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NUR 326 > Urologic Problems > Flashcards

Urologic Problems Flashcards

1
Q

nephro

A

kidney

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2
Q

renal

A

of or belonging to kidney

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3
Q

nephrology

A

study of the kidneys

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4
Q

urology

A

study of the urinary tract

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5
Q

lithos

A

stone

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6
Q

calculi

A

something accidental that doesnt belong in body

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7
Q

parts of urinary tract that can become obstructed

A

bladder
ureters
urethra

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8
Q

factors that determine destruction

A

degree
location
duration
timing

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9
Q

cause of renal pelvis obstruction

A

renal calculi

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10
Q

cause of ureter obstruction

A

renal calculi
pregnancy
tumors

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11
Q

cause of bladder and urethra obstructions

A

bladder cancer
neurogenic bladder
prostatic hyperplasia, cancer
urethra strictures (narrowing of ureters)

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12
Q

two complications of obstructions

A

stasis of urinary flow –> infection
back up pressure –> hydroureter/nephrosis, postrenal acute injury

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13
Q

manifestations of acute obstructions

A

depends on site, cause and speed

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14
Q

which manifestation of obstruction determines the severity of pain

A

site

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15
Q

nephrolithiasis

A

kidney stones

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16
Q

nephrolithiasis definition

A

clumps of crystals in the urinary tract
- crystalized solutes in the urine

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17
Q

where do nephrolithiasis form?

A

urinary pelvis

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18
Q

where are nephrolithiasis?

A

urinary pelvis to urethra

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19
Q

risk factors for nephrolithiasis

A

men
20-30s
white
fam hx
congenital defect
weather
obesity

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20
Q

etiology of nephrolithiasis depends on

A

ind risk factors
characteristics of urine –> diet, meds
type of stone formed

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21
Q

types of kidney stones

A

calcium oxalate
struvite
uric acid

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22
Q

risks for calcium oxalate

A

fam hx
idiopathic
inc calcium, oxalate

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23
Q

risks for staghorn

A

UTI

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24
Q

patho of nephrolithiasis

A

supersaturation w a solute causing crystals to form
- crystal formation enhanced by dehydration, immobility, sedentary lifestyle

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25
Q

clinical manifestations of nephrolithiasis

A

acute renal colic
NV
Diaphoresis
inc HR, RR
lower UTI symptoms

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26
Q

what is renal colic pain?

A

left flank pain that wraps around and goes down right groin
radiates
spasms
intermittent
sharp

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27
Q

pharm for nephrolithiasis

A

pain
- morphine, NSAIDs
- IV fluids
prevention meds
- calcium –> thiazide diuretics
- struvite –> abx
urate –> allopurinol

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28
Q

protective factors for UTI

A

pH –> acidic
presence of urea
sex specific secretions
flow is uni directional
immune system

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29
Q

risk factors for UTI

A

caths
women
older age
pregnancy
sexual activity
obstruction or reflux
immobility
incontinence
dec cognition
bad hygiene

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30
Q

pyelonephritis

A

inflammation of the kidney

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31
Q

cystitis

A

inflammation of the bladder

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32
Q

path of a UTI

A

ascends upwards (lower–>upper)

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33
Q

bacteria that typically causes upper and lower UTIs

A

e coli or blood stream infections

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34
Q

major risk factor for pyelonephritis

A

pregnacy

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35
Q

inflammatory response to pyelonephritis

A

kidney tissue damage and can move to kidney failure

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36
Q

clinical manifestations of upper UTI

A

sudden onset–> fever, chills, CVA tenderness
lower UTI sx
NV
anorexia

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37
Q

complication of pyelonephritis

A

urosepsis

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38
Q

what is urosepsis

A

severe systemic response to UTI

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39
Q

risks for urosepsis

A

elderly pts
DM
immunosuppressed pts

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40
Q

prognosis of urosepsis

A

high mortality

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41
Q

treatment for community acquired UTI

A

single dose
short course
conventional

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42
Q

treatment of UTI varies due to

A

upper vs lower
complications
pregnancy
c and s

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43
Q

ciprofloxacin moa

A

inhibits bacterial reproduction by altering DNA synthesis by interfering with DNA gyrase and topoisomerase

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44
Q

other drugs used for UTI

A

vancomycin

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45
Q

ciprofloxacin adverse effects

A

concentrates in neutrophils
arthropathy –> joint disease
18-60 only

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46
Q

vancomycin moa

A

binds to bacterial cell wall, producing immediate inhibition of cell wall synthesis

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47
Q

vancomycin treats

A

MRSA, PCN resistant orgs, c diff, pseudomembranous colitis

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48
Q

vancomycin adverse effects

A

kidneys eliminate so careful w renal dysfunction
ototoxicity
nephrotoxicity
immune mediated thrombocytopenia
watch w neuromuscular blockades
Red man syndrome

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49
Q

types of urinary cancers

A

kidney
bladder

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50
Q

most common kidney cancer

A

renal cell carcinoma

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51
Q

risk factors for kidney cancer

A

smoking
obesity
age
male
genetics

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52
Q

does kidney cancer metastasize?

A

yes, it is typically not diagnosed until it has manifested somewhere else

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53
Q

renal cell carcinoma clinical manifestations

A

early: none –> why it spreads
late: CVA tenderness, hematuria, palpable abdominal mass
sx related to spread: often travels to bone and lung, so dyspnea, cough, bone pain

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54
Q

treatment for renal cell carcinoma

A

kidney is removed bc it is resistant to chemo

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55
Q

bladder cancer

A

urothelial carcinoma

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56
Q

risk factors for urothelial

A

smoking
male
occupations with exposures to toxins
low fluid intake

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57
Q

clinical manifestations of bladder cancer

A

early: hematuria
late: frequency, urgency, dysuria

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58
Q

treatment for bladder cancer

A

chemo can work at certain stages
- stage 1: intravesical
- advanced: systemic chemo

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59
Q

intravesical therapy

A

BCG vaccine

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60
Q

moa of BCG vaccine

A

stimulates local inflammatory response

61
Q

BCG adverse effects

A

bladder irritation
risk of systemic infection

62
Q

BCG instructions

A

empty bladder
dwell time for 2 hours
turn q 15 mins

63
Q

precautions given with BCG

A

live virus so
- dont give to immunocompromised
- dont be around someone immunocompromised with BCG
- disinfect urine after treatment with bleach

64
Q

hematuria

A

blood in the urine

65
Q

azotemia

A

symptoms appear when the toxins build up

66
Q

oliguria

A

decreased urine output
- less than 400 ml/day

67
Q

proteinuria

A

protein in urine
- due to damaged glomeruli

68
Q

glomerular filtration rate

A

amount of blood that filtered by glomeruli

69
Q

kidney functions

A
  • maintain fluid and electrolyte homeostasis
  • ride the body of water soluble wastes via urine
  • endocrine functions
70
Q

endocrine functions of the kidneys

A
  • produce erythropoietin
  • activate vit D
  • produce renin
71
Q

BUN value

A

10-20

72
Q

Cr value

A

0.5-1.2

73
Q

BUN and Cr ratio

A

10:1

74
Q

GFR value

A

greater than 90 ml/min

75
Q

chronic kidney disease

A

presence of kidney damage from more than 3 months with or without a GFR less than 60 ml/min

76
Q

people w CKD are unable to

A

maintain acid-base balance
remove end products of metabolism
maintain fluid and electrolyte balance

77
Q

what is the GFR for end stage kidney disease

A

less than 15 ml/min

78
Q

causes of CKD

A

1) DM
2) HTN
3) glomerulonephritis and others

79
Q

risk factors for CKD

A

fam hx
inc age (over 60)
male
african american
HTN, DM, smoking
overwt, obesity

80
Q

characteristics of CKD

A

glomerulosclerosis
interstitial fibrosis
interstitial inflammation

81
Q

what plays a role in pathogenesis of CKD

A

complement: causes further destruction
angiotensin II: inc BP which inc damage

82
Q

what stage of CKD are ppl typically diagnosed

A

stage 4: manifestations appear here besides HTN

83
Q

stage 5 CKD characterized by

A

uremia

84
Q

what is uremia

A

retention of metabolic wastes
- urea, Cr, phenols, hormones, electrolytes, water

85
Q

when is uremia often seen

A

GFR less than or equal to 10

86
Q

what is uremia typically measured with

A

BUN

87
Q

clinical manifestations of ESRD

A

affects literally all the other body systems to some degree due to the toxin build up

88
Q

abnormal kidney function: no longer maintain f and e homeostasis

A

edema
hyper K, PO4, Mg
metabolic acidosis

89
Q

abnormal kidney function: no longer rids the body of wastes via urine

A

anorexia
malnutrition
itching
CNS changes

90
Q

abnormal kidney function: dec production of erythropoietin

A

anemia

91
Q

abnormal kidney function: dec activation of vit D

A

renal osteodsytrophy

92
Q

itchy flakey skin as result of toxins in the skin

A

uremic frost

93
Q

how are drugs used to treat CKD

A

HTN: want to keep BP 140/90, typically ACE, ARBs
treat HLP (statins)
treat complications

94
Q

treating volume overload

A

loop diuretic
- used with low Na diet

95
Q

treating hyperkalemia

A

dec K intake, inc diuretics to dec K
- dialysis if needed

96
Q

treating metabolic acidosis

A

sodium bicarbonate (alkaline agent)

97
Q

treating hyperphosphatemia

A

calcium carbonate (phosphate binder)

98
Q

treating renal osteodsytrophy

A

calcitriol (activated vit d)

99
Q

treating anemia

A

erythropoietin –> black box warning, dont give over 10 hgb

100
Q

sodium bicarbonate goals

A

slow progression of CKD
prevent bone loss
improve nutritional status

101
Q

administration of sodium bicarbonate

A

plasma HCO3 < 15 mEq/mL
titrate to HCO2 of 18-20

102
Q

sodium bicarbonate se

A

bloating

103
Q

calcium carbonate moa

A

binds to phosphate

104
Q

calcium carbonate goals of therapy

A

keep phosphate levels normal
reduce mortality

105
Q

calcium carbonate nursing considerations

A

take w meals to bind with phosphate in meal

106
Q

calcium carbonate adverse effects

A

hypercalcemia

107
Q

calcitriol moa

A

activated form of vitamin d that stimulates intestinal absorption of Ca/PO4 and bone mineralization

108
Q

calcitriol adverse effects

A

hypercalcemia
hyperphosphatemia

109
Q

signs of ca toxicity

A

GI upset
bone pain
neuro effects
cardiac arrhythmias

110
Q

complications of CKD drug therapy

A

many drugs are excreted through the kidneys so drugs have to be adjusted to not further affect kidneys
- digoxin, diabetic agents (glyuride, metformin), abx (vanc), opiods (morphine)

111
Q

glomerulonephritis

A

variety of conditions that causes inflammation of the glomeruli
- focal or diffuse
- affects both kidneys equally
- primarily an immune mediated process

112
Q

where does the damage occur in glomerulonephritis

A

glomerulus: delicate network of arterioles in bowmans capsule
tubules: massive consumer of oxygen

113
Q

how do glomeruli work

A

artery and vein with differing pressures that allow wastes to be pushed out of vessel to be excreted

114
Q

what are the alterations in the glomerular capillary

A

dec the diameter of the vessel inc the pressure inside
- afferent: larger D and decent pressure
- efferent: smaller D and high pressure

115
Q

membrane of glomerulus

A

endothelium
basement membrane
podocytes

116
Q

primary glomerulonephritis

A

isolated to the kidneys

117
Q

secondary glomerulonephritis

A

caused by systemic disease
- autoimmune

118
Q

damage to the glomeruli can be

A

diffuse (both kidneys)
focal (only some glomeruli)
local (an area of the glomerulus)

119
Q

type II rxns

A

rxns occurs on cell surface and results in direct cell death or manifestations

120
Q

type III

A

immune complexes are deposited into tissues and the resulting inflammation damages the tissue

121
Q

types of injury w glomerulonephritis

A
  • antibodies attach to antigen of the glomerular basement membrane (GBM antibodies)
  • antibodies react with circulating antigens and are deposited as immune complexes in the GBM
122
Q

both types of glomerulonephritis causes

A

accumulations of antigens, antibodies, and complement
complement activation results in tissue injury

123
Q

characteristics of acute glomerulonephritis

A

abrupt onset of HARP
Hematuria
Azotemia
Retention: Na and water, oliguria, leads to HTN, edema
Proteinuria

124
Q

triggers of acute glomerulonephritis

A

post infection
- poststreptococcal, nonstreptococcal (bacterial, viral, parasitic)
primary diseases
- berger disease
multisystem
- Good pasture syndrome, systemic lupus, erythematous, vasculitis

125
Q

good pasture syndrome

A

lung membrane similar so anti GBM antibodies also attack lung membrane causing respiratory problems on top of renal problems

126
Q

acute glomerulonephritis pathogenesis

A

trigger
immune complexes form
complement activated
release mediators
tissue injury
hematuria, proteinuria, dec GFR

127
Q

what is chronic glomerulonephritis

A

long term inflammation that causes a build up of scare tissue

128
Q

clinical manifestations of chronic glomerulonephritis

A

HARP
- similar to acute

129
Q

prognosis of chronic glomerulonephritis

A

slow progression of destruction
will eventually end in ESKD

130
Q

pharm for glomerulonephritis

A

depends on cause and damage done already
- prednison
- diuretics
- immunosuppressants
- anti HTN (ACE, ARBs)
- dialysis and diet

131
Q

common s/s of chronic glomerulonephritis

A

hematuria
oliguria
fluid retention
labs (inc BUN, Cr, proteinuria, hypoproteinemia (low albumin)

132
Q

glomerulopathy and diabetes

A

high glucose levels causes damage which inc thickness and dec ability to filter
- results in less urine and more toxins

133
Q

glomerulopathy and HTN

A

inc pressure on bv in kidneys causes scarring of glomerulus increases sclerosis of bv and dec renal perfusion

134
Q

nephortic syndrome

A

glomerulus is too permeable to plasma protein
- elimination of less 3 grams of protein/day

135
Q

etiology of nephrotic syndrome

A

glomerulonephritis
DM

136
Q

nephrotic syndrome pathogenesis

A

increased glomerular permeability
proteinuria
hypoalbuminemia
usually protein is too large to pass through vessels

137
Q

nephrotic syndrome clinical manifestations

A

edema (low albumin in bv)
HTN (kidney wants more perfusion/volume)
liver involvement
- hyperlipidemia
- hypercoagulation (loss antithrombin III and plasminogen –> breakdown clots)

138
Q

nephrotic syndrome clinical manifestations

A

edema (low albumin in bv)
HTN (kidney wants more perfusion/volume)
liver involvement
- hyperlipidemia
- hyper coagulation (loss antithrombin III and plasminogen –> breakdown clots)

139
Q

what is the pathophysiology of acute kidney injury

A

ischemic injury related to volume depletion and decreased perfusion
-toxic injury from chemical
-sepsis

140
Q

what does injury cause during acute kidney injury?

A

initiates an inflammatory response, vascular response and cell death

141
Q

3 classifications for AKI

A
  • prerenal
  • intrarenal
  • postrenal
142
Q

prerenal cause

A

inadequate perfusion to kidneys
- hypotension, hypovolemia, sepsis, inadequate CO, renal vasoconstriction, or renal stenosis
- dec GFR –> low glomerular filtration pressure
- failure to restore blood volume, bp, o2 delivery can cause ischemic cell injury and necrosis

143
Q

intrarenal cause

A

acute tubular necrosis related to prerenal AKI, nephrotoxic agents, acute glomerulonephritis and vascular disease
- prerenal AKI –> intrarenal bc kidneys affected at cellular level
- nephrotoxic ATN: abx, heavy metals. contrast dyes, rhabdomyolysis

144
Q

postrenal

A

rare condition that usually occurs with urinary tract obstruction
- bladder outlet obstruction, prostatic hyperplasia, bilateral ureteral obstruction, tumor, neurogenic bladder
*inc pressure caused by blockage

145
Q

what are the values for acute kidney failure

A

sudden decline in function and rapidly progressive
- dec GFR (less than 90 ml/min)
- dec UOP (less than 30 ml/hr)
- inc BUN (over 10-20)
- elevated Cr (over 1.2)

146
Q

is acute injury kidney reversible

A

yes

147
Q

clinical manifestations of acute kidney

A

oliguria less than 400 ml/24 hr
- begins 1 day after hypotensive event and last 1-3 wks

148
Q

pharm treatment goal for acute kidney failure

A

stabilize pt until kidney function is returned

149
Q

pharm management for acute kidney failure

A

correct fluid, electrolyte imbalance (particularly hyperkalemia)
- Lasik clears kidneys
- dextrose and insulin to move K into cells
- binders kayexalate, veltassa, lokelma
correct acid base balance w sodium bicarbonate
manage BP
avoid drugs that are nephrotoxic

NUR 326 (20 decks)

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