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Clinical Chem > Chem Unit 3 > Flashcards

Chem Unit 3 Flashcards

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1
Q

Proteins are too large to fit through what in the kidney?

A

Glomerular membrane

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2
Q

Where are proteins reabsorbed in the kidney?

A

Proximal Convoluted Tubules
Descending Loop of Henele

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3
Q

Where are proteins synthesized?

A

Liver

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4
Q

What proteins are made outside of the liver?

A

Factor 8
Antibodies
Hemoglobin
Peptide hormones

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5
Q

What do proteins provide?

A

Oncotic pressure

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6
Q

What is the most prevalent plasma protein?

A

Albumin

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7
Q

What is the function of albumin?

A

-Buffer for acid
-Increase plasma oncotic pressure to keep fluid in the intravascular space
-Provide a binding site for hormones so they aren’t activated

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8
Q

What produces immunoglobulins?

A

Plasma cells

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9
Q

What produces Hemoglobin?

A

RBCs

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10
Q

How do proteins separate in electrophoresis?

A

Size and charge

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11
Q

What is the reference range for Serum Total Protein?

A

6.0 - 8.3 g/dL

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12
Q

What does Serum Total Protein assess?

A

Pathology
Adequate nutrition

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13
Q

What is the primary function of Albumin?

A

Maintains oncotic pressure
(binds to things as well)

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14
Q

What is the largest peak on Electrophoresis?

A

Albumin

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15
Q

What protein migrates the fastest on Electrophoresis?

A

Albumin

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16
Q

If there is physical injury what happens to albumin?

A

Increased catabolism

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17
Q

What are the reasons for decreased synthesis of Albumin?

A

Primary- liver disease
Secondary- malabsorption/malnutrition

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18
Q

What causes an increased loss of Albumin?

A

Renal Protein Loss

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19
Q

What is the most common Alpha 1 protein called?

A

Antitrypsin (AAT)

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20
Q

What is the role of AAT?

A

remove free elastase from circulation

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21
Q

What can an AAT deficiency cause?

A

Emphysema
Cirrhosis

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22
Q

What are other Alpha 1 proteins?

A

A1-Acid Glycoprotein
Alpha Fetoprotein
A1-Antichymotrypsin

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23
Q

What Globulin is a carrier of cationic drugs?

A

A1-Acid Glycoprotein

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24
Q

What is the major glycoprotein released in inflammation?

A

A1-Acid Glycoprotein

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25
Q

What globulin is found between the A1 and A2 zones on electrophoresis?

A

A1-Antichymotrypsin

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26
Q

What are the Acute Phase Reactants?

A

A1-Antitrypsin
Haptoglobin
CRP
Prealbumin/Transthyretin

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27
Q

What is the role of haptoglobin?

A

Prevents hemoglobin from being removed in the glomeruli

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28
Q

When is haptoglobin increased?

A

Inflammation
Intravascular hemolysis
smoking

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29
Q

What are the Alpha 2 globulins

A

Haptoglobin
Ceruloplasmin
A2-Macroglobulin

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30
Q

What does A2-Macroglobin inhibit?

A

Protease Inhibitor
-Complement
-Coagulation
-Fibrinolytics

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31
Q

What condition will we see a large increase in A2-Macroglobulin?

A

Nephrotic Syndrome

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32
Q

What conditions will we see a decrease in A2-Macroglobulin?

A

Pancreatitis
RA
Multiple Myeloma

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33
Q

What are the main Beta-globulins?

A

Transferrin
CRP
Fibrinogen
Complement
C3, C4
Hemopexin
B-lipoproteins
B-Microglobulin

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34
Q

What are gamma globulins also known as?

A

Antibodies

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35
Q

What is the equation for Globulin?

A

Total Protein - Albumin

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36
Q

What is the normal range for Albumin/Globulin Ratio?

A

1.1 - 1.5

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37
Q

What does low total protein suggest?

A

Liver failure
Glomerular failure
malnutrition/malabsorption

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38
Q

What does elevated protein suggest?

A

Chronic inflammatory states
Autoimmune diseases
Cancers

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39
Q

What does a low A/G ratio <1.1 mean?

A

More globulins than albumin
1. Multiple myeloma
2. cirrhosis
3. Nephrotic syndrome

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40
Q

What does a high A/G ratio >1.5 mean?

A

More albumin than globulins
1. leukemias
2. genetic immunoglobulin deficiencies

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41
Q

What is the role of prealbumin/transthyretin

A

Transport protein

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42
Q
A

Nephrotic Syndrome

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43
Q
A

Acute Phase Reactants

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44
Q
A

Multiple Myeloma

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45
Q

What increases in the urine of multiple myeloma patients?

A

Bence-Jones proteins
(immunoglobulin light chains)

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46
Q

What reflect tubular disorders in the kidneys?

A

Elevated B2-Microglobulin

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47
Q

What are the main causes of hyperproteinuria?

A

Glomerular damage
Post-Streptococcal Glomerulonephritis

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48
Q

Mnemonic for clinical signs of Post-Streptococcal Glomerulonephritis?

A

Sore throat
Pee coke
Face bloat

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49
Q

NephrItic syndrome symptoms

A

Hematuria
Oliguria
Azotemia
Hypertension

*focuses on Inflammation

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50
Q

NephrOtic syndrome symptoms

A

Massive proteinuria
Hypoalbuminemia
Edema
Hyperlipidemia/hyperlipiduria

*focuses on prOteinuria

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51
Q

What is multiple myeloma?

A

Cancer of the plasma cells
**uncontrolled hyperproduction of immunoglobulin

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52
Q

What does multiple myeloma lead to?

A

-Pathological fractures and hypercalcemia
-Decreased A/G ratio
-low A2-macroglobulin
-high B2-microglobulin

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53
Q

Symptoms of multiple myeloma

A

Bone pain
Hypercalcemia
Proteinuria

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54
Q

What syndrome causes frothy urine

A

Nephrotic syndrome

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55
Q

What globulin is increased in nephrotic syndrome

A

A2-macroglobulin

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56
Q

What is the clinical giveaway for hypoproteinemia?

A

Ascites

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57
Q

What can cause hypoproteinemia?

A

Hemodilution
decreased production
increased protein loss
inadequate nutrition
water intoxication
nephrotic syndrome
liver failure

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58
Q

What does a peak in A2 region signify?

A

Acute phase reactants

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59
Q

What does the Biuret reagent contain?

A
  1. NaOH for alkalinity
  2. NaK tartrate
    3.Potassium Iodide
  3. CuSO4
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60
Q

What does the Biuret method interact with to form a purple color

A

In an Alkaline medium
Cupric ions (Cu2+) interact with peptide bonds

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61
Q

What does biuret method assess?

A

The presence of peptide bonds

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62
Q

What are the testing methods for protein

A

Refractometry
Dye-binding

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63
Q

How does the protein dye-binding method work

A

Coomassie blue is in acidic solution. it binds with protein and increases the absorbance at 595 nm

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64
Q

What is the reference range for albumin?

A

3.5 - 5.0 g/dL

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65
Q

What are the dyes used to test for albumin?

A

Bromcresol green (BCG)
Bromcresol purple (BCP)

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66
Q

What does the urine dipstick use to test for protein?

A

tetrabromphenol blue at 3 pH

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67
Q

How does gas chromatography separate proteins?

A

based on differential affinity between the liquid phase migrating up a gel plate and the gel on the plate

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68
Q

What is known as black diapers

A

Alkaptonuria

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69
Q

What is alkaptonuria

A

Body is unable to break down tyrosine and phenylalanine resulting in a buildup of Homogentisic acid.

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70
Q

What are the divalent amino acids

A

Cystine
Lysine
Arginie
Ornithine

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71
Q

What amino acid can result in kidney stones

A

Cystine

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72
Q

What happens in Cystinuria

A

Kidneys can’t reabsorb the divalent amino acids

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73
Q

What is the defect in cystinuria

A

In the amino acid transport system

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74
Q

What are the essential BCAAs

A

Leucine
Isoleucine
valine

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75
Q

What is Maple Syrup Urine Disease (MSUD)

A

Can’t break down branched chain amino acids

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76
Q

What is MSUD deficient in

A

Branched Chain Keto-acid Dehydrogenase Complex (BCKDC)

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77
Q

What is the treatment for MSUD

A

Change diet. Must restrict BCAAs

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78
Q

What disorder causes a mousy urine odor

A

Phenylketonuria (PKU)

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79
Q

What disorder can cause mental retardation?

A

PKU

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80
Q

What can not be metabolized in PKU?

A

Phenylalanine
-an essential AA

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81
Q

What are the Non-Protein Nitrogens in our blood?

A

Urea Nitrogen
Uric acid
Creatinine
Ammonia

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82
Q

What are the % breakdowns of NPN in our blood?

A

45% is Urea
20% is Uric acid
5% Creatinine
.2% Ammonia

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83
Q

What does BUN come from?

A

catabolism of proteins

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84
Q

What is BUN directly related to

A

hydration status
GFR

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85
Q

What is the equation for Urea

A

BUN X 2.14

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86
Q

What is Prerenal Azotemia

A

caused by:
dehydration
impaired blood flow to the kidneys
increased protein catabolism

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87
Q

BUN is inversely correlated with

A

glomerular filtration rate and renal plasma flow

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88
Q

What is renal azotemia

A

Acute renal failure

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89
Q

What is azotemia

A

elevated creatinine in the blood

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90
Q

What is postrenal azotemia

A

obstructive renal disease

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91
Q

What is the reference range for BUN

A

7-18

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92
Q

How long is BUN stable for at RT

A

4 hours

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93
Q

What is the biproduct of the BUN urease method

A

2 NH4 + CO3-

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94
Q

What is Diazine detected at

A

540 nm

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95
Q

What is the Diacetyl (Fearon) Reaction

A

Urea + Diacetyl with Heat = Diazine + 2 H2O

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96
Q

What is the Range for the BUN:Creat Ratio

A

10:1 to 20:1

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97
Q

An increased BUN:Cr ratio indicates?

A

Prerenal azotemia

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98
Q

A decreased BUN:Cr ratio indicates?

A

Intrarenal azotemia

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99
Q

Normal BUN:Cr ratio is seen in what azotemia?

A

postrenal

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100
Q

What AA are Creatinine synthesized in the liver with?

A

Arginine
Glycine
Methionine

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101
Q

In renal disease, excretion of what is decreased?

A

Creatinine

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102
Q

BUN/Cr >30 is usually

A

Prerenal renal failure

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103
Q

BUN/Cr > 40 is definitely what

A

Prerenal

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104
Q

What is the Jaffe Reaction

A

Creatinine and picric acid in alkaline solution

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105
Q

What is the Jaffe Reaction used to measure?

A

Creatinine

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106
Q

What interferes with the Jaffe Reaction

A

Glucose
Uric Acid
Ascorbic Acid
Acetone
Ketoacids
Cephalosporins

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107
Q

Reference Range for Creatinine

A

Men 0.9 -1.2
Women 0.6 - 1.1

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108
Q

What is Lesch-Nyhan Syndrome deficient in?

A

HGPRT
hypoxanthine-guanine phosphoribosyltranferase

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109
Q

What is elevated in Lesch-Nyhan Syndrome

A

Uric Acid

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110
Q

Symptoms of Lesch-Nyhan Syndrome

A

Mental Retardation
Muscle fasciculations
Self-mutilation

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111
Q

Tumor-Lysis Syndrome is caused by

A

Cytotoxic Chemotherapy

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112
Q

What is the result of Cytotoxic Chemotherapy

A

The rapid killing of cells results in DNA damage and Uric Acid production is increased

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113
Q

How does malignancies increase Uric Acid?

A

Rapid formation of cells but they die off quickly resulting in DNA damage and the release of Uric Acid

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114
Q

What method is used for Uric Acid?

A

Xanthine oxidase

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115
Q

What is the Xanthine Oxidase method?

A

Adenine + Guanine are catabolized to Xanthine
+ Xanthine Oxidase
=Uric Acid

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116
Q

What are our sources of Uric Acid?

A

Diet
Endogenously by breaking down cells and destruction of DNA

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117
Q

How does our body remove Uric Acid?

A

Excreted by kidneys
Degraded in GI Tract

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118
Q

What crystals cause Gout

A

Monosodium Urate crystals

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119
Q

What is podagra

A

Pain on the big toe from gout

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120
Q

Factors that contribute to Gout

A

Alcohol
high protein diet
stress
surgery
diuretics

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121
Q

What is Uremia

A

Increased in Urea and creatinine that results in renal failure

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122
Q

What can cause Uremic Frost on patient’s skin

A

Elevated levels of Uric Acid in the blood

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123
Q

What is the color method for Uric Acid

A

PTA method

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124
Q

What is the reaction for PTA method

A

Phosphotungstic Acid + Uric Acid reacting with Na2CO3

Allantoin + CO2 + Tungsten Blue

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125
Q

What is the enzymatic method for Uric Acid

A

Uricase Method

126
Q

What is the reaction for Uricase Method

A

Uric Acid with Uricase

Allantoin + H2O2 + CO2
=
H2O2 + 4-Aminoantipyrine with peroxidase
=chromogen

127
Q

What electrodes are used to assess acid-base disorders?

A

Clarke
Severinghaus
pH electrodes

128
Q

What does the Clarke electrode assess?

A

pO2

129
Q

What does the Severinghaus electrode assess?

A

pCO2

130
Q

What does the pH electrode assess?

A

pH

131
Q

What electrodes are potentiometric?

A

pH and Severinghaus (pCO2)

132
Q

What electrode is amperometric?

A

Clarke (pO2)

133
Q

What measures the O2 reduced in a sample for the amperometric electrode?

A

microammeter

134
Q

What does the ammeter measure?

A

current or the movement of electrons

135
Q

What is acidosis

A

increase of H+ in the body

136
Q

what is acidemia

A

increase of H+ specifically in the blood

137
Q

What is alkalosis

A

increases of HCO3- in the body

138
Q

Reference Range for pH

A

7.35 - 7.45

139
Q

Reference Range for pCO2

A

35 - 45

140
Q

Reference Range for pO2

A

90 - 100

141
Q

Reference Range for HCO3

A

22 - 28

142
Q

Hyperventilation causes?

A

Respiratory alkalosis
-Breathing off all their CO2

143
Q

What disorders cause respiratory acidosis

A

Emphysema
Pneumonia
Bronchiectasis
Atelectasis
ARDS
Pulmonary Edema

144
Q

What disorders cause metabolic alkalosis

A

Hypercortisolism
Adrenal Hyperplasia
Diuretics

145
Q

What disorders cause metabolic acidosis

A

Acute kidney injury
Diabetes
Salicylate Toxicity
Lactic Acidosis

146
Q

What is pKa

A

Dissociation constant of an acid
**how tightly the base will hold on to the Hydrogen ion

147
Q

What enables CO2 and H2O to come together to form BiCarb

A

Carbonic anydrase

148
Q

What are the 3 primary ways that CO2 can travel in blood

A
  1. Dissolved in plasma
  2. Carried in the RBC
  3. Dissolved bicarbonate
149
Q

What is the ratio our body uses to keep pH at 7.4

A

20 bicarbonate to 1 carbonic acid

150
Q

What is a secondary function of Hemoglobin and ALL other proteins?

A

Mop up excess hydrogens

151
Q

Variables that favor Oxygen unloading into the tissues

A
  1. Increased CO2
  2. Acidosis
  3. Increased DPG
  4. Exercise
  5. Increased temperature
152
Q

What does a right shift in regards to O2 mean

A

Easier to unload the O2 into the tissues

153
Q

What is a K+ shift?

A

When there is an excess of H+ surrounding the cell, the cell will accept the H+ in exchange for K+

154
Q

What is a Cl- shift?

A

In acidosis, HCO3- moves out of the cell and Cl- moves in

155
Q

In acidosis what is decreased

A

HCO3-

156
Q

In alkalosis what is increased

A

HCO3-

157
Q

What is a buffer

A

A solution that resists changes in pH when acid or base is added to it

158
Q

What are the primary buffer systems in our body

A
  1. Bicarbonate buffer
  2. Protein buffer
  3. Hemoglobin buffer
  4. Phosphate buffer
159
Q

What is hypoxia

A

We are breathing in less O2 than we need

160
Q

What is hypoxemia

A

Low levels of O2 in our blood

161
Q

What is the Henderson-Hasselbalch Equation

A

pH = pKa +log10 (A-/HA)
**Base over conjugate acid
pH = pKa +log10 (B/BH+)

162
Q

What is the Bicarbonate Buffer System Chemical Equation?

A

HCO3 (Bicarbonate)
<———->
H2CO3 (Carbonic Acid)
<———–>
H2O and CO2

163
Q

What is the most important buffer system

A

Bicarbonate

164
Q

What does the Hemoglobin Buffer System do?

A

Binds CO2 to an amino acid terminal of the protein

165
Q

What does the Protein Buffer System do?

A

Terminal amino acids provide buffering capacity

166
Q

What is Amphoteric compounds

A

Amino acids that are able to act as a base and an acid

167
Q

What is the Phosphate Buffer System

A

-2,3 DPG enable the kidneys to excrete H+
-Helps unload O2 into the tissues by binding to deoxygenated Hgb and stabilizing it

168
Q

Metabolic compensation controls?

A

Bicarbonate concentration by the kidneys
-Occurs after a few days

169
Q

Respiratory compensation controls?

A

pCO2 concentration by the lungs
-occurs immediately

170
Q

Role of Kidneys in Acid-Base Balance

A
  1. NH3 production and NH4+ secretion in the urine
  2. Na-H exchange pumps
  3. Conservation of filtered H2CO3
171
Q

What is more acidic than the blood within the kidney?

A

tubular lumen

172
Q

How is NH4+ created

A

NH3 bind with H+ in the urine filtrate

173
Q

What is Respiratory Compensation

A

How we breath to try and stabilize the acid-base disturbance
**Controlling the level of pCO2 in the blood

174
Q

How does the body handle Metabolic acidosis with respiratory compensation?

A

Decrease levels of pCO2 by breathing faster

175
Q

How does the body handle Metabolic Acidosis with respiratory compensation?

A

Increase the levels of pCO2 by breathing slower

176
Q

How do we tell if there is partial compensation?

A

-pH is outside 7.35 - 7.45
-pCO2 is indicating 1 direction
-HCO3- is indicating another

177
Q

What is Metabolic Compensation?

A

The kidney’s response to help stabilize the acid-base disturbance.

178
Q

How does our body handle Respiratory acidosis with metabolic compensation?

A

Increase the levels of HCO3-

179
Q

How does our body handle Respiratory alkalosis with metabolic compensation?

A

Decrease the levels of HCO3-
*getting rid of CO2

180
Q

What is caused by an overabundance of hydrogen ions caused by decrease in bicarb

A

Metabolic Acidosis

181
Q

When do we see Metabolic acidosis?

A

Lactic acidosis
Cancer
overdose of tylenol, ethanol, aspirin

182
Q

In Metabolic acidosis how do we see Bicarb and pCO2?

A

Low Bicarb
normal to decreased pCO2

183
Q

What is caused by low concentration of hydrogen ions caused by increase in Bicarb?

A

Metabolic Alkalosis
*usually caused by an increase in Bicarb

184
Q

When do we see Metabolic Alkalosis

A

Hyperaldosteronism
Gastric fluid losses (vomitting)
Antacid overdose

185
Q

In Metabolic alkalosis how do we see Bicarb and pCO2

A

High bicarb
normal to increased pCO2

186
Q

When do we see an overabundance of H+ caused by increase of CO2

A

Respiratory Acidosis

187
Q

When do we see respiratory acidosis

A

Respiratory insufficient
-emphysema

188
Q

What are Bicarb and pCO2 levels in respiratory acidosis

A

High pCO2
Normal to increase Bicarb

189
Q

What is it called when alkalosis is caused by a decrease in pCO2 bc the patient is hyperventilating?

A

Respiratory Alkalosis

190
Q

In respiratory alkalosis how is the Bicarb and pCO2?

A

low pCO2
normal to decreased Bicarb

191
Q

What causes a right shift on O2 dissociation curve?

A

CO2
Acidosis
2,3 BPG
Exercise
Increased Temp

192
Q

In Blood Gas analysis what is calculated?

A

HCO3

193
Q

How frequent is Calibration needed for Blood gases?

A

2 points every 8 hrs
1 point every 4 hr

194
Q

Why do we need to calibrate blood gases so frequently?

A

Electrodes drift over time

195
Q

What are the fat soluble Vitamins?

A

A
D
E
K

196
Q

Liver stores what vitamins and minerals

A

Vitamins
A
B12
D
E
K
Minerals
Copper
Iron

197
Q

Where is Thiamine stored

A

RBC

198
Q

Vitamin A is also known as

A

Carotenoid
Beta-carotene
Retindoid

199
Q

What is Vitamin A crucial for

A

vision

200
Q

What does a deficiency in Vitamin A cause

A

Keratomalacia
-retinal epi defect that causes blindness

201
Q

How do we test for Vitamin A

A

HPLC

202
Q

What is on our skin that turns to Vit D from UVs

A

Cholecalciferol

203
Q

Once Vit D gets to the liver what is it changed into

A

25-hydroxylated Vit D

204
Q

What does 25- hydroxy Vit D become once it is in the kidney

A

1,25-hydroxylated Vit D

205
Q

What is the active form of Vit D

A

1,25-dihydroxy Vit D

206
Q

How does Vit D effect Calcium

A

Increases it in the body

207
Q

If we do not get enough Vi D as a child, what can they develop?

A

Rickets

208
Q

Vit D deficiency causes

A

osteoporosis
osteomalacia
osteopenia

209
Q

What vitamin inhibits Platelet aggregation

A

Vit E

210
Q

What is Vit E also known as

A

alpha-tocopherol

211
Q

What is Vit E incorporated into

A

VLDL

212
Q

What does Vit E function as?

A

Antioxidant

213
Q

How is Vit E excreted

A

Transported in bile but can be excreted in urine and bile

214
Q

How do we measure Vit E

A

HPLC

215
Q

Where is Vit K absorbed

A

Small intestines

216
Q

What is the function of Vit K

A

Promote blood coagulation
Factors:
7, 9, 10, 2

217
Q

What happens in Vit K deficiency

A

Malabsorption
Bile duct obstruction
pancreatitis
liver failure

218
Q

What disease is from a deficiency in Vit C

A

Scurvy

219
Q

How do we get Vit C

A

Citrus fruits
veggies
tomatoes
potatoes

220
Q

What is the function of Vit C

A

Antioxidant
Iron Absorption
biosynthesis of carnitine
conversion of dopamine to norepinophrine

221
Q

Symptoms of Scurvy

A

Bleeding
Petechiae
Bloody adrenal glands

222
Q

Too much Vit C causes

A

Elevated ALT, LD, Uric Acid
Kidney stones

223
Q

Thiamine deficiency causes what 3 disorders

A

Dry beriberi
wet beriberi
Wernike-Korsakoff syndrome

224
Q

What are the symptoms of dry beriberi

A

Primarily neurological symptoms

225
Q

What are the symptoms of Wet beriberi

A

Heart failure
Edema

226
Q

Symptoms of Wekike-Korsakoff syndrome

A

Horizontal nystagmus
cerebral ataxia
mental impairment
**long term alcoholism

227
Q

What Vitamin is a cofactor for enzymes to work

A

B1 (Thiamine)

228
Q

What vitamin is for DNA synthesis

A

B12
(Cyanocobalamin)

229
Q

What vitamin needs intrinsic factor to be absorbed in the ileum

A

B12

230
Q

<3.0 serum albumin suggests

A

malnutrition

231
Q

<15 prealbumin suggests

A

protein depletion

232
Q

<200 TIBC suggests

A

protein depletion

233
Q

<0.6 Creatinine suggests

A

Lack of muscle mass
High urine flow rate

234
Q

<6.0 BUN suggests

A

Inadequate protein intake

235
Q

How do we measure vitamins

A

HPLC

236
Q

What are the main organs in Calcium homeostasis

A

Small intestine
Kidneys/liver
Skeleton

237
Q

How much of calcium is protein bound in the serum

A

40-50%

238
Q

How does PTh effect Calcium

A

Increase the circulating ionized Ca

239
Q

How does Vit D effect Calcium

A

increase total body Ca

240
Q

How does Calcitonin effect Calcium

A

Decrease circulating Ca

241
Q

Where does Calcitonin come from

A

Thyroid C-cells

242
Q

What is the main role of Calcitonin

A

Responds to elevated calcium levels and puts the calcium in the bones

243
Q

How does PTH increase calcium

A

-Harvests from bones
-Increase kidney reabsorption
-Removes PO4 from blood
-Increase intestinal absorption

244
Q

What are the renal effects of PTH

A

Conserve Ca and lose PO4

245
Q

What does PTH stimulate

A

1-hydroxylation of 25-hydroxy Vit D in the kidney to the active form 1,25-hydroxy Vit D

246
Q

Calcium correction for hypoalbuminemia

A

Corrected total=
Measured Ca +
(Normal albumin - Patient albumin)
x 0.8

247
Q

The 3 methodologies for Calcium

A
  1. Colorimetric analysis
  2. Atomic Absorption spectrophotometry
  3. Indirect potentiometry
248
Q

What will chelate Ca and give a false low value

A

EDTA

249
Q

What are the 6 main causes of Hypocalcemia

A
  1. PTH deficiency
  2. PTH resistance
  3. Vit D deficient
  4. Deficiencies in bone Mineralization
  5. Renal
  6. Metastatic
250
Q

Other Causes of Hypocalcemia

A

Renal failure
Hypomagnesemia
Sepsis
Extreme physical exertion

251
Q

Causes of Hypercalcemia

A

-Cancer
-Hypercalcemia of Malignancy
-Renal failure
-Immobilization
-Thiazide diuretics
-Lithium
-Vit D toxicosis

252
Q

2 mechanisms of Hypercalcemia of Malignancy

A
  1. Tumors release PTH-related peptide
  2. Osteolytic metases
253
Q

Total Calcium and PTH seen in Secondary HyperPTH

A

Increased total Ca
Increased PTH

254
Q

Total Calcium and PTH seen in Hypercalcemia of Malignancy

A

Increased Ca
Decreased PTH

255
Q

Total Calcium and PTH seen in HypoPTH

A

Decreased Ca
Decreased PTH

256
Q

What is the definition of Electrolyte

A

small ionizable constituents in the body

257
Q

What is the definition of anion

A

negatively charged ion

258
Q

What is the definition of Cation

A

Positively charged ion

259
Q

What are the intracellular ions

A

K
Ca
Mg

260
Q

What are the extracellular ions

A

Na
Cl
HCO3

261
Q

How do we get the Anion Gap

A

Measured Cations and measured anions

262
Q

What are the trace elements

A

Iron
Copper
Zinc

263
Q

How does our body move proteins

A

Oncotic pressure

264
Q

How does our body move ions

A

Osmotic pressure

265
Q

Where does most electrolyte regulation occur

A

Kidneys

266
Q

Where is Na reabsorbed

A

Proximal convoluted tubules

267
Q

What enzyme converts Angiotensinogen to angiotensin 1

A

Renin

268
Q

Where is angiotensin 1 converted to Angiotensin 2

A

in the lungs by Angiotensin Converting Enzyme

269
Q

What does AT2 do in the adrenal cortex

A

Produce aldosterone

270
Q

What does an increased aldosterone level do

A

More Na is reabsorbed in the distal convoluted tubule in exchange for K

271
Q

AT1 and AT2 are involved in

A

Vasoconstriction

272
Q

What is phosphorus regulated by

A

PTH in the kidney

273
Q

What does Phosphorus do to Calcium

A

binds and decreases the plasma free Calcium concentration

274
Q

What does PTH do to Phosphorus

A

Trashes it in the kidney

275
Q

What does Vit D do to Phosphorus

A

increase intestinal absorption

276
Q

How is Copper transported

A

Ceruloplasmin

277
Q

Where is copper stored

A

Liver

278
Q

What do elevated levels of copper cause

A

Neuropathies
hepatitis

279
Q

Decreased Ceruloplasmin is seen in what disease

A

Wilson disease

280
Q

Osmolarity equation

A

2 * Na+
BUN/2.8 +
Glucose/18

281
Q

What is the normal osmolarity range

A

275 - 295 mOsm/L

282
Q

What is the normal Osmolar Gap range

A

5 - 10 mOsm/L

283
Q

What substances can increase Osmolar Gap

A

Ethanol
Methanol
Ethylene glycol
isopropanol
Lactate
B-hydroxy butryate

284
Q

What is SIADH

A

Syndrome of Inappropriate ADH Secretion

285
Q

What happens in SIADH

A

decreased free water excretion and increased thirst

286
Q

In SIADH what would we expect to see in plasma osmolality

A

very low <275

287
Q

In SIADH what would we expect to see in urine osmolality

A

Very high >100

288
Q

What does the free water retention in SIADH do?

A

Dilutes out electrolytes

289
Q

Electrolytes assessed by ISE

A

Na
K
Cl

290
Q

What is ISE membrane made of

A

Valinomycin

291
Q

Hyponatremia can cause<135

A

Hypovolemia
altered mental status
Orthostatic hypotension

292
Q

What causes hypernatremia >150

A

Dehydration
Burns
hypertonic saline

293
Q

Causes of hypokalemia <3.5

A

K shift in treated acidosis
Polyuria
diarrhea
blood dilution
mild dehydration
Lab/sample error

294
Q

Symptoms of hypokalemia

A

EKG changes
Tachycarrhythmias
Dysrhythmias

295
Q

Causes of hyperkalemia >6.1

A

Hypoaldosteronism
Extreme dehydration
Hemolysis

296
Q

Symptoms of hyperkalemia

A

EKG changes
Confusion
Weakness
paralysis

297
Q

Critical values for K

A

<3
>8

298
Q

Hyperchloremia causes
>108

A

Dehyrdation
Intake of Cl exceeds output
Alkalosis

299
Q

Hypochloremia causes
<97

A

Output exceeds intake
Acidosis

300
Q

Dietary sources of Copper

A

Liver
Kidney
Nuts
Cocoa

301
Q

Copper and Ceruloplasmin are what

A

Acute phase reactants which increase during stress

302
Q

Purpose of Copper

A

Metalloprotein and essential for redox reactions

303
Q

What happens in Wilson Disease

A

Low levels of Ceruplasmin
Lots of copper deposits

304
Q

Where does copper deposit in Wilson Disease cause

A

Liver Disease
Neurological disease
Psychiatric symptoms
Kayser-Fleischer rings in eyes

305
Q

Reference range for anion gap

A

7 - 16

306
Q

Anion gap equation

A

Na -
(Cl + HCO3)

307
Q

Causes of metabolic acidosis with elevated anion gap

A

Methanol
Uremia
DKA
Paracetamol
Isoniazid
Lactic Acidosis
Ethanol
Salicylates

308
Q

What is Colligative Properties

A

Properties that are dependent solely upon the concentration of the solvent in solution

309
Q

What occurs when a solute is added to a solution

A

Boiling point elevation
Freezing point depression
Vapor pressure depression

310
Q

When do we use freezing point depression

A

Sweat chloride testing in Cystic Fibrosis in neonates

311
Q

What may be falsely low in lipemic samples

A

Na

Clinical Chem (5 decks)

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