Patho - Alterations in Renal Function Flashcards
what is renal agenesis?
-Failure of 1 or both kidneys to develop before birth
-Rare; associated with other congenital abnormalities.
-Total bilateral agenesis (Potter Syndrome) incompatible with life; found in stillborn infants.
-Unilateral results in compensatory hypertrophy of functional kidney.
-Single normal kidney is sufficient for renal function.
what is polycystic kidney disease?
-Congenital, genetic disorder
-growth of cysts that can expand & disrupt urine formation & flow; localized to one or both kidneys.
-Multiple dilations of collecting ducts, appearing as fluid filled cysts.
-Can lead to renal failure, requiring dialysis or transplant
-ARPKD dx ́d in infants & children—Rare anomaly
-ADPKD dx ́d in adults-more common
pathogenesis of polycystic kidney disease (autosomal recessive forms)
-Evident at birth
-Kidneys enlarged
-Respiratory distress or palpable kidneys on PE
-Severe systemic HTN
-Liver problems
-Diagnosis: inheritance pattern
pathogenesis of polycystic kidney disease (autosomal dominant forms)
-most common
-Symptoms are later in life
-Normal functioning kidney tissue slowly reduced
-Many round cysts of varying sizes
-Other organs can develop cysts, especially liver
polycystic kidney disease CM
-Decreased ability to concentrate urine
-HTN
-Pain: most common
-multiple cystic liver involvement
polycystic kidney disease diagnosis
genetic hx & ultrasonography
polycystic kidney disease treatment
primarily supportive, controlling BP & managing associated pathologies
End-stage renal disease (ESRD): dialysis initiated
what is benign renal neoplasm? what is the diagnosis? treatment?
-Non-metastasizing growths
-Symptoms depend on size; may have no symptoms until large enough to form palpable abdominal mass, hematuria, & flank pain
Diagnosis: renal ultrasound and/or CT scan
Tx: nephrectomy (treatment of choice); laparoscopic and tissue-sparing procedures also being used
what is renal cell carcinoma? CM? treatment?
Kidney cancer that originates in the cells of the kidney tubules
Often familial pattern; risk factors (smoking,obesity,HTN)
Clinical Manifestations: none until advanced
-CVA tenderness, hematuria, palpable mass
Tx: nephrectomy
-Metastases often resistant to radiation, immunotherapy, and chemotherapy
what is nephroblastoma? CM? treatment?
Most common kidney CA in children
Clinical manifestations: Palpable abd. mass; may also have abd. pain, HTN, and/or hematuria
Treatment: nephrectomy, radiation therapy, and chemotherapy
what is acute pyelonephritis?
Infection where bacteria moves from bladder to kidneys, infects renal pelvis/parenchyma usually from ascending UTI
-Major risk factor: pregnancy
acute pyelonephritis CM
CVAT with fever, N/V, chills, anorexia, fever-induced dehydration
Urosepsis: organisms in bloodstream originating from UTI
acute pyelonephritis diagnosis and treatment?
DX: WBC casts in urine indicate upper UTI
TX: prompt antimicrobial tx to avoid decreased renal function
what is chronic pyelonephritis?
-Long-term inflammation of the kidneys usually resulting from recurrent or persistent kidney infections
-Can result in chronic kidney disease
-Associated with reflux or obstruction leading to persistent urine stasis
-Chronic inflammation causes scarring & loss of functional nephrons
chronic pyelonephritis CM
Abd./flank pain, fever, malaise, anorexia
chronic pyelonephritis diagnosis and treatment?
DX: renal imaging
Tx: correct underlying processes & extend abx tx
what is renal calculi (nephrolithiasis)
-Masses of crystalized minerals normally excreted in urine.
-Most composed of Ca+ crystals
-Develop & cause obstruction at any point in urinary system.
-Stationary stones usually asymptomatic; stone migration causes intense renal colic pain abrupt in onset & may radiate; N/V, diaphoresis, hematuria
-Often form in urinary tract d/t solute saturation, low urine volume & abnormal urine pH. (Dehydration favors stone formation)
-High-protein diet predisposes to stone formation in susceptible pts
-Pain d/t distention of ureter, renal pelvis, or renal capsule.
-Most pass spontaneously, but tend to recur
renal calculi (nephrolithiasis) diagnosis and treatment?
Diagnosis: CT scan
TX: fluids, lithotripsy, ureteral stenting, ureteroscopy
-Pain rx needed
what are the major complications of renal calculi (nephrolithiasis)?
-Hydronephrosis (dilation of renal pelvis) & permanent renal damage d/t complete obstruction of ureter, results in backup of urine & buildup of pressure.
-Infection or abscess formation behind partially or completely obstructing stone, which can rapidly destroy the involved kidney.
-Renal damage subsequent to repeated kidney stones.
-HTN results from increased renin production by obstructed kidney.
what are glomerular abnormalities?
-Damage mediated by immune processes.
-Results from alterations in structure & function of glomerular capillary circulation.
-Attraction of immune cells to area of inflammation results in degradation of the basement membrane.
glomerular abnormalities etiology
Autoimmune, drug exposure, vascular or systemic disease. Acute post streptococcal glomerulonephritis is most common form.
glomerulonephritis CM (children, adults)
Children: abruptly develop malaise, fever, nausea, oliguria, & hematuria (smoky or cocoa-colored urine) 1-2 wks after recovery from sore throat, red cell casts in the urine, mild proteinuria, periorbital edema & mild to moderate HTN. 95% pts with eventual total recovery
Adults: onset more likely atypical with sudden appearance of HTN or edema, frequently elevated BUN. Approx. 60% recover promptly.
glomerulonephritis treatment?
-Steroids
-Plasmapheresis
-dietary and fluid management
-Management of systemic and renal hypertension
what is nephrotic syndrome?
-Collection of symptoms caused by glomerular disease.
-Characterized by increase in capillary wall permeability to serum proteins.
-Major loss of proteins in urine.
-Leads to hypoalbuminemia & edema d/t decreased colloid osmotic pressure.
-Tx: manage underlying process.
-Urinary loss of 3 to 3.5 g of protein per day.
what is acute kidney injury?
-Broad range of kidney diseases from minor changes in renal function to complete failure requiring renal replacement tx
-Abrupt reduction in renal function causes accumulation of waste materials in blood.
-Renal function monitored by serum CR & calculated GFR
-Retention of metabolic wastes (azotemia/uremia); monitored by BUN,
widespread systemic effects (uremic syndrome)
-Pt. presents with rapidly rising BUN & CR
acute kidney injury etiology
-Aging
-comorbidities
-insults to kidney
Acute Kidney Injury-Prerenal etiology
Conditions that decrease perfusion to kidney
-Hypovolemia, HTN, heart failure
-Renal artery obstruction
-Fever, vomiting, diarrhea
-Burns
-Overuse of diuretics
-Edema, ascites
-Drugs: ACE inhibitors, angiotensin II blockers, NSAIDs
what is acute tubular necrosis?
-Destruction of tubular cells & loss of renal function.
-Most common cause of ARF
-Rapid decrease in function & urine flow within 24hrs to <400 mL/day.
-Reversible renal lesion arises with inadequate blood flow, marked hypotension & shock
Acute Tubular Necrosis etiology
-Ischemia, d/t decreased or interrupted blood flow
-Acute tubulointerstitial nephritis, commonly d/t hypersensitivity rxn to drugs
-Disseminated intravascular coagulation (DIC)
-Urinary obstruction; tumors, BPH, or blood clots
Acute Tubular Necrosis CM
d/t loss of ability to excrete H20, Na+ & waste
-Early; Fatigue & malaise
-Severe: dyspnea, orthopnea, rales, prominent S3 & peripheral edema. Altered LOC reflects toxic effect of uremia on brain & elevated serum lvls of nitrogenous wastes
Chronic Renal Failure dx
Dx-Elevated BUN, serum CR & GFR <60 ml/minute
-Loss of nephron function over mos to yrs with inability of kidneys to produce enough urine.
-Defined as decreased kidney function or kidney damage of 3 mos duration based on blood tests, urinalysis & imaging studies
Chronic Renal Failure etiology
-glomerulonephritis
-diabetic nephropathy—most common
-HTN
-pyelonephritis (UTI)
-polycystic kidney disease
-nephrotoxic exposure
-obstructive nephropathy
-infection
chronic renal failure pathogenesis?
-Chronic injury results in gradual & irreversible loss of nephrons.
-Greater functional burden by fewer nephrons
-Causes fibrosis & scarring (glomerular sclerosis).
-Progresses to uremia: group of S/S occurring when residual renal function inadequate.
-Functional capacity lost & renal mass is reduced.
-Progressive deterioration of glomerular filtration.
chronic renal failure CM
-Early Stage—symptom free and BUN & CR
-Second Stage—slight rise in BUN and CR, oliguria.
-Third Stage—sharp increase in BUN and CR, oliguria, uremia, multisystem effects.
-Fourth Stage—dialysis
-Fifth Stage—transplant
what are the complications of chronic kidney disease?
-HTN & CVD d/t hypervolemia, escalated atherosclerotic process, increased RAAS and SNS activity.
-Uremic syndrome: d/t retention of metabolic wastes.
-Metabolic acidosis: d/t retention of acidic waste products; kidneys lose
ability to secrete H+ ions and bicarbonate.
-Electrolyte imbalances- Retained K+, Phos., Mg+
-Bone & mineral disorders Elevated Phos. & PTH causes altered bone/mineral metabolism; unable to reabsorb Ca+
-Malnutrition-Decreased intake d/t uremic syndrome, depression, dietary limitations, changes in taste, protein-energy wasting; negative Ntg balance
-Anemia-Lack of erythropoietin; uremia shortens RBCs life; combination of worsening CKD, anemia, & heart failure Pain-Many reasons; disease itself, treatment, comorbidities
-Depression-Co-morbid conditions; disease itself; disruption of social interactions and relationships
