Renal system Flashcards
what are the main things to assess renal function?
Urine smaple: colour, clarity, smell, casts, ph level
blood test: BUN, Creatine,
what is an upper UTI infection?
pyelonephritis, infection of the kidneys
what is a lower urinary tract infection?
urethreitis: infection of the urethra.
Cystitis: infection of the bladder.
inflammatory disorders of the Urinary tract….
Glomerulonephritis: inflammation of the glomerulus in the kidneys
Nephrotic syndrome: increased permeability of the glomerulus usually secondary to diabetes.
pathogenesis for a UTI
1) colonization: bacteria colonize at the periurethra, which allows for bacterial acension up the urethra
2) Uroepithelium penetration:
bacterial fimbrae allow for the attachemet & penetration of the bladder ny way of epithelial cells
3) acencsion: bacterial colonize and ascend through ureters.
4) pyelonephritits: renal parenchyma infected
5) AKI: continued inflammatory response—>interstitial edema
Risk factors for UTIS
women(close proximity of vagina to anus), elderly, incontinent people, ppl w/ catheres, pregnant women, diabetics, immunocompromised, infants.
clinical manifestations of a UTI…
pain when peeing, dysuria (difficult), +urgency, +frequency, nocturia, pee w/ odor and cloudy, pyuria, hematuria, +WBC
process of UTI infection:
starts at the urethra then ascends to the bladder—>ureters—>kidneys
*if peeing well the infection usally does not spread
- physical barriers as well has chemical barriers (ph-) segregate infection from spreading.
patho of pyelonephritits
similar manifestation to UTI, starts unilaterally–>bilateral, the pelvis & calaxes in the kidneys fill with purulent exudate which + the pressure on the ureters obstructing the flow of urine—>AKF
Manifestation of pylonephritis:
- flank pain radiating to the groin, tutbular cells casts in urine, both chronic and acute infections can create scar tissue in cortex, impairs kidney functions
inflammation:glomerunephritis etiology & Patho:
secondary to streptococcal infection (APSGN)
patho: type 3 hypersensitivity response that creates antibodies against bacterial antigens which enter the blood and eventually the kidneys.
APSGN process
1) injury phase: AgAB complex draws tot he complex, which damages the membrane and promotes inflammation
2) proliferative phase: WBC infiltrate, pores get larger allowing bc and proteins to filtrate in urine due to damaged endothelium/BC
3) regenerative phase:
overgrowth of the podocytes impair filtration—>AKf
Patho od APGSN
-strep causes the antibodies to form—> antigen antibodies deposit in the glomerus (inflammation, increased cap permeability), cell proliferation continues to +permeability–>hematuria.Glomerulus swelling –>-GFR, stimulating RAAS to +BP &edema—> AKI/chronic glomerulonephritis
manifestation of glomerulonephritis:
- dark coffee ground urine, +Bp, flank pain, -Urine output, metabolic acidosis, ++edema, decreased urine function
tx: glucocorticoids, antihtn, antibiotics
nephrotic syndrome etiology
caused by; membraneous neuropathy, diabetes, amylodosis etc
- inflammation + permeability of glomerulus