Urologic Problems Flashcards

1
Q

nephro

A

kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

renal

A

of or belonging to kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

nephrology

A

study of the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

urology

A

study of the urinary tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

lithos

A

stone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

calculi

A

something accidental that doesnt belong in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

parts of urinary tract that can become obstructed

A

bladder
ureters
urethra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

factors that determine destruction

A

degree
location
duration
timing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cause of renal pelvis obstruction

A

renal calculi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cause of ureter obstruction

A

renal calculi
pregnancy
tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cause of bladder and urethra obstructions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

two complications of obstructions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

manifestations of acute obstructions

A

depends on site, cause and speed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which manifestation of obstruction determines the severity of pain

A

site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

nephrolithiasis

A

kidney stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

nephrolithiasis definition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where do nephrolithiasis form?

A

urinary pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

where are nephrolithiasis?

A

urinary pelvis to urethra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

risk factors for nephrolithiasis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

etiology of nephrolithiasis depends on

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

types of kidney stones

A

calcium oxalate
struvite
uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

risks for calcium oxalate

A

fam hx
idiopathic
inc calcium, oxalate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

risks for staghorn

A

UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

patho of nephrolithiasis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
clinical manifestations of nephrolithiasis
acute renal colic NV Diaphoresis inc HR, RR lower UTI symptoms
26
what is renal colic pain?
left flank pain that wraps around and goes down right groin radiates spasms intermittent sharp
27
pharm for nephrolithiasis
pain - morphine, NSAIDs - IV fluids prevention meds - calcium --> thiazide diuretics - struvite --> abx urate --> allopurinol
28
protective factors for UTI
pH --> acidic presence of urea sex specific secretions flow is uni directional immune system
29
risk factors for UTI
caths women older age pregnancy sexual activity obstruction or reflux immobility incontinence dec cognition bad hygiene
30
pyelonephritis
inflammation of the kidney
31
cystitis
inflammation of the bladder
32
path of a UTI
ascends upwards (lower-->upper)
33
bacteria that typically causes upper and lower UTIs
e coli or blood stream infections
34
major risk factor for pyelonephritis
pregnacy
35
inflammatory response to pyelonephritis
kidney tissue damage and can move to kidney failure
36
clinical manifestations of upper UTI
sudden onset--> fever, chills, CVA tenderness lower UTI sx NV anorexia
37
complication of pyelonephritis
urosepsis
38
what is urosepsis
severe systemic response to UTI
39
risks for urosepsis
elderly pts DM immunosuppressed pts
40
prognosis of urosepsis
high mortality
41
treatment for community acquired UTI
single dose short course conventional
42
treatment of UTI varies due to
upper vs lower complications pregnancy c and s
43
ciprofloxacin moa
inhibits bacterial reproduction by altering DNA synthesis by interfering with DNA gyrase and topoisomerase
44
other drugs used for UTI
vancomycin
45
ciprofloxacin adverse effects
concentrates in neutrophils arthropathy --> joint disease 18-60 only
46
vancomycin moa
binds to bacterial cell wall, producing immediate inhibition of cell wall synthesis
47
vancomycin treats
MRSA, PCN resistant orgs, c diff, pseudomembranous colitis
48
vancomycin adverse effects
kidneys eliminate so careful w renal dysfunction ototoxicity nephrotoxicity immune mediated thrombocytopenia watch w neuromuscular blockades Red man syndrome
49
types of urinary cancers
kidney bladder
50
most common kidney cancer
renal cell carcinoma
51
risk factors for kidney cancer
smoking obesity age male genetics
52
does kidney cancer metastasize?
yes, it is typically not diagnosed until it has manifested somewhere else
53
renal cell carcinoma clinical manifestations
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
54
treatment for renal cell carcinoma
kidney is removed bc it is resistant to chemo
55
bladder cancer
urothelial carcinoma
56
risk factors for urothelial
smoking male occupations with exposures to toxins low fluid intake
57
clinical manifestations of bladder cancer
early: hematuria late: frequency, urgency, dysuria
58
treatment for bladder cancer
chemo can work at certain stages - stage 1: intravesical - advanced: systemic chemo
59
intravesical therapy
BCG vaccine
60
moa of BCG vaccine
stimulates local inflammatory response
61
BCG adverse effects
bladder irritation risk of systemic infection
62
BCG instructions
empty bladder dwell time for 2 hours turn q 15 mins
63
precautions given with BCG
live virus so - dont give to immunocompromised - dont be around someone immunocompromised with BCG - disinfect urine after treatment with bleach
64
hematuria
blood in the urine
65
azotemia
symptoms appear when the toxins build up
66
oliguria
decreased urine output - less than 400 ml/day
67
proteinuria
protein in urine - due to damaged glomeruli
68
glomerular filtration rate
amount of blood that filtered by glomeruli
69
kidney functions
- maintain fluid and electrolyte homeostasis - ride the body of water soluble wastes via urine - endocrine functions
70
endocrine functions of the kidneys
- produce erythropoietin - activate vit D - produce renin
71
BUN value
10-20
72
Cr value
0.5-1.2
73
BUN and Cr ratio
10:1
74
GFR value
greater than 90 ml/min
75
chronic kidney disease
presence of kidney damage from more than 3 months with or without a GFR less than 60 ml/min
76
people w CKD are unable to
maintain acid-base balance remove end products of metabolism maintain fluid and electrolyte balance
77
what is the GFR for end stage kidney disease
less than 15 ml/min
78
causes of CKD
1) DM 2) HTN 3) glomerulonephritis and others
79
risk factors for CKD
fam hx inc age (over 60) male african american HTN, DM, smoking overwt, obesity
80
characteristics of CKD
glomerulosclerosis interstitial fibrosis interstitial inflammation
81
what plays a role in pathogenesis of CKD
complement: causes further destruction angiotensin II: inc BP which inc damage
82
what stage of CKD are ppl typically diagnosed
stage 4: manifestations appear here besides HTN
83
stage 5 CKD characterized by
uremia
84
what is uremia
retention of metabolic wastes - urea, Cr, phenols, hormones, electrolytes, water
85
when is uremia often seen
GFR less than or equal to 10
86
what is uremia typically measured with
BUN
87
clinical manifestations of ESRD
affects literally all the other body systems to some degree due to the toxin build up
88
abnormal kidney function: no longer maintain f and e homeostasis
edema hyper K, PO4, Mg metabolic acidosis
89
abnormal kidney function: no longer rids the body of wastes via urine
anorexia malnutrition itching CNS changes
90
abnormal kidney function: dec production of erythropoietin
anemia
91
abnormal kidney function: dec activation of vit D
renal osteodsytrophy
92
itchy flakey skin as result of toxins in the skin
uremic frost
93
how are drugs used to treat CKD
HTN: want to keep BP 140/90, typically ACE, ARBs treat HLP (statins) treat complications
94
treating volume overload
loop diuretic - used with low Na diet
95
treating hyperkalemia
dec K intake, inc diuretics to dec K - dialysis if needed
96
treating metabolic acidosis
sodium bicarbonate (alkaline agent)
97
treating hyperphosphatemia
calcium carbonate (phosphate binder)
98
treating renal osteodsytrophy
calcitriol (activated vit d)
99
treating anemia
erythropoietin --> black box warning, dont give over 10 hgb
100
sodium bicarbonate goals
slow progression of CKD prevent bone loss improve nutritional status
101
administration of sodium bicarbonate
plasma HCO3 < 15 mEq/mL titrate to HCO2 of 18-20
102
sodium bicarbonate se
bloating
103
calcium carbonate moa
binds to phosphate
104
calcium carbonate goals of therapy
keep phosphate levels normal reduce mortality
105
calcium carbonate nursing considerations
take w meals to bind with phosphate in meal
106
calcium carbonate adverse effects
hypercalcemia
107
calcitriol moa
activated form of vitamin d that stimulates intestinal absorption of Ca/PO4 and bone mineralization
108
calcitriol adverse effects
hypercalcemia hyperphosphatemia
109
signs of ca toxicity
GI upset bone pain neuro effects cardiac arrhythmias
110
complications of CKD drug therapy
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
glomerulonephritis
variety of conditions that causes inflammation of the glomeruli - focal or diffuse - affects both kidneys equally - primarily an immune mediated process
112
where does the damage occur in glomerulonephritis
glomerulus: delicate network of arterioles in bowmans capsule tubules: massive consumer of oxygen
113
how do glomeruli work
artery and vein with differing pressures that allow wastes to be pushed out of vessel to be excreted
114
what are the alterations in the glomerular capillary
dec the diameter of the vessel inc the pressure inside - afferent: larger D and decent pressure - efferent: smaller D and high pressure
115
membrane of glomerulus
endothelium basement membrane podocytes
116
primary glomerulonephritis
isolated to the kidneys
117
secondary glomerulonephritis
caused by systemic disease - autoimmune
118
damage to the glomeruli can be
diffuse (both kidneys) focal (only some glomeruli) local (an area of the glomerulus)
119
type II rxns
rxns occurs on cell surface and results in direct cell death or manifestations
120
type III
immune complexes are deposited into tissues and the resulting inflammation damages the tissue
121
types of injury w glomerulonephritis
- 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
both types of glomerulonephritis causes
accumulations of antigens, antibodies, and complement complement activation results in tissue injury
123
characteristics of acute glomerulonephritis
abrupt onset of HARP Hematuria Azotemia Retention: Na and water, oliguria, leads to HTN, edema Proteinuria
124
triggers of acute glomerulonephritis
post infection - poststreptococcal, nonstreptococcal (bacterial, viral, parasitic) primary diseases - berger disease multisystem - Good pasture syndrome, systemic lupus, erythematous, vasculitis
125
good pasture syndrome
lung membrane similar so anti GBM antibodies also attack lung membrane causing respiratory problems on top of renal problems
126
acute glomerulonephritis pathogenesis
trigger immune complexes form complement activated release mediators tissue injury hematuria, proteinuria, dec GFR
127
what is chronic glomerulonephritis
long term inflammation that causes a build up of scare tissue
128
clinical manifestations of chronic glomerulonephritis
HARP - similar to acute
129
prognosis of chronic glomerulonephritis
slow progression of destruction will eventually end in ESKD
130
pharm for glomerulonephritis
depends on cause and damage done already - prednison - diuretics - immunosuppressants - anti HTN (ACE, ARBs) - dialysis and diet
131
common s/s of chronic glomerulonephritis
hematuria oliguria fluid retention labs (inc BUN, Cr, proteinuria, hypoproteinemia (low albumin)
132
glomerulopathy and diabetes
high glucose levels causes damage which inc thickness and dec ability to filter - results in less urine and more toxins
133
glomerulopathy and HTN
inc pressure on bv in kidneys causes scarring of glomerulus increases sclerosis of bv and dec renal perfusion
134
nephortic syndrome
glomerulus is too permeable to plasma protein - elimination of less 3 grams of protein/day
135
etiology of nephrotic syndrome
glomerulonephritis DM
136
nephrotic syndrome pathogenesis
increased glomerular permeability proteinuria hypoalbuminemia *usually protein is too large to pass through vessels*
137
nephrotic syndrome clinical manifestations
edema (low albumin in bv) HTN (kidney wants more perfusion/volume) liver involvement - hyperlipidemia - hypercoagulation (loss antithrombin III and plasminogen --> breakdown clots)
138
nephrotic syndrome clinical manifestations
edema (low albumin in bv) HTN (kidney wants more perfusion/volume) liver involvement - hyperlipidemia - hyper coagulation (loss antithrombin III and plasminogen --> breakdown clots)
139
what is the pathophysiology of acute kidney injury
ischemic injury related to volume depletion and decreased perfusion -toxic injury from chemical -sepsis
140
what does injury cause during acute kidney injury?
initiates an inflammatory response, vascular response and cell death
141
3 classifications for AKI
- prerenal - intrarenal - postrenal
142
prerenal cause
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
intrarenal cause
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
postrenal
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
what are the values for acute kidney failure
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
is acute injury kidney reversible
yes
147
clinical manifestations of acute kidney
oliguria less than 400 ml/24 hr - begins 1 day after hypotensive event and last 1-3 wks
148
pharm treatment goal for acute kidney failure
stabilize pt until kidney function is returned
149
pharm management for acute kidney failure
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