Exam 3 Renal Flashcards
CYSTITIS
Signs and Symptoms
Cystitis: Inflammation of the urinary bladder
- S/S: traces of blood in the urine
- dark, cloudy, or strong-smelling urine
- pain just above the pubic bone, in the lower back, or in the abdomen
- burning sensation when urinating
- urinating frequently or feeling the need to urinate frequently
PYELONEPHRITIS
Signs and Symptoms
Pyelonephritis: inflammation of renal pelvis (kidneys)
Aka Kidney infection, upper urinary tract infection. Causes infection in the renal parenchyma, pelvis, and ureters.
- S/S:fever, chills, flank pain
- Cause: Escherichia coli most common pathogen
- Causes may also be from parasitic infections but not commonly seen in this country.
- Significant indication: UTI counts of 10^5 CFU/ml
- See it in pt that are immunosuppressed, diabetic, having undergone multiple antibiotic courses or have traveled to developing countries.
PYELONEPHRITIS
Causes and Treatments
Causes of pyelonephritis are from the Escherichia coli pathogen.
Treatments: antibiotics
- Pyelonephritis: alteration of defense mechanisms increases risk of contracting a UTI.
- Predisposing factors: Factors increasing urinary stasis
- Examples: BPH, tumor, neurogenic bladder
- Foreign bodies
- Examples: catheters, calculi, instrumentation
- Uncomplicated UTI: Occurs in otherwise normal urinary tract, Usually involves only the bladder, Treat with antibiotic for 3 days
- Complicated UTI: Coexists with presence of: Obstruction, Stones, Catheters, Diabetes/neurologic disease, Pregnancy-induced changes, Recurrent infection, Antibiotics 7-10 days
ACUTE
RENAL FAILURE
Usually REVERSIBLE w/sudden loss of kidney function and GFR
Occurs over a period of HOURS to DAYS
3 Categories
PRERENAL:
- Azotemia-nitrogen in blood caused by hypoperfusion of kidney
- Volume depletion:
- due to hemorrhage, renal losses (diuretics, osmotic diuresis), GI losses (vomiting, diarrhea, NG suctioning)
- Impaired cardiac function:
- MI, HF, dysrhythmias, shock
- Vasodilation:
- Sepsis, anaphylaxis, vasodilatory meds-antihypertensives
INTRARENAL:
- Most common cause is ATN (acute tubular necrosis)
- Pigment nephropathy-breakdown of blood cells containing pigments that occlude kidney structures.
- Myoglobinuria- trauma, crush injuries, burns
- Hemoglobinuria- transfusion reaction, hemolytic anemia
- Rhabdomyolysis
- Infectious processes- Pyelonephritis, glomerulonephritis
- Nephrotoxic agents- antibiotics, aminoglycosides, radiopaque contrasts used in CAT scans, heavy metals, arsenic poisoning, NSAID’s, ACE inhibitors
POSTRENAL
Urinary tract obstruction- Calculi (renal stones), tumors, Benign prostatic hyperplasia, urethral strictures, obstructive blood clots
- 4 Stages
- INITIATION PHASE
- last from hours to days
- starts @ time of insult, ends with cellular injury & oliguria develop
- First sign may be DECREASED URINE OUTPUT & HIGH BP
- OLIGURIC PHASE
- Most common early manifestation is OLIGURIA, caused by reduction in GFR
- Usually begins 1-7 days after initial insult, lasts 7-14 days, up to months.
- Need at least 400 mL/day output, this phase is less.
- LONGER OLIGURIA LASTS, POORER the PROGNOSIS
CHRONIC
RENAL FAILURE
- Progressive, IRREVERSIBLE destruction of nephrons in both kidneys
- Can take YEARS
PRE-RENAL
ACUTE RENAL FAILURE
PRERENAL: Azotemia caused by hypo-perfusion of the kidney. Sudden severe drop in BP (shock) or interruption of blood flow to the kidneys from severe injury or illness.
- VOLUME DEPLETION AS A RESULT OF:
- Hemorrhage
- Renal losses: diuretics, osmotic diuresis
- GI losses: vomiting, diarrhea, nasogastric suctioning
- IMPAIRED CARDIAC FUNCTION DUE TO:
- Myocardial infarction, heart failure, dysrhythmias, shock
- VASODILATION RESULTING FROM:
- Sepsis, anaphylaxis, vasodilatory medications- antihypertensives
INTRA-RENAL
ACUTE RENAL FAILURE
INTRARENAL: The renal parenchyma or nephron is damaged. Damage to renal tubules or glomeruli occurs. Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply.
- PROLONGED RENAL ISCHEMIA:
- Most common cause is ATN (acute tubular necrosis)
- Pigment nephropathy (breakdown of blood cells containing pigments that occlude kidney structures)
- Myoglobinuria (trauma, crush injuries, burns)
- Hemoglobinuria (transfusion reaction, hemolytic anemia)
- Rhabdomyolysis
- Infectious processes: Pyelonephritis, Glomerulonephritis
- Nephrotoxic agents such as:
- Aminoglycoside antibiotics- Gentamicin, Tobramycin, Vancomycin
- Radiopaque contrast agents used in CAT scans and Angiograms
- Heavy metals- lead, mercury
- Arsenic poisoning
- NSAID’s, ACE inhibitors
POST-RENAL
ACUTE RENAL FAILURE
POSTRENAL: urine outflow is obstructed. Sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury.
- URINARY TRACT OBSTRUCTION:
- Calculi- renal stones
- Tumors
- Benign Prostatic Hyperplasia (BPH)
- Urethral strictures
- Obstructive blood clots
1st PHASE
of
Acute Renal Failure
- Initiation phase: may last hours to days; begins at time of insult and ends when cellular injury and oliguria develop; first sign may be decreased urine output and elevated blood pressure
2nd PHASE
of
ACUTE RENAL FAILURE
2. Oliguric phase: most common early manifestation of ARF is oliguria caused by a reduction in GFR (glomerular filtration rate); usually begins 1-7 days after initial insult and lasts on average 7-14 days; may last for months; minimum amount of urine needed to rid the body of fluid and metabolic waste products is 400 mL/day; dialysis may be needed temporarily; the loger this stage lasts, the poorer the prognosis for full recovery of renal function
- fluid volume excess: when u/o decreases, fluid retention occurs; patient will have distended neck veins, bounding pulse, edema, HTN; fluid overload may lead to HF, pulmonary edema, pleural effusion; pericardial effusion
- hematologic disorders: anemia due to impaired production of erythropoetin; platelet abnormalities occur (thrombocytopenia)
- metabolic acidosis: when kidneys fail they can’t synthesize ammonia which is necessary for excretion of hydrogen ions and acid products of metabolism; bicarb is use dup trying to buffer hydrogen ions so serum bicarb decreases; patient may develop Kussmaul’s respirations due to increase excretion of carbon dioxide; lethargy and stupor occur if treatment isn’t started
- sodium loss: serum sodium drops as damaged tubules can’t conserve Na+; hyponatremia and water excess can lead to cerebral edema
- potassium excess: Kidney excretion of K+ is impaired; if ARD is caused by tissue trauma, the damaged cells release additional K+ into extracellular fluid; acidosis worsens hyperkalemia as hydrogen ions enter cells and K+ is driven out of cells and into extracellular fluid
- calcium deficit and phosphate excess: results from decreased GI absorption of Ca+; only funcitoing kidneys can activate vitamin D; when low levels of Ca+ occurs, the PTH gland secretes hormone releasing Ca+ from bones; phosphate is also released at this time and causes hyperphosphatemia
- waste product accumulation: urea (end product of protein metabolism) is primarily excreted by the kidneys; creatinine (end product of muscle metabolism) is also excreted by the kidneys; the BUN (blood urea nitrogen) and serum creatinine levels are elevated in kidney failure; BUN can be elevated in dehydration, catabolism, fever, GI bleeding, corticosteroid use; the best serum indicator of renal failure is creatinine!!
- neurologic manifestations: occur as nitrogenous wastes accumulate in the brain and nervous tissue; symptoms may be as mild as fatigue and difficulty concentrating; may be as severe as seizures, stupor, coma
3rd PHASE
of
ACUTE RENAL FAILURE
3. Diuretic phase: begins with a gradual increase in u/o per day to 1-3 L/day; may eventually reach 3-5 L/day; u/o is increasing but nephrons are not fully functioning; kidneys can excrete wastes but can’t concentrate urine; patient may become hypotensive and hypovolemic; BUN and creatinine are still elevated but patient may become hyponatremic, hypokalemic, and dehydrated; phase may last 1-3 weeks
4th PHASE
of
ACUTE RENAL FAILURE
4. Recovery phase: begins when the GFR increases, this allows the BUN and creatinine to plateau and then begin to decrease; major improvements occur in first 2 weeks of recovery phase; complete recovery may take up to 1 year
Clinical manifestations of
CHRONIC RENAL FAILURE
decreased U/O, anemia, increased body weight and blood pressure, grayish colored skin, fatigue, lethargy, Petechiae, pruritus, changes in urine characteristics (proteinuria and casts).
CLINICAL MANIFESTATIONS
of
CHRONIC UREMIA
Hematologic System
- Anemia, Bleeding tendencies, Infection, ↑incidence of cancer
Gastrointestinal System
- Inflammation from excess urea, mucosal ulcerations, metallic taste in mouth, GI bleeding,
- Diarrhea, constipation, nausea, vomiting
Respiratory System
- Pulmonary edema, Pleurisy, Pleural effusions
Cardiovascular System
- Hypertension, ↑ atherosclerotic disease, hyperlipidemia, CHF, arrhythmias, Pericarditis
Neurologic System
- Axonal damage from uremic toxins, neuropathy, encephalopathy, altered mental status, dementia
Musculoskeletal System
- Renal osteodystrophy due to Ca+ and P04 altered metabolism
Integumentary System
- Yellow-gray discolorations of the skin, pruritis
Endocrine System
- Hypothyroidism is common-significance and cause unknown
Reproductive System
- infertility and decreased libido
MEDICAL MANAGEMENT
of
CHRONIC RENAL FAILURE
- Identification of reversible renal disease
- Renal ultrasound
- Renal scan
- CT scan
- Renal biopsy
- Labwork: CBC- Hgb, Hct, Electrolytes, BUN, creatinine
- Urinalysis and urine culture
- Protein-to-creatinine ratio in 1st morning urine
- Correct ECF volume overload or deficit
- Provide nutritional therapy
- Provide erythropoetin supplementation
- Provide calcium supplementation and phosphate binders or both
- Antihypertensive therapy as ordered
- Measures to lower potassium
- Medications need to be adjusted to degree of renal function
Compare and contrast
peritoneal dialysis
and
hemodialysis
