Urine Flashcards
Normally, urine OSM > plasma OSM, why? (2)
What would you think if urine OSM = 280? (1) How about < 280? (1)
Kidney functions to concentrate filtrate to form urine.
Ascending limb is permeable to salt, but not permeable to H2O & urea. Descending limb is the reverse. Therefore, salt diffuses out through the ascending limb to create a hypertonic interstitium, which then forces H2O osmosis through the descending limb.
urine OSM = 280 = plasma OSM, it is called isosthenuria. It implies lost of renal tubule function & urine is generated by passive diffusion.
urine OSM < 280, consider DI (lack of ADH)
State conditions that leads to low EABV. (3)
Explain regulation of EABV by RAA axis & ADH. (9) How about baroreceptor? (2)
Heart Failure, Renal Failure & Nephrotic syndrome
1.Low EABV stimulate juxtaglomerular cells at afferent arterioles to release renin
2.Angiotensinogen from liver is converted to A1 by renin
3.A1 is converted to A2 by Lung ACE
4.A2 stimulate adrenal cortex to release ALDO
#A2 also causes arterial vasoconstriction
5.ALDO stimulates collecting duct to reabsorb NA secrete K
6.reabsorption of NA increases plasma OSM
7.High plasma OSM stimulates posterior pituitary to release ADH
8.ADH stimulates collecting duct to increase H2O permeability
#V2 receptor, aquaporin acting
9.H2O retention results in increased EABV
baroreceptor at the neck (carotid sinus) sense blood pressure. When bp is high, ADH is released & sympathetic nerve to heart is triggered. When bp is low, ADH is not released & parasympathetic nerve to heart is triggered.
What is Porphyria? (1)
State the two main type of Inherited Porphyria (2) What are the main clinical presentations? (2) How can you diagnose them? (2)
How about acquired porphyria? (2)
Porphyria is the accumulation of heme precursor. (1)
Inherited Porphyria can be neuropsychiatric (AIP[PBGD]) or cutaneous (PCT[UROD])
AIP: Bipolar with muscle weakness, high urine PBG
PCT: Skin photosensitivity, high urine UR
Acquired Porphyria can be Pb poisoning, Liver failure, Drug toxicity.
Lead poisoning causes Ferrochelatase inhibition, patient has high urine PBG and sideroblastic anaemia with basophilic stippling.
When is diuretic used? (4) What are the 4 types of diuretic? (4)
Treat patient with fluid overload, including HF, CKD, Edema & Hypertension.
Loop diuretic (mide): inhibit NA reabsorption (PCT,DCT, loop of Henle)
Thiazide diuretic: inhibit NA reabsorption (Early DCT, Ascending loop), increase UA reabsorption (PCT)
K-sparing (spironolactone): ALDO inhibitor
Osmotic (Mannitol): given IV, For cerebral edema & high IOP
Suggest a screening test for PBG. (2)
Watson–Schwartz test
Colour developed with Ehrlich reagent not removed by chloroform
delayed urine sample has higher pH, why? (2) If urine pH>7.5, what would you consider? (1)
After a meat diet, urine pH drops, why? (1) Is it possible for urine pH<4.5? (1)
pH increase due to AMM production & loss of volatile acids
urine pH>7.5 consider renal compensation for respiratory alkalosis
purine in meat metabolized to UA which is excreted through urine, making urine acidic. urine pH<4.5 exceeds the tubular maximum for H+ secretion, so it is not physiologically possible.
Why patient with RTA has NAGMA? (1) Suggest a test that makes you suspect RTA. (1) Describe types of RTA & how they are related to urine pH. (3)
RTA is the loss of HCO3 which is compensated by CL increase, meaning acidosis with anion gap unchanged (NAGMA).
Suspect RTA when high CL with low HCO3 in the absence of diarrhea.
Proximal RTA (Type2): HCO3 reabsorption defect
Distal RTA (Type1): Impaired H+ excretion, most severe
HyperK RTA (Type4): ALDO resistance leading to Impaired H+ excretion
In Type1 RTA, urine pH>5.5 even with severe acidosis
In Type2 & Type4 RTA, urine pH<5.5 in severe acidosis as H+ excretion is still functionable.
In Type4 RTA, K is high as ALDO action is defective
What is the difference between SG & OSM? (1)
Colloids affects SG but not OSM
State principles of all tests on urine dipstick. (9)
Protein: tetrabromophenol blue
ALB: bis-tetrabromosulfonephthalein + CRE-Cu complex peroxide oxidation for CRE
Glucose: GO/H2O2
Ketone: Sodium nitroprusside detecting Acetoacetic acid (AAA)
Hb & Myoglobin: peroxide, and tetramethylbenzidine
Bilirubin: Diazo
urobilinogen: Ehrlich’s aldehyde reagent
nitrite: benzoquinoline
leukocyte: Leukocyte esterase hydrolysis of an ester called indoxylcarbonic acid +diazo = purple
What should be aware of when interpreting urine dipstick result? (8)
Protein:
Alkaline urine causes FP
Globulin (Bence–Jones[MM], Β-microglobulin[PCT]) not detected
Glucose:
Glucose renal threshold is >10 plasma Glucose.
Urine Glucose + when plasma Glucose <10 occurs in pregnancy because high Estrogen can lower the renal threshold
Ketone:
plasma BHB is still necessary as ketone at mostly in BHB form in acidosis, which is not detected by dipstick (AAA & Acetone only)
Hb & Myoglobin:
The two can be separated by ammonium sulphate / column.
Trace corresponds to >3 RBCs/HPF, Hb- RBC+ is a discrepancy
Bilirubin:
Ascorbate FN
urobilinogen:
- = obstructive jaundice
+ = extravascular Hemolysis
Nitrite:
Acidic urine causes FN
70% UTI
Leucocyte:
Trace corresponds to >10 WBC/HPF
TP FN
Patient 24U for CrCl has volume <400mL, give 2 reasons why this happens. (2) Why drinking water is important for this test? (1) State the formula to calculate CrCl. (1) Why do 24U CrCl when eGFR based on plasma CRE is available? (2)
Inappropriate collection procedure
Insufficient hydration before and during the collection period.
dehydration reduces filtration volume, which stimulate CRE secretion to filtrate, increasing urine CRE concentration.
CrCl = U ÷ P × V × 1.73/A
24h CrCl detect a drop of GFR faster than eGFR. It is also useful for patient with extreme muscle mass / accessing renal toxicity of drugs
Why URE/CRE ratio can be used to differentiate pre-renal from renal failure? (2)
Normally, Plasma URE > CRE because 40% URE is reabsorbed
It becomes 70% in pre-renal failure due to reduced flow rate, increasing the URE/CRE ratio.
Name 6 types of renal stone. (6)
CA oxalate
CA PHOS/Carbonate
AMP (Ammonium Magnesium Phosphate)
UA
Cystine
