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PathoPharm 2 > Renal and Urinary Fxn > Flashcards

Renal and Urinary Fxn Flashcards

1
Q

o Alkaline urinary pH: Increases the risk of

A

calcium phosphate stone formation.

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2
Q

o Acidic urine: Increases the risk of

A

uric acid stone

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3
Q

o Potassium citrate, pyrophosphate, and magnesium:

A

Prevent stone formation (Calcium phosphate and oxalate types)..

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4
Q

o Dyssynergia

A

Overactive or hyperreflexive bladder function. * Upper motor neurons dysfxn

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5
Q

o Detrusor hyperreflexia:

A

Uninhibited or reflex bladder * Upper motor neurons dysfxn

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6
Q

o Detrusor hyperreflexia with vesicosphincter (detrusor sphincter) dyssynergia:

A

Both the bladder and the sphincter are contracting at the same time, causing a functional obstruction of the bladder outlet

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7
Q
  • Lower motor neurons dysfxn
A

Detrusor areflexia: Underactive, hypotonic, or atonic bladder

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8
Q

o Detrusor sphincter dyssynergia tx

A

 α-adrenergic blocking and/or antimuscarinic medications or botulinum toxin

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9
Q

o Renal adenomas malignancy

A

benign

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10
Q

most common renal tumor

A

o Renal cell carcinoma

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11
Q

Renal cell carcinoma genetic mutation

A

von Hippel-Lindau (VHL) gene located on chromosome 3p

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12
Q

most common bladder tumor

A

Urothelial (transitional cell) carcinoma

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13
Q

Urothelial (transitional cell) carcinoma genetics

A

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

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14
Q

Urothelial (transitional cell) carcinoma vs Renal cell carcinoma s/s

A

1: Painless microscopic hematuria
2: Hematuria, dull and aching flank pain

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15
Q
  • Pyelonephritis
A

Inflammation of upper urinary tract

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16
Q
  • Cystitis
A

Bladder inflammation

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17
Q

o Inflammation of the urinary epithelium after invasion and colonization by some pathogen in the urinary tract

A

UTI

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18
Q

Tamm-Horsfall protein

A
  • Protective urinary mechanisms
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19
Q

o Ureterovesical junction:

A

Closes to prevent reflux of urine to the ureters and kidneys

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20
Q
  • Protective urinary mechanisms: _ pH and _osmolality of urine
A

low, high

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21
Q
  • Most common pathogens uti
A

o Escherichia coli
o Staphylococcus saprophyticus

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22
Q

Biofilms

A

o Ability to resist the host’s defense mechanisms

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23
Q
  • Cystitis s/s
A

Asymptomatic. Frequency, dysuria, urgency, and low back and/or suprapubic pain

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24
Q

Cystitis dx

A

Urine culture of specific microorganisms with counts of 10,000/ml or more

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25
Q
  • Symptoms of cystitis for longer than 6 weeks’ duration but with negative urine cultures and no other known cause
A

Painful Bladder Syndrome or Interstitial Cystitis

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26
Q

o Acute infection of the ureter, renal pelvis, and/or renal parenchyma

A
  • Acute pyelonephritis
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27
Q

Acute pyelonephritis s/s

A

Flank pain, Fever, chills, Costovertebral tenderness, Purulent urine

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28
Q
  • Chronic pyelonephritis: o Persistent or recurrent infection of the kidneys, leading to
A

scarring of the kidneys, fibrosis, chronic kidney failure

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29
Q

Acute Glomerulonephritis: Thickening of the glomerular basement membrane, but increased permeability to

A

proteins and red blood cells

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30
Q

Most common form OF ACUTE GLOMERULOPATHIE

A

o Immunoglobulin A (IgA) nephropathy (Berger disease):

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31
Q

o Immunoglobulin A (IgA) nephropathy (Berger disease): PATHO

A

 Binding of abnormal IgA to mesangial cells in the glomerulus, resulting in injury and mesangial proliferation

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32
Q

Most common cause of Acute Glomerulonephritis

A

o Membraneous nephropathy

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33
Q

Acute Glomerulonephritis s/s

A

o Hematuria, Proteinuria exceeding 3 to 5 g/day with albumin - Low serum albumin, Edema

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34
Q

o Oliguria

A

Urine output <30 ml/hr or <400 ml/day. efferent arteriolar vasoconstriction

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35
Q
  • Nephrotic Sediment
A

Contains massive amounts of protein and lipids and either a microscopic amount of blood or no blood.

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36
Q
  • Nephritic Sediment
A

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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37
Q

Nephrotic Syndrome

A
  • Excretion of 3.0 g or more of protein in urine. excretion as a result of glomerular injury
38
Q

Nephrotic Syndrome s/s

A

Hypoalbuminemia, Peripheral edema, Prone to infection

39
Q

Decline of renal function to approximately 25% of normal

A
  • Renal insufficiency
40
Q

Significant loss of renal function (less than 15% normal function)

A
  • Renal failure
41
Q

Less than 10% of renal function remains

A
  • End-stage renal failure
42
Q

azotemia tx

A

low protein, high carb diet

43
Q
  • Kidney damage of CKD
A

GFR less than 60 mL/min/1.73 m2 for 3 months or more, irrespective of cause

44
Q

CKD S/S

A

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

45
Q
  • Factors that advance CKD
A

o Proteinuria
o Increased Angiotensin II - Promotes glomerular hypertension, and participates in tubulointerstitial fibrosis and scarring.

46
Q

Kidney develops from three structures

A
  • Pronephros, mesonephros, metanephros
47
Q

Nonfunctional part

A

mesonephros

48
Q

Arises during the third fetal week. Connects the primitive wolffian duct to the cloaca as the foundation for male sexual development.

A
  • Pronephros
49
Q

o Functional kidney

A
  • Metanephros
50
Q
  • Urine formation and excretion begin by
A

third month of gestation.

51
Q

gene - Plays an important role during all the stages of kidney development and the maintenance of kidney function.

A
  • Wilms tumor 1 (WT1) gene
52
Q
  • Wingless type signaling (WNT signaling) transduction pathway
A

important for mesenchyme growth and differentiation.

53
Q

of nephrons at birth

A
  • All nephrons are present at birth, and their number does not increase as the kidney grows and matures.
54
Q
  • Kidney reaches adult size by
A

adolescence

55
Q
  • Blood flow to the kidney in a newborn is primarily to the
A

medullary nephrons.

56
Q
  • Because of the short loops of Henle in the medullary nephrons, an infant produces more
A

dilute urine.

57
Q
  • Infants are in a high anabolic state; therefore their urea excretion is
A

low.

58
Q
  • Infants: Narrow chemical safety margin
    o _ hydrogen ion concentration
    o _ osmotic pressure
    o Limited ability to regulate internal environment
A

high, low

59
Q
  • Immaturity and smaller tubule surface area diminish the water reabsorption response to
A

antidiuretic hormone (ADH).

60
Q

ability to excrete a potassium load, reabsorb bicarbonate, or buffer hydrogen with ammonia Does not become efficient until approximately

A

2 years of age.

61
Q
  • Total electrolyte concentration in extracellular fluids is _in the newborn than in the adult.
A

greater

62
Q
  • Extracellular fluid volume (ECF) of the newborn infant is _ of the adult.
A

nearly double that

63
Q
  • Infants exchange 600 to 700 ml
A

(290% of the total or nearly 50% of the extracellular volume).

64
Q

o Chromosomal disorders commonly associated with urinary tract malformations.

A

especially trisomy 13 (Patau syndrome) and trisomy 18

65
Q
  • Ectopic kidneys
A

Fail to ascend from the pelvis to the abdomen.

66
Q
  • Chordee
A

shortage of skin on the ventral surface, causing the penis to bend or “bow” ventrally.

67
Q
  • Epispadias
A

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.

68
Q

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.

A
  • Exstrophy of the bladder
69
Q

deally, the Exstrophy of the bladder bladder and pubic defect should be closed before the infant is

A

72 hours old.

70
Q

o Cloacal exstrophy

A

 Intestines, genitourinary tract, and spine may be involved.

71
Q
  • Ureteropelvic junction obstruction risk
A

o Increased risk of vesicoureteral reflux

72
Q

o Blockage of the tapered point where the renal pelvis transitions into the ureter

A
  • Ureteropelvic junction obstruction
73
Q
  • Renal agenesis
A

o Absence of one or both kidneys

74
Q

o Potter syndrome

A

(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).

75
Q
  • Polycystic kidney disease (PKD) genetics
A

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

76
Q
  • Poststreptococcal glomerulonephritis (PSGN) occurs after
A

throat or skin infection with certain strains of group A α-hemolytic streptococci.

77
Q

Poststreptococcal glomerulonephritis (PSGN) population and s/s

A

o Mainly occurs in children, 5 to 15 years of age.
o Clinical manifestations – sudden onset of hematuria, edema, hypertension

78
Q

Poststreptococcal glomerulonephritis (PSGN) tx

A

restrict fluid, sodium, and potassium intakes. Administer an antihypertensive medication and diuretic agents

79
Q

Henoch-Schönlein Purpura Nephritis

A

anaphylactoid purpura
o Immune-mediated immunoglobulin A (IgA) vasculitis that causes inflammation and damage to the glomerular blood vessels

80
Q

Henoch-Schönlein Purpura Nephritis s/s

A

Palpable purpura, Arthritis, Abdominal pain, Renal disease, characterized by gross or microscopic hematuria with mild or no proteinuria

81
Q

most common cause of acute renal failure in children; most occur in those younger than 4 years of age.

A

Hemolytic-Uremic Syndrome

82
Q

Hemolytic-Uremic Syndrome Is associated with bacterial and viral agents

A

Escherichia coli O157:H7

83
Q

Hemolytic-Uremic Syndrome patho

A

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
Q

Nephrotic Syndrome congenital, or infantile genetics

A

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.

85
Q

 First clinical manifestation Nephrotic Syndrome congenital

A

Periorbital edema

86
Q

Wilms Tumor

A

embryonal tumor of the kidney. Most common between birth and 5 years of age
* Is also called nephroblastoma.

87
Q

most common solid tumor of childhood

A

Wilms Tumor

88
Q
  • Wilms tumor-suppressor genes WT1 and WT 2 are located on
A

chromosome 11.

89
Q

Vesicoureteral Reflux dx

A

voiding cystourethrogram (VCUG) and an intravenous pyelogram (IVP).
o Is graded I through V. – Slight (I), Mod (II-III), Gross (IV-V)

90
Q

enuresis Medication administration:

A

Desmopressin acetate tablets

91
Q
A

PathoPharm 2 (3 decks)

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