urinary

Question 1

pyelonephritis

Answer 1

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

Question 2

pyelonephritis: rf

Answer 2

preg, recurrent lower uti, abx resistant strain in lower

Question 3

pyelonephritis: cm

Answer 3

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

Question 4

pyelonephritis: tm

Answer 4

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

Question 5

pyelonephritis: complications

Answer 5

urosepsis - elderly
severe systemic response
high mortality
Pregnant more complicated

Question 6

urinary obstruction: nephrolithiasis

Answer 6

location = renal pelvis, ureter, bladder or pelvis

Question 7

urinary obstruction: causes

Answer 7

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

Question 8

urinary obstruction: complications

Answer 8

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

Question 9

urinary obstruction: cm of acute

Answer 9

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

Question 10

nephrolithiasis

Answer 10

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

Question 11

nephrolithiasis: patho

Answer 11

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

Question 12

nephrolithiasis: rf

Answer 12

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

Question 13

nephrolithiasis: types of stones

Answer 13

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

Question 14

nephrolithiasis: cm

Answer 14

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

Question 15

nephrolithiasis: tm

Answer 15

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

Question 16

urologic cancer: kidney

Answer 16

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

Question 17

urologic cancer: kidney - cm

Answer 17

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

Question 18

urologic cancer: bladder

Answer 18

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)

Question 18

urologic cancer: bladder - cm

Answer 18

early = hematuria
later = freq, urgency, dysuria

Question 19

urologic cancer: bladder - tm

Answer 19

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

Question 20

glomerulonephritis

Answer 20

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

Question 21

immune complexes

Answer 21

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

Question 22

glomerulonephritis: etiology

Answer 22

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

Question 23

glomerulonephritis: acute - cm

Answer 23

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

Question 24

glomerulonephritis: acute - triggers

Answer 24

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

Question 25

glomerulonephritis: acute - patho

Answer 25

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

Question 26

glomerulonephritis: chronic

Answer 26

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

Question 27

nephrotic S

Answer 27

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

Question 28

nephrotic S: patho

Answer 28

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

Question 29

nephrotic S: cm

Answer 29

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

Question 30

glomerulopathy

Answer 30

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

Question 31

kidney function

Answer 31

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

Question 32

kidney injury

Answer 32

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

Question 33

acute kidney injury

Answer 33

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

Question 34

AKI: classifications

Answer 34

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)

Question 35

AKI: cm

Answer 35

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

Question 36

AKI: tm

Answer 36

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

Question 37

CKD

Answer 37

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)

Question 38

CKD: rf

Answer 38

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

Question 39

CKD: patho

Answer 39

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

Question 40

CKD: cm

Answer 40

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)