Renal and Urinary Fxn Flashcards
o Alkaline urinary pH: Increases the risk of
calcium phosphate stone formation.
o Acidic urine: Increases the risk of
uric acid stone
o Potassium citrate, pyrophosphate, and magnesium:
Prevent stone formation (Calcium phosphate and oxalate types)..
o Dyssynergia
Overactive or hyperreflexive bladder function. * Upper motor neurons dysfxn
o Detrusor hyperreflexia:
Uninhibited or reflex bladder * Upper motor neurons dysfxn
o Detrusor hyperreflexia with vesicosphincter (detrusor sphincter) dyssynergia:
Both the bladder and the sphincter are contracting at the same time, causing a functional obstruction of the bladder outlet
- Lower motor neurons dysfxn
Detrusor areflexia: Underactive, hypotonic, or atonic bladder
o Detrusor sphincter dyssynergia tx
α-adrenergic blocking and/or antimuscarinic medications or botulinum toxin
o Renal adenomas malignancy
benign
most common renal tumor
o Renal cell carcinoma
Renal cell carcinoma genetic mutation
von Hippel-Lindau (VHL) gene located on chromosome 3p
most common bladder tumor
Urothelial (transitional cell) carcinoma
Urothelial (transitional cell) carcinoma genetics
o Oncogenes of the ras gene family and tumor-suppressor genes including TP53 mutations
o Inactivation of retinoblastoma gene (pRb)
o Loss of heterozygosity at Chromosome 9
Urothelial (transitional cell) carcinoma vs Renal cell carcinoma s/s
1: Painless microscopic hematuria
2: Hematuria, dull and aching flank pain
- Pyelonephritis
Inflammation of upper urinary tract
- Cystitis
Bladder inflammation
o Inflammation of the urinary epithelium after invasion and colonization by some pathogen in the urinary tract
UTI
Tamm-Horsfall protein
- Protective urinary mechanisms
o Ureterovesical junction:
Closes to prevent reflux of urine to the ureters and kidneys
- Protective urinary mechanisms: _ pH and _osmolality of urine
low, high
- Most common pathogens uti
o Escherichia coli
o Staphylococcus saprophyticus
Biofilms
o Ability to resist the host’s defense mechanisms
- Cystitis s/s
Asymptomatic. Frequency, dysuria, urgency, and low back and/or suprapubic pain
Cystitis dx
Urine culture of specific microorganisms with counts of 10,000/ml or more
- Symptoms of cystitis for longer than 6 weeks’ duration but with negative urine cultures and no other known cause
Painful Bladder Syndrome or Interstitial Cystitis
o Acute infection of the ureter, renal pelvis, and/or renal parenchyma
- Acute pyelonephritis
Acute pyelonephritis s/s
Flank pain, Fever, chills, Costovertebral tenderness, Purulent urine
- Chronic pyelonephritis: o Persistent or recurrent infection of the kidneys, leading to
scarring of the kidneys, fibrosis, chronic kidney failure
Acute Glomerulonephritis: Thickening of the glomerular basement membrane, but increased permeability to
proteins and red blood cells
Most common form OF ACUTE GLOMERULOPATHIE
o Immunoglobulin A (IgA) nephropathy (Berger disease):
o Immunoglobulin A (IgA) nephropathy (Berger disease): PATHO
Binding of abnormal IgA to mesangial cells in the glomerulus, resulting in injury and mesangial proliferation
Most common cause of Acute Glomerulonephritis
o Membraneous nephropathy
Acute Glomerulonephritis s/s
o Hematuria, Proteinuria exceeding 3 to 5 g/day with albumin - Low serum albumin, Edema
o Oliguria
Urine output <30 ml/hr or <400 ml/day. efferent arteriolar vasoconstriction
- Nephrotic Sediment
Contains massive amounts of protein and lipids and either a microscopic amount of blood or no blood.
- Nephritic Sediment
Blood is present in the urine with red cell casts, white cell casts, and varying degrees of protein, which is not usually severe.
Nephrotic Syndrome
- Excretion of 3.0 g or more of protein in urine. excretion as a result of glomerular injury
Nephrotic Syndrome s/s
Hypoalbuminemia, Peripheral edema, Prone to infection
Decline of renal function to approximately 25% of normal
- Renal insufficiency
Significant loss of renal function (less than 15% normal function)
- Renal failure
Less than 10% of renal function remains
- End-stage renal failure
azotemia tx
low protein, high carb diet
- Kidney damage of CKD
GFR less than 60 mL/min/1.73 m2 for 3 months or more, irrespective of cause
CKD S/S
Do not occur until renal function declines to less than 25% of normal
Decreased calcium, causing renal osteodystrophies. Hyperphosphatemia
Metabolic acidosis
Retention of sodium, water, and potassium in the late stages
serum protein decrease
Normochromic normocytic anemia, HTN, dyslipidemia, hypercoag
o Malnutrition
o Uremic fetor: Bad breath caused by the breakdown of urea by salivary enzymes
o Uremic gastroenteritis: Bleeding ulcer
o Hyperparathyroidism and uremic skin residues, known as uremic frost: Irritation and pruritus with scratching, excoriation, and increased risk for infection
Low thyroid hormone levels
- Factors that advance CKD
o Proteinuria
o Increased Angiotensin II - Promotes glomerular hypertension, and participates in tubulointerstitial fibrosis and scarring.
Kidney develops from three structures
- Pronephros, mesonephros, metanephros
Nonfunctional part
mesonephros
Arises during the third fetal week. Connects the primitive wolffian duct to the cloaca as the foundation for male sexual development.
- Pronephros
o Functional kidney
- Metanephros
- Urine formation and excretion begin by
third month of gestation.
gene - Plays an important role during all the stages of kidney development and the maintenance of kidney function.
- Wilms tumor 1 (WT1) gene
- Wingless type signaling (WNT signaling) transduction pathway
important for mesenchyme growth and differentiation.
of nephrons at birth
- All nephrons are present at birth, and their number does not increase as the kidney grows and matures.
- Kidney reaches adult size by
adolescence
- Blood flow to the kidney in a newborn is primarily to the
medullary nephrons.
- Because of the short loops of Henle in the medullary nephrons, an infant produces more
dilute urine.
- Infants are in a high anabolic state; therefore their urea excretion is
low.
- Infants: Narrow chemical safety margin
o _ hydrogen ion concentration
o _ osmotic pressure
o Limited ability to regulate internal environment
high, low
- Immaturity and smaller tubule surface area diminish the water reabsorption response to
antidiuretic hormone (ADH).
ability to excrete a potassium load, reabsorb bicarbonate, or buffer hydrogen with ammonia Does not become efficient until approximately
2 years of age.
- Total electrolyte concentration in extracellular fluids is _in the newborn than in the adult.
greater
- Extracellular fluid volume (ECF) of the newborn infant is _ of the adult.
nearly double that
- Infants exchange 600 to 700 ml
(290% of the total or nearly 50% of the extracellular volume).
o Chromosomal disorders commonly associated with urinary tract malformations.
especially trisomy 13 (Patau syndrome) and trisomy 18
- Ectopic kidneys
Fail to ascend from the pelvis to the abdomen.
- Chordee
shortage of skin on the ventral surface, causing the penis to bend or “bow” ventrally.
- Epispadias
o Males: Urethral opening is on the dorsal surface of the penis.
o Females: Cleft along the ventral urethra usually extends to the bladder neck.
o Twice as many boys are affected as girls.
o Herniation of the bladder through the abdominal wall occurs with a failure of the abdominal muscles, pelvic ring, and pelvic floor musculature to fuse in the midline.
- Exstrophy of the bladder
deally, the Exstrophy of the bladder bladder and pubic defect should be closed before the infant is
72 hours old.
o Cloacal exstrophy
Intestines, genitourinary tract, and spine may be involved.
- Ureteropelvic junction obstruction risk
o Increased risk of vesicoureteral reflux
o Blockage of the tapered point where the renal pelvis transitions into the ureter
- Ureteropelvic junction obstruction
- Renal agenesis
o Absence of one or both kidneys
o Potter syndrome
(bilateral renal agenesis) rare disorder that is incompatible with extrauterine life.
Potter syndrome: Is associated with a specific group of facial anomalies (wide-set eyes, parrot-beak nose, low-set ears, and receding chin).
- Polycystic kidney disease (PKD) genetics
o Autosomal dominant (1 in 1000 live births)
o Mutations of two genes, PKD-1 (chromosome 16) and PKD-2 (chromosome 4)
can also be recessive
- Poststreptococcal glomerulonephritis (PSGN) occurs after
throat or skin infection with certain strains of group A α-hemolytic streptococci.
Poststreptococcal glomerulonephritis (PSGN) population and s/s
o Mainly occurs in children, 5 to 15 years of age.
o Clinical manifestations – sudden onset of hematuria, edema, hypertension
Poststreptococcal glomerulonephritis (PSGN) tx
restrict fluid, sodium, and potassium intakes. Administer an antihypertensive medication and diuretic agents
Henoch-Schönlein Purpura Nephritis
anaphylactoid purpura
o Immune-mediated immunoglobulin A (IgA) vasculitis that causes inflammation and damage to the glomerular blood vessels
Henoch-Schönlein Purpura Nephritis s/s
Palpable purpura, Arthritis, Abdominal pain, Renal disease, characterized by gross or microscopic hematuria with mild or no proteinuria
most common cause of acute renal failure in children; most occur in those younger than 4 years of age.
Hemolytic-Uremic Syndrome
Hemolytic-Uremic Syndrome Is associated with bacterial and viral agents
Escherichia coli O157:H7
Hemolytic-Uremic Syndrome patho
o Bacterial toxin from E. coli damages red cells and endothelial cells.
o Arterioles of the glomerulus become swollen and occluded with fibrin clots.
o Causes a decreased glomerular filtration rate with hematuria and proteinuria.
o Swollen vessels damage red cells as they pass.
o Spleen removes the damaged red cells from the circulation, causing acute hemolytic anemia.
o Microcirculation develops numerous thrombi.
Nephrotic Syndrome congenital, or infantile genetics
rare. autosomal recessive mutation of the NPHS1 gene that encodes an immunoglobulin-
like protein, nephrin, at the podocyte slit membrane. Lack of nephrin: Proteinuria
o Is expressed within the first 3 to 12 months of life.
o Infants do not respond to steroidal treatment.
First clinical manifestation Nephrotic Syndrome congenital
Periorbital edema
Wilms Tumor
embryonal tumor of the kidney. Most common between birth and 5 years of age
* Is also called nephroblastoma.
most common solid tumor of childhood
Wilms Tumor
- Wilms tumor-suppressor genes WT1 and WT 2 are located on
chromosome 11.
Vesicoureteral Reflux dx
voiding cystourethrogram (VCUG) and an intravenous pyelogram (IVP).
o Is graded I through V. – Slight (I), Mod (II-III), Gross (IV-V)
enuresis Medication administration:
Desmopressin acetate tablets
