Kidney and Liver Function Tests Flashcards
1
Q
Functions of the urinary system
A
- excretion and elimination (removal of organic waste products from body fluids such as urea, creatinine and uric acid: terminal prods of metabolism)
- homeostatic regulation (water, electrolyte, acid-base balance)
- endocrine function (kidney hormone production)
2
Q
What are some hormones produced by kidneys
A
- renin
- erythropoietin
- 1,25-dihydroxy vitamin D3
- Prostaglandins
3
Q
Main function of kidney (multifunctional)
A
storage of liquids by concentration of urine
4
Q
Urine excreted daily in adults is
A
about 1.5 L (kidney is only 1% of total body weight)
5
Q
Renal blood flow accounts for what % of cardiac output
A
20%
plasma renal flow: 600 ml/min/1.73 meter squared
6
Q
Two processes involved in renal blood flow
A
ultrafiltration (GFR): 180 L/day
Reabsorption (>99% of amount filtered gets reabsorbed)
7
Q
functional units of kidney
A
nephrons
(600,000-1.5 million)
*decrease in functioning nephrons =impaired kidney function
8
Q
number of nephrons an individual is born with which may determine that individual’s susceptibility to renal injury
A
nephron dose
9
Q
Parts of the nephron
A
- Glomerulus
- Distal tubule
- Proximal tubule
- Collecting duct
- Loop of Henle
10
Q
What is formed when collecting ducts ultimately combine? This is where urine collects before passing along the ureter and into the bladder
A
renal calyces
11
Q
Where does transport of solutes and water occur?
A
across and between the epithelial cells that line the renal tubules
12
Q
Kinds of transport observed in nephrons
A
active and passive
*many passive transport are dependent upon active ie sodium transport
13
Q
mediator of filtration which is formed from a specialized capillary network (capillary endothelial cells are ~40 nm thick)
A
glomerulus
14
Q
Purpose of circular fenestrations/pores with diameters of ~60 nmn in glomerulus endothelium
A
Permits virtually free access of plasma solutes to the basement membrane
15
Q
What is the renal threshold for glucose?
A
180 mg/dL
16
Q
What is renal threshold?
A
Blood concentration of a substance that when surpassed, is excreted in urine
17
Q
[Renal threshold]
What is tubular maximum?
A
maximum capacity of the kidneys to absorb a particular substance
*Tm for Glucose = 350 mg/min
18
Q
What is the pre-renal cause of kidney functional disorder?
A
pre-renal: decreased intravascular volume
19
Q
What is the renal cause of kidney functional disorder?
A
acute tubular necrosis
20
Q
What is the post-renal cause of kidney functional disorder?
A
ureteral obstruction
21
Q
What are the terminal products of hemoglobin catabolism?
A
bilirubin
urobilin
22
Q
Hormone metabolites excreted from bloodstream
A
cortisol
testosterone
*other substances: organic acid, drugs, food additives
23
Q
Other mechanisms of excretory function of kidneys
A
- Regulation of blood pressure, circulating volume, and water balance by urine concentration
- Regulation of electrolytes by excretion and resorption
- Maintenance of blood pH in a physiological range by eliminating radical acids, reabsorbing and forming bases
24
Q
[Homeostatic regulation]
What hormone regulates maintenance of water balance
A
antidiuretic hormone
25
[Homeostatic regulation] ADH in maintenance of water balance responds primarily to changes in?
osmolality and intravascular volume
| secreted from posterior pituitary
26
[Homeostatic regulation] What happens when ADH increases permeability of DCT and collecting ducts of water?
Results in increased water reabsorption and excretion of more concentrated urine
27
[Homeostatic regulation] What do the renal tubules do in states of dehydration?
reabsorb water at their maximal rate resulting in production of a small amount of maximally concentrated urine
28
[Homeostatic regulation]
| When do renal tubules reabsorb water at only a minimal rate?
in states of water excess resulting in excretion of large volume of extremely dilute urine
29
hormonal factors affecting regulation of electrolyte concentration
*together with neurogenic stimuli
```
ADH (through detection of osmotic and mechanical stimuli)
Aldosterone
Natriuretic peptides (sodium urinary removal requires h2o removal)
```
30
How does aldosterone affect electrolyte concentration?
| *triggered by decreased blood flow or blood pressure in renal arteriole and decreased plasma sodium
sodium reabsorption and excretion of potassium and hydrogen
31
[homeostatic regulation: electrolyte concentration]
| Thirst sensation causes
osmolality variation by 2%
* increase in thirst = HYPERtonic ECF = lower ICF
* decrease in thirst = HYPOtonic ECF = higher ICF
32
[homeostatic regulation]
| two mechanisms performed by kidney in maintaining blood pH
tubular reabsorption of filter HCO3
| removal of H+ ions produced daily
33
Urinary pH
4.5-5.0 (0.04 mol/L)
34
[homeostatic regulation: maintenance of blood pH] 99% of H+ ions are discarded by
urinary buffer
| [H2PO4 > H+ + HPO42-]
35
Other homeostatic roles of kidneys
4. Government of calcium phosphorus metabolism by secretion and reabsorbing.
5. Regulation of the production of red blood cells.
36
The secretory function of kidneys involve hormones such as
* erythropoietin (regulates RBC prod in BM);
* renin (regulates BP; key part of renin-angiotensin-aldosterone system);
* calcitriol (for calcium reabsorption and bone mineralization; active form of vit. D);
* prostaglandins (PGE1, PGE2, thromboxane)
37
Major renal functions which together, regulate and maintain constant optimal composition of the blood and intracellular fluids
® Glomerular filtration
® Tubular reabsorption (peritubular capillaries)
® Tubular secretion
UE= filtration - reabsorption + secretion
38
[Secretory function]
| Each nephron produces this amount of ultrafiltrate per day
100 μL
*170-200L of ultrafiltrate passes through glomeruli daily
39
[Secretory function] What determines the initial mass on which the nephron must operate to produce and excrete urine?
Bulk transfer of substances from blood to glomerular filtrate
40
Laboratory tests and renal functionality studies
```
• urinary index
• Serum creatinine and creatinine clearance
Estimated GFR (eGFR)
• Proteinuria and diagnosis
• Cistatin C detection
• Electrolytes
• Laboratory and AKI evaluation
```
41
In urine tests*, small, randomly collected urine samples is examined through its:
* Physical: color, odor, appearance, and concentration specific gravity
* Chemical: protein, glucose, and pH
* Microscopic: Cellular elements (RBCs, WBCs, and epithelial cells), Bacteria, Crystals, Casts (structures formed by the deposit of protein, cells, and other substances in the kidneys' tubules)
42
[Urine tests] Additional test for water balance in ECF and plasma
Volume
43
[Urine tests] Additional test for solute regulation (sodium, glucose, urea)
specific gravity and osmolality
44
[Urine tests] Additional test for blood acidity/ alkalinity balance
pH
45
[Urine tests] Creatinine is used to asses what?
glomerular filtration capacity
46
[Urine tests] Solute clearance is used to assess what?
glomerular filtration RATE
47
[Urine tests] These tests are used to assess filtration and/or reabsorption
urine proteins
| urine albumin
48
[Urine tests] test for presence of RBC
hematuria
49
presence of cystatin C in plasma indicates
presence of bence-jones in urine ????
50
[Urine tests]
| Urine 24 hours volume is useful in evaluating
glomerular filtration and tubular functionality
*normal adult range = 800-2000ml/day (normal fluid intake = 2L/day)
51
Adequate homeostasis is maintained with a urine output of
400-2000ml/day
52
Reduced urine volume is caused by
dehydration
not enough fluid intake
some types of chronic kidney disease
53
increased urine volume is caused by
diabetes
high fluid intake
some forms of kidney disease
use of diuretic medications
54
[Abnormal results in urine tests] Anuria or no passage of urine or production of <100 ml per day is often caused by
• Total obstruction of urinary tract
- E.g. prostatic hyperplasia and tumors
• Heart failure or severe hypotension
- E.g. renal ischemia (acute tubular necrosis)
• Glomerular nephritis (acute, subacute, chronic)
• Hemolytic reaction caused by blood transfusion
55
[Abnormal results in urine tests] Oliguria or low output of urine may be due to
no water intake, Prolonged vomit, diarrhea, sweating, ascites, aedema, hypoperfusion, AKI (acute kidney injury), uremic terminal phase of CKD (chronic kidney disease), glomerulonephritis (Diabetic Ketoacidosis, Kidney tubular necrosis- CRI)
56
[Abnormal results in urine tests] Polyuria with increased azotemia (BUN) and creatinine is due to:
* Diabetic ketoacidosis
| * Kidney tubular necrosis (chronic renal insufficiency)
57
[Abnormal results in urine tests] Polyuria with normal azotemia (BUN) and creatinine is due to:
* Polydipsia
* Extreme protein uptake
* Caffeine and alcohol
* Diuretic medication
* Diabetes mellitus e insipidus
* Deficit Anti-Diuretic Hormone (ADH; vasopressin)
58
T or f: Urea is freely filtered from glomerulus and reabsorbed in a variable manner by proximal tubules
true
*not useful GFR marker; good for detection of tissue lesions and cellular damaging (burns) and monitoring renal functionality
59
T or F: urea increases earlier than creatinine and decreases quickly
true
*high values in acute renal insufficiency and terminal stage of chronic renal insufficiency
60
Why is there an increase in serum BUn in azotemia (20-40 mg/dL of BUN)
Kidney is not able to discard nitrogen metabolism's degradation products
61
Pre-renal uremia is usually caused by
outside kidney (upstream of glomerular filtration) such as reduced renal perfusion (shock, dehydration, hemorrhage) and increased protein catabolism (alimentary canal bleeding, burns and fever)
62
Post-renal uremia is usually caused by
consequence of urinary tract obstruction; ureter; bladder and urethra
63
Uremia caused by injury to glomerulus, affecting either renal microcirculation or renal tubules
intra-renal uremia
*also by: Acute or chronic diseases: glomerular nephritis, malignant hypertension, cortical necrosis, drugs or metal nephrotoxicity, pyelonephritis, diabetes mellitus, tubulopathy
64
Compares the density of urine (number and size of particles dissolved) to the density of water (SG=1000)
Urine specific gravity tests
65
usual reference values for adult and child in urine specific gravity tests
adults (1005-1020)
| child (1001-1018)
66
methods of urine specific gravity tests
densimeter, dipsticks (colorimetric reaction), referactometer
67
urine concentration index (urine to plasma ratio of creatinine concentration) is determined by
urea
sodium chloride
sulfates
phosphates
68
When SG is <1005
hyposthenuria
69
Increased urine volume in hyposthenuria is due to
* Insufficiency or absence of ADH
* Pyelonephritis (may progress to chronic kidney disease)
* Diabetes insipidus
*decreased urine volume: glomerulonephritis
70
Hypersthenuria or SG > 1020 is due to
* Diabetes mellitus (increased urine volume)
* Nephrosis
* ADH increases (decreased urine volume)
* Heart diseases
* Toxemia during pregnancy
* Dehydration
71
Dynamic tests
Glomerular filtration rate
| [CKD-EPI (for screening; higher precision)], renal clearance, Creatinine
72
[Dynamic tests] When is GFR* equal to the clearance rate?
*volume per time; best index in both patients and healthy subjects
when any solute is freely filtered and is neither reabsorbed nor secreted by the kidneys
(urine concentrationxurine flow/plasma concentration)
73
e-GFR: the MDRD simplified equation
e-GFR = 175 × SCr
| ^ -1.154 × Age^-0.203 × 1.212(if black) × 0.742(if female)
74
Indirect method of GFR assessment
Estimation by anthropometric, anthropological,
and biochemical parameters
*simple and advantageous; questionable accuracy
75
Direct method/clearance study of GFR measures
```
exogenous substances (inulin, iohexol, iotamatus, Cr51-EDA)
endogenous substances (creatinine)
```
76
Advantages and disadvantages of direct method
accurate, expensive, long-lasting and inapplicable for screening (exo)
blood and urine samples are necessary and careful and timed urine collection is required (endo)
77
GFR level classified as normal in CKD-EPI test
>60ml/min/1.73m
*see eqn in trans
78
• Renal Damage Severity Assessment based on GFR
*same values for KDQI
* Normal Kidney function: GFR >90 mL/min/1.73m2 haematuria and proteinuria detected
* Mildly reduced: GFR 60–89 mL/min/1.73m2
* Moderately reduced: GFR 30–59 mL/min/1.73m2
* Severely reduced: GFR 15–29 mL/min/1.73m2
* Very severe or end stage kidney failure: GFR absent (requires dialysis)
79
CKD stages or renal disease staging is based on
measured or estimated GFR
80
amount of liquid filtered out of the blood that gets processed by the kidneys or the amount of blood cleaned per
time typically recorded in units of volume per time
(renal) clearance
* Urine concentration x collected urine volume / ([plasma creatinine] x time taken to collect urine specimen in minutes)
* ideal marker of clearance
81
Why is renal clearance considered ideal marker?
® Endogenous and constant bio-synthesis
® Metabolically quiescent in vivo and in vitro
® Diffusible in the extracellular space
® Freely filtered by glomerulus
® Not reabsorbed nor synthesized by tubular cells
® Detectable with accurate and sensitive simple methods
® Advantageous cost/ benefit relation
® Simply used in clinical practice
82
interval refence values for males and females for creatinine*
*more accurate marker of kidney function than urea
® Male: 0.6–1.3 mg/dL
| ® Female: 0.5–1.0 mg/dL
83
T or F: Kidney discards creatinine with a low efficiency
false, great
84
T or F: creatinine binds proteins and is water-soluble
false, does not bind protein, water-soluble
85
methods of analysis of creatinine
jaffe method, enzymatic method, reference methods (gas chrom, mass spectro and HPLC)
86
What can interfere in jaffe method?
Proteins, bilirubin, uric, and pyruvic acids and some drugs
87
Restrictions of Creatinine Detection
• Not an early marker of renal functionality loss
• Increase is not related to severity of damage
• Not sensitive enough to little but significant glomerular filtration
rate reduction
• High inter-individual variability: muscle mass, sex, ethnicity, age
88
[Proteinuria]
| Factors which facilitate filtration
• Semipermeable glomerular basement membrane, which has a molecular weight cutoff of < 70kDa
(Water, electrolytes, glucose, amino acids, low-molecularweight
proteins, urea, and creatinine, pass freely through the basement membrane and enter the PCT)
*Other blood constituents, such as albumin, many plasma proteins, cellular elements, and protein-bound substances such as lipids and bilirubin are too large to be filtered
• Molecular configuration
• Negatively charged basement membrane which repels neg molecules such as proteins
89
Proteinuria in renal diseases causes
plasmatic oncotic pressure reduction leading to edema
90
Protein loss from glomerular membranes/ Proteinuria is caused by:
*normal values: 50-150 mg per 24 hrs (adults)
* Electric charges alteration
| * Intracellular pores changing (ø 5-8 nm)
91
Physiological loss of protein
• Albuminuria: < 30 mg/24 h
• On-the-spot testing: <19 mg/L
(10-20% is represented by albuminuria)
• Glomerular damage: proteinuria >1gr/L about 70% is represented by albuminuria
92
Indicators and classification of renal proteinuria
• Selective glomerular proteinuria (glomerulonephritis): M.W. 60-80 KD (1-3 gr/24h)
• Non-selective glomerular proteinuria (nephrotic): M.W. > 100 KD (>3,5 gr/24 h) and Immunoglobulins
• Tubular Proteinuria: M.W. <50 KD (<2 gr/24 h)
• Diabetic nephropathy:
albuminuria >1 gr/24h
93
Type of protein involved in selective glomerular protenuria
albumin and transferrin
94
Type of protein involved in nephrotic proteinuria
albumin
transferrin
immunoglobulins
95
Type of protein involved in tubular proteinuria
Retinol Binding Protein
α1-microglobulin
β2-microglobulin
96
diabetic proteinuria
albumin type of protein present
97
laboratory request for proteinuria serves as
basal investigation (urine total proteins for monitoring of CRI and urine albumin wc is more sensitive and accurate)
98
lab request for proteinuria also serves as differential diagnosis of
tubular or glomerular proteinuria (useful in detecting β2-microglobulin and cystatin C)
99
A specific increase in β2-microglobulin* and cystatin C means?
*need for excluding lymphocytes diseases; plasmatic detection required
proximal tubule reabsorption failure
100
Risk factors present/needed for performing proteinuria assay
* GFR <60/ml/min/1.73m2 (moderate stage)
* Diabetes
* Cardiovascular disorders: myocardial ischemia, chronic cardiac damages, peripheral and cerebral vascular insufficiency
* Stones, prostatic hypertrophy
* LES
* Opportunistic haematuria
101
Low molecular weight protein, it is synthesized by nuclear cells, released in the blood and freely filtered by glomerulus in urines
Plasmatic cistatin c
* not dependent from extrinsic factors
* interferences if increase in PCR, BMI, steroids, hypothyroidism
102
When is Plasmatic Cistatin C a better marker in predicting renal function than creatinine?
Chronic Renal insufficiency
103
Other names for neutrophil gelatinase-associated lipocalin
lipocalin-2 and oncogene 24p3 (human protein encoded by LCN2 gene)
*expressed by multiple human cells ie epithelial cells, neutrophils and organ systems
104
Role of lipocalin-2
- natural immunity protein with antibacterial properties
- may be involved in kidney development
- implicated in renal generation and repair after ischemic injury
- protective effect on kidney from ischemia-reperfusion injury
- effects link role in iron metabolism in growth and differentiation as well as prevention of cellular death
105
Major positive ions/cations in ECF are
Na+ > K+, Mg2+, Ca2+
106
most important negative ions (anions) are
Cl– and HCO3–
107
Electrolytes concentration in ECF and ICF can affect:
* Metabolic process
* Osmotic Status
* Hydration and pH
108
major cation in fluid outside of cells; with osmotic activity
sodium
* freely filtered then reabsorbed by PT
* normal range for serum: 135-153 mEq/L
* normal range for urine: 40-220 mEq/L
* hyponatremia (prevalent electrolyte disorders)
109
T or F: the decreasing rate of sodium is directly proportional to symptoms severity
true
*Moderate psychic changing, asthenia, nausea, muscular cramps, Severe neurological anomalies (disorientation, confusional
status, coma, convulsions)
110
normal ranges for serum and urine potassium
serum: 3.5-5.3 mEq/L
urine: 10-20 mmol
111
Some considerations in potassium
- K+ is not reabsorbed by kidney (descending loop of Henle)
| - K+ serum levels change with pH
112
This is associated with decreasing potassium
chronic alkalosis
*diuretic therapy, vomiting and excess laxatives
113
Kidney function test for following renal function over time
Serum creatinine
114
Kidney function test for checking adequacy of urine collection
creatinine index
115
KFT for assessing GFR, volume status, and protein intake
BUN
116
KFT best estimate for GFR
creatinine clearance
117
Liver is the primary site for
xenobiotic detoxification (drug and toxin metabolism)
118
Other things occuring in liver
ureagenesis (for acid-base balance), protein synthesis, bile secretion, intermediary metabolism processes (gluconeogenesis, glycolysis, ketogenesis, lipid synthesis)
119
Liver functional test to indicate hepatocellular integrity
AST and ALT: more liver-specific (transaminases)
120
LFT for assessing protein synthesis in liver
albumin
| plasma transport protein
121
LFT to test conjugated* and unconjugated bilirubin** for anion transport?
Total bilirubin
* directly measured, polar, water-soluble, found in plasma, unbound or free, reacts with diazotized sulfanilic acid without an accelerator
* *calculated (indirect). non-polar, water insoluble, found in plasma bound to albumin, with accelerator
122
LFT reflecting protein synthetic function by measuring integrity of extrinsic pathway of coagulation
prothrombin time
123
LFT which measures bile flow and isoenzymes
ALP
*ref range varies with age
124
sensitive indicator of liver disorder and cholestasis
GGT
*Induced by many drugs and toxins e.g. C2H5OH, phenytoin, barbiturates, statins
125
Delta fraction of total bilirubin is
conjugated bilirubin bound to albumin and observed in hepatic obstructions
126
Specimen and collection storage for Bilirubin tests
* Serum or plasma preferred
* Temperature sensitive
* Fasting sample preferred (Lipemia increases bilirubin concentrations)
* No hemolysis (Hemolysis decreases the reaction of bilirubin with the diazo reagent)
* Light sensitive (Bilirubin levels decrease by 30-50% per hour)
127
methods of bilirubin analysis
*see ref ranges in trans
* Jendrassik-Grof (for total and conjugate bilirubin; azobilirubin produced from bilirubin pigments in serum reacting with diazo reagent)
* Urine Bilirubin (indicates conjugated hyperbilirubinemia; uses urine dipsticks with diazo reagent embedded; use fresh urine)
128
accelerator used for jendrassik-grof
caffeine benzoate wc accelerates coupling of bilirubin with diazo reagent
* ascorbic acid stops rxn
* alkaline tartrate converts purple azobilirubin to a blue azobilirubin (measured at 600 nm)
129
Advantages of jendrassik-grof
Not affected by pH changes
Maintains optical sensitivity at low bilirubin concentrations
Insensitive to high protein concentrations
130
Indicated by jaundice evident with bilirubin levels 35-70 μmol/L
Hyperbilirubinemia
131
Sources of unconjugated bilirubin (pre-hepatic hyperbilirubinemia)
hemolysis
resolving hematoma
gilbert's syndrome*
crigler-najjar syndrome
*in 5% of popn.; males>females, genetic, exacerbated by fasting and illness
132
Sources of conjugated bilirubin (hepatic/post-hepatic hyperbilirubinemia)
*bilirubinuria present
•Hepatocellular diseases
•Cholestatic diseases
•Benign congenital conjugated hyperbilirubinemia
(Dubin-Johnson syndrome and Rotor’s syndrome
133
Presence of gilbert's syndrome rules these out
hemolysis FBC, reticulocyte count and underlying liver disease
134
causes of neonatal jaundice
kemicterus (brain damage due to uptake of unconjugated bilirubin) ugh pagod na si acoe see trans
135
This is the end product of bilirubin metabolism which is excreted in feces, some reabsorbed and returned to liver
urobilinogen
* increased in hemolytic disease, and defective liver cell funciton
* decreased in biliary obstruction and carcinoma
136
In determining urobilinogen, ehrlich's rxn is used whrein
p-dimethyl aminobenzaldehyde (Ehrlich’s reagent) produces red color
*Performed on fresh urine
• Reference Range: 0.1–1.0 Ehrilch units in two hours
137
Significant enzymes released in liver damage which differentiate between functional or mechanical causes of disease
AST*
ALT*
ALP
GGT (elevated in biliary obstruction and in chronic alcoholism)
5'nucleotidase (elevated in HBD)
LDH (nonspecific marker of cellular injury)
*rise rapidly in most liver diseases; stay elevated for 2-6 weeks, highest in hepa, hepa ischemia and drug/toxin induced necrosis
138
This enzyme differentiates hepatobiliary disease from bone disease
Phosphatases (ALP)
139
Other LFT elevated in liver disease
Prothrombin time
serum ammonia (used for hepa encephalopathy, lacks sensitivity and specificity, and investigation of urea cycle disorders)
Glucose/Galactose tolerance (liver's ability to metabolize carbs)
140
Hepatocellular pattern in LFT shows elevation of
AST/ALt (see causes)
141
Cholestatic pattern in LFT shows elevation of
ALP with GGT +/- bilirubin
| see causes
142
Hepatitis A markers
performed by serological antibodies (IgM = acute infxn, 3-6 mos; IgG= lifelong immunity)
143
Hep B marker in onset of sy,ptoms
HBsAg
144
Hep B marker found in acute infxn
HBcAg
145
Hep B marker found in acute and chronic infxns.
HBeAg
146
Methods used for Hep C testing
- nAnti-HCV detection by EIA
Quantitative nucleic acid (Screening)= positive = exposure to HCV, no diff bet current vs past infxn
- PCR for HCV RNA (Confirmatory)
147
What happens in paracetamol overdose?
hepatic necrosis within 36-72 hrs due to accumulation of breakdown product NAPQI
148
Effective agent in diagnosis and treatment of paracetamol overdose
n-acetylcysteine/parvolex
149
Primary syndromes of iron overload
hereditary hemochromatosis
(autosomal recessive, mutations in HFE gene (C282Y, H63D), 93% assoc with homozygosity of C282Y, 6% with bothe hfe genes, 1% no mutation id)
150
Secondary syndromes of iron overload
* Non-hereditary hemochromatosis cirrhosis
* Ineffective erythropoiesis (Sideroblastic anemia and Thalassemia)
* Multiple transfusions
* Bantu siderosis
* Porphyria Cutanea Tarda
151
autosomal recessive disease in copper poisoning
wilson's disease
*mutation in ATP7B (Cu transportin P type ATPase)
152
clinical presentation of copper poisoning/wilson's disease
(Children and adults usually <40 years)
• CNS: extrapyramidal system, Kayser-Fleisher rings in cornea
• Liver: fatty liver, cirrhosis, acute fulminant hepatic failure
• Kidney, haemolytic anaemia
153
Diagnosis of wilson's disease
low plasma ceruloplasmin
increased urinary copper excretion (via Penicillamine Challenge Test)
Liver biopsy (measure copper content)
154
see cases
see cases
