Unit 5 Flashcards

1
Q

What is heme composed of?

A

Protoporphyrin ring + Fe

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2
Q

What is hemoglobin composed of?

A

Heme + 4 globin chains

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3
Q

What is the storage form of iron?

A

Fe3+
Ferric

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4
Q

What is the functional form of iron?

A

Fe2+
Ferrous

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5
Q

What are porphyrins?

A

Any class of pigments whose molecules contain a flat ring of four linked heterocyclic groups

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6
Q

What is Porphyrias

A

Diseases caused by enzyme deficiencies in the Heme production pathway.
*People will generally look purple.

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7
Q

What is Hemin

A

A black inorganic compound which forms from heme when RBCs are lysed and exposed to air.

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8
Q

What is the most common Primary Porphyrias?

A

Porphyria Cutanea Tarda (PCT)

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9
Q

What is Porphyria Cutanea Tarda deficient in?

A

Uroporphyrinogen Decarboxylase

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10
Q

What test is ordered to confirm PCT

A

Serum porphyrin

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11
Q

What is PCT defined by?

A

Blistering

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12
Q

What is Acute Intermittent Porphyria deficient in

A

PBG Deaminase

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13
Q

What is AIP defined by

A

Blistering
Nerve Impairments

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14
Q

What test is ordered to confirm AIP

A

Urine porphobilinogen

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15
Q

What is Erythropoietic Porphyria deficient in

A

Ferrochelatase

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16
Q

What will Erythropoietic Porphyria show an increase in

A

Total erythrocyte protoporphyrin

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17
Q

What is Erythropoietic Porphyria defined by

A

Blistering

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18
Q

What is the rate limiting step in porphyrin synthesis

A

ALA-Dehydratase

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19
Q

How do we test for ALA-Dehydratase Deficiency

A

Delta-aminolevulinic

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20
Q

What is the most common presenting symptom of ALA-Dehydratase deficiency?

A

Abdominal pain

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21
Q

What does ALA-Dehydratase deficiency cause

A

Accumulation of d-aminolevulinic acid

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22
Q

What does lead poisoning do?

A

Inhibition of most of the enzymes in the synthetic pathway

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23
Q

What secondary porphyria has an elevated level of succinylacetone

A

Hereditary tyrosinemia

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24
Q

What method do we use for Porphobilinogen

A

Watson-Schwartz

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25
Q

What Porphobilinogen method do we not use but is tested on

A

Hoesch

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26
Q

What is a must for all samples being tested for Porphyrins

A

MUST BE LIGHT PROTECTED

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27
Q

How are porphyrins evaluated

A

HPLC

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28
Q

What is a screening test for lead poisoning

A

Ferrochelatase

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29
Q

What form of Bili is lipophilic

A

Indirect/Unconjucated

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30
Q

What form of Bili is hydrophilic

A

Direct/Conjugated

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31
Q

Syndromes from an increase in unconjugated bilirubin

A

Crigler-Najjar
Gilbert

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32
Q

Syndromes when conjugated Bilirubin with biliary obstruction

A

Dubin-Johnson
Rotor

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33
Q

What is delta bilirubin

A

Conjugated bilirubin that is covalently bound to Albumin

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34
Q

How is hem mostly produced

A

Breakdown of RBCs in the spleen

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35
Q

What does Heme Oxygenase in macrophages do

A

Oxidize heme to biliverdin

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36
Q

What does biliverdin reductase in macrophages do

A

Reduces biliverdin to bilirubin

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37
Q

What is bilirubin bound to while being transported

A

Albumin

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38
Q

What conjugates bilirubin

A

UGT1A1
Uridine Diphosphate Glucuronyltranferase

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39
Q

What are the serious autosomal dominant Hyperbilirubinemia disorders

A

Dubin-Johnson (conjugated)
Crigler-Najjar (Unconjugated)

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40
Q

What are the weak sauce autosomal recessive Hyperbilirubinemia disorders

A

Rotor (conjugated)
Gilbert (unconjugated)

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41
Q

What is bilirubin turned into in the gut by bacteria

A

Stercobilin

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42
Q

What is stercobilin turned into after it is reabsorbed

A

Urobilin

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43
Q

What is the main cause of Prehepatic Jaundice

A

Hemolysis

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44
Q

In prehepatic jaundice what are the levels of Unconjugated and conjugated bilirubin

A

Unconjugated will be drastically increased

Conjugated will be normal or mildly increased

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45
Q

What can cause an increased amount of unconjugated bilirun be caused by

A

decreased bilirubin uptake by liver cells

Increased bilirubin burden

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46
Q

What is posthepatic jaundice is from?

A

Failure of liver to excrete conjugated bilirubin

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47
Q

In posthepatic jaundice what are the levels of Unconjugated and conjugated bilirubin

A

Both will be increased

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48
Q

Why is there jaundice when there is a blocked duct or biliary tract problems?

A

The body is reabsorbing bilirubin due to bile sludging and bc it can’t get out of the body.

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49
Q

What are the tests that measure bilirubin

A

Evelyn-Malloy

Jendrassik-Grof

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50
Q

What does Evelyn-Malloy use as an accelerator

A

Methanol

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51
Q

What does Jendrassik-Grof use as an accelerator

A

Cafferine-benzoate-acetate

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52
Q

What is the pH for Evelyn-Malloy method?

A

1.2

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53
Q

What is the absorbance for the Evelyn-Malloy method?

A

red-purple chromagen at 560nm

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54
Q

What is the absorbance for the Jendrassik-Grof method?

A

Blue chromagen at 600 nm

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55
Q

What is needed to reduce alcohol interference in a sample?

A

To be fasting

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56
Q

How does lipemia affected bilirubin

A

Falsely increases

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57
Q

What does hemolysis do to the bilirubin method

A

decrease the reaction with diazo reagent

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58
Q

How much bilirubin will be lost in an hour if exposed to light?

A

50%

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59
Q

How long can bilirubin be stored?

A

Off cells:
2 days RT
1 week fridge
forever if frozen

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60
Q

What is Hgb electrophoresis first performed on?

A

Cellulose acetate strip

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61
Q

What is used with cellulose acetate for Hgb electrophoresis?

A

alkaline buffer (pH 8)

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62
Q

To distinguish Hgb what is the electrophoresis performed on?

A

Citrate Agar Gel with Acid buffer (pH 6)

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63
Q

What is the order of Hgb from slowest to fastest?

A

C
S
F
A

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64
Q

What hemoglobins are considered fast Hgb?

A

Hgb H
Barts

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65
Q

What is Hgb H made out of?

A

4 beta chains (Beta globin tetramer)

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66
Q

What is Barts Hgb made out of?

A

4 gamma chains

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67
Q

Standard alkaline and acid electrophoresis can’t distinguish what 2 Hgbs?

A

Hgb D and G

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68
Q

How is Hgb E made?

A

Mutated Beta chain

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69
Q

What is HgbA1C?

A

Glycated hemoglobin

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70
Q

What is carboxyhemoglobin

A

carbon monoxide binds to hemoglobin and displaces oxygen

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71
Q

What is methemoglobin

A

Alkaline media or oxidizing agents transform normal Fe2+ into Fe3+, conferring a inability to reversibly bind oxygen

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72
Q

What is Sulfhemoglobin

A

Sulfation of hemoglobin casues an inability to bind oxygen

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73
Q

Steps in Iron Spectrophotometry Method?

A
  1. Release Iron from transferrin with addition of acid
  2. Reduction of Fe3+ to Fe2+ with ascorbic acid
  3. React Fe2+ with a chromogen
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74
Q

How much of a carrier protein is bound to Iron

A

66%

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75
Q

What is the quantitative defect of Hgb

A

alpha thalassemia

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76
Q

Alpha thalassemia trait has how many genes missing?

A

2 genes

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77
Q

Hgb H Ds has how many genes

A

1
3 missing

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78
Q

What Alpha Thalassemia results in utero death?

A

Hgb Barts/Hydorps fetalis
-All genes are missing

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79
Q

How do we get Hgb H disease?

A

Inadequate alpha globin production so body produces beta hemoglobin that form together

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80
Q

What is Beta+

A

reduced beta hgb production

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81
Q

What is B0?

A

complete lack of beta hgb production

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82
Q

paracentesis fluid is from where?

A

peritoneal cavity

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83
Q

thoracentesis fluid is from where?

A

pleural cavity

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84
Q

Athrocentesis fluid is from where?

A

joint

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85
Q

What is ascites

A

Pathological accumulation of fluid in the peritoneal cavity

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86
Q

What is effusion

A

Pathological accumulation of fluid in most other body cavities

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87
Q

what is transudate

A

an effusion which is a filtrate of the plasma

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88
Q

what is exudate

A

an effusion which is protein-rich and usually caused by an infection or cancer
*likely has inflammatory cells and occassionally pus

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89
Q

What is Xanthrochromia

A

a yellowish tinge to CSF
*indicates prior bleeding in the CSF

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90
Q

What is pseudochylous

A

an effusion which has high levels of cholesterol

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91
Q

What can be found in refridgerated joint aspirations and urine samples

A

crystals

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92
Q

What can increase due to anaerobic metabolism of cells

A

Lactate

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93
Q

What is a spinal tap used to diagnosis?

A

Multiple Sclerosis
Hemorrhage
Meningitis
Other infections of CNS

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94
Q

Where does a spinal tap occur?

A

Epidural space between L4/5

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95
Q

What is the CSF tube order

A

1st- Storage/Cytology
2nd- Chemistry/Serology
3rd-Micro
4th- Heme

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96
Q

Milky consistency in Pleural Effusion indicates?

A

Chylothorax (lymphatic obstruction)

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97
Q

What does a putrid odor in Pleural Effusion indicate?

A

Anaerobic Empyema

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98
Q

What is glucose directly correlated with in Pleural Effusions?

A

pH bc the products of glycolysis are acidic

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99
Q

What does Black Pleural fluid suggest

A

-Malignant melanoma
-non-small cell lung carcinoma
-ruptured pancreatic pseudocyst
-charcoal-containing empyema

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100
Q

Peritoneal fluid is usually taken from patients with?

A

Ascites

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101
Q

What is ascites?

A

Abnormal collection of fluid in the peritoneal cavity due to either portal hypertension or low serum osmolality

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102
Q

What is transudates Specific Gravity

A

<1.010

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103
Q

What is Exudates Specific Gravity

A

> 1.020

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104
Q

Why would the rare pericardial fluid test be ordered?

A
  1. Therapeutic pericardiocentesis for cardiac temponade
  2. Clinical suspicion of purulent, tuberculosis, or neoplastic pericarditis
  3. Large pericardial effusions of unknown etiology
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105
Q

What are the 4 categories of Synovial Effusions

A
  1. Inflammatory
  2. Noninflammatory
  3. Hemorrhagic
  4. Septic
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106
Q

What are the routine Synovial testing

A

Gross examination
leukocyte count
gram stain and bacterial cx
crystal examination
uric acid

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107
Q

When is amniotic fluid traditionally taken?

A

15-18 weeks

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108
Q

Why would we collect amniotic fluid

A

Assess for Genetic disorders

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109
Q

How can we distinguish between urine and amniotic fluid

A

Urea
Glucose
Creatinine
Protein
**Urine has higher value of Urea and Creatinine

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110
Q

Preeclampsia signs and sypmtoms

A

Hemolysis- Elevated AST, ACP, LD
Elevated Liver Enzymes- AST, ALT, ALP
Low Platelets- profound thrombocytopenia

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111
Q

What is the only reason to evaluate seminal fluid

A

Infertility

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112
Q

What are the ways we assess seminal fluid

A

Ejaculate Volume
Total Sperm Count
Concentration
Shape of the head
Movement of the Sperm

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113
Q

What is traumatic tap

A

The first tube is quite bloody and the blood lessens in each subsequent tube

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114
Q

What is subarachnoid hemorrhage

A

The first tube is quite bloody and the last tube is just as bloody

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115
Q

What does yellow or brown CSF indicate

A

The old, oxidized blood is present

116
Q

What do 10% of bacterial meningitis begin with?

A

Lymphocytosis

117
Q

In bacterial meningitis what is elevated in CSF?

A

Protein
WBCs
Neutrophils

118
Q

In Viral infection what is elevated in CSF?

A

Protein
WBCs
Lymphocytes

119
Q

In bacterial meningitis what is decreased in CSF?

A

Glucose

120
Q

In viral infection was is decreased in CSF?

A

Glucose

121
Q

In Brain Tumor was in elevated in CSF?

A

Protein
Malignant Cells

122
Q

In Brain tumor what has a normal value in CSF?

A

Glucose
WBCs

123
Q

In a traumatic tap what is elevated in CSF

A

Protein
WBCs
All cells

124
Q

What is has a normal value in a traumatic tap in CSF

A

Glucose

125
Q

In multiple sclerosis what is elevated in CSF?

A

Protein
IgG
T Cells

126
Q

In multiple sclerosis what has a normal value in CSF?

A

Glucose
WBCs

127
Q

What is the normal CSF IgG Index

A

<0.73

128
Q

What indicates multiple sclerosis in CSF

A

Oligoclonal bands

129
Q

How do we get the CSF IgG index

A

(CSF IgG/Serum IgG)
/
(CSF albumin/serum albumin)

130
Q

An intact blood brain barrier has what index

A

<9

131
Q

How do we get BBB index

A

CSF/serum albumin index =
CSF albumin / serum albumin

132
Q

What is an effusion

A

Pathological accumulation of serous fluid in a body cavity

133
Q

What is edema

A

accumulation of serous fluid in the tissues

134
Q

What can cause the accumulation of serous fluid

A

-Decreased plasma oncotic pressure
-increased capillary hydrostatic pressure
-increased capillary permeability

135
Q

What are the values for normal pleural fluid

A

Clear
<2 g/dL: Protein
<1000 WBCs
Glucose at normal serum levels
Pleural LDH < 50% plasma LDH

136
Q

Bacterial Pleural Effusion Values

A

Cloudy
»2 Protein
»1000 WBCs
Glucose «120
Pleural LDH&raquo_space;50% plasma LDH

137
Q

Pleural fluid glucose < 30-50 mg/dL suggests

A

Malignant effusion

138
Q

Pleural LDH levels > 1000 indicate

A

Rheumatoid effusion
malignant effusion
Pneumocytstis jiroveci
empyema

139
Q

Why do we perform paracentesis

A
  1. remove serous fluid from compressing a vital organ
  2. determine pathologic cause of effusion
  3. classify the effusion as either transudate or exudate
140
Q

If Serum to Ascites Albumin Gradient (SAAG) is > 1.1 it is?

A

Portal Hypertension

141
Q

If Serum to Ascites Albumin Gradient (SAAG) is < 1.1 it is?

A

NOT portal hypertension

142
Q

what are the 2 methods that form ascites

A
  1. high blood pressure in the portal veins pushes some fluid into the peritoneum
    *usually transudate
  2. Serum is drawn into the peritoneal membrane by low plasma oncotic pressure and higher oncotic pressure in the abdominal cavity. *liver failure
143
Q

Peritoneal Fluid Amylase will be increased due to?

A

Pancreatitis or bowl perforation up to 2000 IU/L

144
Q

Peritoneal Fluid LDH will be increased due to?

A

Bacterial Peritonitis 1:1
Ratio above 1 = infection, bowl perforation, or tumor

145
Q

Serum Pro-BNP will be elevated in Peritoneal Fluid bc?

A

Heart failure

146
Q

Pericardial Effusion is usually ordered with what tests?

A
  1. Serum electrolytes
  2. CBC
  3. Cardiac biomarker levels
  4. Other markers of inflammation
147
Q

Synovial fluid should be ran how fast?

A

Within 2 hours

148
Q

What can Synovial fluid be diluted with if necessary?

A

Saline

149
Q

Gout is made up of what crystals

A

monosodium urate

150
Q

Pseudogout is made out of what crystals

A

Calcium pyrophosphate

151
Q

Synovial Fluid Normal Values

A

Transparent
Clear
0-150 WBC
<25 PMN
0 RBC
0-10 Glucose

152
Q

Synovial Fluid Group 1 noninflammatory values

A

Transparent
Xanthochromatic
<3000 WBC
<30 PMN
0 RBC
0-10 glucose

153
Q

Synovial Fluid Group 2 inflammatory values

A

Transparent/Opaque
Xanthochromatic to bloody
3000-75,000 WBC
>50 PMN
0 RBC
0-40 Glucose

154
Q

Synovial Fluid Group 3 Infectious Values

A

Opaque
White
50,000-200,000 WBC
>90 PMN
Yes RBC
20-100 Glucose

155
Q

Synovial Fluid Group 4 Hemorrhagic Values

A

Opaque
Red/brown to Xanthochromatic
50-10,000 WBC
<50 PMN
Yes RBC
0-20 Glucose

156
Q

Spectrophotometry for bilirubin and HDFN is detected at

A

Abs 450

157
Q

What is the range of absorbances for bilirubin

A

350-550
*but peaks at 450

158
Q

When does AFP peak in the amniotic fluid

A

13-15 weeks gestation

159
Q

What cutoff suggests a neural tube defect

A

> 2.5 MoMS AFP
The higher the level the more brain is exposed

160
Q

What is preeclampsia

A

Toxemia of pregnancy

161
Q

Diagnosis for preeclampsia

A

BP >140/90
Protein >5 in 24 hr urine
Oliguria <500 mL/24 hr urine
Thrombocytopenia <100,000

162
Q

What is L/S ratio

A

Lecithin Sphingomyelin ratio that is used for fetal lung maturity

163
Q

<1.5 L/S ratio indicates

A

Lung Immaturity

164
Q

> 2.0 L/S ratio indicates

A

Lung Maturity

165
Q

What are other tests to evaluate surfactant production of the fetus

A
  1. Phosphatidylglycerol
  2. Foam Stability Index
166
Q

Why would we do a sweat chloride test on infants

A

Presence of CFTR mutation

167
Q

Elevated sweat chloride is seen in

A

cystic fibrosis

168
Q

Decreased sweat sodium concentration is seen in

A

SIADH
Liddle Disease
Hypoaldosteronism

169
Q

Transudate values

A

Straw colored to amber
Clear
Normal glucose
Normal protein
Normal WBC

170
Q

Exudate values

A

Brown, yellow, green
Milky
Low glucose
High protein
High WBC

171
Q

To officially diagnosis exudate the specimen MUST have

A

Elevated total protein ratio and LD ratio
>0.6

172
Q

What causes transudate

A

Decreased relative serum oncotic pressure (hepatitis)
Increased hydrostatic pressure (CHF)
Renal Failure

173
Q

What causes Exudate

A

Infection
Autoimmune disease
Occasionally cancer

174
Q

Hemoglobin A1 is composed of

A

2 Alpha
2 Beta

175
Q

Hemoglobin A2 is composed of

A

2 alpha
2 delta

176
Q

What is fetal hemoglobin composed of

A

2 alpha
2 gamma

177
Q

What is Coproporphyrinogen 3 seen in

A

Heme synthesis

178
Q

What is the purpose of HMB synthase

A

Converts PBG (Porphobilinogen) to HMB (Uroporphyrinogen I)

179
Q

What is the purpose of ALA dehydratase

A

Convert Aminolevulinic Acid to PBG (Porphobilinogen)

180
Q

What is the purpose of Ferrochelatase

A

Convert Protoporphyrin IX to Heme with Fe2+

181
Q

what is AIP classified as?

A

Serious Acute Neurological disease
*life threatening

182
Q

What are the most common hemoglobins

A

S
C
D
E

183
Q

About 70% of all hemoglobinopathies have a defective

A

Beta globin chain

184
Q

What are the serous fluids

A

Pleural fluid
Pericardial fluid
Peritoneal fluid

185
Q

Exudative Pleural Effusion Criteria

A

Pleural fluid protein/serum protein >0.5
Pleural Fluid LDH/Serum LDH >0.6

186
Q

Peritoneal SAAG <1.1 and Neutrophil count >250 indicates

A

Peritonitis

187
Q

What makes fluid Serous

A

they are from dialyzing of the plasma

188
Q

What are the Non-Serous fluids

A

CSF
Amniotic Fluid
Sweat analysis
Synovial fluid

189
Q

What makes fluid non-serous

A

Cells that secrete this fluid and they manipulate the constituents inside the fluid

190
Q

What forms CSF

A

Choroid plexuses in each of the ventricles of the brain

191
Q

What is Therapeutic Drug Monitoring

A

measuring specific drugs at designated intervals to maintain a stable concentration in a patient’s bloodstream

192
Q

What is toxicology

A

The study of substances that cause adverse effects in a human
i.e. xenobiotic

193
Q

What is Pharmacodynamics

A

what the DRUG does to the body

194
Q

What is pharmacokinetics

A

What the BODY does to the drug

195
Q

What is steady state

A

the rates of addition and subtraction of a drug are equal

196
Q

what is half life

A

time it takes for the drug to decrease by half

197
Q

what is therapeutic range

A

the concentration window at which a drug can achieve its desired effect

198
Q

what is peak

A

the highest concentration of drug in the body, usually 30 min to 2 hrs after the last dose

199
Q

what is trough

A

the lowest concentration of drug in the body, usually just prior to the next dose

200
Q

what is the most common cause of treatment failure in TDM

A

noncompliance

201
Q

What are the 4 biological events for Pharmacokinetics

A
  1. Absorption
  2. Distribution
  3. Metabolism
  4. Excretion
202
Q

Absorption increases with what factors?

A
  1. Increased surface area for absorption
  2. increased contact time with the absorptive surface
  3. increased blood flow
  4. increased solubility of the drug
203
Q

What is bioavailability

A

The extent and rate at which administration of the drug increases the blood concentration

204
Q

What is therapeutic window

A

Below the min effective concentration for the adverse effect
Above the min effective concentration for the desired effect

205
Q

What factors decide on distribution of the drug

A

Blood flow
capillary permeability
drug binding in tissues
target tissue volume

206
Q

Tissue distribution depends on?

A
  1. partitioning of drug between blood and the tissue of interest
  2. lipid solubility
  3. pH gradient
207
Q

What is biotransformation

A

Change the polarity, activate, or inactivate molecules to regulate their effect on our bodies

208
Q

Phase 1 reactions are

A

Oxidation
Reduction
Hydrolysis
**made water soluble and quickly excrete in urine

209
Q

Phase 2 Reactions

A

Add a functional group by a covalent bond
*render drug inactive
Excrete in urine or feces

210
Q

What is volume of distribution

A

A measure of how broadly the body distributes the drug

211
Q

What is volume of distribution dependent upon

A

total amount of drug in the body and the plasma concentration

212
Q

What type of drug will have a large volume of distribution

A

Fat soluble

213
Q

How do we get the Vd (volume of distribution)

A

total amount of drug in body/ plasma concentration

214
Q

what type of drug will have a small volume of distribution

A

water soluble

215
Q

Protein bound water soluble drugs have what Vd

A

similar to that of ordinary water soluble drugs

216
Q

What is the active portion of a drug?

A

The free portion

217
Q

What are the proteins that bind most of the circulating drugs

A

Albumin
a1-glycoprotein

218
Q

Overdose of a drug can happen in liver disease because?

A

Hypoalbuminemia allowing more free drug to circulate

219
Q

What organ is the primary route for drug excretion

A

kidneys

220
Q

Clearance is co-dependent on?

A

Renal perfusion and renal function

221
Q

What is first pass effect

A

Meds that are ingested enter the enteric circulation and go to the liver which will metabolize, partition, or excrete many compounds. Drugs can be inactivated before they reach their target location.

222
Q

What is the major drug metabolism system

A

P450 Oxidase system

223
Q

What does P450 Oxidase system do?

A

Serves as the terminal electron donor

224
Q

Creation of conjugation compunds usually involves

A

Sulfation
Acetylation

225
Q

What do sulfates or acetates do to the drugs

A

inactive them

226
Q

In order to absorb drugs what does it need to come in contact with?

A

Circulatory system

227
Q

What do we need to do with drugs that have an active metabolite

A

decrease the dose as the drug is still active after it starts the metabolic process

228
Q

How many half lives does it take to achieve a steady state

A

5 half lives

229
Q

Upon cessation of the drug how many half lives until the body eliminates the drug

A

5 half lives

230
Q

What is zero order elimination

A

the same amount of drug is eliminated per unit of time. regardless of the plasma concentration.
*elimination rate is constant

231
Q

What is first order elimination

A

The same proportion of the drug is eliminated per unit of time. This leads to a variable amount of eliminated based on the plasma concentration.
*as concentration drops so does the elimination rate

232
Q

What is agonist

A

accentuates the intended response and second messengers of the receptor

233
Q

What is antagonist

A

prevents the intended response from occurring or causing an opposing effect

234
Q

What may agonists and antagonists do at the same site

A

compete for binding

235
Q

If the substrate can’t fit at the active site it is

A

Noncompetitive

236
Q

What is the dosing rate equation

A

Clearance x Steady State Concentration

237
Q

What are the toxicity symptoms from Aminoglycosides

A

Neurotoxicity
Ototoxicity
Renal Impairment

238
Q

What are the toxicity symptoms from Vancomycin

A

Ototoxicity
Nephrotoxicity
Red Man Syndrome

239
Q

What are the toxicity symptoms from Phenytoin

A

Nystagmus
ataxia
slurred speech
seizures
coma

240
Q

What are the toxicity symptoms from Methotrexate (MXT)

A

Aplastic anemia
spontaneous GI hemorrhage

241
Q

What are the toxicity symptoms from Digoxin

A

Palpitations
nausea
vomiting
drowsiness

242
Q

What are the toxicity symptoms from Lithium

A

Seizures
Hypopnea
Dysrhythmias
Anemia

243
Q

What is the toxicity symptom from Cyclosporin A

A

Nephrotoxic

244
Q

What is the MOA for Aminoglycosides

A

Inhibits bacterial protein synthesis by binding 30S ribosomal subunit and misreading of the genetic code

245
Q

What type of organism is Aminoglycosides used for

A

Gram + and Gram =
Can be used against Fungi

246
Q

What is the MOA for Vancomycin

A

Binds to the bacterial cell wall causing disruption in the glycopeptide polymerization, results in immediate cessation of cell wall synthesis

247
Q

What is vancomycin produced by

A

Bacterium

248
Q

What is the MOA for Phenytoin

A

Limitation of seizure propagation along the neurons by reduction of nerve impulse potentiation

249
Q

What is the use for Phenytoin

A

Anticonvulsant
*control tonic-clonic (grand mal) seizures

250
Q

What is the MOA for Methotrexate

A

Folate analog that inhibits dihydrofolate reductase, which inhibits purine synthesis and thereby, DNA synthesis

251
Q

What is MXT used for

A

To treat cancers

252
Q

What is Lithium used for

A

Treatment of mania, depression and bipolar disorder

253
Q

What do Tricyclic Antidepressants do

A

Inhibit the neural reuptake of Norepinephrine and 5-HT

254
Q

What are some examples of Tricyclic Antidepressants

A
  1. amitriptyline
  2. desipramine
  3. doxepin
  4. imipramine
  5. notriptyline
255
Q

When is Theophylline assessed

A

At the PEAK

256
Q

What was Theophylline used for

A

treatment of respiratory disorders bc it relaxes the bronchial smooth muscles
***NO LONGER USED

257
Q

What is the MOA for Digoxin

A

blocks the Na/K- ATPase in the cardiac myocyte, improves contractability

258
Q

What is Digoxin used for

A

CHF

259
Q

Digoxin overdose causes

A

Vision changes

260
Q

What is Cyclosporine A also called?

A

Calcineurin Inhibitors

261
Q

What is the MOA for Warfarin

A

Inhibits Vit K oxide reductase which impairs the prodcution of Vit K dependent coag factors (FVII, IX, X, II, Proteins C & S)

262
Q

What phase is 1st in Acetaminophen metabolism

A

Phase 2

263
Q

What is for Acetaminophen elimination

A

Rumack-Matthew Nomogram

264
Q

If the point of Acetaminophen is below the line on the Nomogram what will likely NOT be depleted

A

Glutathione

265
Q

What can an Acetaminophen overdose do

A

Lead to oxidative stress and depletion of glutathione, which creates reactive oxygen species and may cause liver failure

266
Q

Routes of drug administration

A

Enteral (mouth)
Parenteral
Pulmonary
Rectal
Topical

267
Q

What are the Parenteral routes of administration

A

IV (100% bioavailability)
IM
Subcutaneous
Intraarterial
Intrathecal

268
Q

What is the gold standard confirmation method for positive drug screens

A

GC/MS

269
Q

What does alcohol increase in our body

A

Estrogen

270
Q

What are common indicators of alcohol abuse

A

GGT
AST
AST/ALT ratio >2
HDL
MCV

271
Q

What is cocaine metabolized to

A

Benzoylecgonine

272
Q

How long can cocaine be detected after a single use

A

up to 3 days

273
Q

In chronic, heavy users of cocaine how long can it be detected

A

20 days

274
Q

How long can THC be detected

A

5 days after a single use
4 weeks in chronic use

275
Q

How is THC screened

A

Immunoassay

276
Q

Where are toxicities seen in Carbon Monoxide

A

brain and heart

277
Q

Why is elimination of mercury slow

A

Highly protein bound

278
Q

What is qualitative testing

A

does not give a value
Yes/ No

279
Q

What is quantitative testing

A

actually tells you how much of a substance is present

280
Q

What is Xenobiotic

A

chemicals that are not normally found in humans

281
Q

What is Poison

A

eXogenous agents that have an adverse effect

282
Q

what is toxin

A

eNdogenous substances that have an adverse effect

283
Q

What is effective dose 50 (ED50)

A

dose at which 50% of all patients taking this drug see clinical benefit

284
Q

What is toxic dose 50 (TD50)

A

dose at which 50% of all patients taking this drug experience a specific side effect

285
Q

What is lethal dose 50 (LD50)

A

dose at which 50% of all patients taking this drug experience death as a side effect

286
Q

What is acute toxicity

A

exposure to a dose high enough to elicit immediate short term effects

287
Q

what is chronic toxicity

A

repeated or frequent exposure at low doses which are insufficient to cause an immediate acute response