urinary Flashcards
pyelonephritis
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
pyelonephritis: rf
preg, recurrent lower uti, abx resistant strain in lower
pyelonephritis: cm
sudden onset: fever, chills, CVA tenderness
lower UTI s (dysuria)
possible hematuria
n/v, anorexia
pyelonephritis: tm
abx: trimethoprim/sulfamethoxazole, cirpofloxacin, nitrofurantoin
recurrent = longer regimen
IV if more serious
urinalysis, C+S
pyelonephritis: complications
urosepsis - elderly
severe systemic response
high mortality
Pregnant more complicated
urinary obstruction: nephrolithiasis
location = renal pelvis, ureter, bladder or pelvis
urinary obstruction: causes
renal calculi: renal pelvis
ureter: renal calculi, preg, tumor
bladder and urethra: bladder cancer, neurogenic bladder, prostatic hyperplasia, prostate cancer, urethral strictures
urinary obstruction: complications
stasis of urine -> may flow but not freely, infection!
back up P: hydroureter (in ureter), hydronephrosis (in kidney), post renal acute kidney injury
urinary obstruction: cm of acute
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
nephrolithiasis
kidney stone
clumps of crystals in urinary tract
size: sand -> golf ball
smooth or jagged
most common cause = renal obstruciton
nephrolithiasis: patho
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
nephrolithiasis: rf
m
20s - 30s
white
fam hx
congenital defect
weather (hot - dehyd)
obesity (immobile)
nephrolithiasis: types of stones
Ca oxalate or CaP -> fam hx, idiopathic, hyperCa, oxaluria (diet)
struvite -> UTI
uric acid -> gout
nephrolithiasis: cm
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
nephrolithiasis: tm
acute pain = morphine/NSAIDs, IVF (dilute urine and move stones through)
preventative: Ca = thiazide diuretics, struvite = abx, urate = allopurinol
urologic cancer: kidney
renal cell carcinoma -> rare
rf = smoking!, obese, age, male, genetics
prognosis depends on metastasis
urologic cancer: kidney - cm
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
urologic cancer: bladder
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)
urologic cancer: bladder - cm
early = hematuria
later = freq, urgency, dysuria
urologic cancer: bladder - tm
chemo -> depends on stage!
stage 1 = intravesical
advanced stages = systemic chemo
glomerulonephritis
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
immune complexes
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
glomerulonephritis: etiology
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
glomerulonephritis: acute - cm
abrupt onset (HARP)
Hematuria
Azotemia (build up of waste)
Retention (Na + H2O, oliguria, lead to htn and edema)
Proteinuria -> bc membrane damage
glomerulonephritis: acute - triggers
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
glomerulonephritis: acute - patho
trigger, immune complex, complement activated, mediators released, tissue injury, hematuria, proteinuria, decrease GFR (azotemia)
glomerulonephritis: chronic
long term inflam -> scar tissue, cant filter effectively, diminished kidney function
cm like acute -> depends on damage
slow progressive destruction -> ESRD (will need dialysis)
nephrotic S
can develop from glomerulonephritis
glomerulus too permeable to plasma proteins
eliminate >3g of protein/day
etiology: glomerulonephritis, DM
nephrotic S: patho
increased glomerular perm, proteinuria (albumin, but too large to pass so stay in circ), hypoalbuminemia (3rd spacing)
nephrotic S: cm
edema (3rd spacing), htn (want to increase kidney perfusion), liver (spilling proteins)
hld, hypercoag - loss of antithrombin 3 and plasminogen
DVT and PE
glomerulopathy
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
kidney function
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
kidney injury
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
acute kidney injury
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
AKI: classifications
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)
AKI: cm
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
AKI: tm
address cause and we treat manifestations (replace volume, OD, antidote, flush, E imbalance, fluid shift)
monitor labs and chronic issues
CKD
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)
CKD: rf
fam hx, >60, m, black/AA, htn, DM, smoke (endothelial damage), overweight, obese
other vascular diseases: CAD, hld, atherosclerosis
CKD: patho
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
CKD: cm
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)
