renal - patho - Exam 2 Flashcards
pyelonephritis etiology
inflammation of the kidneys caused by infection ascending up the urinary tract or from a bloodstream infection
risk factors of pyelonephritis
pregnancy, recurrent lower UTIs, or develop a abx resistant strain
what is the most common pathogen of pyelonephritis
E.coli
chronic pyelonephritis can lead to what if severe enough
chronic kidney disease or sepsis
pyelonephritis characteristics of the kidney
swollen, abscesses can form and necrosis can develop which impairs renal function
clinical manifestations of pyelonephritis
sudden onset of fever, chills, CVA tenderness + lower UTI symptoms and possible hematuria (if systemic then also N/V & anorexia)
treatments for pyelonephritis
ABX -> bactrim (trimeth + sulfa), ciproflozacin, nitrofurantoin
bactrim
-class: sulfonamides
-inhibits bacterial growth by stopping synthesis of folic acid
-1st choice for UTIs
-sulfa allergies start w/ a fever then rash
-do not use during pregnancy
ciprofloxacin
-class: Fluoroquinolones
-alters bacterial DNA
-UTIs & STIs
-arthropathy (non reversible joint point) do not give <18 or >60
-do not use during pregnancy
complications of pyelonephritis
urosepsis -> more likely in elderly w/ high mortality rates
locations for urinary obstruction + most likely cause
-renal pelvis; renal calculi
-ureter; renal calculi, pregnancy, tumors
-bladder or urethra; bladder cancer, neurogenic bladder, prostate cancer, urethral strictures
what is the potential complication of urine stasis
infection
what does back up pressure cause
when the kidneys are still making urine but there is a blockage -> hydroureter, hydronephrosis, or postrenal acute kidney injury
hydronephrosis & hydroureter
enlarged areas d/t urine back up -> fix the blockage to treat
emergency & usually needs surgical intervention
what does manifestation of an obstruction depend on
-site
-cause
-speed of onset
which factor of obstruction determines severity of pain
speed of onset
what is nephrolithiasis
renal calculi / kidney stones
clumps of crystals in the urinary tract
nephrolithiasis pathogenesis
urine is a solution of solvent (water) and solutes (particles) -> w/ stones we get super saturation w/ a solute and we begin to form crystals in the nephron
what enhances formation of crystals
-pH changes (UTI)
-excessive concentration of insoluble salts in the urine (dehy, bone disease, gout, renal disase)
-urinary stasis (immobility)
nephrolithiasis risk factors (7)
-male
-ages 20-30s
-white
-family history
-congenital defect (kidneys or urinary sys)
-weather (hot)
-obesity
what are the 3 types of stones
1) calcium (oxalate or phosphate); 70-80%
2) struvite; 15%
3) uric acid: 7%
causes of/risks calcium stones (4)
family hx, idiopathic, increased calcemia, increased oxaluria
what diet is a risk factor for calcium stones
high Na
high oxalate (beets, strawberries, carrots, caffeine, chocolate, oats)
high protein
causes of/risks struvite stones
urinary tract infections
causes of/risks of uric acid stones
gout
clinical manifestations of nephrolithiasis (+describe pain felt)
pain / acute renal colic
- flank region that radiates to the lower abd & groin
- spasms, lasts 20-60 min
- intermittent
- sharp
+ N/v, dysuria, chills & fever w/ infection, hematuria, foul smelling urine, diaphoresis
what is the treatment goal of nephrolithiasis
treat pain
nephrolithiasis treatment
acute pain: morphine, NSAIDs, IV fluids
preventive meds for nephrolithiasis
-thiazide diuretics for calcium stones
-abx for struvite
-allopurinol for urate
urologic cancer
kidney cancer , rare
-renal cell carcinoma (85%)
-usually not caught before it metastasizes & if not caught in early stages 5 yr survival rate is <10%
renal cell carcinoma risk factors (5)
-smoking (#1 reason)
-obesity
-age
-male
-genetics hx
clinical manifestations of renal cell carcinoma
early: none
late: CVA tenderness, hematuria (cola colored), possible palpable abdominal mass
renal cell carcinoma signs of metastasis
usually will spread to bones or lungs so bone pain or dyspnea/difficult breathing
renal cell carcinoma treatment
resistant to chemo -> surgery to remove kidney
bladder cancer
-fourth most common cancer in med
-urothelial carcinoma (within bladder lining)
risk factors for bladder cancer (4)
-smoking (#1 cause)
-male
-occupations w/ exposure to toxins (rubber or paint factories)
-low fluid intake (toxins sit in low concentration of urine & sit longer)
bladder cancer clinical manifestations
early: hematuria
later: frequency, urgency, dysuria
bladder cancer treatment
chemo based on stages
- stage 1: intravesical chemo
- advanced stage: systemic chemo
glomerulonephritis
a variety of conditions that cause inflammation of glomeruli
-can be focal or diffuse
-3rd leading cause of kidney failure
-primarily an immune process
where does damage occur with glomerulonephritis
-glomerulus: a delicate network of arterioles within the bowman’s capsule (all blood goes through)
-Tubules
glomerular blood flow
there are 2 renal arteries -> an afferent artery that takes blood in and an efferent artery that return blood
pressure difference that helps push chemicals, toxins, ect out of the vessels to filter the blood and sends them to the urine
what organ takes up a large amount of the bodies cardiac output
the kidney
needs high enough BP to profuse the kidney and allow glomeruli to work
what cells help with the production of urine
podocytes
3 layers of the capillary membrane in the glomerulus
1) endothelium
2) basement membrane (most issues happen here)
3) podocytes
production of urine
starts by podocytes -> fluid travels the nephron -> particles are excreted and reabsorbed -> final concentration of urine
type 2 sensitivity rx
reactions occur on the cell surface and result in direct cell death or malfunction
type 3 sensitivity rx
immune complexes are deposited into tissues and the resulting inflammation destroys the tissue
etiology of glomerulonephritis
1) antibodies attach to antigens of the glomerular basement membrane (anti GBM antib’s) type 2 rx ~5%
2) antibodies react w/ circulating antigens and are deposited as immune complexes in the GBM type 3 rx ~90%
characteristics of acute glomerulonephritis
-abrupt onset
HARP
-hematuria
-azotemia (build up of waste products)
-retention (edema, oliguria, HTN)
-proteinuria
acute glomerulonephritis triggers
-post infections (strep)
-primary disease (berger disease)
-multisystem disease aka secondary (goodpasture syndrome, systemic lupus, vasculitis)
bergers disease
antibody IGA builds up in the kidney which causes inflammation within the glomerulus
goodpasture syndrome
a disorder where a person has anti GBM antibodies (the 5% cause) -> the glomerular basement membrane looks very similar to the basement membrane of the lungs so these pts present to the hospital w/ a hemoptysis bc the anti GBM are not only attacking the glomerular but also the lungs basement membrane causing the pts to cough up blood
resp & renal problems -> look for anti GBM antibodies
acute glomerulonephritis pathogenesis
trigger -> immune complexes form -> complement activated -> release of mediators -> tissue injury -> hematuria, proteinuria & decreased GFR
chronic glomerulonephritis
- long term inflammation of the glomerulus (scare tissue which cannot filter or produce urine effectively)
-presents like acute
-prognosis: slow then ESRD
nephrotic syndrome
the glomerulus is too permeable to plasma proteins which is measured by elimination of >3g of protein per day
do 24hr urine
nephrotic syndrome etiology
glomerulonephritis
DM
nephrotic syndrome pathogenesis
increased glomerular permeability -> proteinuria -> hypo albuminemia
specifically lose a lot of albumin
result of losing large amount of albumin w/ nephrotic syndrome
third spacing because fluid begins to shift
nephrotic syndrome clinical manifestations
-edema
-htn (kidneys want more volume so activate raas)
-liver problems (hyperlid, hypercoag, loss of antithrombin 3 & plasminogen)
why do we see liver problems w/ nephrotic syndrome
we are spilling protein and losing fluid so the liver will have increased lipid levels & some proteins lost include antithrombin 3 and plasminogen (precursor to plasmin which helps breakdown clots -> risks for PEs & DVTs
glomerulopathy
DM & HTN complications
glomerulopathy: DM comps
-major complication
-gross thickening of the GBM (so doesn’t filter particles & fluid as effectively) -> less urine & more toxin build up
-leads to ESRD
glomerulopathy: HTN comps
decreased renal perfusion -> sclerotic glomerular changes d/t increased pressure on the blood vessels
glomerulopathy manifestations
hematuria, oliguria (<400ml/d), fluid retention, increased BUN/Cr, proteinuria and low albumin
