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Clinical Chemistry 1 > Protien Catabolism & Nitrogenous Waste Excreation > Flashcards

Protien Catabolism & Nitrogenous Waste Excreation Flashcards

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1
Q

Functions of EPO?

A

Anti apoptosis function
Produce more RBC 

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2
Q

_____________ recycles HCO3

A

Kidneys

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3
Q

How can kidney disease lead to lysed RBCs?

A

Decreased EPO—> anemia and decreased bicarb ——> acidosis ——> causes membrane damage of RBCs and ruptures the cells

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4
Q

What is the most abundant serum protein?

A

Albumin

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5
Q

What is A:G ratio?

A

Albumin : total globulin

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6
Q

NPNs…

Non-protein

A

-cholesterol
-glucose
-urea nitrogen
-uric acid
-creatinine
-iron

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7
Q

Albumin range

A

3.4-5.0 g/dl

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8
Q

Total globulin range

A

2.2- 4.0 g/dl

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9
Q

Transferrin

A

250 mg/dl

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10
Q

Haptoglobin range

A

30- 205 mg/ dl

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11
Q

Ceruloplasmin range

A

25-45 mg/dl

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12
Q

Ferritin range

A

15- 300 ug/ dl

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13
Q

Hemopexin range

A

50- 100 mg/dl

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14
Q

Cholesterol range

A

140-250 mg/dl

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15
Q

Glucose range

A

70- 110 mg/dl

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16
Q

Urea nitrogen

A

6-23 mg/dl

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17
Q

Uric acid range

A

4.1- 8.5 mg/dl

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18
Q

Creatinine range

A

0.7- 1.4 mg/dl

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19
Q

Iron range

A

50-150 ug/dl

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20
Q

What can be a source of oxidative stress when not bound?

A

Haptoglobin when not bound to alpha globin chain

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21
Q

Free haptoglobin ______ can tell if if alpha is defective

A

G

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22
Q

_____________ becomes toxic when not bound

A

Transferrin

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23
Q

-can bind to free heme
-delivered to liver to be recycled

A

Haptoglobin
Hemopexin

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24
Q

Source of NPNs

A

Amino acids

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25
Q

Urea is synthesized in the ___________ from NH3 (Bacterial metabolism and got it and AA deamination) 

A

Liver

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26
Q

More protein ———-> more _____________ in GI.

A

Ammoniagesin

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27
Q

Why is determination important metabolic process?

A

Allows product (protein?) to be used for energy or to be converted into carbs or fat

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28
Q

urea in circulation is reported as ….

A

Blood urea nitrogen (BUN) 

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29
Q

BUN is increased with….

A

High protein diets and tissue breakdown

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30
Q

BUN is decreased with…

A

Protein synthesis, chronic and progressive renal insufficiency (No reabsorption), low protein intake and severe liver disease

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31
Q

Urea filtered in the kidney (______% reabsorbed in collecting duct, ____% excreted in urine)

A

40-50
50-60

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32
Q

Because BUN increased or decreased while GFR is normal, BUN is a _____________ Indicator of renal function.*****

A

Nonspecific **
(Compared to other markers) 

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33
Q

C.f. Urea production > Urea excretion: Urea remains in system —-> Degraded to ______ by intestinal bacteria and process by liver and cleared.

A

NH4

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34
Q

What is the most abundant NPN?

A

BUN

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35
Q

What are the three types of acute renal failure?

A

-Prerenal (Hypovolemia or poor perfusion) Before kidneys
-Renal (Rapid deterioration, e.g. Acute tubular necrosis) at kidneys
-post Renal (Obstructions, When osmolarity becomes the same in blood and tubule Filtration stops) After kidneys 

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36
Q

Pre-renal acute failure is usually due to altered ____________ function. 

A

Cardiovascular

(given ACE or angiotensin)

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37
Q

In normal serum, what is the year BUN/urea: Creatinine ratio? ***

A

10:1 - 20:1*

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38
Q

If both BUN and creatinine is elevated, ratio will still be normal bit could indicate…

A

Renal disease

  • Both can be out of range but have normal ratios
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39
Q

What is the most common cause of increased BUN in middle aged men? 

A

G.I. bleeding

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40
Q

What can cause an abnormal urea to creatine ratio?

A

Increase amino acid breakdown as in muscle wasting, high protein diet or G.I. bleeding

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41
Q

Serum BUN serum creatinine ratio greater than 20:1 Is observed in patients with…

A

• pre-renal azotemia*** (Accumulation of nitrogenous products in blood)
• Gastrointestinal bleeding
• Excessive protein intake

-Post-renal azotemia

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42
Q

BUN is absolute for determining renal function. true or false?

A

False! 

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43
Q

What is used to determine urea BUN ratio? 

A

-Berthelot reaction
-enzymatic glutamate dehydrogenase (340nm)
-Conductance
-protentiometric
-diacetyl monoxime
-O-phthalaldehyde 

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44
Q

-absorption maximum measured at 560 nm
-Performed directly on blood, serum or urine

A

Berthelot Reaction (rarely used)

(Urea methodology) 

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45
Q

Why is Berthelot Reaction rarely used? What’s the disadvantage?

A

Difficult to automate, lack of specificity, beers law narrow range

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46
Q

Beers law?

A

A =  epsilon b c ?

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47
Q

Berthelot Reaction test can be monitored at _____nm and Produces a bluish color from indophenol complex

A

560

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48
Q

-Method used quite frequently in clinical labs
-Conductivity increases with formation of

Urea ——Urease —->(NH,),COg —->2NH, +CO,
-Conductively measured at the same time

A

Conductance (Urea methodology)

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49
Q

-NH3 ISE Monitors urease reaction
-Urease covalently linked to electrode, converts urea to NH3
-Change in pH measured by electrode
-Very specific but not commonly use due to possibility of contamination***

A

UREA METHODOLOGY: POTENTIOMETRY

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50
Q

-Direct chemical analysis of urea (Instead of using urease)
-Commonly used

A

***Diacetyl Monopxime (urea methodology) 

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51
Q

Reference interval (BUN) for Diacetyl Monopxime?

A

8-26 mg/dl

(A lot of fluctuation in numbers, lab sets their own range) 

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52
Q

What is the disadvantage of Diacetyl Monopxime?

A

-Photosensitivity of product
-large dilution of sample required for beers law
-Corrosive reagents

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53
Q

Diacetyl Monopxime:

Yellow Diazine
-chromagen _____nm
-Fluorescence _____ nm 

A

550
415

no use of enzymes in this test

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54
Q

-Rarely used because of interference with other primary amines

A

O-phthalaldehyde*

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55
Q

A group of atoms and electrons forming part of an organic molecule that causes it to be colored

A

Chromophore

(At 510 nm with O-phthalaldehyde)

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56
Q

Why is O-phthaladehyde rarely used for urea? 

A

Interference with other primary amines 

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57
Q

What are the benefits of using dry slide urease-pH indicator?

A

-excellent accuracy
-Little interference from other biochemicals

  • Commonly used and can use different dyes 
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58
Q

What specimen is used for urea testing?

A

Serum or heparinized plasma or diluted urine

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59
Q

When testing for urea, CANNOT use ___________ (Inhibits urease reaction) or ___________ (Causes artificial elevation)

A

Fluoride, NH4 heparin***

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60
Q

What is the storage requirements for urea?

A

serum and plasma is stable for one week at 4°C or six months at -20°C

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61
Q

Creatinine is proportional to…

A

Muscle mass

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62
Q

What lab marker is important in liver disease?

A

Creatinine

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63
Q

CK requires ______. It is important for diagnosis of many diseases (ex: CK1, CK2, CK3)

A

ATP

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64
Q

Creatinine is formed from __________ creatine and creatine ________.**

A

Muscle
Phosphate

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65
Q

Creatinine in serum is proportional to…

A

Muscle mass. Generally increased in males compared to females

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66
Q

Serum concentrations of creatinine depends on?

A

-rate of production
-Rate of removal

*** Does not change dramatically, very stable!

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67
Q

There is little effect on serum creatinine from diet, urine volume and exercise
-plasma creatinine is stable with less than 10% variation in a day because….

A

-concentration in muscle is constant
-Rate of spontaneous breakdown is constant

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68
Q

Measure _____________ Clearance to determine filtration GFR**

A

Creatinine

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69
Q

How is creatinine filtered in the kidneys?Is creatinine reabsorbed?

A

-Freely filtered
-Not REABSORBED (5 to 20% may be secreted, from tubular secretion, not filtration)

  • Urinary excretion is directly proportional to muscle mass



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70
Q

About _____ mmol/creatinine excreted/kg of muscle mass

A

5

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71
Q

Exercise __________ Increases creatinine in serum and or urine

A

Slightly

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72
Q

Protein deficiency long-term ___________ Decreases creatinine in serum

A

Decreases

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73
Q

Tubular secretion ____________ as creatinine in serum increases in patients with renal insufficiency

A

Increases

Increased renal insufficiency = increased secretion of creatinine

74
Q

Because rate of production and removal are constant, creatinine is used to assess….

A

GFR (Renal function) 

75
Q

Creatinine clearance is a good estimate of GFR but still not…

A

The best method

(creatinine clearance more specific?) 

76
Q

Creatinine clearance is more sensitive for determining renal function than Creatinine _________ levels Because based on rate of excretion.

A

Serum

77
Q

Volume of plasma from which an amount of creatinine is removed in a specific amount of time (1 min) 

A

* creatinine clearance**

78
Q

Formula for creatinine clearance (Urine and serum: 24 hour test) 

A

Creatinine clearance (mL/min) = (Ux*V/Px)

Ux: Urine concentration
Px:  Plasma concentration
V: Urine volume or flow rate

79
Q

What is the reference intervals for creatinine clearance (Corrected for surface area) = 

A

90-120 mL/min

80
Q

What is the average persons body surface area?

A

1.73/BSA (m^2)

81
Q

BSA formula?

A

•BSA (m^2) = SQRT [height(cm) x weight (kg) ] / 3600)

•BSA (m^2) = SQRT [height(in) x weight (lb)] / 3131)

Creatinine clearance x BSA (m^2)

82
Q

Three methods for creatinine measurements

A

•Jaffe’s reaction
•Enzymatic Creatinine amidohydrolase & Creatinine deaminase
•Partial enzymatic

83
Q

Jaffe’s reaction is conducted at _____ degrees Celsius

A

30 or 37

Increase temperature can cause picrate to react with glucose, uric acid, ascorbic acid, cephalosporin, guanidine, ketone body, pyruvate, protein.

84
Q

Jaffe’s reaction….

A

Creatinine + picrate ——OH- ——-> Janovoski complex (orange-red) absorbance 510-520 nm

85
Q

What does Jaffe’s reaction require?

A

A protein free filtrate
-Fullers earth (Floridin) Added to increase Specificity


86
Q

Oldest clinical chemistry method that is still in use?

A

Jaffe’s reaction

87
Q

What is the advantage of Jaffe’s reaction?

A

Automated and low cost

88
Q

Disadvantage of Jaffe’s reaction?

A

-Fuller’s earth needs to be added “manually”
-pyruvate and oxaloacetate at high concentrations can interfere

89
Q

Enzymatic creatinine deaminase impartial enzymatic:

-can monitor NADPH reaction
-use dry slide technology to assay NH3 (Immobilized aminohydrolase Converts creatinine to NH3 —-> Detected via__________________.

A

Bromophenol Blue dye complex (670 nm)

-Requires Centribution Of endogenous NH3 to be subtracted

90
Q

Used as a point of care testing device

A

Enzymatic-creatinine deaminase and partial enzymatic

91
Q

Enzymatic creatinine Deaminaseand partial enzymatic: 

Dry slide technology has shown that __________ Creatinine from patients on 5-fluorocytosine (fungal medication) 

A

Increased

92
Q

Creatinine is cleared and _______ Reabsorbed.

A

Not

93
Q

What is the specimen collection in handling for creatinine?

A

-serum, plasma or diluted urine (1:100)
-No interference from fluoride, but NH4-heparin Should be avoided
-If using NH3 Detecting methodology, remove RBC ASAP 

94
Q

Four Jaffe’s assay, Samples are stable for _____ week at ____ Degrees Celsius

A

1, 4

95
Q

Can you function can be assessed by the ability of the kidney to….. 

A

Clear a substance

96
Q

Definition of clearance? 

A

Volume (ml) Of plasma from which a substance completely removed / Unit of time (1 min) **

97
Q

Why does serum sodium decrease when the liver is not working?

A

Decrease in albumin, more free sodium that then gets filtered out (not bound to proteins so gets Eliminated faster) 

98
Q

What are the three renal disease clearance test?

A

-para-amino hippurate
-Inulin
-Creatinine (Does not buying to protein in free filters) 

para-amino hippurate and Inulin are exogenous substances, need to be injected by IV

99
Q

What is the criteria That makes a good marker for renal disease determination? 

A
  1.  renal tubular secretion and reabsorption do not contribute to elimination of the compound
  2. Plasma protein binding should be negligible
100
Q

For the clearance test it requires?

A

-accurate measurement of both plasma and urinary marker
- reliable urine collection (Urine flow must be adequate, collection. Should be long enough duration (More than four hours), Complete bladder emptying achieved

101
Q

Collection. Should be more than ______ hours For clearance tests.**

A

Four

102
Q

How is para-amino hippurate (PAH) cleared?

A

By binding to proteins

103
Q

para-amino hippurate (PAH) is not good for GFR because?

A

Carrier proteins mediated excretion

104
Q

how is para-amino hippurate (PAH) administered? 

A

By IV infusion, cannot eat for this test

105
Q

Exogenous substance used to determine Reno plasma slow/amount of blood passing through the kidney

A

para-amino hippurate (PAH)

106
Q

PAH is both filtered and secreted to such an extent that
greater than ______ % of the substances removed from the blood
in a single pass through the kidney

A

90

107
Q

why does para-amino hippurate (PAH) not need to be calculated for body surface area?

A

Comes from a plant source

108
Q

Exogenous substance that is the reference molecule for assessing GFR it must be infused

A

Inulin 

109
Q

Anyone is freely filtered by glomerulus and is neither….

A

Reabsorbed nor secreted 

110
Q

Faster and better than Creatinine clearance test

A

Inulin clearance test*

111
Q

Creatinine can be ___________ by tubule. 

A

Secreted

112
Q

When is Cystatin C elevated?

A

When increased Inflammation, increase in heart and brain conditions, increased very high in renal disease

113
Q

Neither PHA nor inulin or quick laboratory measurements, the leaves __________ As the next best convenient tool

A

Creatinine clearance (Cystatin C or cysteine 3)

114
Q

Creatinine is an ______________ Substance and tests are easy to perform

A

Endogenous

115
Q

What prohibits creatinine from being the perfect marker for GFR?**

A

Tubular secretion of creatinine

116
Q

Creatinine clearance is used to diagnose…..

A

Acute and chronic renal failure

117
Q

Results closely parallel inulin until renal failure progresses where
[creatinine] serum ___________ significantly and then creatinine clearance
decreases as renal functions fail.

A

Increases

118
Q

What are the disease profiles of renal diseases? **

A

-chronic renal failure (Uremic syndrome,final stage of renal failure)
-Acute renal failure
-Acute glomerulonephritis
-nephrotic syndrome
-renal tubular defects
-Urinary track infection (pyelonephritis, cystitis)
-Nephrolithiasis (Kidney stone)
-Renal hypertension

119
Q

What disease causes huge gaps so Albumin can go through, increases osmotic pressure, no osmotic gap, filtration can stop

A

Nephrotic syndrome

120
Q

Chronic renal failure is more than _______ months with implications of health

A

3

121
Q

chronic renal failure causes metabolic __________.

A

Acidosis***

122
Q

Symptoms of chronic renal failure

A

Weakness, fatigue, loss of appetite, nausea and vomiting, muscle wasting, tremors, abnormal mental function, and shallow respiration and metabolic acidosis

123
Q

GFR:
<60 ml/min/1.73 m2 =
<15ml/min/1.73 m2 =

A

Decreased renal function
Renal failure

124
Q

What results from decreased glomerular filtration and tubular function?

A

Increase in NPN, hyperphosphateuria, hypocalcemia, acidosis in hyperkalemia

125
Q

Calcium and phosphorus are _____________ Related. 

A

Inversely

If increase of calcium and phosphorus = stone 

126
Q

Caused by inability to secrete normal H+ production

A

Uremia–acidosis

127
Q

Retained nitrogenous waste, ____________ both BUN and creatinine in serum. 

A

Increase

128
Q

Loss of tubular reabsorption —-> 

A

Inability to concentrate urine is reflected in decreased urine Osmolality

129
Q

What happens in chronic renal failure and uremic syndrome?

A

-Uremia acidosis
-Retained nitrogenous waste
-Loss of tubular reabsorption
-Abnormal endocrine function (Secondary hyperparathyroidism, anemia/EPO)
-Diabetes mellitus
-Increased proteinuria


130
Q

In chronic renal failure and uremic syndrome:
Which of the following are elevated and which are decreased?

HCO3-, Na+, Ca2+, pH, K+, Cl-, P-, Mg2+

A

Decreased: HCO3-, Na+, Ca2+, pH

Increased: K+, Cl-, P-, Mg2+

(Na+ due to renin not being produced by damage kidneys) 

131
Q

Defined as rapid and severe reduction of GFR with oliguria and Edema. 
Caused by prerenal, Renal, post-renal effects

A

Acute renal failure

132
Q

What are examples of acute renal failure causes?

A

Hypovolemia, Heart failure, acute tubular necrosis, or urinary tract obstruction

133
Q

What are clinical findings associated with acute renal failure?

A

-Hyperkalemia with cardiac arrhythmia
-Metabolic acidosis (Decreased bicarbonate)
-Increase monophosphate, decreased calcium that leads to secondary hyperparathyroidism
-Bone disease
-Increased BUN and creatinine
-Possible anuria (<100ml/day) 

134
Q

Where is EPO produced?

A

At the border line area between the cortex and medulla of kidney

135
Q

Inflammation of glomerular membrane, sometimes due to ____________ disease

A

poststreptococcal

136
Q

acute glomerularnephritis:

Early stage resembles pre-renal __________ With normal tubular function.
Later stage tubular damage resembles __________ Syndrome.

A

Azotemia

Uremic

137
Q

Clinical findings of acute glomerulonephritis:

Urine…

A

Hematuria, RBC cast, proteinuria, Decreased GFR, oliguria

138
Q

Clinical findings of acute glomerulonephritis:

Serum…

A

Increased urea and creatinine (Normal ratio)

Decrees complement factors such as C3 and CH 50 (Overall compliment activity and body)

139
Q

Clinical findings of acute glomerulonephritis:

Overall…

A

Increase sodium and water retention that results in Edema, hypertension

  • anemia also 
140
Q

Excessive permeability to plasma proteins = 

A

Renal failure

141
Q

What happens to BUN and creatinine in nephrotic syndrome? 

A

Not affected until renal failure (in this case goes up)

142
Q

How does nephrotic syndrome affect urine?

A

Massive proteinuria > 3.5 per day, lipiduria (oval fat bodies produced, granulated renal tubular cells)

143
Q

How does nephrotic syndrome affect serum?

A

Increase sodium and water retention, offered to macro guardians, TG and cholesterol (secondary to Lipo proteins alterations)

144
Q

What is the overall effect of nephrotic syndrome?

A

Loss of serum proteins, decreased oncotic pressure (Caused by proteins) and shifts water from vascular to interstitial (edema) 

145
Q

Sodium __________ and volume __________ in Nephrotic syndrome. 

A

Retention, expansion

146
Q

_______________ and oliguria may be present With nephrotic syndrome.

A

Hematuria

147
Q

Renal tubular defects:
Decrease reabsorption or secretion with normal ______.

A

GFR

148
Q

What is the most important clinical disorder associated with renal tubular defects?

A

Renal tubular acidosis (Types one through four)

149
Q

Renal tubular acidosis type…..

Decrease proximal tubules bicarbonate reabsorption
Hyperchloremia acidosis with normal AG, also may observe hypouricemia, hypophosphatemia, aminoaciduria, And renal glucosuria
Fanconi syndrome

A

Proximal RTA type II

150
Q

Rare, excess glucose (Reabsorption is affected), phosphate, bicarbonate.

Uric acid, potassium and some amino acids can be excreted in urine and bicarb

A

Fanconi syndrome***

Associated with proximal RTA type two

151
Q

Renal tubular acidosis type where tubular cells cannot secrete hydrogen that leads to metabolic acidosis

A

Distal RTA type one

152
Q

What are the clinical findings in renal tubular defects?

A

Urine: Normal or slightly decreased GFR, proteinuria (aminoaciduria), glucosuria
and phosphouria
• Serum: increased BUN & creatinine, potassium & H*, hypophosphatemia

153
Q

RTA type that is secondary to aldosterone deficiency or resistance to aldosterone

A

 RTA type 4

154
Q

Mixed RTA proximal and distal

A

RTA type 3 

155
Q

Urinary track infection, usually resulting in cystitis. Most severe, associate with fever and pain over her kidneys

A

Pyelonephritis

156
Q

Bacterial infection of the bladder

A

Cystitis

157
Q

Clinical findings of cystitis and pyelonephritis 

A

Greater than 100,000 bacterial colonies per ML, increased WBC and WBC cast and pyuria(pus)
Increased number of RBC in urine

158
Q

Causes of stone formation?

A

-after urinary track infection
-Increase calcium from primary hyperparathyroidism (Calcium oxalate is the most common)
-Uric acid/gout
-Cystine (cystinuria)
- Magnesium/ammonia/phosphate or xanthine 

159
Q

What are the effects of renal hypertension?

A

Decreased renal perfusion, increase renin secretion, increase angiotensin II, increased blood pressure

160
Q

145/95

A

Hypertensive nephrosclerosis

161
Q

Clinical findings of renal hypertension

A

Urine: increase aldosterone
Serum: Increased renin, aldosterone, hypernatremia, hypokalemia

162
Q

Chronic renal failure can lead to ________ retention That causes Renal hypertension

A

Sodium and water

163
Q

Which Diabetes is insulin dependent?

A

Diabetes mellitus type one

164
Q

What is the leading cause of mortality for diabetes mellitus type one patients?

A

Severe renal system Issues

165
Q

What are the stages of diabetes mellitus type one?

A
  1. Glucosuria and polyuria that leads to proteinuria that develops approximately 17 Years after initial diagnosis
  2. Decreased GFR and hypertension develops 1 to 2 years later
  3. Eventually renal failure
166
Q

High molecular weight proteins enter filtrate-glomerulonephritis, Streptococcal infection, nephrotic syndrome, or diabetic nephropathy (> 2 g/day excreted)

A

Glomerular proteinuria*

(window is bigger, proteins goes through) 

167
Q

Initial filtrate, proteins not altered, but defect in reabsorption results in
1 to 3 g per day of low molecular weight proteins and albumin being
excreted

A

Tubular proteinuria

168
Q

Hemolysis, hemoglobin diuresis, multiple myeloma (Abnormal antibodies, immunoglobulins), crush injuries

A

Overload proteinuria

169
Q

bladder infections and tumors

A

Post renal protein 

170
Q

___________ renin released from chronically damage kidneys

A

Increased

171
Q

In renal hypertension the cardiovascular system is…..

A

Normal?

172
Q

Purines are excreted as…

A

Uric acid

173
Q

Major product of Catabolism of the adenosine and guanosine (purines) 
2,6,8-Trihydroxypurin

A

Uric acid

174
Q

Net urinary excretion of uric acid is about______% Of amount filtered

A

6-12

175
Q

Renal handling of uric acid

A

-filtration of virtually all uric acid in the capillary plasma entering glomerulus
-almost 100% reabsorption at the proximal tibial
-Subsequent secretion throughout the tubule
-Further reabsorption at the distal tubule 

176
Q

Inherited disorders of purine metabolism are very rare. Either hyperuricemia or hypouricemia 

Abnormal uric acid could result in…

A
  1. Kidney failure or stone (Child or a young adult)
  2. Gravel in an infant diaper
  3. Unexplained neurological problems
  4. Gout (Younger than 30 years of age) 
177
Q

What are the methods for assessing uric acid?

A

-phosphotungifstic acid (PTA)
-Uricase
-HPLC 

178
Q

Method for assessing uric acid:
-PTA —> Reduce by uric acid under alkaline condition —->Tungsten blue (chromongen, blue)
-Absorbance at 650 to 700 nm
-disadvantage: Too many interference

A

Phosphotungstic acid method

179
Q

Method for assessing Uric acid:
-More sensitive than PTA method
-High quality and low cost
-Absorbance at 293 nm*
-A reference method, but require high quality spectrophotometer

A

Uricase method

  • The concentration of uric acid in serum increases about 10% between ages of 20 and 60
180
Q

Method for assessing Uric acid:
• Ion exchange or reversed phase column to separate and quantify uric
acid.
• Column effluent is monitored at 293 nm to detect luting uric acid.
• Retention time of uric acid is less than 6 min.
• Also considered as a reference method.

A

High performance liquid chromatography
(HPLC)

181
Q

Increase intracellular calcium results in increased…

A

Contraction

Clinical Chemistry 1 (9 decks)

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