UTI Flashcards
(27 cards)
IGA Nephropathy BERGER
IgA complex deposition causing glomerulonephritis
IgA-Mucus in GI. Deposit lead to inflammation
Pop.- young adults, M
S/S- gross hematuria (bright red), URI, ILI, GI sx
TX- NONE. Resolves on own
Nephrotic Sydrome
Inc protein spilling/permeable w/in Glomerolus
Lipids, protein-normally too large, but cells open to filtrate, tubules keep in side lumen, excreted
Albumin- small gets resorbed, but gets filtered, not resorbed to blood, out in urine. Most abundant
RISK of infxn, d/t antibodies spilled/proteins
POP- kids (prime), adults (2nd to dz)
S/S- proteinuria, lipiduria, hypoalbuminenmia, edema hyperlipidemia. Mineral, protein, electroyte defincines
Salt/water rention
Minmal Change DZ
Def- loss of podyctes 2-6y peak. Absence of GM microscopic damage
S/S- h/o URI, allergy, immune
Focal segmental sclerosis
Focal scarring, Idipathic
S/S- hyposxia, SCD, HIV, HTN, reduced renal FX
Risk- advance to ESRD
Glomerulonephritis Injury
gm or renal tube-MC cause of renal failure in US.
SLE, DM
Antibody or complex sticks to membrane. Or overreact
Complement deposit w AB, which activates inflam
Alters permeability, membrane normally neg charge, turn positive charges on membrane.
Proteins and RBC pass freely into tubule bc of neg. charge themself
Immune system attacks d/t trigge
Scarring reduces GFR- filtration dependent on BF
forms less filtrate, dec urine
Findings RBC cast- membrane changed to neg charged Dec GFR-inc BUN Dec Urine HTN
Acute Cystiis. UTI
inoculation of e.coli, gram +. Asc to UT
S/s- irrative voiding, frequency, urgency, suprapubic discomforr
Prostatitis
Gram - rods (e.coli), pseudos, occ enterocci
Infected urine into prostate
S/S- fever, perineal pain, obstrutive sx. ASX for awhile
PE- no acute findings
UA- normal, INc Leukocytes
Epididymitis
<40y CT/NG cause
>40y nonSTI cause relaed to UTI/Prostatic
S/S- sperm cord radiates to Flank. Fever, scortal swelling
Prostadynia
Sx of voiding dfx, and pelvic floor dysfunction w/o infect or inflam. Similar to prostattis
DX- Clean UA, urodynamic test
Interstitial cystis
Pain w/ bladder filling, relief with emptying. Not single disorder,
Some abnormal protein
Sx- dysuria and frequency,
BPH
obstructive, irratitive voiding
enlarged on DRE
S/s- no UTI, stricture, malignancy
Metabolic Acidosis
Dec pH^
Dec. CO2*
Dec. HCO3*
N-pO2
Deficit in HCO3
S/S- inc. RR, RF- BUN/CR inc. growth stop, anorexia, wt. loss, weak, lack of enthusiasm
Correction
Inc. ventilation, blow off CO2. limit the bicarb reacton to dissocaiton.
Metabolic Alkalosis
Inc. pH^
Inc. CO2*
Inc. HCO3* >29
N-PO2
S/S- ASX or volume depletion (vomiting or Na loss)or hypokalemia
Neuro sx, HYPOventaliion (inc CO2 correct w/ more acide)
Sever- RDS, CV, Seizures, coma
Respiratory Alkalosis
Inc. pH^
Dec. CO2*
Dec. HCO3*
Dec.pO2
Respiratory Acidosis
Dec pH^
Inc. CO2*
Inc. HCO3*
dec.pO2
Normal Acid Balance
pH- 7.4
pCO2-40
HCO3-24
PO2- 90
Respiratory Distress Syndrome
RDS dec. pH inc. CO2 N-HCO3 dec. PO2
Renal Failure
dec. pH
N- CO2
dec. HCO3
N- PO2
Compensaton
None are perfect
None correct underlying problem
Pulmonary fast, but less efficient d/t dec drive as normal ph is approached
Metabolic Acidosis Causes:
Extrinsic, INtrinsic, Other
Causes: Extrinsic DKA- inc nonvolatile extrinsic Excessive HCO3 loss diarrhea (kidney cant replace fast as colon secretes. Stomach inc. acid Inc. Chloride love H+
Intrinsic-dec. acid (H+) secretion by kidney (CKD)
Renal Tubular Acidoiss-effects resorb of bicarb, and excretion of H+
Other
Lactic acidosis- MSK, exercise, sepsis, seizures
Ketoacidosis
Ingesiton- asprin l/t Res. Akl, then Kidney sercrete bicarb, K, Na l/t Met Acidoisis
Methaonl, ethlene glycol-antifreeze
Inc. loss of HCOR-impaired conservation
Hypercholremic-abnormal absorbion by kidney or meds
Proximal tubule acidosiss
Chronic metabolic acidosis
Resorbing defect
Loss of bicarb reduces serum levels
Loss of Na- changes filtration rate due to dec. vol.
1.l/t dec BV__Aldosteroine (inc. NA/K pump) secretion___K+loss__
Distal site function ok
Acidemia- growth slows down, FANCONI
Distal Renal Tubular Acidosis
Chronic metabolic acidosis CLINCAL- Hypokalemia, hyperchloremic metabolic acidosis, defect in acidification of urine nephrocalcinosis, nephrolithiasis with osteomalacia rickets
failure of acid secretion to acidify urine
Failure to secrete acid=loss of Sodium bicarbonate
Fluid volume is reduced, aldosterone is released causing hypokalemia
Acidosis leads to loss of calcium from bone resulting in release of PTH (secondary hyperparathyroidism), osteomalacia, bone pain, impaired growth in children, stones.
Seconday HPTH– Dialysis pt get bone loss
Soda
phosphate is a preservative PH loves calcium, soak all CA Stimulate release of CA via PTH to fix the loss Resorbs/breaks down true bone Viscous cirlce
Metobolic Alkalosis
1 MC excess alkali is CAcarbonate used a buffer if dialysis pt.s= low potassium from diuretics
2nd MC acid-base dx in Hospital Pts
loss of H+, CL
Gain of HCO3- Kidney generates or resorbs more from fitrate
PCT 99%, (but some release in urine)
