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SMUSPG-PHY1 > UTI > Flashcards

UTI Flashcards

1
Q

IGA Nephropathy BERGER

A

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

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2
Q

Nephrotic Sydrome

A

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

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3
Q

Minmal Change DZ

A

Def- loss of podyctes 2-6y peak. Absence of GM microscopic damage

S/S- h/o URI, allergy, immune

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4
Q

Focal segmental sclerosis

A

Focal scarring, Idipathic

S/S- hyposxia, SCD, HIV, HTN, reduced renal FX

Risk- advance to ESRD

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5
Q

Glomerulonephritis Injury

A

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
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6
Q

Acute Cystiis. UTI

A

inoculation of e.coli, gram +. Asc to UT

S/s- irrative voiding, frequency, urgency, suprapubic discomforr

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7
Q

Prostatitis

A

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

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8
Q

Epididymitis

A

<40y CT/NG cause
>40y nonSTI cause relaed to UTI/Prostatic

S/S- sperm cord radiates to Flank. Fever, scortal swelling

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9
Q

Prostadynia

A

Sx of voiding dfx, and pelvic floor dysfunction w/o infect or inflam. Similar to prostattis

DX- Clean UA, urodynamic test

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10
Q

Interstitial cystis

A

Pain w/ bladder filling, relief with emptying. Not single disorder,
Some abnormal protein

Sx- dysuria and frequency,

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11
Q

BPH

A

obstructive, irratitive voiding
enlarged on DRE

S/s- no UTI, stricture, malignancy

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12
Q

Metabolic Acidosis

A

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.

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13
Q

Metabolic Alkalosis

A

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

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14
Q

Respiratory Alkalosis

A

Inc. pH^
Dec. CO2*
Dec. HCO3*
Dec.pO2

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15
Q

Respiratory Acidosis

A

Dec pH^
Inc. CO2*
Inc. HCO3*
dec.pO2

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16
Q

Normal Acid Balance

A

pH- 7.4
pCO2-40
HCO3-24
PO2- 90

17
Q

Respiratory Distress Syndrome

A 
RDS
dec. pH
inc. CO2
N-HCO3
dec. PO2
18
Q

Renal Failure

A

dec. pH
N- CO2
dec. HCO3
N- PO2

19
Q

Compensaton

A

None are perfect
None correct underlying problem
Pulmonary fast, but less efficient d/t dec drive as normal ph is approached

20
Q

Metabolic Acidosis Causes:

Extrinsic, INtrinsic, Other

A 
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

21
Q

Proximal tubule acidosiss

A

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

22
Q

Distal Renal Tubular Acidosis

A 
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

23
Q

Soda

A 
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
24
Q

Metobolic Alkalosis

A

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)

25
Q

Metibolic Alkalosis pathophys

A

Aldosterone- enhances NA/k pump, NA retained, K LOST AND H+ LOST, INC. DIURESIS, BUT HIGH SOLUTE CONCENTRAION

Thiazide diurects- block NA/CL cotransport in lumen membrane_DEC NA resorbtion (Less volume_Less filtraion__slow filtraion mean INC IN RESORBTION HCO3

CAI- prevent resorb of NAHCO3 by limiting counter transport of NA w/ H+ ion-promotes diuresis

DIRURESIS__INC H+ RELASE
THUS HIGH HCOR

26
Q

Vomiting

A

secretion of stomach acid

INc. risk of Metabolic alkalosis via inc HCO3 resorption

27
Q

Hyperaldosterone

A

Cushing Dz
inc. H+ secretion
Inc Na and HCO3 resorption (conserving solutes)
Loss of K+ inc. alkalosis

SMUSPG-PHY1 (15 decks)

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