Week 11 Flashcards

1
Q

Advantages of urinalysis

A

Non-invasive diagnosis
Easily obtained- feasible in local GP practice
Normal composition is mostly known
For pre renal or renal diseases
Changes in levels of what should be present including material that normally occurs only at low basal levels

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2
Q

Collection

A

Clean/sterile containers
+/- preservatives- may affect analysis
Random samples: clean catch midstream specimen timing of sampling depends on test required; test as soon as possible
24 hours specimen- empty bladder first

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3
Q

Volume in 24h

A

Depends on body size, diet and fluid intake
0.8-2.0l

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4
Q

General appearance

A

Pale yellow and clear. Urobilin
Concentrated urine (eg dehydration) ; dark
Red urine: blood
-blood- urethra (early), throughout (bladder), end (prostate)
Pseudohematuria: free Hb, myoglobin, porphyrins, drugs (laxatives, desferrioxamine, rifampicin, anti-inflammatories)
Red/brown: conjugated bilirubin
Black: melanin (disseminated melanoma)
Other hues: foods, drugs, supplements …
See if urine darkens on standing: eg alkaptonuria and porphyria

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5
Q

Microscopic examination

A

Centrifuge a mixed sample of urine. Examine sediment for:
-Bacteria: confirm dipstick tests for nitrate production; then culture to quantitate
-Cells: white cells—> kidney infection. Red—> damage
- Casts: eg hyaline (composed primarily of Tamm-Horsfall mucoprotein secreted by tubules) or fine granular
Normal finding esp. post exercise; appearance not proteinuria
1 red cell cast- always pathological
- crystals

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6
Q

Crystals

A

Oxalate crystals
Cystine
“Triple phosphate” NH4MgPO4.6H2O
Amorphous crystals

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7
Q

PH range 4.5-8

A

Acidic: much meat in diet. uncontrolled diabetes, starvation, respiratory discords can cause acidic. uric acid, cystine risk of stones.
Alkaline: citrus fruits and vegetables in diet. Urinary tract obstruction, some respiratory disorders, hyperventilation cause. Ca/MgPO4, CaCO3 risk of stones

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8
Q

Creatinine clearance as a GFR indicator

A

In muscles, phosphocreatine acts as a major energy reserve
1-2% muscle pool, spontaneous degradation to creatinine daily,~constant rate in good health. And glomerular filtration with minimal tubular reabsorption/secretion
Creatinine clearance CC is a commonly used fair GFR approximation in healthy subjects
CC is less useful when levels of excreted creatinine vary:
-increase. excessive meat diet
-decreased excretion. Wasting disease, malnutrition (or strict vegetarianism), Poor renal blood flow or function.

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9
Q

Two kinds of disorder cause abnormal solute excretion

A

Pre-renal: kidney function is normal
-overspill due to:
—increased solute filtration-> increased production in body
—abnormal metabolite (no suitable transporter)
-decreased solute filtration:
—decreased production in body
—decreased delivery (cardiac failure, haemorrhage, burns)

Renal: kidney is abnormal
-Glomerular malfunction:
—infection, autoimmune disease, inflammation. Leakage (proteins)
-tubular malfunction:
—infection, autoimmune disease, inflammation, necrosis, drugs, toxins
—defective reabsorption eg glucose
—defective secretion eg H+

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10
Q

Changed output of Urea

A

Urea: non toxic end product of nitrogen metabolism
Factors increasing excretion:
-Excess protein intake- surplus excreted
-factors that trigger greater protein catabolism:
—protein energy malnutrition
—uncontrolled Type I diabetes
—infections, burns, wasting disease, trauma including surgery or a broken limb/GI bleeding
Factors decreasing urea excretion:
-low protein diet, severe liver disease/genetic defects
-glomerular nephritis, acute tubular necrosis
-poor renal blood supply or renal obstruction-stones , tumour
Outcomes:
-hyperammonaemia, NH4+ crosses BBB
—lethargy, irritability, finally coma

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11
Q

Urinary excretion of materials normally in very low amounts or “absent”

A

Glucose:
-reagent strip (glucose oxidase)
-excrete <0.2% of the glucose normally
-filtered by the glomerulus (0.03-0.g/d)

-metabolic hyperglycaemia (normal renal threshold). Diabetes mellitus type I; anxiety or stress
Phaeochromocytoma (and adrenaline)
-reduced renal threshold
Pregnancy or renal glycosuria (genetic)
-Tubular malfunction
Generalised tubular dysfunction- secondary to other damage, Fanconi syndrome

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12
Q

Other sugars abnormally excreted in urine

A

Galactose- galactosemia (spill over of Gal 1-P) positive test for reducing substances
Lactose- lactation; primary lactase deficiency; coeliac disease
Fructose- fructose intolerance, essential fructosuria
Pentoses- essential pentosuria

Ketones: uncontrolled diabetes type I, starvation

Amino acidurias: generalised tubular damage, specific transporter defects (cystinuria, Hartnup’s disease), raised plasma amino acids (PKU, cystinosis)

Conjugated bilirubin: eg liver damage/obstructed bile ducts

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13
Q

Phaeochromocytoma

A

Prerenal disorder
-increased end product (overspill) excretion
-secreting adrenal medulla tumour
-occasionally ectopic
-excessive secretion of adrenaline causes:
—hypertension, headaches, sweating, anxiety, palpitations, tachycardia, anorexia, hyperglycaemia, high plasma FFAs
Diagnosed by excessive adrenaline breakdown products in urine metadrenaline and VMA (vanillyl mandelic acid)
-therapy by surgery (adrenal)
—blockers (phenoxybenzamine, propanolol)

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14
Q

Proteinuria

A

Glomerular basement membrane restricts protein entry to glomerulus
Both size and charge selectivity normally allow passage of small proteins
Plasma content: 35000mg/l; glom.filtrate ~30mg/l … 0.1% filtered
Normal excretion <200mg/24h

Proteinuria> 200mg/24h of proteins. 3.5g/24h is severe in nephrotic syndrome
Single most sensitive indicator of renal disease

Also orthostatic proteinuria:
-usually a benign condition affecting children and young adults
-protein is not detectable in morning on voiding immediately after rising
-proteinuria develops only after subject has been standing upright
-insignificant if proteinuria is detected only in some of the urine samples passed when subject is out and about

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15
Q

Mechanisms of proteinuria

A

Prerenal problem: overflow: due to presence in plasma of a high concentration of a low molecular weight protein which is filtered in a quantity exceeding tubular reabsorptive capacity eg Bence Jones protein
Renal problem:
-glomerular: due to increased glomerular permeability eg albumin
-tubular- due to impaired or saturated reabsorption of protein filtered by normal glomeruli eg B2-microglobulin
-secreted- due to secretion by kidneys or epithelium of urinary tract eg Tamm-horsfall protein

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16
Q

Protein size discriminates between pre-renal vs renal problem

A

Low Mr—> kidney is typically normal eg myoglobin
Medium- high Mr—> damaged kidney eg albumin

17
Q

Phenylketonuria PKU

A

Prerenal disorder
Results in excretion of phenylpyruvate
-Phe —> protein synthesis; converted by the Phe hydroxylase to tyrosine
Genetic deficiency of the Phe hyroxylase results in classical PKU
Relatively common in Britain- homozygotes 1:10000
Early symptoms: irritability, fits
Later: mental retardation, observable after 4-6months
- Phe hydroxylase deficiency —> accumulation of hydrophobic Phe which adversely affects the brain
-build up of transamination byproducts: Phe pyruvate, Phe acetate
-Phe acetate overspills into urine: “mousey” urine
-diagnosis includes urinalysis for phenylketones
-early diagnosis is vital to minimise neurological damage
—strict dietary management

18
Q

Continence

A

Somatic system active
Keeps striated sphincter contracted
Sympathetic system active
Constricts smooth muscle sphincters
Keeps storage element relaxed
Parasympathetic system inactive

19
Q

Voiding

A

Somatic system and sympathetic systems switched off
Sphincters relax
Parasympathetic system activated storage element wall contracts