: Diabetes & Hypertension Complications
oDiabetic Nephropathy: Major complication, Gross thickening of the GBM; Ultimately leading to ESRD
oHypertensive Glomerular Disease: Decreased renal perfusion ->sclerotic glomerular changes
CM: Hematuria, Oliguria, Fluid retention, Increased BUN/Cr ratio, Proteinuria, Low albumin [hypoproteinemia]
KIDNEY CANCER: risk factors, prognosis, manifestations, and chemotherapy treatment of renal cell carcinoma.
RF: SMOKING, obesity, age, male, genetics
Prognosis: depends on metastasis
Manifestations: Early: none
Late: CVA tenderness, hematuria, possible palpable abdominal mass.
Metastasis usually occurs in bone = bone pain or lungs = dyspnea, coughing.
Chemo tx: usually resistant to chemo if metastasized, surgery to remove kidney if not metastasized.
BLADDER CANCER: risk factors, manifestations, and chemotherapy treatment
RF: SMOKING, male, occupation with exposure to toxins, low fluid intake
Manifestations: Early: hematuria
Later: frequency, urgency, dysuria
Chemo: depends on stage
Stage 1= intravesical chemo
Advanced stages= systemic chemo
intravesical therapy for bladder cancer
Drug Name: BCG vaccine
MOA: simulates inflammatory response in the bladder, goal is for immune system to recognize cancerous cells and attack
SE: bladder irritation, systemic infection
Patient instructions: 1: empty bladder. 2: instill BCG vaccine into the bladder (dwell time 2 hours). 3: change positions q15 minutes
Safety: disinfect urine for 6hrs post treatment; watch for infection.
Describe the functions of the kidney, including the endocrine functions
Maintain F&E homeostasis
Rid the body of water-soluble wastes via urine
3 endocrine functions: Produces erythropoietin- stimulates RBC production, Activates vitamin D, Produces renin, which helps regulate BP
Explain why humans can live with only 1 kidney
Each kidney contains >1 million nephrons
Nephron is the functional unit of the kidneys.
We can function with 10-25% of nephrons
Describe the 3 major tissues of the kidney
Renal pelvis: Large collecting area for urine that drains from the nephrons
Medulla: Contains 8-12 pyramids that consist of: Collecting tubules, Collecting ducts, Loops of Henle & capillaries
Renal cortex: Contains all glomeruli and 85% of nephron tubules
A nephron must:
Filter water-soluble substances from the blood
Reabsorb filtered nutrients, water, and electrolytes
Secrete wastes and excesses.
Each nephron has a glomerulus and a tubule
glomerulus
Filters fluid from the blood into tubules
Prevents passage of RBC’s and proteins
Surrounded by a Bowman’s capsule
The overall glomerular filtration rate is about 125 mL/min
ureters
Two Ureters
Narrow tubes, 10-12 inches long
Drain urine from renal pelvis to bladder
bladder
Reservoir for urine
Normal output is 1500 mL/day
urethra
Small muscular tube from bladder neck to meatus
Female = 1-2 inches; Male = 8-10 inches long.
