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MLS > Chemistry Exam 1 > Flashcards

Chemistry Exam 1 Flashcards

1
Q

The proximal convoluted tubule (PCT) reabsorbs

A

Glucose, Amino acids, Proteins

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2
Q

Disease state: High ADH

A

Inappropriate ADH Secreation

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3
Q

Disease state: Low ADH

A

Diabetes insipidus

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4
Q

ADH is secreted when

A
  • high plasma sodium
  • low plasma water
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5
Q

ADH causes what effect to happen where

A

Water reabsorption to increase in the Collecting Ducts of the Kidneys

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6
Q

Osmolality

A

Measure of osmotic pressure across body membranes

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7
Q

Osmolarity

A

Measure of osmoles of solute (dissolved particles) per kilogram of solvent

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8
Q

When are osmolality and osmolarity equivalent?

A

When the solvent is water, like in the body

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9
Q

Formula 1 for Osmolality

A

2.0[Na+] + [glucose]/20 + [BUN]/3

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10
Q

Units for Osmolality formula

A

[Na] in mEq/L
[Glu] and [BUN] in mg/dL

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11
Q

Osmolar Gap - definition and significance

A
  • Difference between calculated and measured osmolalities
  • May indicate unaccounted for solutes, most commonly alcohol, mannitol, glycine, methanol, or ethylene glycol
  • Larger gap = poorer prognosis
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12
Q

Colligative Properties

A

More dissolved particles causes:
- Freezing point down
- Vapor pressure down
- Boiling point up
- Osmotic pressure up

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13
Q

1000 mOsmole results in how much freezing point depression?

A

1.86 °C

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14
Q

What are the body’s fluid compartments? What do they include?

A
  • Intracellular Fluid Compartment (ICF) - fluid within cells
  • Extracellular Fluid Compartment (ECF) - plasma and interstitial spaces
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15
Q

Creatinine Clearance formula

A

UV/P x 1.73/A

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16
Q

Renal threshold for glucose

A

160-180 mg/dL

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17
Q

Classifications of Renal Disease

A
  • Pre-renal (cardiac output)
  • Renal (kidneys)
  • Post-renal (blockage like stones or tumors)
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18
Q

Non-protein Nitrogen (NPN) compounds

A
  • BUN
  • Uric Acid
  • Creatinine/creatine
  • Ammonia
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19
Q

Increase in one more more NPN is called

A

Azotemia

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20
Q

Creatinine vs Creatine for disease states

A
  • Creatinine = Renal Disease
  • Creatine = Muscular Disorders
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21
Q

Jaffe Reaction

A

Detects creatinine by color formation as it complexes with alkaline picrate

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22
Q

Ornithine Cycle

A

Ammonia from protein degradation is converted to BUN, which is soluble for excretion in urine

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23
Q

How are azotemia and uremia related?

A
  • Azotemia is high BUN in plasma
  • Uremia is high BUN in urine (renal failure)
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24
Q

High BUN occurs in

A
  • Low Renal Perfusion
  • Renal Disease
  • High Protein Intake
  • Dehydration
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25
Q

Low BUN occurs in

A
  • Low protein intake
  • sever liver disease
  • Sever vomiting or diarrhea
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26
Q

Urease converts

A

Urea to ammonia

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27
Q

Berthelot reaction

A

Detects BUN indirectly by converting to ammonium with urease, then reacting with phenol. Indophenol is produced, which is a blue chromophore.

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28
Q

BUN Enzymatic Assay

A

Detects BUN indirectly by converting to ammonium with urease, then reacting with enzyme to convert NADPH to NADH. NADPH is more colored than NADH, so more BUN = less color in the products.

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29
Q

BUN Chemical Method

A

Urea reacted directly with diacetyl. Produces diazine chromaphore.

30
Q

BUN:Creatinine Ratio

A
  • Healthy = 10:1 to 20:1
  • Pre-renal azotemia = 20:1 to 30:1
  • Post-renal azotemia =&raquo_space;20:1 with high creatinine (proportional increase)
  • Low BUN from liver disease or malnutrition = <10:1
31
Q

Uric Acid Chemical Method

A

Uric Acid + Phosphotungstic acid to make Tungsten blue

32
Q

Uric Acid Enzymatic Method

A

Uricase converts uric acid to allantoin and peroxide. Peroxide reacts with NADP to make NADPH chromagen

33
Q

What organ converts ammonia to BUN?

34
Q

Ammonia Methodology

A

Ion Selective Electrode

35
Q

“Lytes” includes

A
  • Na+
  • K+
  • CL-
  • HCO3-
36
Q

Major Extracellular Cation

37
Q

Where is Aldosterone produced? What does it control?

A
  • Produced in adrenal gland
  • Sodium reabsorption in kidneys
38
Q

Disease State: low aldosterone

A

Addison’s Disease

39
Q

Disease State: high aldosterone

A

Cushing’s Disease

40
Q

Name and Function of ACE

A
  • Angiotensin Converting Enzyme
  • Converts Angiotensin I to Angiotensin II
41
Q

What activates the renin-angiotensin system? What is the result of this activation?

A
  • Juxtaglomerular Apparatus
  • Increase to blood pressure and sodium levels
42
Q

Major Intracellular Cation

43
Q

Low Potassium is caused by

A
  • low intake
  • insulin excess
  • vomiting or diarrhea
44
Q

Potassium Critical Values

A

<2.8 or >6.0 mmol/L

45
Q

High Potassium is caused by

A
  • high intake
  • tissue destruction
  • hemolysis of sample
  • impaired renal excretion
46
Q

Major Extracellular Anion

47
Q

Cl- ion shift

A

is secondary to Na+ and HCO3- movement in and out of cells

48
Q

Low Chloride is associated with

A
  • prolonged vomiting
  • skin trauma/burns
  • renal lost to diuretics
  • metabolic acidosis
49
Q

High Chloride is associated with

A
  • dehydration
  • renal tubular acidosis
  • loss of NaHCO3
  • salicylate intoxication (aspirin)
50
Q

Equation for equivalence of H2CO3 to pCO2 in the blood

A

H2CO3 = 0.03 x pCO2

51
Q

Sweat Chloride Testing

A
  • Screening test for cystic fibrosis (high in these patients)
  • Measured with pilocarpine iontophoresis
52
Q

2nd largest anion in the ECF

A

Bicarbonate (HCO3-)

53
Q

Control of HCO3- levels happens in

A
  • Kidneys through reabsorption
  • Lungs through respiration rate
54
Q

Low HCO3- results in

A

Metabolic Acidosis

55
Q

High HCO3- results in

A

Metabolic Alkalosis

56
Q

Anion Gap formula

A

[Na+] - ([Cl-] + [HCO3-])

57
Q

The body pH centerpoint is

58
Q

The Krebs Cycle produces

A

ATP + H2O + CO2 (acid)

59
Q

What cation moves with HCO3-?

60
Q

Bicarbonate Buffer System Equillibrium

A

CO2 + H2O <-> H2CO3 <-> HCO3- + H+

61
Q

Phosphate Buffer System Equillibrium

A

(HPO4)2- + H+ <-> (H2PO4)-

62
Q

Effect of Acidosis on CNS

A

Suppression

63
Q

Effect of Alkalosis on CNS

A

Excitation

64
Q

pKa of Bicarbonate

65
Q

Where is the respiratory center of the brain?

A

Hypothalmus

66
Q

Respiratory Acidosis

A

Increased pCO2
- issues breathing
- barbiturate poisoning
- brain damage

67
Q

Metabolic Acidosis

A

Decreased bicarbonate
- loss to diarrhea
- ethylene glycol/methanol poisoning
- decreased kidney function

68
Q

Respiratory Alkalosis

A

Decreased pCO2 from hyperventilation
- oxygen deficiency
- anxiety
- aspirin overdose
- brain damage

69
Q

Metabolic Alkalosis

A

Increased bicarbonate
- Loss of acid (vomiting)
- Cushing’s Disease
- Citrate toxicity from massive transfusion

70
Q

A patient is compensating for acid/base imbalance if

A
  • they are within the reference range
  • the levels of pCO2 and HCO3- are on the same side of normal (both high/both low)
71
Q

Respiratory Compensation

A
  • occurs in minutes, maxed within hours
  • can’t handle long-term stress
72
Q

Metabolic Compensation

A
  • occurs in hours, maxed within days
  • better handles long-term stress

MLS (18 decks)

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