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Chem&Haem > Random Questions > Flashcards

Random Questions Flashcards

1
Q

Tests performed at PMH Chem Toxicology (>4,13)

A

SPE for MM
Urine CAT (Strip pH<2>5 cancel, LC-MS, sample preparation: Column extraction)
Urine Toxic (sample preparation: dilution)
Urine Myoglobin (CK<200 / >23000 cancel, Strip HB+ cancel,rhabdomyolysis)
Cryo (1:IgM MM;2:Infection[HepC],3:Autoimmune[SLE,RA])
Urine 5-HIAA & HVA (Neuroblastoma,carcinoid tumors)
Plasma acylcarnitine (fatty acid oxidation)
Urine Metabolic profiling (LCMSMS)
Urine Sulfite (sulfite oxidase deficiency)
Urine Chyle (lymphatic obstruction)
Urine Mucopolysaccharide (E, MPS1, Hurler’s syndrome)
Urine Porphobilinogen / Porphyrin(HPLC) / Urobilinogen (porphyrias / heme production)
Urine reducing substance (galactosemia)

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2
Q

Organs involved in Vitamin D synthesis & analytical utility of 25OH & 1,25 OH (2)

A

Skin, Liver, Kidney
25OH for vitamin D deficiency / excess
1,25OH for sarcoidosis

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3
Q

Test to differentiate osteoporosis from osteomalacia & discuss VDDR vs VDRR (2)

A

ALP

VDDR:
1 alpha hydroxylase deficiency (Liver, vitD Low)
vitD R deficiency (Bone, vitD High)

VDRR:
PHOS reabsorption deficiency (CA normal, PHOS Low)

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4
Q

Reference range of GLU, 4 diagnostic criteria for DM & OGTT for GDM (6)

A

3.9–5.5

  1. fasting GLU >7 * 2 [5.5~7 = IFG]
  2. random GLU >11 + polyuria / increased thirst / weight loss
  3. 2h 75g OGTT >11 [7.8~11 = IGT]
  4. HbA1C>=6.5%

GDM screening
1h 50g OGTT >7.8

GDM confirmatory
1. 3h 100g OGTT
-fasting GLU>5.5
-1h >10
-2h >8.6
-3h >7.8
[Any 2]
2. 2h 75g OGTT
Same cutoff as 3h OGTT

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5
Q

Why use HK+G6PD rather than GO, how POCT differs in terms of assay & interference (4)

A

Although GO is more specific, H2O2 is prompt to interference, so use HK+G6PD

POCT is amperometric and uses either GDH (FAD+/NAD+/PQQ) or GO (H2O2).
As POCT uses whole-blood, high HCT causes falsely low result, bias can be corrected by measuring sample conductivity

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6
Q

Name 5 hormone which affects glucose level & the mechanism behind the effect (10)

A

Insulin:
Glucose uptake, Lipid & Glycogen synthesis, X Glucose synthesis

GH & Cortisol:
Glucose synthesis

EPI:
Glycogen breakdown

Glucagon:
Both Glucose synthesis & Glycogen breakdown

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7
Q

Why are we doing C-peptide, Insulin, Urine mucopolysaccharide, Urine reducing sugar, and D-xylose absorption test (5)

A

C-peptide: exogenous insulin source
Insulin: insulinoma, Reactive hypoglycemia
Urine mucopolysaccharide: MPS1 (iduronidase deficiency)

Urine reducing sugar:
GSD: Accumulation of Glycogen due to G6P deficiency
1.Von Gierke (L,UA,HB)
2.Pompe (Cardiac)
3.Cori (Mild)
4.Andersen (L,child death)
5.McArdle (Muscle)
6.Hers (~Von Gierke)
1,4,6 = Liver
2,5,7 = Muscle

D-xylose absorption test: Differentiate Pancreatic insufficiency from malabsorption

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8
Q

When is Iron in Fe2+ (3) / Fe3+ (1) form? In what condition is Iron absorption increased (3) / decreased (1)?

A

Fe2+: absorption, Ferrozine binding, in Hb
Fe3+: transferrin binding, MetHb

Absorption increase in alcoholism, low gastric pH, IDA
Absorption decreased in IDA

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9
Q

Can you determine if a patient is having Iron deficiency based on a single measurement? (1) How about Ferritin? (2) Name a test that is helpful for IDA diagnosis in difficult cases. (1)

A

No, because Iron is elevated by hemolysis and is subject to diurnal variation (higher during work)

Low Ferritin is specific but not sensitive for IDA, as Ferritin is elevated in malignancy, infection, and inflammation, masking the Low Ferritin caused by IDA.

sTfR increase suggest IDA, this increase is not affected by inflammation

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10
Q

How can you differentiate IDA, Iron overload & ACD using Iron panel? (3) Why Iron panel result in Iron overload is similar to hemolytic & sideroblastic anaemia? (2) How about Nephrosis, Hepatitis & Pregnancy? (3)

A

Fe is high in Iron overload
TIBC is high in IDA but low in ACD

Fe is released in hemolysis, resembling a state of Iron overload

Nephrosis: urinary loss of Fe & Transferrin

Hepatitis: ferritin release & transferrin synthesis decrease

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11
Q

Where are Heme, BILI & conjugated BILI produced respectively? (3)

A

Heme: Bone & Liver
BILI: Spleen & Liver
conjugated BILI: Liver

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12
Q

What is δ Bilirubin? How would it affect DB results? (2)

A

δ BILI = irreversibly albumin bound BILI

δ is not a Conjugated BILI but is measured as DB
High δ Bilirubin to Conjugated BILI ratio indicate effective of biliary drainage, which rule out cholestasis.

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13
Q

Why is Urine Urobilinogen high in AIHA but low in cholestasis? (2)

A

High in extravascular hemolytic anemias (Splenic removal, in AIHA / HS) as more BILI is released to GI & be converted to urobilinogen by enteric bacteria

Low in cholestasis because urobilinogen can’t be produced without BILI being released to GI

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14
Q

Bilirubin can be affected by drugs, name 2 of them. (2)

A

Barbiturates lowers BILI, it is used in treatment of jaundice
Chlorpromazine increases BILI, it is an antipsychotic that causes cholestasis

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15
Q

DB should be measured faster, TB measurement involves caffeine, why? (3)

A

To prevent unconjugated BILI from reacting during DB measurement, measure within 3 minutes OR reduce diazo group using ascorbate to stop reaction

Accelerator is required for unconjugated BILI to react during TB measurement

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16
Q

Why do some labs measure NB with bichromatic spectrophotometric methods? (2) Why Neonate has high BILI? (1)

A

Negative interference persist as Hb itself inhibit diazo reaction
NB are usually Hemolyzed, consider Direct bichromatic spectrophotometric methods (454 nm and 540 nm) for NB to prevent underestimation of BILI

Physiological hyperBILI in neonate is due to hemolysis & relative UGT deficiency, the BILI is mostly unconjugated, persist for 1 weeks for normal / 2 weeks for prematures babies

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17
Q

Enzymatic method for BILI measurement uses different pH for DB & TB, explain. (2) Name a bedside method. (1)

A

At pH 8, both conjugated, unconjugated, and delta bilirubin react with the enzyme
At pH 4, only the conjugated form reacts.

At bedside, there is Multiwavelength reflectance photometry for transcutaneous bilirubin assay

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18
Q

Why is DB high in hepatitis when liver function is low? (1)

A

Although theoretically liver dysfunction causes conjugation problem leading to increase in unconjugated BILI, DB is also high due to re-excretion failure and cholestasis

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19
Q

High BILI may be attributed to diseases related to bile transport & UGT deficiency, name 5 of them. (5)

A

Bile transport: Dubin–Johnson, Rotor
UGT deficiency: Crigler–Najjar, Gilbert’s, Lucey–Driscoll

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20
Q

CRE tends to overestimate GFR, especially for men having low GFR, why is that? (1)

A

CRE is 100% filtered by the glomeruli, in addition, secretion especially at low filtration rate. Low GFR means more CRE secretion, so the apparent plasma CRE is lower, overestimating the actual GFR.

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21
Q

Why do men & women have different reference ranges for CRE? (1)

A

They has different muscle mass

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22
Q

Why is CrCl measurement with plasma & 24h CRE prone to preanalytical error? (4) How about calculated CrCl? (1)

A

CrCl = U/P X V X 1.73/A (A differs so use separate RI for M / F / Child)
Not empty bladder at start (Falsely High)
Adopt MSU procedure (Falsely Low)
Not empty bladder before end (Falsely Low)
<400mL 24H urine due to dehydration (secretion, Falsely High)

Cockcroft-Gault: drug dosing adjustment
calculation depends on age, gender, weight
CrCl, mL/min = (140 – age) × (weight, kg) × (0.85 if female) / (72 × Cr, mg/dL)

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23
Q

Name 2 method for eGFR calculation & comment on the major difference. (2) What are the variables in their calculation? (3)

A

MDRD:
underestimate for eGFR>60, invalid for child & elderly & seriously ill

CKD-EPI:
more accurate for eGFR>60, choice for adult CKD monitoring

For MDRD & CKD-EPI, calculation depends on age, gender, race

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24
Q

What are the main concerns of Jaffe’s reaction over enzymatic methods in measuring CRE? (2) How can we reduce those concerns? (3) How would it potentially affect our patients if those concerns are not tackled? (1)

A

BILI negative interference, minimized by sample dilution, rate-blanking, or manual deproteinization

ascorbate, ketone & protein positive interference, compensated by subtracting a constant value

Falsely Low CRE can lower MELD score can delay liver transplant for patient in need

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25
Q

Why CHO and LDL is high in nephrotic syndrome?

A

Low ALB upregulates HMG CoA Reductase and downregulate LPL

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26
Q

Name 5 causes of low MG. What will happen when a patient has low MG? (4)

A

Alcoholism, GI tract disease, Diarrhea/Vomiting, parenteral feeding, DKA
Hyperactive including seizures, tremor, tachycardia, swallowing problems

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27
Q

Why is plasma urea useful for accessing prerenal cause of decreased renal function? (1)

A

Urea reabsorption is filtration rate dependent

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28
Q

If the patient has renal & liver failure simultaneously, how would plasma urea change? (1)

A

No change, liver failure reduces urea synthesis, renal failure reduces urea excretion.

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29
Q

Can we measure URE without using enzymes? (1)

A

Yes.
Electrochemical method measures current increases caused by NH4+ production

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30
Q

Name 7 conditions related to aminoaciduria? (7)

A

1.PKU is accumulation of phenylalanine due to phenylalanine hydroxylase deficiency

2.Fanconi syndrome is inherited renal-type due to renal tubule defects

3.Homocystinuria is inherited overflow-type due to cystathionine synthase deficiency

4.Wilson’s disease is inherited overflow-type due to urea cycle failure

5.Hepatitis is acquired overflow-type due to urea cycle failure

6.Alkaptonuria is due to homogentisic acid oxidase deficiency

7.MSUD is due to branched-chain decarboxylase deficiency, leading to Valine, leucine, and isoleucine accumulation

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31
Q

Name 4 methods for AA measurement, which is most common? (5)

A

ESI-MS-MS, HPLC, CE, 2D TLC (SiO2polar, mobile phase basic & acidic)

ESI-MS-MS

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32
Q

Why would someone have a high AMM? (2) Why is it not good? (2) Anything to consider before taking blood for AMM? (3)

A

Hepatic coma (severe liver necrosis)
ammonia increases central nervous system pH and is coupled to glutamate (neurotransmitter)

Venous stasis and prolonged storage cause peripheral deamination of amino acids
Smoking can double AMM, fasting is recommended

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33
Q

Apart from Renal, Cancer & Gout, UA is also high in ketoacidosis & lactic acidosis, why is that? (1) Suggest an urgent condition that requires UA measurement (1)

A

They compete with uric acid for renal excretion.

Uric acid calculi obstructing ureter

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34
Q

What is the full name of A & B antigen, and Anti-H? (3)

A

A = N-acetyl-D-galactosamine
B = D-galactose
Anti-H = ulex europaeus

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35
Q

Do ABO causes HDFN? (1) How? (1) Is it serious? (1)

A

ABO induced HDFN is common but weak (DAT weak+, as fetal RBC has weak ABO expression)

Due to IgG Anti-A,B from O mom.

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36
Q

What would you do if reverse A is 1+ and you suspect it is the culprit of ABO discrepancy? (1)

A

Add Anti-A1 Lectin to determine if the patient is A2 subgroup

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37
Q

Order of H abundance (1) What is the use of adding Anti-H to A1 cell? (1)

A

O> A2 > B > A2B > A1 > A1B

As a negative control when solving ABO discrepancy with Anti-H.

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38
Q

Why sometime rouleaux is observed in forward & reverse grouping? (1) what would you do? (1)

A

High protein in plasma (MM)
Use washed patient’s RBC suspension for forward
Add ALB to dilute the mixture for reverse.

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39
Q

What would you do if forward groupings are all positive? (1)

A

Do AC (patient RBC+ patient plasma) to rule out AutoAb

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40
Q

Why is plasma urea useful for accessing prerenal cause of decreased renal function? (1)

A

Urea reabsorption is filtration rate dependent

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41
Q

If the patient has renal & liver failure simultaneously, how would plasma urea change? (1)

A

Urea can be normal. RF reduces urea excretion, LF reduces urea synthesis

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42
Q

Can we measure URE without using enzymes? (1)

A

Yes.
Electrochemical method measures current increases caused by NH4+ production

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43
Q

Name 7 conditions related to aminoaciduria? (7)

A

PKU is accumulation of phenylalanine due to phenylalanine hydroxylase deficiency

Fanconi syndrome is inherited renal-type due to renal tubule defects

Homocystinuria is inherited overflow-type due to cystathionine synthase deficiency

Wilson’s disease is inherited overflow-type due to urea cycle failure

Hepatitis is acquired overflow-type due to urea cycle failure

Alkaptonuria is due to homogentisic acid oxidase deficiency

MSUD is due to branched-chain decarboxylase deficiency, leading to Valine, leucine, and isoleucine accumulation

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44
Q

Name 4 methods for AA measurement, which is most common? (5)

A

ESI-MS-MS, HPLC, CE, 2D TLC (SiO2polar, mobile phase basic & acidic)

ESI-MS-MS

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45
Q

Why would someone have a high AMM? (2) Why is it not good? (2) Anything to consider before taking blood for AMM? (3)

A

Hepatic coma (severe liver necrosis)

ammonia increases central nervous system pH and is coupled to glutamate (neurotransmitter)

Venous stasis and prolonged storage cause peripheral deamination of amino acids
Smoking can double AMM, fasting is recommended

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46
Q

Apart from Renal, Cancer & Gout, UA is also high in ketoacidosis & lactic acidosis, why is that? (1) Suggest an urgent condition that requires UA measurement (1)

A

They compete with UA for renal excretion.
Uric acid calculi obstructing ureter

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47
Q

What is the full name of A & B antigen, and Anti-H? (3)

A

A = N-acetyl-D-galactosamine, B = D-galactose
Anti-H = ulex europaeus

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48
Q

Do ABO causes HDFN? (1) How? (1) Is it serious? (1)

A

Yes.
Anti-A,B from O mom.
ABO induced HDFN is common but weak (DAT weak+, as fetal RBC has weak ABO expression)

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49
Q

What would you do if reverse A is 1+ and you suspect it is the culprit of ABO discrepancy? (1)

A

Anti-A1 Lectin is useful in determine if the patient is A2 subgroup

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50
Q

Why sometime rouleaux is observed in forward & reverse grouping? (1) what would you do? (1)

A

High plasma protein (MM)
Use Washed RBC for forward
Dilute reverse mixture

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51
Q

What would you do if forward groupings are all positive? (1)

A

Do AC (patient RBC+ patient plasma) to rule out AutoAb

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52
Q

What would you do if reverse O is positive? (2)

A

consider Bombay, or cold agglutinin

Anti-H to Patient’s cell to rule out Bambay

Prewarm to warm out cold Ab such that Ab screen & ID reflects AlloAb

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53
Q

What are the common Rh phenotypes in the Asian population? (2)

A

R1, R2

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54
Q

Chromosome for ABO & Rh? (2)

A

ABO: 9
Rh: 1

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55
Q

Practically, how to demonstrate weak D? (2) how about partial D? (1) If you have only 1 unit O- blood, who would you give it to? (1)

A

weak/partial D: weak reaction with Anti-D
partial D = more reactive with another brand of Anti-D
Give it to patient with partial D as their plasma contain Anti-D

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56
Q

Pregnant women often tested Anti-D+, why is that?(1)

A

RhIg is prescribed for O- mom to prevent RhD immunization

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57
Q

Describe the function of enzyme-treatment (3) & AET (1)

A

Enhanced:
ABO (ABO/H,Lewis,I,P1PK)
Rh
Kidd

Decreased:
MNS
Duffy

Unchanged:
Kell

AET treated cells denatures Kell Ag

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58
Q

In CMC, what would you do if ColdAutoAb is suspected? (1) is there risk of doing so? (1) how about WarmAutoAb? (1) What would RC do for the specimen you send to them? (1)

A

ColdAutoAb: Prewarm.
Risk of removing clinically significant Ab with wide thermal amplitudes (anti-Vel)

WarmAutoAb: Ab screen & ID would always be +, proceed to phenotyping & give patient with phenotype-matched IAT-compatible blood after physician consent.

RC would use techniques like Autoadsorption, Alloadsorption (homozygous M cells for ColdAutoAb), and Enzyme-treatment to confirm their presences.

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59
Q

Jka is notorious for not being detected & causing DHTR, why is that? (1) Why is DAT positive in HTR? (1)

A

Antibody produced in primary immune response decreases in titer and become indetectable at Ab screen before 2nd transfusion, so the transfusion proceed and HTR occurs due to secondary immune response.

DAT suggests IgG coated on RBC, which triggers hemolysis.

60
Q

Why is Frequency data useful when you want Antigen-negative blood but don’t want to wait? (1)

A

Frequency data from Red Cross may be used to calculate the estimated number of random XM required before a match can be found

61
Q

If you issue 1 unit of O+ blood to O- mother, is it absolute that she will develop Anti-D?(1)

A

There is 22% chance for Rh- patients to develop Anti-D after 1 unit Rh+ RBC transfusion.

62
Q

For panagglutinin with AC+ we would consider warmAutoAb, if it is AC-, what would you suspect? (1)

A

consider multiple Ab to low frequency Ag if reaction strength differs.

consider Ab to high frequency Ag like Anti-k, k is not phenotyped in routine practice because k- is very rare.

63
Q

Why is phenotyping of SCD patients possible even after transfusion?(1)

A

Patient with SCD who is transfused recently can still be phenotyped after treatment with hypotonic saline, as transfused RBC are all lyzed by osmosis

64
Q

What are the 3 rules when interpreting ABO discrepancy? (3) Give 5 examples of ABO discrepancy (5)

A
  1. Always correlate Clinical history
  2. weak reaction = discrepancy
  3. Ab problems are more common than Ag problems

4+ 4+ 2+ 0 = A2B
0 0 0 0 = Immunocompromised
4+ 4+ 2+ 2+ = Cold agglutinin
4+mf 4+mf 0 0 = AB patient received O blood
4+ 2+ 0 4+ = Acquired B due to GI disease, no longer a problem with current Anti-B

65
Q

In a case of Ab- with Anti-Jkb history, you proceed to XM with Jkb- blood, it is 1+, give 2 possible explanations to this. (2)

A
  1. Ab to high frequency Ag (Anti-k) in patient plasma.
  2. DAT+ donor cell.
66
Q

In a case of Ab- without history, you issue blood by CXM & the blood is transfused. Next Ab screen shows DAT+(mf) suggesting DHTR, is it your fault? (1)

A

No, there is systemic risk of DHTR following protocol of giving CXM blood to Ab screen - patient.
Antibody produced in primary immune response decreases in titer and become indetectable at Ab screen before 2nd transfusion, so the transfusion proceed and HTR occurs due to secondary immune response.

67
Q

When panagglutination is encountered, always do AC & DAT, why? (1)

A

AC+ & DAT+ confirm WarmAutoAb case and rule out Ab to high frequency Ag (Anti-k, although not likely)

68
Q

When you see Ab(?), what would you suspect? (1) What would you do to prove your suspicion? (1) What to do next if your suspicion is likely? (1)

A

ColdAutoAb
DAT + (C3d+)
Prewarm for Ab screen, ID & XM

69
Q

A patient is DAT+, does it mean he has AIHA? (1)

A

AutoAb != AIHA, AIHA ~= AutoAb

70
Q

Aetiology of TTP, HUS, DIC. (3) State 1 thing you should do & 1 thing you should never do for TTP patients. (2) How to differentiate TTP & HUS? (2) Why is ITP not related to schistocytes? (1) How to rule out DIC? (1)

A

TTP : ADAMTS13 deficiency (<10%)
HUS: E. coli O157:H7 OR complement-mediated HUS
DIC: APL / Sepsis / Malignancy

perform plasma exchange & avoid PLT transfusion for TTP suspected cases

TTP: Neurological
HUS: Renal

ITP is caused by viral infection, Ab opsonization of RBC facilitate extravascular removal at spleen.

Absence of D-dimer elevation & PT/APTT prolongation rule out DIC.

71
Q

Patient is having panagglutination with AC+ DAT+, XM incompatible for units tested, what should you suggest when immediate blood transfusion is indicated? (1), when blood transfusion is indicated later? (1)

A

unmatched O / group-specific blood.
When phenotype is available, phenotype-matched incompatible IAT can be issued with physician consent.

72
Q

Patients having ITP received PLT but PLT count remains low, what would you recommend the physician to prescribe that can potentially improve the condition? (1)

A

Try IVIG(Anti-D), macrophage engulf excess IVIG, sparing opsonized PLT.

Steroid + IVIG(Anti-D), TPO R agonist, Fostamatinib (Sky inhibitor, inhibit Anti-PLT production & Macrophage opsonization), splenectomy, immunosuppression

73
Q

O- women called MTP, BB only have 4 units of O- blood, what would you do? (2)

A

If MTP is really massive, skip O- blood, give O+ blood instead. women is going to be sensitized anyway due to the shortage of O-, so we better reserve O- for other patients.

If MTP is not massive, give the O- blood, consider give A2- as well if it is available (A2 cell contain least A Ag), then transit to O+ blood.

74
Q

A- man with Anti-D called MTP, BB only has Rh+ blood, what would you do? (2)

A

Give Rh+ blood, monitor hemolysis, transit to Rh- post-operative.

75
Q

Elution helps in TR investigation, DTT helps in patients receiving daratumumab, prewarming & cord blood helps in Cold Ab investigation, homozygous cell helps in Ab ID of Ag having dosage effect. Describe how. (4)

A

Elution: detach IgG from RBC, then perform Ab ID on eluate

DTT: remove CD38 & Kell Ag from RBC, facilitate detection of AlloAb after daratumumab[Anti-CD38] treatment

cord cell: i Ag predominant, used to confirm Anti-I

homozygous cell: homozygous cell usually has two alleles for the Ag (not always), so its reaction with Ab is stronger.

76
Q

Name 6 antihyperlipidemic medications & explain how they work. (5)
What are their side effects? (5)

A
  1. Ezetimide (inhibit CHO absorption)
    -diarrhea
  2. Statin (inhibit HMA-CoA R)
    -liver toxicity, rhabdomyolysis
  3. Fibrate (stimulate LPL)
    -liver toxicity, Gall stone
  4. bile acid sequestrant [Cholestyramine] (inhibit bile acid reabsorption)
    -Fat malabsorption, Gall stone
  5. Niacin (inhibit lipolysis, inhibit VLDL secretion)
    -Flushing (Give aspirin), High UA (renal excretion competition), High GLU (insulin resistence)
  6. PCSK9 I (Antibodies, PCSK9 cleaves LDL R on hepatocytes)
77
Q

How hemolyzed sample affects the result? (1)

A

High H index:
1. Color interference (colorimetric assay with similar wavelength)
2. Release of RBC content (LDH, PHOS, K, AST, FOL, ALT, MG, FE)
3. Sample dilution [>3g HB] (ALB, BILI, GLU, NA)
4. Chemical interference (competition, inhibition, ppt., Protease[Cathepsin E: Low Insulin, BNP])

78
Q

Name 6 acute TR & 4 delayed TR. (10)

A

Acute TR:
1. Allergic (sensitive to donor plasma protein)
2. FNHTR (HLA, cytokine)
3. Septic (donor unit with bacteria)
4. TACO (Excess volume of transfusion)
5. HTR (Incompatible)
6. TRALI (Anti-HLA from donor attacks patient’s lung)

Delayed:
1. DHTR (2nd immune response, Jka,CcEe)
2. GVHD (proliferation of donor Lymphocyte in patient’s BM)
3. Viral (window period, product recall)
4. FE overload (repeated transfusion [aplastic anaemia, THAL major])

79
Q

Indications of giving RBC, PLT, Plasma, CRYO & Leukocytes. (5)

A

RBC:
1. HB<7
2. HB>10 who can’t tolerate anaemia

PLT:
1. PLT<10
2. PLT<20 with sepsis
3. PLT<50 with mucosal bleeding
4. PLT<100 with CNS bleeding
5. PLT<50 for premature neonates (PLT<100 for sick)
6. Suspected PLT dysfunction / deficiency after MTP
#Avoid giving PLT in MAHA cases

Plasma:
1. TTP
2. Warfarin reversal (consider PCC if available)
3. PT/APTT>1.5X + HaemophiliaA/B OR DIC OR hepatic failure
4. Suspected Factor deficiency after MTP

CRYO (1,8, vWF,13):
1. vWF (consider DDAVP if available, beware of Low NA)
2. FIB deficiency
3. Factor 13 deficiency

Leukocytes:
1. N<0.5 with no response to antibiotic >2d

80
Q

Indication of irradiated, CMV-, Rh- RBC. (3)

A

Irradiated for BMT (Lymphocyte division is inhibited to prevent GVHD)

CMV- for CMV- pregnant / BMT patient, and patient with HIV

Rh-
1. HDFN Anti-D+
2. Rh- Anti-D+
3. Rh- women
4. Rh? white women
5. Rh-

81
Q

What is epilepsy? (1)
Name anti-epilepsy drugs & their mechanism of action. (8)
Why taking anti-epilepsy drugs with oral contraceptive is a bad idea? (1)
Give two consideration for when prescribing anti-epilepsy drugs to pregnant women. (2)

A

chronic seizures (synchronous depolarization)
+involuntary muscular movement = convulsion

For neuron, + entry = depolarization (activation), CA enter causes release of neurotransmitter
ALB is carrier of most drugs, so Low ALB (L/R disease) increase drug toxicity

anti-epilepsy:
Carbamazepine: Na
Phenytoin & Valproic acid: Na & CA
Ethosuximide: CA
Barbiturate: CL[GABA] (duration)
Benzodiazepine: CL[GABA] (frequency)
ViGABAtrin: GABA transaminase inhibition
Topiramate: AMPA(NA) Glutamate R inhibition
Felbamate: NMDA(CA) Glutamate R inhibition

anti-epilepsy drugs (except Valproic acid) upregulate P450, increasing rate of OCP metabolism

Anti-epilepsy drugs are teratogen & interfering folate absorption. Order AFP (neural tube defect) & give folate.

82
Q

What are pre-eclampsia & eclampsia? (2) Name 4 organs affected. (4)
How to prevent eclampsia? (1)

A

pre-eclampsia: narrowing of Uteroplacental artery induces pro-inflammatory protein release causing vasoconstriction.

Kidney: High UTP
Eye: Scotoma
Liver: HELLP (Hemolysis, Elevated Liver enzyme, low PLT)
Brain: cerebral edema causing seizures (eclampsia)

Give MgSO4 to patient with pre-eclampsia

83
Q

We use BCG for ALB measurement. Is BCG specific for ALB? How about BCP? (2) Name 1 interference for BCG & BCP respectively (2)

A

No. BCG react faster with ALB but also react with Globulin.
BCP has higher specificity for ALB.

BCG: Penicillin
BCP: Organic acid in renal dialysis patients

84
Q

Kjeldahl Method measures Nitrogen content & converts it to TP. Why do we use Biuret instead of Kjeldahl for routine TP measurement? (1) tartrate & KI exist in Biuret reagents, why? (2)

A

Kjeldahl requires tedious titration & boiling steps.
Tartrate salt prevents turbidity
KI prevents Cu autoreduction (favorable in alkaline)

85
Q

I want to measure UTP without using turbidity by Benzethonium chloride, how? (1)

A

Folin–Lowry modification of Biuret method may be used, it has increased sensitivity.

86
Q

Why do ward patients have lower TP, ALB, HCT & CA? (1)

A

They are laying down instead of sitting/standing.
Standing patient has 10% higher TP, ALB(CA), CHO, WBC, RBC due to shifting of water out of blood vessel.

87
Q

Plasma protein is higher than serum protein, why? (1)

A

FIB is used during clot formation, forming serum.

88
Q

Name 1 condition that causes High ALB & Low ALB respectively (2)

A

High ALB: dehydration
Low ALB: Inflammation, after ruling out cirrhosis, loss (burn, hemorrhage)

89
Q

State SPE fractions from fastest to slowest. (5) which fraction is related to the Iron panel, hemolysis & cystic fibrosis respectively? (3)

A

ALB, alpha1, alpha2, beta, gamma
Iron panel: beta (transferin)
hemolysis: alpha2 (haptoglobin)
cystic fibrosis: alpha1 (alpha1 antitrypsin)

90
Q

Point the finding in SPE for Cirrhosis, Wilson’s, Malignancy/RA, MM, Inflammation, & CF (5)

A

ALB Low whenever inflammation is involved

Cirrhosis: β-γ bridging (IgA)
Wilson’s: Low α2 (ceruloplasmin)
Malignancy/RA: Polyclonal γ + inflammation
MM: Monoclonal γ (sometimes β / α2)
Inflammation: α1 (α1-antitrypsin), α2 (haptoglobin)
CF: α1 Low, α2 (chronic emphysema[Inflammation]), γ (Cirrhosis)

91
Q

Why low buffer ionic strength increases analyte mobility?(1)

A

When ionic strength decreases, current decreases, but the current force is used to move analyte, increasing analyte mobility.

92
Q

Why are Serum SPE & Urine bence jones protein both required for MM screening? (1) Why is the Serum light chain used in MM monitoring? (1)

A

24h Urine bence jones protein is necessary to rule out MM because 25% MM patient has heavy chain gene deletion and the remaining monoclonal light chain is filtered & can be detected only in urine. polyclonal gammopathies can cause false positive

Serum-free light chain immunoassay is sensitive in detecting early monoclonal gammopathies, good for monitoring also due to shorter plasma half life than intact Ig

93
Q

Why do CSF SPE? (1) How to treat the CSF sample before SPE? (1) How can you confirm the bands in CSF SPE only exist in CSF?(1)

A

For MS, IgG index is sensitive but not specific. gamma oligoclonal banding in SPE in 90% MS patient .

CSF sample should be Concentrate 100 times to increase sensitivity.

gamma oligoclonal banding observed in CSF SPE should be absent in serum SPE.

94
Q

What is the K/L ratio & why is it important in MM diagnosis? (2)

A

Normal K : L ratio ~= 2:1. Alteration implies monoclonal Antibody.

95
Q

How does SDS-PAGE differ from agarose gel? (1) Apply them to Lipoprotein separation. (1)

A

SDS-PAGE: based on size
– Chylomicrons→pre-β(VLDL) →β(LDL)→α(HDL) +
agarose gel: based on size & charge
– Chylomicrons →β(LDL)→pre-β(VLDL)→α(HDL) +

96
Q

Haptoglobin is not useful in diagnosing hemolysis in a state of inflammation, suggest another test in this case. (1)

A

Haptoglobin binds free Hb after hemolysis, but its synthesis increase in inflammation as an APR, masking the drop in Hp, consider Hemopexin to confirm hemolysis in this case

97
Q

In PMH, Hb pattern is performed using HPLC, describe the procedure. (6)

A

PMH uses bio rad variant ii for Hb pattern
1. Select sample (MCV&MCH Low, No history, No Transfusion)
2. Check RT & Area for Cal, F & A2 results for QC
3. Early elution peak existence = HbH likely = re-H if -
4. HbH>3%/Early peak/Hb variants = Alk Gel
5. HbSCED for confirm = Acid Gel
6. unresolved cases / OBS&IVF cases = CE (Sebia)

98
Q

Describe the 4 types of inherited hyperlipoproteinemia & the 3 types of acquired hyperlipoproteinemia (7)

A

Inherited
1. LPL deficiency
2. apo-B100 mutation (Young patient with MI)
3. apoE mutation
4. excess VLDL release
#Xanthomas, acute pancreatitis

Acquired
1. Cholestasis (accumulation)
2. Nephrotic syndrome (Liver compensate for lost of ALB)
3. DM (insulin induces LPL, lack of insulin causes VLDL accumulation)

99
Q

Describe the Apo affected in Abetalipoproteinemia & Tangier disease respectively (2)

A

Abetalipoproteinemia: Apo B48 / Apo B100
-fat-soluble vitamin deficiency (A: retinitis, D: osteomalacia, E: acanthocytosis)
Tangier disease: Apo A1, Low HDL

100
Q

Name 7 lysozymal storage disease (7)

A
  1. Fabry
    galactosidase, ceramide
    My fabrite activity is ceramics. We made a galaXy
  2. Gaucher
    glucocerebrosidase, glucocerebroside
    oh my Gauch, he’s such a Bro (tissue paper cytoplasm)
  3. Tay-Sachs
    hexoaminidase, ganglioside
    A Gang of 6 small Jews (no splenomegaly)
  4. Niemann Pick
    sphinogomyelinase, sphinogomyelin
    pick your big nose with your sphinger
  5. Krabbe’s
    galactocerebrosidase, galactocerebroside
    the Krabbe is out of this world (globoid cell)
  6. Hunter’s
    iduronate sulfatase, dermatan sulfate
    X-marks the spot (no corneal clouding)
  7. Hurler’s
    L-iduronidase, dermatan sulfate

Cherry-red macula: Tay-Sachs & Niemann Pick

101
Q

What are the 4 classes of antiarrhythmic? (4)
Are there other drugs? (3)

A
  1. NA (CAB) [0]
    -A = SLE, B = Post-MI
  2. NA/K (ol) [4]
    -hypoglycemic masking
  3. K (AIDS) [3]
    -TFT,PFT,LFT
    -phlebitis
  4. CA [0,3,4]
    -Edema

Other drugs:
1. Digoxin
-inhibit NA/K&raquo_space; 2nd NA/CA&raquo_space; High CA = High contractility&raquo_space; CHF
-vagus nerve&raquo_space; SA&raquo_space; AF
2. Adenosine
-Acute IV for SVT
3. MgSO4
-de pointes & Digoxin induced arrhythmia

102
Q

What is the upper limit of TG for the Friedewald equation? (1) Suggest another formula with a higher upper limit. (1)

A

4.52, that’s why LDL measurement is required for sample with TG>5.2.

Sampson-NIH2 equation (TG<=9 mmol/L)

103
Q

LDL by either calculation or measurement are not appropriate for non-fasting samples, why? (2)

A

In non-fasting, chylomicron present, so not all TG are on VLDL, so never use non-fasting sample to determine LDL by calculation (LDL itself increase after meal, so it is not acute even by measurement)

104
Q

What is 1U of enzyme activity? (1)

A

1IU = quantity of enzyme that Converts 1 μmol of substrate to product per minute

105
Q

State enzymes that requires Mg2+, Ca2+, and vitamin B6 as cofactor respectively (3)

A

Mg2+: CK ALP
Ca2+: AMY
B6: AST, ALT

106
Q

Why is ALP & GGT increase in cholestasis when no actual cell damage is done? (1)

A

In cholestasis, ALP & GGT release is based on secretion rather than necrosis

107
Q

CK & AMY results often become higher after dilution / decrease mode, why is that? (1)

A

Higher than expected result after dilution is common due to endogenous inhibitors of CK & AMY

108
Q

State where LDH1~5 exists in the body. (5) How would LDH level be affected for freezed sample? (1)

A

1: Heart
2: RBC
3: Brain, pancreas, lung, spleen, kidney
4: kidney, pancreas, placenta
5: Liver, muscle

Freezing cause deterioration of LD-5

109
Q

What is the URL of hsTnI based on? (1) How can physicians rule out MI using hsTnI? (1)

A

99% percentile of population with CV<10%

0min: Myoglobin / HsTnI
3h & 6h & 12h: HsTnI / CK-MB

110
Q

What is the use of measuring NT-proBNP? (1) Why don’t we measure BNP instead? (1)

A
  1. CHF&raquo_space; increased intracardiac blood volume&raquo_space; BNP released by ventricles
  2. preproBNP&raquo_space; proBNP&raquo_space; BNP & NT-proBNP (inactive)
  3. High BNP + ischemia&raquo_space; Higher risk of MI
  4. NT-proBNP value not affected by nesiritide (BNP for treating CHF)
111
Q

State the order of cardiac markers increases after MI. (1) Why is hsTnI still the best even if it is not the first to rise? (1)

A

Myoglobin, WBC, hsTnI, CK, AST, LDH.　見張っとく気ある？
hsTnI persist 7 days, with high clinical specificity

112
Q

Interpret High results with AST>ALT vs ALT>AST. (2)

A

AST>ALT:
1. Alcoholism (mitochondrial AST)
2. acute hepatitis (half life of AST)

113
Q

2-amino-2-methyl-1-propanol exists in ALP reagents, why? (1)

A

Pi product inhibition on ALP activity
Add 2-amino-2-methyl-1-propanol to bind Pi

114
Q

State the 3 ALP isoenzymes & suggest a way to separate them (4)

A

Heat labile to stable:
Placental / lung cancer ALP > liver ALP > bone ALP

Placental / lung cancer ALP retain activity after 65° C for 10 minutes
If activity <20% after 56°C for 10 minutes, consider bone ALP

115
Q

Suggest 3 conditions that can be diagnosed by ACP (3)

A

prostatic ACP: seminal fluid, sexual assault
TRAP: hairy cell leukaemia (AP in Lymphocyte), bone cancer (AP in osteoclast)

116
Q

Is AMY specific for pancreatitis? (2) Why measure UAMY & Lipase on top of AMY? (2)

A

No. It also rise in peptic ulcer, and there is S-type AMY rise in Mumps / ectopic pregnancy.

In acute pancreatitis, AMY rise at 2h & peaks at 12h (5X), return to normal after 4 days, UAMY rise higher & persist 1 week

Lipase rise higher than amylase (~50X)

117
Q

How about chronic pancreatitis? (4)

A

AMY & Lipase synthesis is compromised in chronic pancreatitis.

Sensitivity of AMY & Lipase in detecting chronic pancreatitis is <50%, consider faecal fat increase & trypsin / chymotrypsin / elastin decrease

118
Q

Explain why Le(a-b+) patient won’t develop Anti-Lea (1)

A

Lea still exist in patient plasma, just the quantity is insufficient to adsorb to RBC & be detected as phenotype.
In Se(w) patient, less Ag is converted to H so less is further converted to Leb, and more Ag is available to be converted to Lea, therefore patient phenotype can be Le(a+b+).

119
Q

Describe 3+3 rule in Antigram interpretation (1) How WarmAutoAb & Dosage effect influence Antigram interpretation? (2)

A

3+3 rule for Ab ID is based on 1/20 probability by chance as calculated using Fisher’s exact method, meaning 95% confidence in correct Ab ID, other combination is ok as long as the p is <= 1/20

heterozygous panel cell, along with weak Ab, Anti-C’, and Ag not in panel cell, are the reasons of -ve AbID.

WarmAutoAb causes panagglutination (ALL +ve AbID), with DAT+.
If DAT-, possibility of Multiple AlloAb, Anti-H, Anti-high frequency Ag should be considered.

120
Q

Suggest a possible culprit of warm AIHA & cold AIHA respectively (2)

A

-warm AIHA can be Anti-e, although in most cases its specificity can’t be determined. Finding e- blood is difficult e is has frequency in population. SLE is a cause of warm AIHA.

-cold AIHA can be Anti-I / i, which can be confirmed with negative reaction with cord blood as it contains only i antigen, Anti-i ~= mononucleosis (EBV)

121
Q

Weak Panagglutination with AC-, what would you suspect? (1) How to prove? (1)

A

Anti-high frequency Ag with HTLA characteristic.
For HTLA, serial dilution of plasma would affect the strength of its reaction, but all reactions are weak.

122
Q

Anti-Lua vs Anti-Lub, which is more common? (1)

A

-Anti-Lua usually exist as Lua is low frequency antigen, Lub is high frequency antigen & Anti-Lub is rare & may cause hemolysis.

123
Q

Why don’t we use EDTA samples for the Cold agglutinin test? (1)

A

-For Cold agglutinin test, store at 4C<48h is recommended for C’ activity. Plasma sample is inappropriate as anticoagulant chelate Ca required for C’ actions.

124
Q

State Ab involved for PCH, CAD, IM(EBV), M. pneumoniae. (3) How about PNH? (1)

A

PCH: IgG (IgM / A) Anti-I / P, also called Donath–Landsteiner antibody
-biphasic: Attach RBC at 4C, Hemolysis at 37C

CAD: IgM Anti-I

IM(EBV): IgM Anti-i, mostly child
M. Pneumoniae: Anti-I, mostly adult
#titer >64 = +

PNH: Not Ab induced. It is PIGA mutation causing CD55/59 deficiency, which weaken C’ inhibition, this apply to WBC & PLT as well (Pancytopenia)

125
Q

Why did we Irradiate RBC? (1)

A

Lymphocyte division is inhibited to prevent GVHD

126
Q

State the WBC standard of Leukocyte-reduced RBC, the PLT standard of apheresis PLT (2)

A

WBC < 5 * 10^6

> 3.0 × 10^11 PLT (10^9 for PLT count)

127
Q

Which blood product is indicated for patients with IgA deficiency? (1)

A

Patient with IgA deficiency may develop Anti-IgA, which is an allergic transfusion reaction, consider giving washed RBC

128
Q

Can I transfuse O+ plasma to O- women? (1)

A

Yes.
Rh is irrelevant in plasma transfusion

129
Q

O- mom with Anti-D -, rosette test -, dose of RhIg? (1)

A

-rosette test (FMH,+Anti-D to maternal blood, add indicator cell to form a rosette)&raquo_space; kleihauer test (HbF in maternal circulation, based on HbF resistance to acid)

rosette test negative = no fetal blood in maternal circulation = give 1 dose RhIg

130
Q

O- mom with Anti-D -, rosette test +, kleihauer (25 fetal cell / 4000 maternal cell), dose of RhIg? (1)

A

-kleihauer test calculation:
x fetal cell / 2000 maternal cell counted * 5000 / 30
n (0.1~0.4): +1; n (0.5~0.9): +2
#5000mL is maternal BV, 30mL is protection volume by 1 vial RhIg
#Calculate maternal BV based on weight using 70mL/kg

=1.04 (+1) = 2

131
Q

Suggest 3 actions that can be taken when maternal Anti-K is detected for Foetus with K antigen. (3)

A
  1. Early labour
  2. Plasmapheresis
  3. Intrauterine transfusion (>20weeks with fetal hemolysis observed)
132
Q

Why should a Kleihauer test be performed to prove Maternal weak D? (1)

A

The weak D can be caused by fetal RBC & not reflecting maternal phenotype

133
Q

Normal CSF GLU & Protein compared to plasma. (2) When you see GLU low & Protein high, what would you consider? (4)

A

CSF Glu = 60% Plasma Glu
CSF Protein is trivial compared to Plasma Protein, *2 for neonate

Low GLU High TP:
SAH, MS, malignancy, bacterial (High Lactate) / fungal meningitis

134
Q

Name 2 tests of CSF requiring urgent sendout to MICRO. (2) Why is it urgent & how are they performed? (3)

A

Cell count & Gram stain.

Detect Pleocytosis & DC to determine infection type
-always perform DC for newborn & patient with WBC> 5/μL
-Cytocentrifugation to concentrate the sample before Wright’s stain
N = bacterial, L = viral, both = TB/fungal
MS & leukaemia

-Pleocytosis in traumatic tap should have WBC count corrected by RBC count in CSF
-Corrected WBC count = WBCs in CSF – [(Blood WBCs × CSF RBCs) ÷ Blood RBCs]

Neonate
Group B Streptococcus
E. coli

Children
Haemophilus influenzae
S. pneumoniae
N. meningitidis

Elderly
S. pneumoniae

135
Q

Name two ways to differentiate Traumatic tap vs SAH (2)

A

visual Xanthochromia for SAH
Low opening pressure during CSF collection implies decreased CSF volume (Traumatic tap)

136
Q

Describe two tests for MS, which is more specific? (3)

A

-For MS, IgG index is sensitive but not specific, gamma oligoclonal banding in SPE in 90% MS patient (those band should be absent in serum SPE)
-IgG index = (CSF/Plasma IgG) / (CSF/Plasma ALB) ; >0.85 = MS / infection

137
Q

Can you send aliquot for CSF CHEM to MICRO? (1)

A

No.
1st aliquot CSF send to CHEM as contamination is likely, 2nd aliquot sent to MICRO

138
Q

After a car accident, there is colourless discharge from the patient’s nose, how to tell if it is CSF? (1)

A

β-2 transferrin (tau protein) in CSF only

139
Q

What are the 4 steps of hemostasis? (4)
PLT plug formation steps. (3)
Based on the mechanism, suggest why aspirin, clopidogrel, Abciximab, & dipyridamole are antithrombotic. (4)
Also, correlate BSS, vWD, TTP, GT, ITP to the story.

A
  1. v.c.
  2. PLT aggregation
  3. Coagulation (Fibrin formed trap RBC)
  4. Fibrinolysis

PLT plug formation
1. Adhesion (S.E.C exposed, GP1b~vWF)
2. Activation (PLT granule release, Ca dependent)
-ADP&raquo_space; P2Y12 R - ADP &raquo_space; activate GP2b/3a
-TXA2&raquo_space; PLT aggregation & v.c. (Gi: cAMP Low: CA High)
3. Aggregation (GP2b/3a-Fibrinogen)

aspirin is COX I, causing TXA2 inhibition.
clopidogrel is P2Y12 RI, blocking ADP action.
Abciximab is Anti-Gp2b/3a.
dipyridamole is PDE I, preventing cAMP degradation.

GP1b defective in BSS. vWF defective/deficient in vWD. vWF excess in TTP due to ADAMTS13 deficiency.
GP2b/3a defective in GT, it is also the target in ITP.

140
Q

What are the inducers & inhibitors of P450? (11)

A

CRAP GPS induces my rage
C: Carbamazepine (anti-epilepsy)
R: Rifampin (antibiotic)
A: Alcohol
P: Phenytoin (anti-epilepsy)
G: Griseofulvin (anti-fungal)
P: Phenobarbital (anti-epilepsy)
S: Sulfonylurea (insulin inducer)

inhibitor:
Valproic acid (anti-epilepsy)
Isoniazid (anti-TB)
Amiodarone (class 3 antiarrhythmic)
Grapefruit juice

P450 is for metabolism of drugs, so P450 inducer causes low drug level, and P450 inhibitor causes high drug level.

141
Q

Give 5 P450 subtypes & the drug they metabolize respectively. (5)

A

CYP1A2: ACET (2A)
CYP2E1: Ethanol (21y for alcohol)
CYP2C9: Warfarin (2,7,9,10,C,S)
CYP2D6: cardiovascular drug (2D echo)
CYP3A4: Others

142
Q

When you suspect patient has alcohol intoxication, both Osmolal gap & Anion gap should be calculated, why? (2)
Name 1 drug for treating alcohol intoxication. (1) What if the hospital don’t have this drug? (1)

A

Alcohol DH is an enzyme that convert Alcohol to metabolites.
Ethanol&raquo_space; Acetic acid&raquo_space; CO2
Ethylene glycol (anti-freeze)&raquo_space; Glyoxylic acid
Methanol (moonshine)&raquo_space; Formic acid
Isopropyl alcohol (hand sanitizer)&raquo_space; Acetone

Alcohol = OSM gap, Metabolites = Anion gap.
Therefore, OSM gap decreases & Anion gap increases after ingestion.
Except Isopropyl alcohol as Acetone is ketone, not acid

Fomepizole prevents Alcohol DH action so no toxic metabolites are formed.
Give Ethanol (vodka), as Alcohol DH preferentially metabolize Ethanol, which forms non-toxic CO2.

143
Q

Sulfonylurea & Metformin are both DM drugs, what is the main difference between them. (2)
What is the order of drugs prescribed for patient with different level of DM? (3)

A

Sulfonylurea: Insulin release
Metformin: Insulin sensitivity, causes LA when RF compromised by contrast.

For DM1, give insulin.
Rapid: LAG
Short: Regular
intermediate: NPH
Long: GD

For DM2:
IFG (Diet)&raquo_space; DM (Metformin + 1 + 2)&raquo_space; Insulin
1. Sulfonylurea / Meglitinide (-ide)
2. DPP4 I (High GLP1, High Insulin) (-liptin)
3. GLP1 agonist (-tide)
4. SGLT2 I (-flozin) (UTI)
5. alpha-glucosidase I (Acarbose) (GI upset)
6. Thiazolidinedione (TZD) (-glitazone) (bind PPAR-gamma)
7. Amylin analog (help Insulin)

144
Q

Name 2 foods & 1 condition that causes gout. (2)
Treatment of acute & chronic gout is different, explain. (5)

A

Treating the inflamed joint, not lowering UA

Red meat & Alcohol&raquo_space; purine&raquo_space; UA
TLS: chemotherapy lysis cancer cell, releasing DNA&raquo_space; purine&raquo_space; UA

Acute gout:
NSAIDs
Cochicine
#Treating Inflammation, no effect on UA

Chronic gout:
Eat less red meat & Alcohol
Allopurinol (XO I)
Rasburicase (break down UA)

145
Q

Name 1 condition for falsely high & low HbA1C respectively (2)
What test would you recommend to resolve this? (1)

A

Falsely high: IDA (RBC life span increase)
Falsely low: Dialysis (Blood loss, RBC life span decrease)

GA >20% = DM

146
Q

Explain how IgG, C3C4, and ANA are used to screen for Autoimmune diseases (SLE, RA, SS, SSc).

Suggest follow up tests for SLE, RA, SS, SSc.

A

IgG high in SS & SLE, although infection, MM & hepatitis should be ruled out first. IgG low after taking steroid.

C3C4 low in SLE (consumption), although cirrhosis should be ruled out first. C3C4 high in inflammation.

ANA high in 100% SLE cases, and 50% RA & MS & SSc cases.

SLE: Anti-dsDNA, Anti-Sm (Any 1 + rash)
RA: Anti-CCP, RF
SS: Anti-SSa/b
SSc: Anti-centromere, Anti-Scl-70

147
Q

What are P-ANCA & C-ANCA test for? (2)
How about Anti-mitochondria, Anti-IF, Anti-smooth muscle, and Anti-GAD.

A

Different types of vasculitis.
P-ANCA is Anti-PR3
C-ANCA is Anti-MPO
They are inside neutrophil granule until priming by IL-1 & TNF-alpha, when it travels to cell surface & react with their respective Autoimmune Ab, causing neutrophil degranulation & subsequent ROS induced vasculitis.

Specifically, C-ANCA is for granulomatosis with polyangiitis, & P-ANCA for other types of vasculitis.

PBC, pernicious anaemia, AIH, Type1 DM.

Chem&Haem (17 decks)

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