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nur 326 > urinary > Flashcards

urinary Flashcards

1
Q

pyelonephritis

A

upper UTI -> kidney
inflam of kidneys -> kidney damage
ascending (starts lower) or blood stream infection (systemic)
e coli
usually acute but can be chronic
kidneys are swollen and filled with exudate, severe issues if obstruct renal artery -> necrotic, abscesses (sepsis, CKD)
abscesses and necrosis -> impair renal function

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2
Q

pyelonephritis: rf

A

preg, recurrent lower uti, abx resistant strain in lower

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3
Q

pyelonephritis: cm

A

sudden onset: fever, chills, CVA tenderness
lower UTI s (dysuria)
possible hematuria
n/v, anorexia

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4
Q

pyelonephritis: tm

A

abx: trimethoprim/sulfamethoxazole, cirpofloxacin, nitrofurantoin
recurrent = longer regimen
IV if more serious
urinalysis, C+S

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5
Q

pyelonephritis: complications

A

urosepsis - elderly
severe systemic response
high mortality
Pregnant more complicated

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6
Q

urinary obstruction: nephrolithiasis

A

location = renal pelvis, ureter, bladder or pelvis

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7
Q

urinary obstruction: causes

A

renal calculi: renal pelvis
ureter: renal calculi, preg, tumor
bladder and urethra: bladder cancer, neurogenic bladder, prostatic hyperplasia, prostate cancer, urethral strictures

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8
Q

urinary obstruction: complications

A

stasis of urine -> may flow but not freely, infection!
back up P: hydroureter (in ureter), hydronephrosis (in kidney), post renal acute kidney injury

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9
Q

urinary obstruction: cm of acute

A

depends on…
site: less pain if in renal pelvis bc more room (more difficulty peeing), migrate to ureter -> pain in waves; internal or external blockage
cause: stone, prostate
speed of onset: quickly = less tolerable

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10
Q

nephrolithiasis

A

kidney stone
clumps of crystals in urinary tract
size: sand -> golf ball
smooth or jagged
most common cause = renal obstruciton

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11
Q

nephrolithiasis: patho

A

urine is solution of solvent (water) and solutes (particles)
problem = super saturation with solute -> crystals begin forming in nephron
formation enhanced by: pH changes -> UTI, excess [] of insoluble salts in urine (dehyd, bone disease, gout, renal); urinary stasis -> immobility/sedentary

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12
Q

nephrolithiasis: rf

A

m
20s - 30s
white
fam hx
congenital defect
weather (hot - dehyd)
obesity (immobile)

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13
Q

nephrolithiasis: types of stones

A

Ca oxalate or CaP -> fam hx, idiopathic, hyperCa, oxaluria (diet)
struvite -> UTI
uric acid -> gout

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14
Q

nephrolithiasis: cm

A

pain of acute renal colic
location = flank
radiation = lower abd and groin
spasms = colicky (20 - 60 min)
intermittent = ureter spasms
sharp = calculi scrape ureter wall
n/v, dysuria, chills, fever (infection only!), hematuria, foul smelling urine, diaphoresis

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15
Q

nephrolithiasis: tm

A

acute pain = morphine/NSAIDs, IVF (dilute urine and move stones through)
preventative: Ca = thiazide diuretics, struvite = abx, urate = allopurinol

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16
Q

urologic cancer: kidney

A

renal cell carcinoma -> rare
rf = smoking!, obese, age, male, genetics
prognosis depends on metastasis

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17
Q

urologic cancer: kidney - cm

A

early cm -> none
late cm -> CVA tenderness, hematuria, possible palpable abd mass
metastasis in bone or lung -> dyspnic, bone pain, cough, difficulty breathing
usually chemo resistant (+ radiation with metastasis) -> sx to remove kidney likely

18
Q

urologic cancer: bladder

A

4th most common in m, urithelial carcinoma
rf: smoking, M, occupations with exposure to toxins (bc kidneys filter; rubber, paint), decreased fluid intake (toxins are high [] in urine and stay longer)

18
Q

urologic cancer: bladder - cm

A

early = hematuria
later = freq, urgency, dysuria

19
Q

urologic cancer: bladder - tm

A

chemo -> depends on stage!
stage 1 = intravesical
advanced stages = systemic chemo

20
Q

glomerulonephritis

A

a variety of conditions that cause glomeruli inflam
glomerular disorder: alterations in glomerular cap
focal or diffuse
KF -> may end up on dialysis
primarily an immune process
damage of glomerulus delicate network of arterioles w/n bowmans capsule: cap membrane layers = endothelium, basement membrane, podocytes (special epithelial cells)
damage of tubules: massive consumer of O2
efferent = higher P

21
Q

immune complexes

A

type 2 = rxn on cell surface by antibodies, direct cell death or malF
type 3 = immune complexes (antibody-antigen) deposited into tissues, resulting inflam destroys tissue

22
Q

glomerulonephritis: etiology

A

2 types of injury (based on immune reponse)
type 2 = antibodies attach to antigens of glomerular basement membrane (anti GBM antibodies)
type 3 = antibodies react with circulating antigens and are deposited as immune complexes in GBM
in common: accumulation of antigens, antibodies, complement; complement activation results in tissue injury

23
Q

glomerulonephritis: acute - cm

A

abrupt onset (HARP)
Hematuria
Azotemia (build up of waste)
Retention (Na + H2O, oliguria, lead to htn and edema)
Proteinuria -> bc membrane damage

24
Q

glomerulonephritis: acute - triggers

A

post infection: strep, or non strep - bacterial, viral, parasitic; antibodies mistake GBM as infection and attack
primary disease: berger -> buildup of antibody IGA - inflam
multisystem disease -> come from systemic problems (good posture S, systemic lupus erythematosus SLE, vasculitis)
SLE = autoimmune
good posture S = anti GBM antibodies, confused for lungs -> present with hemoptysis, resp and renal issues

25
Q

glomerulonephritis: acute - patho

A

trigger, immune complex, complement activated, mediators released, tissue injury, hematuria, proteinuria, decrease GFR (azotemia)

26
Q

glomerulonephritis: chronic

A

long term inflam -> scar tissue, cant filter effectively, diminished kidney function
cm like acute -> depends on damage
slow progressive destruction -> ESRD (will need dialysis)

27
Q

nephrotic S

A

can develop from glomerulonephritis
glomerulus too permeable to plasma proteins
eliminate >3g of protein/day
etiology: glomerulonephritis, DM

28
Q

nephrotic S: patho

A

increased glomerular perm, proteinuria (albumin, but too large to pass so stay in circ), hypoalbuminemia (3rd spacing)

29
Q

nephrotic S: cm

A

edema (3rd spacing), htn (want to increase kidney perfusion), liver (spilling proteins)
hld, hypercoag - loss of antithrombin 3 and plasminogen
DVT and PE

30
Q

glomerulopathy

A

uncontrolled DM and htn
DM nephropathy: major complication, gross thickening of GBM (cant filter so toxin buildup), lead to ESRD
htn glomerular disease: decreased renal perfusion (high P) -> sclerotic glomerular changes
cm: hematuria, oliguria, fluid retention, high BUN/cre, proteinuria, low albumin

31
Q

kidney function

A

F+E, rid body of water-soluble wastes via urine
endocrine function: produce erythropoietin (stim rbc production), activate vit D (Ca abs and bone health), productive renin which helps regulate BP

32
Q

kidney injury

A

needy! -> 1L/min
so injury can be sudden and rapid but can be reversible
renal insuf = 25% of normal GFR (25-30) -> indicate kidney injury
normal >90

33
Q

acute kidney injury

A

usually ischemic injury r/t loss of V -> decreased perfusion (also toxins with drug OD or sepsis - third spacing)
kidney function can be mildly-severely affected
increased inflam -> lots of vascular change, lots of cell death

34
Q

AKI: classifications

A

pre-renal: r/t v loss
intrarenal (direct kidney injury): acute tubular necrosis (chm, kidney cell death) - toxins, drug OD, glomneph, nephrotoxic ANT (meds)/vascular (htn, DM)
post renal: not as common, obstruction causing cell death (blockage/tumor)

35
Q

AKI: cm

A

oliguria: <30mL/hr or 400mL/24hr, begin 1 day after hypotensive event (sx, blood loss, dehyd) and lasts 1-3wk, FVE (edema, more advanced state), met acidosis, hypoNa, hyperK, waste product accumulation (azetemia, uremia), neurologic disorders

36
Q

AKI: tm

A

address cause and we treat manifestations (replace volume, OD, antidote, flush, E imbalance, fluid shift)
monitor labs and chronic issues

37
Q

CKD

A

can be caused by acute injury
stage determined by GFR (1+2 likely asymptomatic; 3 = htn; severe 4+ 5: other manifestations (uremic = urea in blood)
stages 1-3: diagnose, moderate and treat, risk reduction -> DM, htn, AKI
prevention is best treatment -> control rf (htn, DM, AKI, glomneph)

38
Q

CKD: rf

A

fam hx, >60, m, black/AA, htn, DM, smoke (endothelial damage), overweight, obese
other vascular diseases: CAD, hld, atherosclerosis

39
Q

CKD: patho

A

starts with renal ischemia
proteinuria = inability of kidney to reuptake protein (leaky basement membrane, contribute to further tubal interstitial injury (proteins accumulate in interstitial space), leads to more inflam
more angiotensin 2 = powerful vasoconstrictor (arteriolar - leads to more proteinuria)
cyclic
proteinuria and high A2 = worsening CKD

40
Q

CKD: cm

A

almost every body system effected, increased inflam
neuro: fatigue, HA, sleep disturbance, encephalopathy
CV: htn, HF, CAD, pericarditis, peripheral artery disease
GI: anorexia, n/v, GI bleed, gastritis
Integumentary: pruritus, ecchymosis, dry, scaly skin
anx and depression, pulm edema (need dialysis)
F+E imbalance: edema, hyperK!!, hyperP, hyperMg, met acid
waste buildup: anorexia, malN, itch (toxin build up), cns changes
decreased erythropoetin: anemia
decreased vit D activation: renal osteodystrophy (break bones)

nur 326 (45 decks)

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