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UA > Urinary Disease & Findings > Flashcards

Urinary Disease & Findings Flashcards

1
Q

congenital anatomical variations affecting urinary tract (3)

A

duplicate set of ureters
horseshoe kidney
vesicoureter reflux

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2
Q

acquired anatomical variations affecting urinary tract (2)

A
  • accidents/injuries damaging kidney or urinary tract

- benign prostatic hyperplasia (BPH)

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3
Q

MC renal congenital abnormality

A

duplicated ureter

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4
Q

additional ureter may result in

A

ureterocele (distal ureter balloons) or ectopic ureter

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5
Q

congenital anatomical variations MC affect ______ and could be important predisposing factor for

A

females (around 4th week of fetus development)

UTIs in newborn or children

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6
Q

renal fusion or super kidney that affects 1 in 400 people

A

horseshoe kidney

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7
Q

horseshoe kidney is MC seen with (2) disorders

A

Turner Syndrome

Trisomy 18

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8
Q

genetic disorder seen in GIRLS, where all or part of X chromosome is absent or has abnormalities

A

Turner Syndrome

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9
Q

___ % of girls with Turner Syndrome aka _____ have horseshoe kidney;

A

15%

45, X0

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10
Q

serious chromosomal abnormality characterized by defects in nearly all organs and systems, develops horseshoe kidney in ___% of kids affected

A

trisomy 18

20%

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11
Q

in horseshoe kidney, the isthmus is found at ___ level

A

L4/L5

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12
Q

(2) characteristics of horseshoe kidney

A

MC in men

usually asymptomatic

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13
Q

horseshoe kidney increases risk for development of (5) as result of POOR DRAINAGE

A 
kidney obstruction
hydronephrosis
pyelonephritis
urolithiasis
kidney cancer
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14
Q

abnormal retrograde movement of urine from bladder to ureters; can be primary or secondary

A

vesicoureteral reflux

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15
Q

vesicourteral reflux may result in (2)

A

hydronephrosis

pyelonephritis

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16
Q

MC hospital acquired infection

A

UTI

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17
Q

UTI affects

A

bladder- cystitis

kidneys- pyelonephritis

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18
Q

female-male ratio for UTI and age range

A

female to male 4:1

ages 16-35

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19
Q

etiology of BACTERIAL UTI, (can also be a viral or fungal infection)

A
  • E.Coli = 80-85%
  • other gram - rods
  • staphylococcus epidermis
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20
Q

risk factors for UTI

A
  • urinary tract obstruction in pregnancy, urolithiasis, prostate enlargement, or tumors
  • catheterization
  • diabetes mellitus
  • congenital anatomical abnormalities
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21
Q

2 ways that bacteria can reach kidney in UTI’s

A
  • from lower urinary tract (ascending infection usually due to cystitis) = MC
  • through blood stream
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22
Q

signs of acute cystitis

A 
dysuria
increased frequency of urination
increased urinary urgency
lower abdominal pain
(RARELY causes systemic symptoms)
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23
Q

signs of pyelonephritis

A
  • causes systemic symptoms (fever, chills, nausea)
  • flank pain
  • dysuria
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24
Q

urinalysis of UTI includes:

A 
increases leukocytes (neutrophils)
positive leukocyte esterase
bacteria
MAY have positive nitrite
WBC casts- maybe (indicate kidney infection)
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25
Q

urinary tract stone formation is called

A

urolithiasis

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26
Q

kidney stones are common cause of _____ obstruction; can cause severe pain called ______

A

UPPER urinary tract

ureteral (renal) colic

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27
Q

classic presentation for acute ureteral colic

A

sudden onset of severe pain originating in flank, back and radiating inferior and anteriorly towards groin

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28
Q

with urolithiasis, change of position _________; at least 50% of patients will also have (2)

A
  • does NOT relieve pain
  • systemic symptoms
  • dysuria due to obstruction of urinary tract
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29
Q

urinalysis of ureteral colic includes:

A

hematuria
WBC, leukocyte esterase
crystals

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30
Q

chemical substances that form stones

A
  • calcium oxalate with combination of calcium phosphates (75% of all stones)
  • Magnesium ammonium phosphate ( aka Triple Phosphate, Struvites)
  • Uric acid
  • Cystine
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31
Q

HTN resulting in damage of blood vessels of kidney is called ______: ____ accumulates in wall of small arterioles producing the thickening of their walls and narrowing of lumen causing ischemia –>

A

benign nephrosclerosis
hyaline
reduction of renal function

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32
Q

hyaline arteriosclerosis/benign nephrosclerosis leads to (3)

A

tubular atrophy
interstitial fibrosis
glomerular alterations

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33
Q

urinalysis of HTN nephropathy shows:

A

multiple hyaline casts
cell casts
proteinuria
hematuria

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34
Q

in HTN nephropathy, there is decrease in GFR –> blood ELEVATION of (2)

A

creatinine

blood urea nitrogen

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35
Q

diabetes mellitus is manifested by (7)

A 
polyuria
polydipsia
malaise
fatigue
micoangiopathies (small blood vessels of body injured)
diabetic nephropathy
peripheral neuropathy
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36
Q

diabetic nephropathy characterized by (3) and is OFTEN manifested by ____ syndrome

A

glomerular lesions
renal angiopathy
pyelonephritis
nepHROTIC syndrome

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37
Q

changes in urine w/ diabetic nephropathy

A 
polyuria
increased specific gravity
glycosuria
ketonuria
albuminuria
lipiduria
cell, fatty, and waxy casts
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38
Q

if diabetic nephropathy is complicated by pyelonephritis, urinalysis includes (4)

A

gross hematuria
pyuria
bacteriruai
trace albuminuria

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39
Q

nephritic and nephrotic syndrome are present in people with

A

glomerular diseases

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40
Q

glomerular diseases are associated with (2); can be genetic or acquired, acute or chronic

A

immunopathological processes

AI diseases

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41
Q

_____ is associated with paradoxical increased permeability of glomeruli for RBCs and REDUCED permeability for water

A

nephRITIC syndrome

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42
Q

signs and symptoms of nephRITIC syndrome

A 
hematuria
oliguria
azotemia
HTN
proteinuria
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43
Q

immunopathological condition- type III hypersensitivity, that may arise 14-21 days after exposure to BETA-HEMOLYTIC GROUP A STREPTOCOCCUS

A

acute proliferative glomerulonephritis

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44
Q

acute proliferative glomerulonephritis is manifested by ______, develops MC in ____ with high rate of recovery, elevated _____ found in blood

A

nephrRITIC syndrome,
kids
anti-streptolysin O titre

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45
Q

in acute proliferative glomerulonephritis, immune complexes become lodged btwn _____ and ______ below the podocyte foot processes; complement _____ leads to destruction

A

magnesium
glomerular basement membrane
activation

46
Q

molecular size of glomerular basement membrane pores in kids is ____ nm, and the streptococcus- antibody complex is ___ nm which makes it easy for complex to be lodged into GBM pore

A

2-3 nm

15 nm

47
Q

changes in urine for acute proliferative glomerulonephritis are typical for _____ syndrome; including (4)

A 
nepHRITIC
hematuria
oliguria
edema
cast cells
(may be HTN or azotemia)
48
Q

kidney disorder characterized by rapid loss of renal fxn, acute renal failure, and death within months

A

rapidly progressive (crescentic) glomerulonephritis

49
Q

rapidly progressive (crescentic) glomerulonephritis may develop with (4) AI diseases:

A

goodpasture’s syndrome
systemic lupus
wegener granulomatosis
polyarteritis nodosa

50
Q

morphologically, rapidly progressive glomerulonephritis crescents develop from proliferation of ______ and then crescents eventually __________

A

parietal epithelial cells of bowman’s capsule

obliterate Bowman’s space and compress glomerular tuft

51
Q

rapidly progressive (crescentic) glomerulonephritis is manifested by _____ syndrome with symptoms such as (6); but may also manifest with symptoms similar to _____ syndrome with symptoms such as ____

A 
nephrITIC syndrome
- severe hematuria
- dark, smoky colored urine
- RBC casts
- oliguria, anuria
- proteinuria less than 3 g/d
- HTN
nephrOTIC syndrome
- heavy proteinuria
- generalized edema
52
Q

AI disease characterized by formation of antibodies against glomerular and alveolar basement membranes

A

goodpasture’s syndrome

53
Q

in goodpasture syndrome, (2) organs affected; ______ could occur within 2 weeks

A

lungs and kidneys

renal failure

54
Q

symptoms in lungs for goodpasture’s syndrome

A

hemoptysis
dyspnea
hypoxia of tissue

55
Q

symptoms in kidneys for goodpasture’s syndrome

A 
hematuria
RBC casts
oliguria
HTN
proteinuria
azotemia
56
Q

disease that is characterized by deposition of IgA and IgA immune complexes into misangium with distraction of GBM

A

Berger’s Disease (IgA Nephropathy)

57
Q

Berger’s diseases begins 1-2 days within (3) and is manifested by ________ which subsides in several days spontaneously and ____

A 
acute respiratory 
acute GI
UTI
gross hematuria
nepHRITIC syndrome
58
Q

berger’s disease turns into _____ in 25-30% of patients

A

chronic glomeronephritis

59
Q

______ is MC cause of glomerulonephritis world-wide

A

IgA nephropathy

60
Q

syndrome associated with increased permeability of glomeruli for PROTEINS, predominately albumins

A

nephROTIC syndrome

61
Q

signs and symptoms for nephROTIC syndrome

A 
heavy proteinuria (> 3.5 g/d)
HYPOalbuminemia
generalized edema
lipidemia and lipiduria
fat goblets and casts
62
Q

MC disease associated with nephROTIC syndrome in adults; characterized by _______

A

membranous glomerulonephritis

diffuse thickening of glomerular capillary wall

63
Q

signs and symptoms of membranous glomerulonephritis (5)

A 
proteinuria
hematuria
edema
mild HTN
nocturia
64
Q

characterized by thickening of glomerular basement membrane and leukocyte infiltration, usually present with nePHROTIC syndrome,

A

membranoproliferative glomerulonephritis

65
Q

50% of membranoproliferative glomerulonephritis develops into

A

chronic renal failure

66
Q

signs and symptoms of membranoproliferative glomerulonephritis

A 
proteinuria
edema
hematuria
dark urine- tea/cola colored
HTN
oliguria
67
Q

relatively benign disorder that is MC cause of nephrOTIC syndrome in KIDS; peak btwn 2-6 y.o.

A

minimal change disease (lipoid nephrosis)

68
Q

diffuse loss of foot processes of podocytes that cannot be detected by light microscopy, but can be found by electron microscopy

A

minimal change disease (lipid nephrosis)

69
Q

minimal change disease is clinically associated with

A

respiratory infections

prophylactic immunization

70
Q

minimal change disease has symptoms similar to adult ______ syndrome, but with much better prognosis; symptoms include

A 
nephrOTIC syndrome
massive proteinuria
hypoalbuminemia
generalized edema
no HTN
no hematuria
71
Q

_____ are very effective with minimal change disease

A

corticosteroids

72
Q

lesion that is characterized by sclerosis of some, but not all glomeruli and in affected glomeruli only a portion of capillary tuft is involved

A

focal segmental glomerulosclerosis

73
Q

focal segmental glomerulosclerosis is frequently accompanied by

A

nephROTIC syndrome or heavy protein uria

74
Q

electron microscopy for focal segmental glomerulosclerosis shows:

A

pronounced focal detachment of visceral epithelial cells with denudation of underlying GBM

75
Q

focal segmental glomerulosclerosis affects ____ with better prognosis, and has higher incidence in ___ & ____

A

kids
males
african americans

76
Q

end stage of glomerular disease; results from continued glomerular inflammation, worsening destruction of glomeruli, and progressive loss of kidney fxn leading to kidney failure (usually develops in years or decades)

A

chronic glomerulonephritis

77
Q

progression of chronic renal failure varies from ____ to ___ ; tested using

A

several months to several years

GFR

78
Q

4 stages of chronic renal failure

A

1 diminished renal failure apprx 50% normal GFR
2 renal insufficiency 20-50% normal GFR
3 renal failure GFR less than 20% normal
4 End stage less than 5% normal

79
Q

signs/symptoms of chronic renal failure

A 
oliguria
nausea, vomiting
loss of appetite
anemia
fatigue, weakness
sleep problems
decreased mental sharpness
easy bruising
muscle twitching/cramping
feet/ankle swelling
persistent itching
chest pain
shortness of breath
high BP
80
Q

genetic condition characterized by kidney disease, loss of hearing before 30 y.o., eye abnormalities, affects mostly MALES

A

alport syndrome

81
Q

destruction of tubular epithelial cells of nephron, present with acute toxic kidney injury and ischemia

A

acute tubular necrosis

82
Q

acute tubular necrosis is USUALLY ______; lab findings include:

A 
reversible
reduced GFR
increased blood levels of BUN and creatinine
severe oliguria
hematuria
casts
83
Q

diseases (genetic, congenital, or acquired) of PROXIMAL renal tubules of kidneys with inadequate reabsorption of AA, uric acid, glucose, phosphates, bicarbonates

A

Fanconi’s syndrome

84
Q

urinalysis of Fanconi’s syndrome

A

mild proteinuria/aminoaciduria
glycosuria
hyperuricosuria
(may result in renal tubular acidosis)

85
Q

group of disorders involving either decreased ability to secrete hydrogen ions in distal tubules or decreased ability to reabsorb bicarbonate in proximal tubules

A

renal tubular acidosis

86
Q

renal tubular acidosis may result in chronic metabolic acidosis including:

A 
potassium depletion and wasting
muscle weakness
calcium loss in bones
elevated urine calcium
kidney stones
renal failure
87
Q

kidney tubules defect that affects ability to respond to ADH

A

nephrogenic diabetes insipidus

88
Q

nephrogenic diabetes insipidus is in contrast to _______, which is caused by INSUFFICIENT levels of ADH

A

central/neurogenic diabetes inspidus

89
Q

patient passes LARGE volume of urine with LOW specific gravity; usually affects MEN

A

nephrogenic diabetes insipidus

90
Q

autosomal recessive disorder that involves inadequate reabsorption of glucose due to proximal tubules dysfunction; ketones are NEVER present; renal histology is normal

A

renal glycosuria

91
Q

form of nephritis affecting interstitium of kidneys surrounding tubules; interferes with kidney function

A

acute interstitial nephritis

92
Q

acute interstitial nephritis results from (3)

A

allergic reactions to meds
infection
intoxication

93
Q

acute interstitial nephritis is manifested by

A 
hematuria
increased WBCs in urine
fever
rash
increased or decreased urine output
mental status changes
nausea, vomiting
94
Q

acute onset in patients with severe liver diseases; progressively intense VASOCONSTRICTION which leads to oliguria, elevated BUN, creatinine and renal failure

A

hepatorenal failure

95
Q

urinary findings for hepatorenal failure

A 
oliguria
dark color urine
increased specific gravity
low sodium
no proteinuria or abnormal crystals
96
Q

autosomal recessive diseases occurring rarely; due to non-production of enzyme phenyalanine hydrolase, blockage of normal conversion to tyrosine

A

phenylketonuria (PKU)

97
Q

in PKU, several intermediates are excreted in large amounts in urine and sweat (3) and cause ____ odor

A

phenylpyruvic acid
phenylactic acid
phenylacetic acid
musty/mousy odor

98
Q

___ tests detect PKU early; people affected usually have ___ skin and ___ hair

A

blood
pale skin
blonde hair

99
Q

autosomal recessive disorder, in which there is a lack of enzyme homogentisic acid oxidase in tyrosine pathway –> accumulation of homogentisic acid in tissues

A

alkaptonuria

100
Q

color of urine with alkaptonuria

A

black

101
Q

accumulation of homogentisic acid in cartilage results in its degeneration- this is called:

A

ochronosis

102
Q

rare, inherited metabolic disorder in which patients cannot breakdown leucine, isoleucine or valine; AA and their ketone-acids are excreted

A

maple syrup urine disease

103
Q

maple syrup urine disease can be controlled if detected before the _____

A

11th day after birth

104
Q

symptoms of maple syrup urine disease

A 
brain damage
cataracts
jaundice
enlarged liver
kidney damage
105
Q

inherited disease that is characterized by inadequate reabsorption of AA in PROXIMAL convoluted tubules

A

cystinosis (cystine disorders)

106
Q

cystinuria exists in 2 forms in cystinosis

A
  1. lysine, arginine, ornithine, and cystine cannot be reabsorbed
  2. only lysine or cystine cannot be reabsorbed
107
Q

inherited disorders in which clusters of noncancerous cysts develop primarily within the kidney

A

polycystic kidney disease (PKD)

108
Q

PKD is associated with

A

aortic aneurysms
brain aneurysms
cysts in liver, pancreas and testes
diverticula of colon

109
Q

______ PKD often develops btwn 30-40 yo; only one parents needs to have disease, MC

A

autosomal dominant

110
Q

_____ PKD appears shortly after birth, both parents must have it, less common

A

autosomal recessive

111
Q

symptoms of PKD

A 
high BP
back pain
headache
increase in size of abdomen
lood in urine
frequent urination
kidney failure
UTIs

UA (9 decks)

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