Clinical Chemistry Boards

Front 1

Gilbert's Syndrome/Disease

Back 1

Benign elevation of unconjugated bilirubin. Typically no more specific symptoms than mild jaundice on occation. Total bili ranges from 1.2 to 5.3 mg/dL, with high unconjugated/indirect bili.

Front 2

Hendeson-Hesselbach Equation

Back 2

pH=pKa+Log([Base]/[Acid])

Front 3

H-H Eqn for blood acid-base balance

Back 3

pH=6.1+Log([HCO3-]/(0.03*pCO2))

Front 4

RPM to RCF

Back 4

RCF=1.12xr(mm)x(RPM/1000)^2

Front 5

Osmolality from freezing point

Back 5

Osm=dT/1.86 (in mol/kg)

Front 6

MCV

Back 6

HCT*10/RBC

Front 7

MCH

Back 7

Hgb*10/RBC

Front 8

MCHC

Back 8

Hbg*100/HCT or MCH*100/MCV

Front 9

Affect of high pH, pCO2, or T on pO2

Back 9

High pCO2 and T lower pO2, high pH increases it (aka low pCO2, an acid)

Front 10

Autoimmune Hepatitis 1 antibodies

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Anti-Smooth Muscle and Anti-Nuclear

Front 11

Autoimmune Hepatitis Type 2 Antibodies

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Anti-liver-kidney-microsomal and Anti-liver cytolosol

Front 12

Peptide hormones sharing their alpha subunit

Back 12

TSH, hCG, LH, and FSH

Front 13

Dubin-Johnson Disease

Back 13

Conjugated Hyperbilirubinemia. High conjugated/direct and total (2-5). Otherwise normal LFTs, typically benign.

Front 14

AlkPhos heat denaturation mnemonic

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Bone burns, liver lingers, placental persists

Front 15

Which antibodies activate complement via which path?

Back 15

IgA - alternative. IgG and IgM - classical

Front 16

Test for in vitro hemolysis

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Haptoglobin (low in in vivo, normal for in vitro)

Front 17

Most common interference for Jaffe reaction

Back 17

Cephalosporins (all start with 'Cef', such as Cefclidine)

Front 18

Changes in beta-Thal

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microcytic anemia, elevated HbA2, and HbF

Front 19

Changes in alpha-Thal

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Microcytic anemia, no change in A2 or F

Front 20

Standard test for CO poisoning

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CO-oximetry. Pulse oximetry will not work.

Front 21

Result of cyanide poisoning

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Lactate-driven metabolic acidosis with anion gap

Front 22

Light's Criteria

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LDH > 2/3 ULN for serum or >200, used to determine if effusion is exudative or not. Positive by light's criteria denotes exudative.

Front 23

Respiratory Alkylosis

Back 23

High pH with low pCO2. May also have low bicarb (compensation)

Front 24

Metabolic alkylosis

Back 24

High pH with high bicarb. Typically will also have high pCO2 (compensation).

Front 25

Respiratory acidosis

Back 25

Low pH with high pCO2. May also have high bicarb (compensation)

Front 26

Metabolic acidosis

Back 26

Low pH with low bicarb. Typically will also have low pCO2 (compensation)

Front 27

Actions of Renin

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Converts Angiotensinogen to angiotensin I, which results in increased blood pressure both directly and through increased Na (and water) reabsorption.

Front 28

Crigler-Najar syndrome, type 1

Back 28

Defect in the enzyme that conjugates bilirubin, resulting in very high (>20 mg/dL) serum and unconjugated (indirect) bilirubin. Can be fatal.

Front 29

Crigler-Najar Syndrome, Type II

Back 29

Caused by a similar defect as type I (conjugating enzyme) but less severe, also leads to high serum bili and unconjugated (indirect) bili, but to a lesser extent (typically 7-20 mg/dL). Can be distinguished through phenobarb treatment, which is only helpful in Type II.

Front 30

Calculated LDL

Back 30

LDL=TC-HDL-TG/4. Not usable if TG is greater than 400.

Front 31

INR

Back 31

INR=(PTpatient/PTaverage)^ISI

Front 32

Total Body Burden

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TBB = Vd*Body Mass*Cs, where Vd is volume of distribution and Cs is serum concentration

Front 33

Rumak-Mathew Nomogram

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Chart used to judge a patient's risk of acetaminophen toxicity

Front 34

Serum Anion Gap

Back 34

AG = Na + K - Cl - HCO3

Front 35

Serum Osmolality

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Osm = 2×Na + Glucose/18 + BUN/2.8

Front 36

Effects of PTH

Back 36

Increase Bone resorption, Ca resportion (and thus Serum calcium), and 1,25-Vit D production. Decreases Ph resorption and thus serum Ph.

Front 37

Clearance

Back 37

Cl=Cu*Vu/Cs, where Cu and Cs are urine and serum concentration respectively, and Vu is volume of urine. Expressed in mL/min.

Front 38

Factor V Leiden

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Mutation in Factor V leading to activated protein c resistance, an excessive clotting state.

Front 39

Sensitivity

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Sens = TP/(TP+FN), where TP is true positive and FN is false negative

Front 40

Specificity

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Spec = TN/(TN+FP), where TN is true negative and FP is false positive.

Front 41

Positive Predictive Value

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PPV = TP/(TP+FP), where TP is true positive and FP is false positive.

Front 42

Negative Predictive Value

Back 42

NPV = TN/(TN+FN), where TN is true negative and FN is false negative.

Front 43

Likelyhood Ratio

Back 43

LR = Sens/(1-Spec)

Front 44

Chylomicrons

Back 44

First stop for triglycerides, they're formed in the gut, circulate, and then are absorbed as remnants by the liver. Contain ApoE, c-11, and B-48.

Front 45

Remnants

Back 45

The leftover particles after chylomicrons have lost most of their TGs and ApoC-11. Typically absorbed by the liver.

Front 46

VLDL

Back 46

'Very Low Density Lipoprotein', the largest intrinsic lipid particles. Contain ApoE, C-11, and B-100, and is mostly TGs

Front 47

IDL

Back 47

'Intermediate Density Lipoprotein', size between that of VLDL and LDL. Contains ApoE and B-100, and is an even mix of TGs and cholesterol.

Front 48

LDL

Back 48

'Low Density Lipoprotein', density below IDL, this is the last step before intrinsic lipid particles become HDL, and mostly cholesterol. Contains ApoB-100.

Front 49

HDL

Back 49

'High Density Lipoprotein', the smallest of the intrinsic lipid particles, mostly composed of cholesterol. Also contains ApoA-1 and A-11.

Front 50

ApoE

Back 50

Apolipoprotein E, found on most particles, but most important for remnants and HDL, as it regulates uptake by the liver.

Front 51

ApoA-I

Back 51

The main component of HDL, and a cofactor for LCAT, which forms cholesterol esters from cholesterol.

Front 52

ApoA-II

Back 52

Next major constituent of HDL after A-I, and an inhibitor of LCAT and activator of hepatic triglyceride lipase.

Front 53

ApoA-IV

Back 53

Present on newly formed chylomicrons, and possibly an activator of LCAT.

Front 54

ApoB-48

Back 54

Present on chylomicrons and remnants, allows for secretion and absorption.

Front 55

ApoB-100

Back 55

Present on VLDL, IDL, and LDL, this is involved with secretion and absorption in the liver.

Front 56

ApoC-I

Back 56

Associated with something, possibly activates LCAT. Not much known.

Front 57

ApoC-II

Back 57

Associated witb VLDL, IDL, HDL, and chylomicrons, this protein activates LPL, which allows lipoprotein molecules to be hydrolized and absorbed by various tissues.

Front 58

ApoE

Back 58

Found in chylomicrons, remnants, VLDL, and IDL, this allows to liver to absorb these paritcles. Several isoforms are known, and an E2/E2 genetic state is associatdled with Type III hyperlipidemia.

Front 59

Type I Hyperlipidemia

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Increased chylomicrons, associated with clear plasma and cream layer after centifuging. Caused by LPL or C-II deficiency or LPL inhibition.

Front 60

LPL

Back 60

Lipoprotien lipase, protein in peripheral crlls which allow them to break down and absorb tiglycerides.

Front 61

Type IIA Hyperlipidemia

Back 61

Increase in LDL, associated with clear plasma on centrifugation. Can be caused by many things, most notably mutations in LDL-R, defective B-100, overproduction of B-100, hyperabsorption of sitosterol, or caused by DM, nephrosis, biliary tract disease, or hyperthroidism.

Front 62

Type IIB Hyperlipidemia

Back 62

Similar to IIA, with increased LDL and VLDL (and thus increased TG), associated with turbid plasma upon centrifugation. Increase in LDL, associated with clear plasma on centrifugation. Can be caused by many things, most notably mutations in LDL-R, overproduction of B-100, hyperabsorption of sitosterol, or caused by DM, nephrosis, biliary tract disease, or hyperthroidism.

Front 63

Type III Hyperlipidemia

Back 63

Increaed IDL, thus increased TG and LDL. Associated with turbit plasma upon centrifugation. Caused either by ApoE deficiency (rare) or an E2/E2 phenotype.

Front 64

Type IV Hyperlipidemia

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Increased VLDL, thus increased triglycerides and associated with turbid plasma upon centrifugation. Caused by hypothyroidism, DM, FHC, FCH, deficiency of adipose tissue, or various causes of liver damage or renal disease.

Front 65

Type V Hyperlipidemia

Back 65

Increased VLDL and chylomicrons, thus very high TG. Associated with turbid plasma and a cream layer. Caused by multiple Type IV causing conditions, such as DM and alcoholism.

Front 66

LPL deficiency

Back 66

Autosomal recessive disorder, affects 1 in 1 mil. Causes an increase in chylomicrons (type I hyperlipidemia) from reduced clearance.

Front 67

ApoC-II deficiency

Back 67

Similar to LPL deficiency, an autosomal recessive disorder that results in increased cylomicrons (type 1 hyperlipidemia) from reduced clearance.

Front 68

Familial Hypercholesterolemia

Back 68

Autosomal Dominant disorder, affecting about 1 in 500 people. Caused by a mutation in LDL-R that causes an LDL increase (type IIA hyperlipidemia) from reduced clearance and possibly secretion. Homozygous is highly affected and deadly by 20s.

Front 69

Familial defective B-100

Back 69

Autosomal dominant condition affecting about 1 in 500. Results in reduced clearance of LDL (type IIA hyperlipidemia). Not as severe as familial hypercholesterolemia.

Front 70

Familial Combined Hyperlipidemia

Back 70

Autosomal dominant overproduction of ApoB-100, affecting about 1 in 250 people. Since B-100 is overproduced, results in overproduction of VLDL, IDL, and LDL, causing type IIA, IIB, or IV hyperlipidemia.

Front 71

Autosomal Recessive Hypercholesterolemia

Back 71

As the name implies, a rare autotsomal recessive hyperlipidemia where LDL-R is not properly coupled to endocytotic machinery. Leads to Type IIA hyperlipidemia (high LDL) as ApoE clears VLDL and IDL properly.

Front 72

Polygenic Hypercholesterolemia

Back 72

Almost a diagnosis of exclusion, result of multiple low-level genetic causes with lifestyle aggrevation that leads to a relatively mild LDL increase.

Front 73

Sitosterolemia

Back 73

Rare genetic condition that results in hyperabsorption and decreased secretion of sitosterol and modified cholesterol synthesis which can lead to Type IIA/B hyperlipidemia, though it is hard to diagnose (need to test for phytosterols specificially).

Front 74

Homozygous E2

Back 74

A condition caused by having a homozygous E2 phenotype (out of possible E2, E3, or E4 allels), affecting about 1 in 5000. Considerably raises the risk for Type III hyperlipidemia (high IDL).

Front 75

ApoE deficiency

Back 75

Very rare disorder which results in the decreased clearance of IDL particles, resulting in Type III hyperlipidemia.

Front 76

Familial Hypertriglyceridemia

Back 76

An autosomal dominant condition resulting in high VLDL from excess hepatic production or LPL deficiency. Affects about one in 100 people.

Front 77

Transmittance to absorption

Back 77

Either A=Log10(1/T) (not percent!) or A=2-Log10(%T)

Front 78

Crockcroft Gault Eqn

Back 78

Simple equation for estimation of clearance from plasma creatinine -> Cl(ml/min)=((140-age(y))xBodyWeight(kg)x1.3)/PlasmaCreatinine(umol/L))x0.85(if female).

Front 79

4v-MRD

Back 79

Four variable equation for estimation of GFR -> GFR(mL/min/1.73m^2)=186×(SerumCreat(umol/L)x0.011312)^-1.154×age(y)^-0.203×(1.21 if black)×(0.742 if female).

Front 80

Fractional excretion

Back 80

Fraction of a substance excreted at each pass through the glomeruli. Can be calculated by (Cu,x×Cp,creat)/(Cu,creat×Cp,x) or (Cu×Vu)/(Cp×GFR)

Front 81

Elimination rate constant

Back 81

Typically shown by the variable k, it is slope of a first order elimination and is related to half-life by k=0.693/t.5 or Cl/Vd or (LnCp1-LnCp2)/(t2-t1), where Cp is plasma concentration, t2 and t1 are timepoints, and t.5 is half life.

Front 82

Maintenence Dose

Back 82

The dose required to maintain a steady state of drug in the body, typically given per hour (impatient) or per 12 or 24 hours. Can be calculated with MD=(Cp×Cl×T)/(S×F), where T is the time between doses, S is salt fraction, and F is bioavailability.

Front 83

Mixed Elimination Model Eqn

Back 83

Equation based on MM kinetics to estimate Maintenance Dose for non-first-order substances. Dose=(Vmax×CpxT)/((Km+Cp)×S×F), where T is the time between doses, S is salt fraction, and F is bioavailability.