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Clinical Chemistry > Kidney and Liver Function Tests > Flashcards

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)
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2
Q

What are some hormones produced by kidneys

A
  • renin
  • erythropoietin
  • 1,25-dihydroxy vitamin D3
  • Prostaglandins
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3
Q

Main function of kidney (multifunctional)

A

storage of liquids by concentration of urine

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4
Q

Urine excreted daily in adults is

A

about 1.5 L (kidney is only 1% of total body weight)

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5
Q

Renal blood flow accounts for what % of cardiac output

A

20%

plasma renal flow: 600 ml/min/1.73 meter squared

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6
Q

Two processes involved in renal blood flow

A

ultrafiltration (GFR): 180 L/day

Reabsorption (>99% of amount filtered gets reabsorbed)

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7
Q

functional units of kidney

A

nephrons
(600,000-1.5 million)
*decrease in functioning nephrons =impaired kidney function

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8
Q

number of nephrons an individual is born with which may determine that individual’s susceptibility to renal injury

A

nephron dose

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9
Q

Parts of the nephron

A
  • Glomerulus
  • Distal tubule
  • Proximal tubule
  • Collecting duct
  • Loop of Henle
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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

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11
Q

Where does transport of solutes and water occur?

A

across and between the epithelial cells that line the renal tubules

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12
Q

Kinds of transport observed in nephrons

A

active and passive

*many passive transport are dependent upon active ie sodium transport

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13
Q

mediator of filtration which is formed from a specialized capillary network (capillary endothelial cells are ~40 nm thick)

A

glomerulus

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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

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15
Q

What is the renal threshold for glucose?

A

180 mg/dL

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16
Q

What is renal threshold?

A

Blood concentration of a substance that when surpassed, is excreted in urine

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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

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18
Q

What is the pre-renal cause of kidney functional disorder?

A

pre-renal: decreased intravascular volume

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19
Q

What is the renal cause of kidney functional disorder?

A

acute tubular necrosis

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20
Q

What is the post-renal cause of kidney functional disorder?

A

ureteral obstruction

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21
Q

What are the terminal products of hemoglobin catabolism?

A

bilirubin

urobilin

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22
Q

Hormone metabolites excreted from bloodstream

A

cortisol
testosterone
*other substances: organic acid, drugs, food additives

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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
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24
Q

[Homeostatic regulation]

What hormone regulates maintenance of water balance

A

antidiuretic hormone

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25
Q

[Homeostatic regulation] ADH in maintenance of water balance responds primarily to changes in?

A

osmolality and intravascular volume

secreted from posterior pituitary

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26
Q

[Homeostatic regulation] What happens when ADH increases permeability of DCT and collecting ducts of water?

A

Results in increased water reabsorption and excretion of more concentrated urine

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27
Q

[Homeostatic regulation] What do the renal tubules do in states of dehydration?

A

reabsorb water at their maximal rate resulting in production of a small amount of maximally concentrated urine

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28
Q

[Homeostatic regulation]

When do renal tubules reabsorb water at only a minimal rate?

A

in states of water excess resulting in excretion of large volume of extremely dilute urine

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29
Q

hormonal factors affecting regulation of electrolyte concentration

*together with neurogenic stimuli

A 
ADH (through detection of osmotic and mechanical stimuli)
Aldosterone 
Natriuretic peptides (sodium urinary removal requires h2o removal)
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30
Q

How does aldosterone affect electrolyte concentration?

*triggered by decreased blood flow or blood pressure in renal arteriole and decreased plasma sodium

A

sodium reabsorption and excretion of potassium and hydrogen

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31
Q

[homeostatic regulation: electrolyte concentration]

Thirst sensation causes

A

osmolality variation by 2%

  • increase in thirst = HYPERtonic ECF = lower ICF
  • decrease in thirst = HYPOtonic ECF = higher ICF
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32
Q

[homeostatic regulation]

two mechanisms performed by kidney in maintaining blood pH

A

tubular reabsorption of filter HCO3

removal of H+ ions produced daily

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33
Q

Urinary pH

A

4.5-5.0 (0.04 mol/L)

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34
Q

[homeostatic regulation: maintenance of blood pH] 99% of H+ ions are discarded by

A

urinary buffer

[H2PO4 > H+ + HPO42-]

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35
Q

Other homeostatic roles of kidneys

A
  1. Government of calcium phosphorus metabolism by secretion and reabsorbing.
  2. Regulation of the production of red blood cells.
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36
Q

The secretory function of kidneys involve hormones such as

A
  • 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)
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37
Q

Major renal functions which together, regulate and maintain constant optimal composition of the blood and intracellular fluids

A

® Glomerular filtration
® Tubular reabsorption (peritubular capillaries)
® Tubular secretion

UE= filtration - reabsorption + secretion

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38
Q

[Secretory function]

Each nephron produces this amount of ultrafiltrate per day

A

100 μL

*170-200L of ultrafiltrate passes through glomeruli daily

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39
Q

[Secretory function] What determines the initial mass on which the nephron must operate to produce and excrete urine?

A

Bulk transfer of substances from blood to glomerular filtrate

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40
Q

Laboratory tests and renal functionality studies

A 
• urinary index
• Serum creatinine and creatinine clearance
Estimated GFR (eGFR)
• Proteinuria and diagnosis
• Cistatin C detection
• Electrolytes
• Laboratory and AKI evaluation
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41
Q

In urine tests*, small, randomly collected urine samples is examined through its:

A
  • 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)
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42
Q

[Urine tests] Additional test for water balance in ECF and plasma

A

Volume

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43
Q

[Urine tests] Additional test for solute regulation (sodium, glucose, urea)

A

specific gravity and osmolality

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44
Q

[Urine tests] Additional test for blood acidity/ alkalinity balance

A

pH

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45
Q

[Urine tests] Creatinine is used to asses what?

A

glomerular filtration capacity

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46
Q

[Urine tests] Solute clearance is used to assess what?

A

glomerular filtration RATE

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47
Q

[Urine tests] These tests are used to assess filtration and/or reabsorption

A

urine proteins

urine albumin

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48
Q

[Urine tests] test for presence of RBC

A

hematuria

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49
Q

presence of cystatin C in plasma indicates

A

presence of bence-jones in urine ????

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50
Q

[Urine tests]

Urine 24 hours volume is useful in evaluating

A

glomerular filtration and tubular functionality

*normal adult range = 800-2000ml/day (normal fluid intake = 2L/day)

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51
Q

Adequate homeostasis is maintained with a urine output of

A

400-2000ml/day

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52
Q

Reduced urine volume is caused by

A

dehydration
not enough fluid intake
some types of chronic kidney disease

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53
Q

increased urine volume is caused by

A

diabetes
high fluid intake
some forms of kidney disease
use of diuretic medications

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54
Q

[Abnormal results in urine tests] Anuria or no passage of urine or production of <100 ml per day is often caused by

A

• 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

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55
Q

[Abnormal results in urine tests] Oliguria or low output of urine may be due to

A

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)

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56
Q

[Abnormal results in urine tests] Polyuria with increased azotemia (BUN) and creatinine is due to:

A
  • Diabetic ketoacidosis

* Kidney tubular necrosis (chronic renal insufficiency)

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57
Q

[Abnormal results in urine tests] Polyuria with normal azotemia (BUN) and creatinine is due to:

A
  • Polydipsia
  • Extreme protein uptake
  • Caffeine and alcohol
  • Diuretic medication
  • Diabetes mellitus e insipidus
  • Deficit Anti-Diuretic Hormone (ADH; vasopressin)
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58
Q

T or f: Urea is freely filtered from glomerulus and reabsorbed in a variable manner by proximal tubules

A

true

*not useful GFR marker; good for detection of tissue lesions and cellular damaging (burns) and monitoring renal functionality

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59
Q

T or F: urea increases earlier than creatinine and decreases quickly

A

true

*high values in acute renal insufficiency and terminal stage of chronic renal insufficiency

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60
Q

Why is there an increase in serum BUn in azotemia (20-40 mg/dL of BUN)

A

Kidney is not able to discard nitrogen metabolism’s degradation products

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61
Q

Pre-renal uremia is usually caused by

A

outside kidney (upstream of glomerular filtration) such as reduced renal perfusion (shock, dehydration, hemorrhage) and increased protein catabolism (alimentary canal bleeding, burns and fever)

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62
Q

Post-renal uremia is usually caused by

A

consequence of urinary tract obstruction; ureter; bladder and urethra

63
Q

Uremia caused by injury to glomerulus, affecting either renal microcirculation or renal tubules

A

intra-renal uremia

*also by: Acute or chronic diseases: glomerular nephritis, malignant hypertension, cortical necrosis, drugs or metal nephrotoxicity, pyelonephritis, diabetes mellitus, tubulopathy

64
Q

Compares the density of urine (number and size of particles dissolved) to the density of water (SG=1000)

A

Urine specific gravity tests

65
Q

usual reference values for adult and child in urine specific gravity tests

A

adults (1005-1020)

child (1001-1018)

66
Q

methods of urine specific gravity tests

A

densimeter, dipsticks (colorimetric reaction), referactometer

67
Q

urine concentration index (urine to plasma ratio of creatinine concentration) is determined by

A

urea
sodium chloride
sulfates
phosphates

68
Q

When SG is <1005

A

hyposthenuria

69
Q

Increased urine volume in hyposthenuria is due to

A
  • Insufficiency or absence of ADH
  • Pyelonephritis (may progress to chronic kidney disease)
  • Diabetes insipidus

*decreased urine volume: glomerulonephritis

70
Q

Hypersthenuria or SG > 1020 is due to

A
  • Diabetes mellitus (increased urine volume)
  • Nephrosis
  • ADH increases (decreased urine volume)
  • Heart diseases
  • Toxemia during pregnancy
  • Dehydration
71
Q

Dynamic tests

A

Glomerular filtration rate

[CKD-EPI (for screening; higher precision)], renal clearance, Creatinine

72
Q

[Dynamic tests] When is GFR* equal to the clearance rate?

*volume per time; best index in both patients and healthy subjects

A

when any solute is freely filtered and is neither reabsorbed nor secreted by the kidneys
(urine concentrationxurine flow/plasma concentration)

73
Q

e-GFR: the MDRD simplified equation

A

e-GFR = 175 × SCr

^ -1.154 × Age^-0.203 × 1.212(if black) × 0.742(if female)

74
Q

Indirect method of GFR assessment

A

Estimation by anthropometric, anthropological,
and biochemical parameters
*simple and advantageous; questionable accuracy

75
Q

Direct method/clearance study of GFR measures

A 
exogenous substances (inulin, iohexol, iotamatus, Cr51-EDA)
endogenous substances (creatinine)
76
Q

Advantages and disadvantages of direct method

A

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
Q

GFR level classified as normal in CKD-EPI test

A

> 60ml/min/1.73m

*see eqn in trans

78
Q

• Renal Damage Severity Assessment based on GFR

*same values for KDQI

A
  • 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
Q

CKD stages or renal disease staging is based on

A

measured or estimated GFR

80
Q

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

A

(renal) clearance

  • Urine concentration x collected urine volume / ([plasma creatinine] x time taken to collect urine specimen in minutes)
  • ideal marker of clearance
81
Q

Why is renal clearance considered ideal marker?

A

® 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
Q

interval refence values for males and females for creatinine*
*more accurate marker of kidney function than urea

A

® Male: 0.6–1.3 mg/dL

® Female: 0.5–1.0 mg/dL

83
Q

T or F: Kidney discards creatinine with a low efficiency

A

false, great

84
Q

T or F: creatinine binds proteins and is water-soluble

A

false, does not bind protein, water-soluble

85
Q

methods of analysis of creatinine

A

jaffe method, enzymatic method, reference methods (gas chrom, mass spectro and HPLC)

86
Q

What can interfere in jaffe method?

A

Proteins, bilirubin, uric, and pyruvic acids and some drugs

87
Q

Restrictions of Creatinine Detection

A

• 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
Q

[Proteinuria]

Factors which facilitate filtration

A

• 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
Q

Proteinuria in renal diseases causes

A

plasmatic oncotic pressure reduction leading to edema

90
Q

Protein loss from glomerular membranes/ Proteinuria is caused by:

*normal values: 50-150 mg per 24 hrs (adults)

A
  • Electric charges alteration

* Intracellular pores changing (ø 5-8 nm)

91
Q

Physiological loss of protein

A

• 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
Q

Indicators and classification of renal proteinuria

A

• 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
Q

Type of protein involved in selective glomerular protenuria

A

albumin and transferrin

94
Q

Type of protein involved in nephrotic proteinuria

A

albumin
transferrin
immunoglobulins

95
Q

Type of protein involved in tubular proteinuria

A

Retinol Binding Protein
α1-microglobulin
β2-microglobulin

96
Q

diabetic proteinuria

A

albumin type of protein present

97
Q

laboratory request for proteinuria serves as

A

basal investigation (urine total proteins for monitoring of CRI and urine albumin wc is more sensitive and accurate)

98
Q

lab request for proteinuria also serves as differential diagnosis of

A

tubular or glomerular proteinuria (useful in detecting β2-microglobulin and cystatin C)

99
Q

A specific increase in β2-microglobulin* and cystatin C means?
*need for excluding lymphocytes diseases; plasmatic detection required

A

proximal tubule reabsorption failure

100
Q

Risk factors present/needed for performing proteinuria assay

A
  • 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
Q

Low molecular weight protein, it is synthesized by nuclear cells, released in the blood and freely filtered by glomerulus in urines

A

Plasmatic cistatin c

  • not dependent from extrinsic factors
  • interferences if increase in PCR, BMI, steroids, hypothyroidism
102
Q

When is Plasmatic Cistatin C a better marker in predicting renal function than creatinine?

A

Chronic Renal insufficiency

103
Q

Other names for neutrophil gelatinase-associated lipocalin

A

lipocalin-2 and oncogene 24p3 (human protein encoded by LCN2 gene)

*expressed by multiple human cells ie epithelial cells, neutrophils and organ systems

104
Q

Role of lipocalin-2

A
  • 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
Q

Major positive ions/cations in ECF are

A

Na+ > K+, Mg2+, Ca2+

106
Q

most important negative ions (anions) are

A

Cl– and HCO3–

107
Q

Electrolytes concentration in ECF and ICF can affect:

A
  • Metabolic process
  • Osmotic Status
  • Hydration and pH
108
Q

major cation in fluid outside of cells; with osmotic activity

A

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
Q

T or F: the decreasing rate of sodium is directly proportional to symptoms severity

A

true

*Moderate psychic changing, asthenia, nausea, muscular cramps, Severe neurological anomalies (disorientation, confusional
status, coma, convulsions)

110
Q

normal ranges for serum and urine potassium

A

serum: 3.5-5.3 mEq/L
urine: 10-20 mmol

111
Q

Some considerations in potassium

A
  • K+ is not reabsorbed by kidney (descending loop of Henle)

- K+ serum levels change with pH

112
Q

This is associated with decreasing potassium

A

chronic alkalosis

*diuretic therapy, vomiting and excess laxatives

113
Q

Kidney function test for following renal function over time

A

Serum creatinine

114
Q

Kidney function test for checking adequacy of urine collection

A

creatinine index

115
Q

KFT for assessing GFR, volume status, and protein intake

116
Q

KFT best estimate for GFR

A

creatinine clearance

117
Q

Liver is the primary site for

A

xenobiotic detoxification (drug and toxin metabolism)

118
Q

Other things occuring in liver

A

ureagenesis (for acid-base balance), protein synthesis, bile secretion, intermediary metabolism processes (gluconeogenesis, glycolysis, ketogenesis, lipid synthesis)

119
Q

Liver functional test to indicate hepatocellular integrity

A

AST and ALT: more liver-specific (transaminases)

120
Q

LFT for assessing protein synthesis in liver

A

albumin

plasma transport protein

121
Q

LFT to test conjugated* and unconjugated bilirubin** for anion transport?

A

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
Q

LFT reflecting protein synthetic function by measuring integrity of extrinsic pathway of coagulation

A

prothrombin time

123
Q

LFT which measures bile flow and isoenzymes

A

ALP

*ref range varies with age

124
Q

sensitive indicator of liver disorder and cholestasis

A

GGT

*Induced by many drugs and toxins e.g. C2H5OH, phenytoin, barbiturates, statins

125
Q

Delta fraction of total bilirubin is

A

conjugated bilirubin bound to albumin and observed in hepatic obstructions

126
Q

Specimen and collection storage for Bilirubin tests

A
  • 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
Q

methods of bilirubin analysis

*see ref ranges in trans

A
  • 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
Q

accelerator used for jendrassik-grof

A

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
Q

Advantages of jendrassik-grof

A

Not affected by pH changes
Maintains optical sensitivity at low bilirubin concentrations
Insensitive to high protein concentrations

130
Q

Indicated by jaundice evident with bilirubin levels 35-70 μmol/L

A

Hyperbilirubinemia

131
Q

Sources of unconjugated bilirubin (pre-hepatic hyperbilirubinemia)

A

hemolysis
resolving hematoma
gilbert’s syndrome*
crigler-najjar syndrome

*in 5% of popn.; males>females, genetic, exacerbated by fasting and illness

132
Q

Sources of conjugated bilirubin (hepatic/post-hepatic hyperbilirubinemia)

A

*bilirubinuria present
•Hepatocellular diseases
•Cholestatic diseases
•Benign congenital conjugated hyperbilirubinemia
(Dubin-Johnson syndrome and Rotor’s syndrome

133
Q

Presence of gilbert’s syndrome rules these out

A

hemolysis FBC, reticulocyte count and underlying liver disease

134
Q

causes of neonatal jaundice

A

kemicterus (brain damage due to uptake of unconjugated bilirubin) ugh pagod na si acoe see trans

135
Q

This is the end product of bilirubin metabolism which is excreted in feces, some reabsorbed and returned to liver

A

urobilinogen

  • increased in hemolytic disease, and defective liver cell funciton
  • decreased in biliary obstruction and carcinoma
136
Q

In determining urobilinogen, ehrlich’s rxn is used whrein

A

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
Q

Significant enzymes released in liver damage which differentiate between functional or mechanical causes of disease

A

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
Q

This enzyme differentiates hepatobiliary disease from bone disease

A

Phosphatases (ALP)

139
Q

Other LFT elevated in liver disease

A

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
Q

Hepatocellular pattern in LFT shows elevation of

A

AST/ALt (see causes)

141
Q

Cholestatic pattern in LFT shows elevation of

A

ALP with GGT +/- bilirubin

see causes

142
Q

Hepatitis A markers

A

performed by serological antibodies (IgM = acute infxn, 3-6 mos; IgG= lifelong immunity)

143
Q

Hep B marker in onset of sy,ptoms

144
Q

Hep B marker found in acute infxn

145
Q

Hep B marker found in acute and chronic infxns.

146
Q

Methods used for Hep C testing

A
  • 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
Q

What happens in paracetamol overdose?

A

hepatic necrosis within 36-72 hrs due to accumulation of breakdown product NAPQI

148
Q

Effective agent in diagnosis and treatment of paracetamol overdose

A

n-acetylcysteine/parvolex

149
Q

Primary syndromes of iron overload

A

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
Q

Secondary syndromes of iron overload

A
  • Non-hereditary hemochromatosis cirrhosis
  • Ineffective erythropoiesis (Sideroblastic anemia and Thalassemia)
  • Multiple transfusions
  • Bantu siderosis
  • Porphyria Cutanea Tarda
151
Q

autosomal recessive disease in copper poisoning

A

wilson’s disease

*mutation in ATP7B (Cu transportin P type ATPase)

152
Q

clinical presentation of copper poisoning/wilson’s disease

A

(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
Q

Diagnosis of wilson’s disease

A

low plasma ceruloplasmin
increased urinary copper excretion (via Penicillamine Challenge Test)
Liver biopsy (measure copper content)

154
Q

see cases

Clinical Chemistry (9 decks)

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