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Y3R1 - DALR ✋🏻 > Lab Medicine 👨‍🔬 > Flashcards

Lab Medicine 👨‍🔬 Flashcards

1
Q

Blood elements

A
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2
Q

What does a CBC measure?

A
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3
Q

What is Hematocrit?

A
  • The ratio of the volume of red blood cells to the total volume of blood.
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4
Q

What is Mean corpuscular volume (MCV)?

A

The average volume of single RBC

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5
Q

What is Mean corpuscular Hemoglobin (MCH)?

A

The average amount of Hb present in single RBC

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6
Q

What is Mean corpuscular Hemoglobin Concentration (MCHC)?

A

The % ratio of Hb concentration in a single RBC in relation to its volume

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7
Q

What is the definition of anemia?

A
  • Reduction of the red cell mass due to decrease in Hb concentration And, or RBCs count below the normal for age & sex.
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8
Q

Classification of anemia

A
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9
Q

Examples of Microcytic, Hypochromic anemia

A
  • Iron deficiency
  • Thalassemia.
  • Sideroblastic anemia.
  • Anemia of chronic disease.
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10
Q

Examples of Normocytic, Normochromic anemia

A
  • Hemolytic anemia: Except thalassemia.
  • Aplastic anemia.
  • Acute hemorrhage.
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11
Q

Examples of Macrocytic anemia

A

Megaloblastic anemia:
* B12 & folic acid deficiency.

Non-megaloblastic anemia:
* Liver disease.
* Acute hemolysis.
* Acute blood loss.
* Hypothyroidism.

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12
Q

What is the most common form of anemia?

A

IRON DEFICIENCY ANEMIA

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13
Q

Pathophysiology of iron deficiency anemia

A

Iron deficiency leads to decrease in the Production of hemoglobin.

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14
Q

Lab diagnosis of iron deficiency anemia

A
  • Blood exam
  • BM Exam
  • Iron Studies
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15
Q

Blood exams in iron deficiency anemia

A

Anemia: typically, Microcytic Hypochromic.

Blood indices: Decrease in (MCV + MCH + MCHC).

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16
Q

Bone marrow exam in iron deficiency anemia

A
  • Erythroid hyperplasia.
  • Absence of iron stores.
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17
Q

Iron studies in iron deficiency anemia

A
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18
Q

What are the best test for iron deficiency anemia?

A

Serum ferritin

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19
Q

Classification of megaloblastic anemia

A
  • Vit B12 deficiency.
  • Folic acid deficiency.
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20
Q

Pathophysiology of megaloblastic anemia due to vitamin B12 deficiency

A

B12 deficiency —> Impaired nucleic acid synthesis in all cells (including RBCs) —> Defect in maturation of RBCs (Megaloblastic erythropoiesis) & Neurological damage (so called pernicious anemia).

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21
Q

Blood exam of megaloblastic anemia

A

Hemogram shows:
* Macrocytic anemia (MCV > 100 fl).
* Moderate neutropenia (Dec in Neutrophil).
* Thrombocytopenia (Dec in Platelet count).

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22
Q

Laboratoey Diagnosis of megaloblastic anemia

A
  • Blood Exam
  • BM Exam
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23
Q

What does blood film of megaloblastic anemia show?

A
  • Howell -Jolly bodies.
  • Oval macrocytes.
  • Anisopoikilocytosis: RBCs different sizes & shapes.
  • Large hyper segmented neutrophils.
  • Giant platelets.
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24
Q

What does bone marrow exam show for megaloblastic anemia?

A
  • Hypercellular (Due to erythroid hyperplasia).
  • Megaloblasts (Large than normoblast, with large nucleus).
  • Atypical megakaryocytes (With hyper-segmented nuclei).
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25
Q

Types of hemolysis

A
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26
Q

What is the structure of hemoglobin?

A
  • 4 globin chains + 4 heme molecule.
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27
Q

What are hemoglobin variants?

A
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28
Q

What is thalassemia and what causes it?

A
  • Inherited (Autosomal recessive) & chronic hemolytic anemia
  • Due to globin chain imbalance.
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29
Q

Classification of thalassemia

A
  • Acc to the type of the globin chain that is produced at reduced rate into Alpha & Beta Thalasemia
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30
Q

Blood exam of beta thalassemia major

A
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31
Q

Compare between alpha thalassemia, and Beta thalassemia

A
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32
Q

Bone marrow exam of beta thalassemia major

A
  • Intense erythroid hyperplasia.
  • With marked ineffective erythropoiesis.
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33
Q

Definitive tests for diagnosis of beta thalassemia major

A
  • Hb electrophoresis –> Inc in Hb F (10-90%)
  • Molecular characterization of globin gene mutation.
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34
Q

Blood exam of Thalassemia minor

A

Blood indices: decrease in (MCV + MCH) & Normal RDW.

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35
Q

Definitive tests for Thalassemia minor

A
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36
Q

What is Sickle cell anemia?

A
  • Autosomal recessive disorder due to amino acid substitution in beta globin chain.
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37
Q

Pathophysiology of Sickle cell anemia

A

Point mutation in the B-globin gene (chromosome 11) —> glutamic acid replaced with valine (single amino acid substitution) —> 2 a-globin & 2 mutated B-globin subunits create pathological hemoglobin S (HbS).

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38
Q

Clinical features of Sickle cell anemia

A

Carriers (sickle cell trait):
- are usually normal (symptom-free).

Patient:
- suffer from many types of crises:
* Hemolytic.
* Aplastic.
* Vaso-occlusive.
* Spleen sequestration.

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39
Q

Lab diagnosis of Sickle cell anemia

A
  • Blood Exam
  • RBCs fragility test
  • Definitive tests
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40
Q

Blood exam of Sickle cell anemia

A

CBC shows Normocytic normochromic anemia.

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41
Q

RBCs osmotic fragility test for Sickle cell anemia

A

Decreases

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42
Q

Definitive tests for diagnosis of Sickle cell anemia

A
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43
Q

Pathophysiology of hereditary Spherocytosis

A

Abnormality in membrane cytoskeleton leads to decrease in RBC deformability (flexibility).

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44
Q

Presentation of hereditary Spherocytosis

A
  • At neonatal, adult or even old age.
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45
Q

Lab diagnosis of hereditary Spherocytosis

A
  • Blood Exam
  • RBCs osmotic fragility test
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46
Q

Blood exam of hereditary Spherocytosis

A
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47
Q

RBCs osmotic fragility test for hereditary Spherocytosis

A
  • Increases
    (Specific test for spherocytosis)
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48
Q

Enzymopathies related to blood disorders

A
  • G6PD deficiency (Favism)
  • Pyruvate kinase deficiency
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49
Q

What is the most common hemolytic anemia?

A
  • G6PD enzyme deficiency (favism)
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50
Q

Inheritance of G6PD deficiency (Favism)

A

X- linked recessive: So most often affects males.

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51
Q

Presentation of G6PD deficiency (Favism)

A
  • Neonatal or infancy period
  • In Between attacks the child is completely normal.
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52
Q

Risk factors of G6PD deficiency (Favism)

A

Precipitating agents of hemolytic crisis:
- Drugs.
- Acidosis.
- Infection.
- Fava beans or their pollens.

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53
Q

Definitive tests for diagnosis of G6PD deficiency (Favism)

A

Assay for G6PD enzyme activity

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54
Q

Blood exam of G6PD deficiency (Favism)

A
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55
Q

Definition of anemia due to Pyruvate kinase deficiency

A
  • Congenital non-spherocytic hemolytic anemia
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56
Q

CBC of Pyruvate kinase deficiency

A

CBC shows:
- Hb: usually 7-10 g/dI.
- Blood smear: No characteristic changes

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57
Q

definitive test for pyruvate kinase deficiency

A

Determination of pyruvate kinase enzyme activity.

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58
Q

Why are white blood cells called leukocytes?

A

as they are colorless, Due to lack of Hemoglobin.

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59
Q

Lifespan of white blood cells

A
  • Few hours to a few days.
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60
Q

Total leukocytic count

A
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61
Q

Differential leukocytic count

A
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62
Q

Compare between white blood cells and red blood cells in stained preparation

A
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63
Q

What are blood cells derived from?

A

hematopoietic stem cells

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64
Q

Differentiation of hematopoietic stem cells

A
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65
Q

Definition of acute leukemias

A

A heterogeneous group of malignant neoplasms of the precursors of blood cells resulting in appearance of the blast cells in the blood & bone marrow.

(Blast cells = partially developed WBCs)

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66
Q

Classification of acute leukemia

A
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67
Q

Etiology of acute leukemias

A

It is unknown but theories are implicated:
- lonizing radiation.
- Drugs & chemicals: as immunosuppressive agents & benzene.
- Genetics: chromosomal abnormalities.
- Infection: Retrovirus.
- Immune status: increased incidence of immunosuppressed individuals

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68
Q

Types of acute leukemia

A
  • According to the type of the affected blast cells)
  1. (Acute Lymphoblastic Leukemia (ALL) -› Mainly in infants.
  2. (Acute Myeloblastic Leukemia (AML) -> Mainly In adults.
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69
Q

FAB classification of acute lymphoblastic leukemia (ALL)

A
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70
Q

Pathophysiology of acute leukemias

A

mutation (e.g. chromosomal translocation) in the blast in bone marrow —> Which affect cell division & function.

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71
Q

FAB classification of acute myeloblastic leukemia (AML)

A
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72
Q

Cytochemistry of acute lymphoblastic leukemia (ALL)

A
  • MPO (Myeloperoxidase): Negative.
  • PAS stain (Periodic Acid Schiff): Positive.
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73
Q

Cytochemistry of acute myeloblastic leukemia (AML)

A
  • MPO: Positive.
  • PAS: Negative.
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74
Q

Immunophenotyping for acute Lymphoblastic leukemia (ALL)

A
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75
Q

Immunophenotyping for acute myeloblastic leukemia (AML)

A

CD13, CD33, CD117 & others.

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76
Q

Cytogenes of acute Lymphoblastic leukemia (ALL)

A

t (12;21)] & [t (8;14)].

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77
Q

Cytogenes for acute myeloblastic leukemia (AML)

A
  • M3: [t(15;17) ]. & Other cytogentic abnormalities in different FAB Subtypes e.g. inv 16: [t(8;21 )].
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78
Q

Hematological Findings of acute leukemia

A
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79
Q

Bone marrow findings of acute leukemia

A
  • Hypercellular & infiltrated with blast cells (>20%).
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80
Q

Biochemical findings in acute leukemia

A
  • Increased Serum uric acid.
  • Increased Serum LDH.
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81
Q

What are Lymphoproliferative disorders (LPDS)?

A
  • A group of both malignant (clonal) lymphoid disorders.
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82
Q

What should Lymphoproliferative disorders (LPDS) Be diffrentiated from?

A

from reactive (polyclonal) lymphoid disorders

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83
Q

What do Lymphoproliferative disorders (LPDS) Include?

A
  • Chronic lymphocytic leukemia (CLL).
  • Hairy cell leukemia (HCL).
  • Plasma cell leukemia (PCL).
  • Non-Hodgkin’s lymphoma (NHL).
  • Large granular lymphocytosis.
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84
Q

Epidemiology of Chronic Lymphocytic leukemia (CLL)

A

Age:
- Affect older people (>50 years old).
- Incidence increases with age.

Sex:
- Male predominance.

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85
Q

Diagnostic criteria for Chronic Lymphocytic leukemia (CLL)

A
  • Peripheral blood: Absolute lymphocytosis > 5.0 × 10°9 /L.
  • Bone marrow: Lymphocytosis > 30% of total bone marrow cells.
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86
Q

What is the difference between absolute lymphocytosis and relative lymphocytosis?

A
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87
Q

Definition of plasma cell dyscrasias

A
  • A group of disorders characterized by abnormal proliferation of the same type (=single clone =monoclonal) of a plasma cell (Immunoglobulin-selecting cells).
  • That may also secrete a single homogenous immunoglobulin (ig) and/or immunoglobulin fragment (e.g., light chain) -› increase in their serum level.
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88
Q

What do plasma cells Dyscrasias include?

A
  • Multiple Myeloma.
  • Waldenstrom’s macroglobulinemia.
  • Solitary Plasmacytoma.
  • Others.
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89
Q

What are myeloproliferative disorders?

A
  • Related hematopoietic stem cell malignancies from myeloid lineage.
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90
Q

Diagnostic criteria for multiple myeloma (plasma cell myeloma)

A
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91
Q

Classification of myeloproliferative disorder

A
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92
Q

Diagnostic criteria for chronic myeloid leukemia (CML)

A
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93
Q

Philadelphia chromosome

A
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94
Q

Definition of polycythemia vera

A
  • Increased Erythrocyte cell mass leads to increase in hematocrit, blood volume & blood viscosity with subsequent thrombotic or hemorrhagic problems.
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95
Q

Diagnostic criteria for polycythemia vera

A
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96
Q

Etiology of myloid metaplasia (myelofibrosis)

A
  • Unknown so called agnogenic
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97
Q

Pathophysiology of myloid metaplasia (myelofibrosis)

A
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98
Q

What characterizes (symptoms) myloid metaplasia (myelofibrosis)?

A
  • Extramedullary hematopoiesis (Formation of blood outside the BM as in spleen).
  • Splenomegaly.
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99
Q

Natural History of myloid metaplasia (myelofibrosis)

A

Two phases:

  • Initial cellular phase (early phase).
  • Pancytopenic phase (late phase): due to progressive bone marrow failure (fibrosis.
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100
Q

Diagnostic criteria for myloid metaplasia (myelofibrosis)

A
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101
Q

Clinical features of essential Thrombocytopenia

A

The increased blood platelets lead to episodic symptoms:

  • Thrombosis.
  • Bleeding (as majority of newly formed platelets are dysfunctional).
  • Acute leukemia (in < 1 %).
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102
Q

Diagnostic criteria for essential Thrombocytopenia

A
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103
Q

Janus kinase (JAK)

A
  • An intracellular tyrosine kinase
  • Mutations in the JAK2 gene are associated with certain myeloproliferative neoplasms, including polycythemia vera, primary myelofibrosis, and essential thrombocythemia.
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104
Q

Definition of hemoglobin electrophoresis

A
  • It is a test that measures the different types of hemoglobin in the blood.
  • It also looks for abnormal types of hemoglobin.
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105
Q

Principle of hemoglobin electrophoresis

A
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106
Q

What is the charge of hemoglobin in electrophoresis?

A

Negatively charged at alkaline pH

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107
Q

Results of hemoglobin electrophoresis (interpretation)

A
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108
Q

Steps of sickling test

A
  • Mixing blood with reducing agent –> (Sodium metabisulphite)
  • This will induce sickling insusceptible cells.
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109
Q

Results of sickling test

A
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110
Q

Steps of sickle solubility test

A

Mix Hb with a reducing solution
(sodium dithionite)

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111
Q

Results of solubility test

A
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112
Q

Definition of osmotic fragility test

A
  • A measure of the resistance of erythrocytes to hemolysis by osmotic stress.
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113
Q

Results of osmotic fragility test

A
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114
Q

Principle of immunophenotyping analysis

A
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115
Q

Steps of immunophenotyping analysis

A
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116
Q

Definition of cytogenetics

A
  • The study of chromosome & the related disease states caused by abnormal chromosome number and/or structure.
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117
Q

Definition of bone marrow aspiration

A
  • The removal of a small amount of Bone Marrow (in semi-liquid form for examination)
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118
Q

Sites of bone marrow aspiration

A
  • Iliac crest.
  • Sternum.
  • Tibial plateau.
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119
Q

Tool used in bone marrow aspiration

A
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120
Q

Definition of bone marrow biopsy

A
  • The removal of a small amount of:
  • Bone.
  • Fluid & cells.
    (From inside the bone.)
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121
Q

Sites of bone marrow biopsy

A
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122
Q

Tool used in bone marrow biopsy

A
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123
Q

Definition of normal hemostasis

A
  • Mechanism by which bleeding from an injured vessel is arrested by formation of a thrombus.
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124
Q

Function of normal hemostasis

A
  • To maintain the blood in fluid state.
  • In intact vessels → Prevent clots.
  • In injured vessels → Arrest bleeding
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125
Q

Components of normal hemostasis

A
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126
Q

Diagnosis of bleeding disorders

A
  • History
  • Clinical examination
  • Laboratory investigation
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127
Q

Precautions during sample collection

A
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128
Q

Steps of blood sample collection

A
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129
Q

Which anti-coagulant is used during blood sample collection?

A

Trisodium citrate (1:9)

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130
Q

What are lab tests related to hemostasis?

A
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131
Q

Read notes about intrinsic and extrinsic pathways of coagulation

A
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132
Q

Significance of prothrombin time (PT)

A

Reflects: efficiency of extrinsic pathway.

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133
Q

Principle of prothrombin time (PT)

A
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134
Q

What is prothrombin time (PT) Sensitive to?

A
  • Change in factor V - VII - X (Mostly)
  • Change in factor I - Il (Lesser)
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135
Q

What causes prolonged prothrombin time (PT)?

A
  • Deficiency of factor VII - X - V - II - I.
  • Vit K Deficiency.
  • DIC.
  • Oral anticoagulant.
  • Liver disease especially obstructive jaundice.
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136
Q

Range of prothrombin time (PT)

A
  • With rabbit thromboplastin → 11 - 16 sec
  • With human thromboplastin → 10 - 12 sec
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137
Q

Why should activated partial thromboplastin time (APTT) be done without the addition of tissue thromboplastin?

A
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138
Q

Significance of activated partial thromboplastin time (APTT)

A

Reflects: efficiency of intrinsic pathway

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139
Q

What is activated partial thromboplastin time (APTT) Sensitive to?

A

Sensitive to:
* Changes in factor VIII - IX - XI - XII.
* Heparin & circulating anticoagulant.

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140
Q

Range of ** activated partial thromboplastin time (APTT)**

A

26 to 40 sec.

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141
Q

What causes prolonged APTT?

A
  • Deficiency of Factor VIII (Hemophilia A).
  • Deficiency of FIX (Hemophilia B).
  • DIC.
  • Heparin therapy.
  • Circulating anticoagulant.
  • Liver disease.
  • Massive transfusion of plasma depleted blood.
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142
Q

Significance of Bleeding time

A

Assess: primary hemostatic defect (vessel wall or platelet)

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143
Q

What does Bleeding time Depend on?

A

Adequate functioning of platelet
& Blood Vessels.

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144
Q

Method of Bleeding time

A
  • Ivy’s method.
  • Duke’s (not recommended).
  • Template method.
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145
Q

Ranges of Bleeding time

A
  • Ivy’s method →2 to 7 mins.
  • Template method → 2.5 to 9.5 mins.
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146
Q

Causes of prolonged Bleeding time

A
  • VWD = Von Willebrand Disease.
  • Thrombocytopenia.
  • Platelet function disorder.
  • Disorders of blood vessels.
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147
Q

Tests for bleeding disorders

A
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148
Q

what is the most common cause of bleeding disorders?

A

vascular

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149
Q

Definition of blood transfusion

A
  • Injection of a volume of blood or blood products obtained from a healthy person (donor) into the circulation of a patient (recipient) whose blood is deficient in quantity or quality.
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150
Q

What is donated blood subjected to after collection?

A
  • Donated blood is usually subjected to processing after collection & separated into blood components by differential centrifugation.
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151
Q

Blood components

A
  • Whole blood (donor & recipient must be ABO identical).
  • Packed RBCs.
  • Platelet concentrates.
  • Fresh frozen plasma.
  • Cryoprecipitate.
  • Protein solution.
  • Factor concentrate.
  • Granulocyte concentration.
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152
Q

Blood after centrifugation

A
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153
Q

Storage of whole blood

A
  • At 4°C.
  • For up to 35 days.
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154
Q

Indications of whole blood

A
  • Hemorrhage: Sudden loss of 25% or more of blood volume.
  • Patients undergoing exchange transfusion.
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155
Q

Storage of Packed RBCs

A
  • At 4°C.
  • For up to 42 days.
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156
Q

Benefits of Packed RBCs

A

1 unit of packed cell: increases the level of
- Hb by 1g/dl.
- Hematocrit by 3%.

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157
Q

Indications of Packed RBCs

A
  • Acute blood loss: Sudden loss of 30% or more of blood volume.
  • Symptomatic chronic anemia without hemorrhage.
  • Cardiac failure.
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158
Q

Storage of Platelets

A
  • At 20-24°C (room temp)
  • For up to 5 days.
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159
Q

Benefits of Platelets

A

1 unit /10kg of body weight → increases count of platelet by 50,000.

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160
Q

Preparation of Platelets

A
  • It is the precipitate after platelet-rich plasma is centrifugated at 3000 rev/min.
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161
Q

Indications of Platelets

A
  • Patients with thrombocytopenia or platelet function defect.
  • correction of coagulopathy (if platelet count <50,000/ml).
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162
Q

Storage of fresh frozen plasma

A
  • At -18 °C or colder.
  • For up to 12 months.
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163
Q

Preparation of fresh frozen plasma

A

It is the supernatant liquid portion when fresh blood is centrifugation at 3000 rev/min.

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164
Q

Indications of fresh frozen plasma

A
  • Deficiencies of coagulation factors.
  • Emergency TTT of vit k deficiency.
  • TTT of TTP.
  • TTT of DIC.
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165
Q

What are TTP & DIC short for respectively?

A

TTP = Thrombotic Thrombocytopenic Purpura
DIC = Disseminated Intravascular Coagulation

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166
Q

Preparation of Cryoprecipitate transfusion

A

Precipitate formed when Fresh Frozen Plasma (FFP) is thawed at 4°C

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167
Q

Importance of Cryoprecipitate transfusion

A
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168
Q

Types of blood transfusion complications

A
  • Acute transfusion reaction
  • Delayed transfusion reaction
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169
Q

Duration of acute transfusion reaction

A

Within 24hrs

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170
Q

Types of acute transfusion reactions

A

Immunologic

  • Hemolytic transfusion reaction.
  • Febrile non-hemolytic reaction.
  • Allergic reaction.
  • TRALI = Transfusion - Related Acute Lung injury

Non-immunologic

  • Bacterial contamination.
  • Transfusion - associated circulatory overload.
  • Acute hypotensive reaction.
  • Physical hemolysis: Hypothermia, Hyperkalemia & Acidosis
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171
Q

Duration of delayed transfusion reactions

A

After 24hrs

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172
Q

Types of delayed transfusion reactions

A

Immunologic

  • DHTR = Delayed Hemolytic Transfusion Reaction.
  • Post-transfusion thrombocytopenic purpura.
  • Alloimmunization (RBCs - WBCs - platelet)
  • GVHD = Graft Versus Host

Non-immunologic

  • Hemosiderosis = Iron overload.
  • Citrate
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173
Q

What are Transfusion related infections?

A
  • Viral hepatitis (A-B-C-D).
  • Syphilis.
  • Malaria.
  • HIV (AIDS).
  • CMV infection
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174
Q

How will lab imact this patient care??

A
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175
Q

Urine analysis

A
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176
Q

What is Neutrophil Estrase?

A
  • an enzyme produced by WBC.
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177
Q

What forms Nitrite in urine?

A
  • Formed by reducing nitrate by the action of gram -ve bacteria (e.g., E. Coli).
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178
Q

Interpreration of urine tests

A
179
Q

TTT of UTI

A
  • antibiotic with dose adjustment
180
Q

What are renal function tests?

A
181
Q

What are tubular functions tests?

A
  • Water deprivation test
  • DDAVP test
  • Urine acedification test
182
Q

Principle of Water Deprivation test

A

The ability of the tubules to reabsorb water (Concentrate the urine)

183
Q

Importance of Water Deprivation test

A
  • Indicates the Prescence or absence of diabetes insipidus.
184
Q

Principle of DDAVP test

A
  • DDAVP is a synthetic analogue of desmopressin.
185
Q

Importance of DDAVP test

A
  • Determine the type of diabetes insipidus (Neurogenic or
    Nephrogenic)
186
Q

Principle of Urine Acidification test

A
  • The ability of the tubules to excrete H (Excrete acidic urine).
187
Q

Importnace of Urine Acidification test

A
  • Indicates if the cause of metabolic acidosis is tubular or not.
188
Q

What are glomerular function tests?

A

Clearance test

189
Q

Def of GFR

A
  • Amount of the plasma that filtered through the glomeruli each minute.
190
Q

Normal Range of GFR

A
  • 100-125 ml/min for a body surface area of 1.74 m2
191
Q

Factors that decrease GFR

A
192
Q

Def of Substance Clearance

A
  • The volume of plasma in ml. cleared of this substance in 1 min through urine.
193
Q

What are factors that affect Substance Clearance?

A
194
Q

Substance used in Substance Clearance

A

Creatinine & not inulin is preferred why?

  • As creatinine is an endogenous substance.
195
Q

Calculation of Substance Clearance

A
196
Q

Importance of Creatinine Clearence

A

Assessment of GFR.

197
Q

Calculation of Creatinine Clearence

A

CLcr Equation

198
Q

Normal Range of Creatinine Clearence

A

90-110 ml / min

199
Q

Sample collection for Creatinine Clearence

A
  • Urine sample: (24h sample collection).
  • Blood sample: Serum Creatinine analysis.
200
Q

Interpretation of Creatinine Clearence

A

Decrease in CLcr —> decrease in GFR —-> (So decrease drug dose)

201
Q

Relation between Creatinine Clearence And Antibiotic dosing

A
202
Q

What are Blood Estimates?

A
203
Q

Blood Urea

  • Formation
  • Excretion
  • Test
  • Increases in cases of
A
204
Q

Uric Acid

  • Formation
  • Excretion
  • Test
  • Increases in Cases of
A
205
Q

What happens to plasma proteins in Nephrotic Syndrome?

A
  • accompanied by a marked lowering of the plasma, protein concentration, particularly albumin
206
Q

Def of Arterial Blood Gas (ABG)

A
  • A test used to measure 02 saturation, Co2 & bicarbonate blood levels.
207
Q

Significance of Arterial Blood Gas (ABG)

A
  • It provides quick assessment of acid-base balance.
208
Q

Normal level of Plasma pH

A

7.4 (Range 7.35 - 7.45).

  • Corresponding to H+ concentration of 40 nmol/L (range 36 - 43 nmol/L.)
209
Q

How is Plasma pH Maintained?

A

maintained within these narrow limits through strict regulations by:

  • Body buffers.
  • Respiratory mechanisms.
  • Renal tubular mechanisms.
210
Q

What are acid-base disorders?

A
211
Q

How are Acid-Base Disorders maintained?

A
212
Q

Collection of ABG sample

A
213
Q

What are requirments for MI diagnosis?

A

Requirements of MI diagnosis:
- Panel of markers.
- Serial measurement.
- Timing of sample from onset of chest pain is important.

Sample Collection:
1. A venous blood sample was withdrawn into plain tube without additive.

  1. Then clotting of blood sample & serum is separated.
214
Q

What are Cardiac markers?

A
215
Q

Lab tests of Cardiac markers

A
216
Q

What is POCT?

A

(Point Of Care Testing):
* Rapid test performed where healthcare is provided close to or near the patient.

217
Q

Kinetics of Cardiac markers after AMI

A
218
Q

What is Troponin?

A
  • A regulatory protein in striated muscle.
219
Q

What is the most sensitive & Specific (Definitive) Cardiac Marker?

A

Troponin

220
Q

What is the last marker to dissapear?

A

Troponin

221
Q

What is the first marker to appear?

A

Myoglobin (4 Hrs after AMI)

222
Q

Why isn’t Myoglobin specific?

A

as it increases in…
* Acute myocardial infarction (AMI).
* Muscle damage.
* Renal failure.

223
Q

CK

A
224
Q

LDH

A
225
Q

What are Acute Phase Proteins?

A

Plasma proteins whose concentrations If by enhanced synthesis & release following inflammations.

226
Q

What causes increase in Acute Phase Proteins?

A
227
Q

What are Commonly measured Acute Phase Proteins?

A
  • C-reactive protein. (Especially hs-CRP)
  • Complement.
  • a1 antitrypsin.
  • Fibrinogen.
  • Haptoglobins.
  • a 2 macroglobulin.
228
Q

Serum Creatinine

  • Formation
  • Excretion
  • Test
  • Increases in Cases of
A
229
Q

Synthetic Liver Function tests

A
  • Plasma proteins.
  • Prothrombin time.
230
Q

Test for integrity of hepatocytes

A
  • Transaminases (ALT & AST).
231
Q

Liver Function tests

A
  • Excretory
  • Synthetic
  • Integrity of hepatocytes
  • Tests for cholestasis
232
Q

Tests for cholestasis

A
  • Alkaline Phosphatase (ALP).
  • Gamma Glutamyl Transferase (GGT).
233
Q

Excterory Liver Function tests

A
  • Serum bilirubin.
  • Urinary Bile Pigment.
  • Bile acids.
234
Q

Metabolism of Hb

A
235
Q

How does Bilirubin exist in the serum?

A
  • Unconjugated (indirect) bilirubin
  • Conjugated (Direct) bilirubin
236
Q

Compare between unConjugated & Conjugated bilirubin in terms of:

  • Normal Site
  • Solubility
  • Fate
A
237
Q

What is the Fate of urobilinogen?

A
  • Most of it converted into stercobilin & excreted in feces (brown color).
  • Part of it oxidized to urobilin & excreted in urine (yellow color).
238
Q

Def of Delta-Bilirubin

A
  • Conjugated bilirubin covalently bound to albumin.
239
Q

Level of Delta-Bilirubin

A
  • Normally: Absent or present in very small amount.
  • Increases in: cholestasis (in parallel with other fractions).
240
Q

Clearence of Delta-Bilirubin

A
  • Cleared slowly from circulation to urine so:
  • When jaundice resolves the delta fraction (which is not filtered) still present & bilirubin testing may become -ve in spite of high serum level.
241
Q

Causes of increased unconjuguated bilirubin

A
242
Q

Causes of increased Conjugated bilirubin

A
243
Q

What is Gilberts Syndrome?

A

Most common cause of Unconjugated hyperblirubinemia

  • Deficiency of uridinediphosphoglucuronyl transferase enzyme (UDP-GT).
  • There is defect in the uptake by hepatocytes.
244
Q

What is Dubin-Johnson Syndrome?

A
  • A defect in excretion of bilirubin by hepatocyte.
245
Q

Site of formation of plasma proteins

A

Most of them: in liver.

Except gamma globulins: in plasma cells.

246
Q

Level of albumin

A
  • Represent: 60% of total serum protein.
  • Level: 3.5 - 5.0 g/di.
247
Q

What happens to synthetic liver function tests in advanced hepatic affection?

A
248
Q

What happens in patients with hepatocellular damage?

Concerning Blood coagulation factors

A

Decrease in Coagulation factors → Increase Prothrombin time [PT] (an early abnormality in this disease).

249
Q

What forms blood coagulation factors?

A
  • Most of coagulation factors (except factor VIII) & fibrinolytic enzymes → by the liver.
  • Factor VIII → by spleen.
250
Q

Normal site of ALT & AST

A

Inside Hepatocytes

251
Q

What hapens to serum Levels of ALT & AST in hepatitis?

A
252
Q

What is Preicteric phase?

A
  • the period prior to appearance of jaundice
253
Q

What happens to serum level of ALP in Obstructive Jaundice?

A

In obstructive jaundice “serum level is markedly elevated (>3 URL)”

254
Q

What are other causes of elevated GGT?

A

Alcohol & barbiturates

255
Q

What happens to serum level of GGT in cholestasis & Liver cirrhosis?

A

Serum Level: Inc. in cholestasis & liver cirrhosis (but the rise is marked in cholestasis).

256
Q
A
257
Q

Types of Plasma amaylase

A
  • Salivary (S-isoenzyme)
  • Pancreatic (P-isoenzyme): More specific & sensitive for diagnosis of acute pancreatitis.
  • Total amylase activity > 10 times URL is virtually diagnostic of acute pancreatitis.
258
Q

Definition of Tumor Markers

A
  • A substance found in an increased amount in (blood - other body fluids - body tissues) that may suggest the presence of a type of cancer.
259
Q

Method of measurment of Tumor Markers

A
  • Qualitatively or quantitatively by chemical, immunological or molecular biological methods (PCR) to identify the presence of cancer.
260
Q

Uses of Tumor Markers

A

Screening in general population:
- It is of limited value as it doesn’t confirm diagnosis.
- May aid diagnosis in high-risk people.

Differential diagnosis in symptomatic individuals:
- But must be in conjunction with clinical & radiological evidence.

Prognostic indicator of disease progression:
- As the plasma concentration correlates with the tumor mass.

Monitoring of response to therapy & detecting recurrence.

261
Q

Categories of Tumor Markers

A
  • Enzymes
  • Hormones
  • Oncofetal Antigens
  • Blood Group Antigens
  • In addition to : Proteins, Hormone Receptors, Genetic markers
262
Q

Enzyme Tumor Markers

A
263
Q

Oncofetal antigins as Tumor Markers

A
264
Q

Hormonal Tumor Markers

A
265
Q

Blood group antigens as Tumor Markers

A
266
Q

What is a Sample?

A

A biological material taken from a patient for diagnostic, prognostic or therapeutic monitoring.

267
Q

Types of samples

A
  • Blood.
  • Sweat.
  • Urine & other fluids.
  • Semen.
    Feces.
    Tissue.
268
Q

Collection site of blood samples

A
269
Q

Types of blood samples

A
  • Venous sample.
  • Capillary sample.
  • Arterial sample.
270
Q

In Blood sample collection, Avoid the hand with ……

A
  • Extensive scarring.
  • Burn.
  • Hematoma.
  • Containing I.V. access for I.V. infusion.
  • Infection.
  • On the side of mastectomy.
  • Edema.
271
Q

Cleansing of venipuncture site

A
272
Q

Types of urine samples

A
273
Q

Outcomes of Improper sample collection

A
274
Q

Specimen Quality & Markers for rejection

A
275
Q

Tests to assess thyroid function

A

TSH (Thyroid Stimulating Hormone).
Free T3.
Free T4.

276
Q

What are other tests to assess the function of thyroid gland?

A

TSI

277
Q

Aim of TSI Testing

A

to determine the cause of the disease.

278
Q

Lab results of TSI

A
279
Q

Thyroid Disorders and T4,T3 & TSH levels

A
280
Q

What are Variables affecting (T3- T4 - TSH) testing?

A
  • Hospitalized patient & recovery from Iliness.
  • Pediatric & neonate.
  • Pregnancy.
  • Drug treatment.
  • Assay interference.
  • Reference range.
  • Follow up test selection.
281
Q

Def of Euthyrold sick syndrome (ESS)

A
  • Abnormal levels of thyroid hormones despite normal thyroid gland function.
282
Q

Synonyms of Euthyrold sick syndrome (ESS)

A
  • Sick Euthyroid Syndrome (SES).
  • Non-Thyroidal tilness syndrome (NTI).
283
Q

Etiology of Euthyrold sick syndrome (ESS)

A

Occurs in severe illness or severe physical stress Most common in intensive care patients”

284
Q

Pathophysiology of Euthyrold sick syndrome (ESS)

A
285
Q

Patterns of Euthyrold sick syndrome (ESS)

A
286
Q

Neonatal Thyroxine Levels at birth

A
287
Q

Clinical features of Euthyrold sick syndrome (ESS)

A

No symptoms of hypothyroidism (as It Is a temporary state).

288
Q

TTT of Euthyrold sick syndrome (ESS)

A

Once the person recovers from the Iliness → thyrold hormone returns to normal.

289
Q

Neonatal Thyroxine Levels then

A
290
Q

Examples of Conditions causing Increase of plasma TBG

A

Cases associated with Increased estrogen:
* Pregnancy.
* Oral contraceptives.

291
Q

Effect of Conditions causing Increase of plasma TBG

A

Lead to false inc. of Total T4 & T3.

292
Q

Reliable test in Conditions causing Increase of plasma TBG

A

Free T3 & Free T4 reliable In these cases.

293
Q

Effect of Conditions causing Decrease of plasma TBG

A

Cause a false dec of Total T4 & T3.

294
Q

Examples of Conditions causing Decrease of plasma TBG

A

Protein losing states

295
Q

What are Drugs that interfere with thyroid function leading to thyroid disfunction (Hypo or hyperthyroidism)?

A
296
Q

Reliable test in cases of Conditions causing Decrease of plasma TBG

A

Free T3 & Free T4 reliable In these cases.

297
Q

Def of Assay Interference

A
  • A nonspecific binding with assay reagents leading to false increase in concentration of the measured substance.
298
Q

Thyroid assay interference

A
299
Q

What is Thyroid Assay?

A

An animal anti-body against thyroid hormones used to determine their serum level.

300
Q

Def of reference Range

A

A set of values that Includes upper & lower limits of a lab test based on a group of otherwise healthy people.

301
Q

Is reference Range Age related?

A

yes

302
Q

reference Range Must be trimester related in pregnancy

A

..

303
Q

What test is used in follow up in cases of thyroid dysfunction?

A
304
Q

Refer to Liver Case Scenario in Notes

A

..

305
Q

Refer to Thyroid Case Scenario in Notes

A

..

306
Q

Diurnal Variation in tests

A
  • Time of day, month or year may affect lab test results
  • Some tests must be collected at specific times or days in order to provide meaningful clinical information.
307
Q

Examples of diurnal variation in tests

A
308
Q

What are adrenal disorders?

A
  • Hyperfunction: Cushing syndrome.
  • Hypofunction: Adrenal insufficiency.
309
Q

Levels of cortisol And ACTH in blood

A
  • Cortisol & ACTH levels fluctuate throughout the day

Peak levels: In the early morning.

Lowest levels in the late evening around bedtime.

310
Q

sample collection for cortisol

A

We collect 2 samples:

  • 1st sample: At 8:00 AM.
  • 2nd sample: At 8:00 PM “in the same day”
311
Q

Serum cortisol levels & salivary cortisol in late night in patients with cushing syndrome

A

Elevated

312
Q

Besides time, name other biologic variables that may affect lab test results

A
  1. Age.
  2. Gender.
  3. Race.
  4. Exercise.
  5. Diet.
  6. Posture.
  7. Stress (venipuncture).
  8. Genetic predisposition.
313
Q

Tests to diagnose adrenal insufficiency

A
  • Basic chemistry profile.
  • CBC (Complete Blood Count).
  • Urinalysis.
314
Q
A
315
Q

Other Variables affecting cortisol and ACTH testing

A
  • Emotional stress.
  • Estrogens containing oral contraceptive.
  • Steroid therapy:
  • Stopped within 12 h before the test.
  • If not possible (as in Addison disease dexamethasone should be prescribed (As it doesn’t cross react with cortisol assay) & not-prednisolone.
316
Q

Time of sample collection for cortisol & ACTH

A
  • 2 Samples (because of daily circadian rhythm).
  • Morning: 8 - 10 AM.
  • Evening: 10 - 12 PM.
317
Q

Time of sample collection for Sex hormones & Gonadotropins

A

Monthly circadian rhythm in female.

318
Q

Blood sample Collection

  • Additive on sample
  • Test done on
A
319
Q

insulin sample collecion

A

separated immediately and kept in fridge

320
Q

Def of Competitive binding techniques

A

The method where the hormone competes with labelled one for binding sites in vitro.

321
Q

Binding sites in Competitive binding techniques

A
  1. Antibody.
  2. Binding proteins.
  3. Receptor.
322
Q

Labelling in Competitive binding techniques

A
  • Radioisotope.
  • Enzymes.
  • Fluorochrome.
323
Q

Examples of Competitive binding techniques

A
  1. Radioimmunoassay (RIA)
  2. Enzyme linked immunosorbent assay (ELISA)
  3. Fluoro immunoassay (FIA)
324
Q

Chromatography

A

This is a reference method.

325
Q

Samples for Catecholeamines Testing

A

Blood & Urine

326
Q

Blood sample for Catecholeamines Testing

A
  • Measurement of plasma catecholamines.
  • A sensitive test that needs specialized equipment’s.
327
Q

Urine sample for Catecholeamines Testing

A
  • The reliable test: Measurement of urinary vanillymandelic acid (VMA).
  • VMA: Is the end stage metabolite of catecholamines,
    Excreted in urine.
328
Q

blood Sample collection for Catecholeamines Testing * In patients with paroxysmal attacks of hypertension

A

Basal measurements should be made once in between attacks & another estimation, when the next attack occurs.

329
Q

Cautions during collection & timing of urine specimens (24 hours) for VMA for catecholeamines testing

A

The diet excluded the following Items:
1. Caffeine as in (coffee - tea - cocoa - chocolate)

  1. Amines as in (bananas - walnuts - avocados - fava beans - cheese - beer * red wine).
  2. Vanilla (in foods or fluids)
  3. Licorice
  4. Nicotine (4 hours before collection of urine and during the urine collection),
  5. Alcohol (ethanol) & cocaine.
  6. These analytes are sensitive to drugs (azathloprine).
330
Q
A
331
Q

Def of Autoimmunity

A
  • The process where the host immune system ceases to recognize one or more of the body’s normal constituents as self, creates autoantibodies that starts to attack its own (Cells - Tissues - Organs) causing inflammation & damage.
332
Q

Examples of Autoimmunity

A
  • Systemic Lupus Erythematosus (SLE).
  • Rheumatoid Arthritis.
333
Q

Causes of Autoimmunity

A

Mostly Unknown

334
Q

Def of Autoantibodies

A
  • Proteins created by the immune system when it fails to distinguish between self-antigens & non-self-antigens (foreign antigens) e.g. bacterial or viral.
335
Q

what are Autoantibodies directed against?

A

These autoantibodies may be directed against a variety of substrates including:

  • Intra-cellular antigens.
  • Cell surface antigens.
  • Extracellular antigens.
336
Q

SLE

A
337
Q

Immunological testing for SLE

A
  • Antinuclear antibodies (ANA)
  • SLE specific antibodies
  • Complement proteins
  • Anti-platelet antibodies & Anti-erythrocyte antibodies
  • Anti-histone antibodies
  • RF (Rheumatoid factors)
338
Q

Antinuclear antibodies (ANA) in Testing for SLE

A
  • Highly sensitive (Seen in large proportion of patients).
  • But not specific (Seen in other autoimmune diseases).
339
Q

SLE specific antibodies in Testing for SLE

A
340
Q

Complement proteins in Testing for SLE

A
  • Decrease Serum complement (C3-C4)
  • Due to its consumption.
341
Q

Anti-platelet antibodies & Anti-erythrocyte antibodies in Testing for SLE

A
  • Present in about 70% of patients.
  • Responsible for hemolytic anemia & thrombocytopenia.
342
Q

Anti-histone antibodies in Testing for SLE

A
  • Present in drug induces lupus.
343
Q

RF (Rheumatoid factors) in Testing for SLE

A

+ve in 30% of patients.

344
Q

Def of Rheumatoid Arthritis

A
  • Chronic systemic inflammatory auto immune disease that affect the joints.
345
Q

Immunological testing for Rheumatoid Arthritis

A
  • Specific tests
  • Others
346
Q

Specific tests for Rheumatoid Arthritis

A
  • Rheumatoid factors (RF): Positive in 75% of patients.
  • Anti-CCP autoantibodies (Anti-Cyclic Citrulinated Peptide)
347
Q

Charaters of Anti-CCP autoantibodies (Anti-Cyclic Citrulinated Peptide) in testing for RA

A
  • Highly specific for RA (96%).
  • They appear before the onset of RA symptoms.
348
Q

Other tests for RA

A
  • Serum complement: Decrease in presence of vasculitis.
  • Antinuclear antibodies (ANA): May be positive.
  • Hypergammaglobulinemia & Cryoglobulinemia.
349
Q

Def of Immunodeficiency disorders

A
  • Deficiency of one or more of the 4 major components of the immune system (B lymphocytes - T lymphocytes - phagocytic cells - complement system).
  • Which protect the individual against different viral, bacterial, fungal and protozoal infections.
350
Q

what are Primary Immunodeficiency disorders?

A
  • B cell Immunodeficiency Disorders.
  • T cell Immunodeficiency Disorders.
351
Q

Classification of Immunodeficiency disorders

A
  • Primary immunodeficiency diseases (Presented from birth)
  • Secondary immunodeficiency diseases (Acquired due to infection as AIDS).
352
Q

Examples of B-Cell Immunodeficiency disorders

A
353
Q

Examples of T-Cell Immunodeficiency disorders

A

DIGEORGE’S SYNDROME

(CONGENITAL THYMIC APLASIA)

354
Q

Clinical Features of T-Cell Immunodeficiency disorders

A
355
Q

Laboratory assessment of immune competence

A
  • Complement assay
  • Evaluation of Humoral (B cells) mediated immunity
  • Evaluation of Cellular (T cells) mediated immunity
  • Assessment of phagocytic function
356
Q

Methods of Complement assay

A
  • Immunoassay “Assay of C3 & C4 levels”
  • Functional “Hemolytic assay CH50”
357
Q

Methods of Immunoassay “Assay of C3 & C4 levels”

A
  • Electro immunodiffusion
  • Rate nephelometry
  • ELISA
  • Single radial diffusion
358
Q

Methods for Evaluation of Humoral (B cells) mediated immunity

A
  • Protein electrophoresis
  • Quantitative immunoglobulins level
  • IgG subclasses level
  • Total B cell count
  • Specific antibody response after immunization in vivo
  • Stimulation of B cells in vitro
359
Q

Methods of Quantitative assessment of immunoglobulins level

A
  • Radial immunodiffusion
  • Nephelometry
  • ELISA
360
Q

Methods of assessment of IgG subclasses level

A

ELISA

361
Q

Methods of assessment of Total B cell count

A
  • Using Flow cytometry
  • Normally 10 - 20% of total circulating lymphocytes
362
Q

Specific antibody response after
immunization in vivo

A

Principle: Immunization with tetanus or pneumococcal polysaccharide Antigens

363
Q

Stimulation of B cells in vitro

A
  • By Mitogen or Antigen, and assessment of immunoglobulin release
364
Q

Evaluation of Cellular (T cells)
mediated immunity

A
  • Total Lymphocytes count
  • Monoclonal antibodies to T cell subsets
  • Total T cell count
  • Delayed cutaneous hypersensitivity skin test in vivo
  • Lymphocyte response in vitro
365
Q

MOAs = Method of assessment

MOAs of Total Lymphocytes count

A

Normally > 1200/ul “At any age”

366
Q

MOAs of Monoclonal antibodies to T cell subsets

A

Using Flow cytometry

367
Q

MOAs of Total T cell count

A
  • Using Flow cytometry
  • Normally >60% of total circulating lymphocytes
368
Q

MOAs of Delayed cutaneous hypersensitivity skin test in vivo

A
  • Using PPD
  • Used to evaluate specific cellular immunity to antigen
369
Q

MOAs of Lymphocyte response in vitro

A
  • By Mitogen or Antigen
370
Q

Assessment of phagocytic function

A
  • Nitro-blue tetrazolium test
  • Chemiluminescence
  • Chemotaxis
  • Assessment of superoxide production
  • Enzyme tests
  • Genetic analysis
371
Q

what is Nitro-blue tetrazolium test used in?

A

Used lo diagnosis of CGD

372
Q

Chemiluminescence

A

Albnormal in…
* CGD
* Myeloperoxidase deficiency

373
Q

MOAs of Chemotaxis

A
  • Principle: Measure ability of neutrophils to move in a directed, migratory pattern toward chemotactic substance
374
Q

when is Chemotaxis abnormal?

A
  • Abnormal in various disorders “Not specific”
375
Q

Superoxide production in CGD

A
  • Absenl in CGD
  • Defective in other syndromes
376
Q

Genetic analysis

A

Available for
* CGD
* LAD
* Chediak Higashi syndrome

377
Q

Indication of Enzyme tests

A
  • e.g., G6PD - Myeloperoxidase
378
Q

Intro To Nucleic Acids

A
379
Q

Def of PCR

A

An enzymatic method, Used for making multiple copies of a pre-selected segment of DNA /RNA.

380
Q

RNA Extraction

A
381
Q

what are The primary materials (reagents) used in PCR?

A
382
Q

what should happen before PCR?

A

We need to extract the nucleic acid from the cell at first.

383
Q

DNA Extraction

A
384
Q

Cyclic reactions

A
  • There are 3 major phases, which are repeated for 20 to 40 cycles.
  • This is done on an automated Thermal Cycler.
385
Q

Phases of Cyclic reactions

A
386
Q

Verification of PCR products

A
  • Agarose gel electrophoresis.
  • Hybridized with a labelled probe.
387
Q

Clinical applications of PCR

A
388
Q

Def of Infectious Diseases

A
  • Clinically evident diseases resulted from the presence of pathogenic microorganisms with the potential of transmission from a person to another.]
  • Infectious Diseases are many but limited by our knowledge, facilities, & ignorance.
389
Q

what are causes of Infectious Diseases?

A
  • Bacterial.
  • Viral.
  • Fungal.
  • Parasitic.
390
Q

Samples will be subjected to:

A
  • Phenotypic microbiological analyses.
  • Immunological-serological analyses.
  • Genotypic-Molecular biological analyses.
391
Q

Types of samples

A
  • Blood.
  • Sputum.
  • Urine.
  • CSF.
  • Stool.
  • Pus.
392
Q

Phases of diagnosis

A
393
Q

Preanalytical phase of diagnosis

A
394
Q

Importance of Sampling

A

(good sample = true result)

  • The successful identification of microbe depends on sampling.
  • The specimen is the beginning:
    As all diagnostic information from the laboratory depends upon the knowledge by which specimens are chosen & the care with which they are collected & transported.
395
Q

Proper selection of type of sample

A

Collect the appropriate type of specimen for diagnosis of the infectious disease.

396
Q

what does the quality of the sample Depend on?

A
  • Proper Selection
  • Proper Collection
  • Proper Transport
397
Q

Proper collection of sample

A

Avoid harming the patient & causing discomfort

Site:
- Collected from: site of pathogen is most likely to be found
- collected into: sterile containers

Time:
- The acute stage is the best.
- Before antimicrobial therapy has begun.

Quanlity:
- Sufficient quantity.

398
Q

proper transport of sample

A
  • Specimens should be protected from heat & cold.
  • Specimen transported promptly Within 2 hours.
  • Use of transport media especially for anaerobic culture.
399
Q

Def of Direct methods of diagnosis

A
  • Detection of organisms, their structural components & their products.
400
Q

Clinical specimens from various organs

A
  • Circulatory System.
  • (Skin- Abscess - Wound) Specimens.
  • Eyes & Ears.
  • Respiratory System.
  • Central Nervous System.
  • Urinary Tract.
  • Genital Tract.
  • Oral Cavity.
  • Gastrointestinal Tract.
  • Body Fluids.
401
Q

Examples of Direct methods of diagnosis

A
  • Macroscopic evaluation.
  • Microscopy (Unstained & Stained).
  • Culture & biochemical reactions.
  • Detection of microbial antigens & products.
  • Molecular identification of nucleic acids (PCR & DNA probe technology).
402
Q

Def of InDirect methods of diagnosis

A
  • Detection of antibodies against the microorganism in the patient’s serum.
403
Q

Examples of InDirect methods of diagnosis

A
  • Serologic method
404
Q

Macroscopic examination of samples

A
405
Q

Microscopic examination of samples

A
406
Q

Def of Culture

A

The process of growing & propagating organisms in a media that is conducive for their growth.

407
Q

Importance of Culture

A

It Reproduce the organism for use for additional testing

408
Q

Types of Culture

A
409
Q

Identification of bacteria

A
  1. Morphology.
  2. Growth requirements.
  3. Biochemistry.
  4. Enzymes.
  5. Antigens.
410
Q

Rapid identification of bacteria

A

Automated bacterial identification & Antimicrobial susceptibility systems.

411
Q

Example of Automated bacterial identification and antimicrobial susceptibility systems

A

VITEK system.

412
Q

Principle of Automated bacterial identification and antimicrobial susceptibility systems

A
413
Q

Time of results of Automated bacterial identification and antimicrobial susceptibility systems

A

Available within 6-8 hours.

414
Q

Drawbacks of Culture of Pathogenic Microbes

A
415
Q

Diagnosis of infection with slow-growing or non-culturable bacteria tends to rely on….

A

Direct: by molecular methods (PCR).

Indirect: by serodiagnosis (antibody detection).

416
Q

Diagnostic Methods through time

A
417
Q

Def of Direct Antigen detection

A

Assays are available for rapid detection of

  • Bacterial Antigens (surface antigen - soluble antigen).
  • Or toxin in biological fluids e.g. (CSF - blood - urine).
418
Q

When are Direct Antigen detection useful?

A
  • Prior antibiotic therapy has been initiated & cultures are negative after 24 hours of incubation.
  • Rapid results in critical ill patients e.g. meningitis.
419
Q

Principle & Types of Direct Antigen detection

A
420
Q

Def of Molecular biology Techniques

A

Molecular detection techniques for bacterial, viral and fungal DNA.

421
Q

Importance of Molecular biology Techniques

A
422
Q

Disadvantages of Molecular biology Techniques

A
423
Q

Def of MULTIPLEX PCR

A

Simultaneous detection of dozens of targets from one patient sample

424
Q

Characters of MULTIPLEX PCR

A
425
Q

Def of Indirect tests (serodiagnosis & Immune status tests)

A

Tests for detection of specific antibody for infectious agents including (IgM - IgG - IgA).

426
Q

What is diagnostic in Indirect tests (serodiagnosis & Immune status tests)?

A

Rising antibody titer (at least 4 folds) is diagnostic.

427
Q

Time of sample collection in Indirect tests (serodiagnosis & Immune status tests)

A

Samples are withdrawn at acute & convalescent stages (within 14 days).

428
Q

Techniques of Indirect tests (serodiagnosis & Immune status tests)

A
429
Q

Advantages of Indirect tests (serodiagnosis & Immune status tests)

A
  • Inexpensive.
  • Easy to perform.

——-
- Allows identification of:
* Acute infection → IgM.
* Past infection → IgG.

430
Q

Disadvantages of Indirect tests (serodiagnosis & Immune status tests)

A
  • Delayed response.
  • False negative results during sero-conversion window.
  • Time of infection not always clear.
431
Q

Sampling for mycological examination

A
  • Clean the site with alcohol 70%.
  • Sterile scalpel is used for scrapping.
  • Sterile scissor is used for trimming the nails.
  • Scales are transferred in clean dark paper.
432
Q

Inoculation of fungal infections

A
433
Q

Sampling for viral examination

A

Time: Sample should be collected during the most active stage of the disease.

Transport:
* Samples as (urine - stool - sputum - CSF) are transported directly to the lab.
* Swaps from (throat - nose - vesicles - cervix) are transported in viral transport medium.

434
Q

Biohazard label should be used for containers of …..

A

(HBV - HCV - HIV)

435
Q

Methods of viral detection

A
436
Q

Def of MIC (minimum inhibitory concentration

A

The lowest concentration of antimicrobials that will inhibit the growth of organisms.

437
Q

importance of MIC (minimum inhibitory concentration

A

Confirm resistance of organisms to an antimicrobial agent.

438
Q

Methods of MIC (minimum inhibitory concentration

A
439
Q

Post-Analytical phase of diagnosis

A
  • Reporting of:
  • Identification.
  • Antibiotic sensitivity.
  • Treatment
440
Q

Def of Rapid Detection Tests

A

Tests that give results in minutes to 1-2 hours.

441
Q

Characters of Rapid Detection Tests

A
  • Accurate.
  • Simple to use.
  • Low cost.
  • Stable under extreme conditions.
  • Little or no processing.
  • Culturally acceptable “Give the same result of the culture”.
  • Easy to interpret.
442
Q

Revolution in Direct Detection of Infections

A
  • Direct antigens.
  • Direct antibody.
  • Nucleic Acid (NA) based technology.
443
Q

Check conclusion

A

..

444
Q

Check take home messages

A

..

Y3R1 - DALR ✋🏻 (4 decks)

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