Renal and Urinary Fxn Flashcards
(91 cards)
1
Q
o Alkaline urinary pH: Increases the risk of
A
calcium phosphate stone formation.
2
Q
o Acidic urine: Increases the risk of
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uric acid stone
3
Q
o Potassium citrate, pyrophosphate, and magnesium:
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Prevent stone formation (Calcium phosphate and oxalate types)..
4
Q
o Dyssynergia
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Overactive or hyperreflexive bladder function. * Upper motor neurons dysfxn
5
Q
o Detrusor hyperreflexia:
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Uninhibited or reflex bladder * Upper motor neurons dysfxn
6
Q
o Detrusor hyperreflexia with vesicosphincter (detrusor sphincter) dyssynergia:
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Both the bladder and the sphincter are contracting at the same time, causing a functional obstruction of the bladder outlet
7
Q
- Lower motor neurons dysfxn
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Detrusor areflexia: Underactive, hypotonic, or atonic bladder
8
Q
o Detrusor sphincter dyssynergia tx
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α-adrenergic blocking and/or antimuscarinic medications or botulinum toxin
9
Q
o Renal adenomas malignancy
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benign
10
Q
most common renal tumor
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o Renal cell carcinoma
11
Q
Renal cell carcinoma genetic mutation
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von Hippel-Lindau (VHL) gene located on chromosome 3p
12
Q
most common bladder tumor
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Urothelial (transitional cell) carcinoma
13
Q
Urothelial (transitional cell) carcinoma genetics
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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
14
Q
Urothelial (transitional cell) carcinoma vs Renal cell carcinoma s/s
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1: Painless microscopic hematuria
2: Hematuria, dull and aching flank pain
15
Q
- Pyelonephritis
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Inflammation of upper urinary tract
16
Q
- Cystitis
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Bladder inflammation
17
Q
o Inflammation of the urinary epithelium after invasion and colonization by some pathogen in the urinary tract
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UTI
18
Q
Tamm-Horsfall protein
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- Protective urinary mechanisms
19
Q
o Ureterovesical junction:
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Closes to prevent reflux of urine to the ureters and kidneys
20
Q
- Protective urinary mechanisms: _ pH and _osmolality of urine
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low, high
21
Q
- Most common pathogens uti
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o Escherichia coli
o Staphylococcus saprophyticus
22
Q
Biofilms
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o Ability to resist the host’s defense mechanisms
23
Q
- Cystitis s/s
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Asymptomatic. Frequency, dysuria, urgency, and low back and/or suprapubic pain
24
Q
Cystitis dx
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Urine culture of specific microorganisms with counts of 10,000/ml or more
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* 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
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o Acute infection of the ureter, renal pelvis, and/or renal parenchyma
* Acute pyelonephritis
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Acute pyelonephritis s/s
Flank pain, Fever, chills, Costovertebral tenderness, Purulent urine
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* Chronic pyelonephritis: o Persistent or recurrent infection of the kidneys, leading to
scarring of the kidneys, fibrosis, chronic kidney failure
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Acute Glomerulonephritis: Thickening of the glomerular basement membrane, but increased permeability to
proteins and red blood cells
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Most common form OF ACUTE GLOMERULOPATHIE
o Immunoglobulin A (IgA) nephropathy (Berger disease):
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o Immunoglobulin A (IgA) nephropathy (Berger disease): PATHO
Binding of abnormal IgA to mesangial cells in the glomerulus, resulting in injury and mesangial proliferation
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Most common cause of Acute Glomerulonephritis
o Membraneous nephropathy
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Acute Glomerulonephritis s/s
o Hematuria, Proteinuria exceeding 3 to 5 g/day with albumin - Low serum albumin, Edema
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o Oliguria
Urine output <30 ml/hr or <400 ml/day. efferent arteriolar vasoconstriction
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* Nephrotic Sediment
Contains massive amounts of protein and lipids and either a microscopic amount of blood or no blood.
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* 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.
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Nephrotic Syndrome
* Excretion of 3.0 g or more of protein in urine. excretion as a result of glomerular injury
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Nephrotic Syndrome s/s
Hypoalbuminemia, Peripheral edema, Prone to infection
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Decline of renal function to approximately 25% of normal
* Renal insufficiency
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Significant loss of renal function (less than 15% normal function)
* Renal failure
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Less than 10% of renal function remains
* End-stage renal failure
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azotemia tx
low protein, high carb diet
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* Kidney damage of CKD
GFR less than 60 mL/min/1.73 m2 for 3 months or more, irrespective of cause
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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
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* Factors that advance CKD
o Proteinuria
o Increased Angiotensin II - Promotes glomerular hypertension, and participates in tubulointerstitial fibrosis and scarring.
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Kidney develops from three structures
* Pronephros, mesonephros, metanephros
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Nonfunctional part
mesonephros
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Arises during the third fetal week. Connects the primitive wolffian duct to the cloaca as the foundation for male sexual development.
* Pronephros
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o Functional kidney
* Metanephros
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* Urine formation and excretion begin by
third month of gestation.
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gene - Plays an important role during all the stages of kidney development and the maintenance of kidney function.
* Wilms tumor 1 (WT1) gene
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* Wingless type signaling (WNT signaling) transduction pathway
important for mesenchyme growth and differentiation.
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of nephrons at birth
* All nephrons are present at birth, and their number does not increase as the kidney grows and matures.
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* Kidney reaches adult size by
adolescence
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* Blood flow to the kidney in a newborn is primarily to the
medullary nephrons.
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* Because of the short loops of Henle in the medullary nephrons, an infant produces more
dilute urine.
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* Infants are in a high anabolic state; therefore their urea excretion is
low.
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* Infants: Narrow chemical safety margin
o _ hydrogen ion concentration
o _ osmotic pressure
o Limited ability to regulate internal environment
high, low
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* Immaturity and smaller tubule surface area diminish the water reabsorption response to
antidiuretic hormone (ADH).
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ability to excrete a potassium load, reabsorb bicarbonate, or buffer hydrogen with ammonia Does not become efficient until approximately
2 years of age.
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* Total electrolyte concentration in extracellular fluids is _in the newborn than in the adult.
greater
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* Extracellular fluid volume (ECF) of the newborn infant is _ of the adult.
nearly double that
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* Infants exchange 600 to 700 ml
(290% of the total or nearly 50% of the extracellular volume).
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o Chromosomal disorders commonly associated with urinary tract malformations.
especially trisomy 13 (Patau syndrome) and trisomy 18
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* Ectopic kidneys
Fail to ascend from the pelvis to the abdomen.
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* Chordee
shortage of skin on the ventral surface, causing the penis to bend or “bow” ventrally.
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* 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.
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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
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deally, the Exstrophy of the bladder bladder and pubic defect should be closed before the infant is
72 hours old.
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o Cloacal exstrophy
Intestines, genitourinary tract, and spine may be involved.
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* Ureteropelvic junction obstruction risk
o Increased risk of vesicoureteral reflux
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o Blockage of the tapered point where the renal pelvis transitions into the ureter
* Ureteropelvic junction obstruction
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* Renal agenesis
o Absence of one or both kidneys
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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).
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* 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
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* Poststreptococcal glomerulonephritis (PSGN) occurs after
throat or skin infection with certain strains of group A α-hemolytic streptococci.
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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
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Poststreptococcal glomerulonephritis (PSGN) tx
restrict fluid, sodium, and potassium intakes. Administer an antihypertensive medication and diuretic agents
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Henoch-Schönlein Purpura Nephritis
anaphylactoid purpura
o Immune-mediated immunoglobulin A (IgA) vasculitis that causes inflammation and damage to the glomerular blood vessels
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Henoch-Schönlein Purpura Nephritis s/s
Palpable purpura, Arthritis, Abdominal pain, Renal disease, characterized by gross or microscopic hematuria with mild or no proteinuria
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most common cause of acute renal failure in children; most occur in those younger than 4 years of age.
Hemolytic-Uremic Syndrome
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Hemolytic-Uremic Syndrome Is associated with bacterial and viral agents
Escherichia coli O157:H7
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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.
84
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.
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First clinical manifestation Nephrotic Syndrome congenital
Periorbital edema
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Wilms Tumor
embryonal tumor of the kidney. Most common between birth and 5 years of age
* Is also called nephroblastoma.
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most common solid tumor of childhood
Wilms Tumor
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* Wilms tumor-suppressor genes WT1 and WT 2 are located on
chromosome 11.
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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)
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enuresis Medication administration:
Desmopressin acetate tablets
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