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Clinical Lab > Tomaiuolo > Flashcards

Tomaiuolo Flashcards

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1
Q

Why is Laboratory medicine useful

A
  1. Diagnostic test (60% of clinical actions are influenced by lab tests)
  2. Formulate prognosis
  3. Monitor therapeutic decisions
  4. Change therapies
    etc.
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2
Q

Efficacy

A

The ability to obtain a result

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3
Q

Efficiency

A

Ability to complete a task quickly, using the minimal amount of resources/time/money

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4
Q

Effectiveness

A

Effect of the same intervention, but in a specific population (real world condition)

It is patient centered, whereas efficacy and efficiency are within the lab (internal dimension)

Ie. the efficacy of a test is always the same, but the effectiveness might change since its related to the clinical condition of the patient.

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5
Q

TTP

A

Total testing process

5 different phases:
1. Pre-pre analytical
2. Pre analytical
3. analytical
4. Post analytical
5. Post post analytical

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6
Q

Pre-pre analytical phase

A

the clinician orders the test
Risks involving appropriateness, the clinician must ask for the right test at the right time

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7
Q

Pre analytical phase

A

Collection of sample (type depends on the test to be performed)

Accounts for 46-68% of errors - transport, sample collection etc.

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8
Q

Sampling errors

A

Incorrect technique, prolonged stasis, wrong sample container, insufficient, inappropriate withdrawal site, incorrect storage

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9
Q

Analytical phase

A

Analysis of the sample
Least prone to error - computerized labs nowadays
Sample lost, mix up, analytical errors however can still occur

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10
Q

TLA

A

Total Lab automation
refers to an automation process that include pre analytical, analytical and post analytical phases
Help reduce around 30% of time and cost

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11
Q

Serum work area

A

refers to ALL analytical sectors within the core laboratory where the analysis is carried out on the serum

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12
Q

Consolidation

A

Refers to reducing the number of analytical platforms, to reduce preanalytical and analytical variability

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13
Q

System components (of the core lab)

A
  1. Control unit
  2. central unit
  3. Analytical modules
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14
Q

Post analytical phase

A

Obtain a medical report
Values are compared with the physiological/reference value

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15
Q

Post post analytical phase

A

Communication phase from lab to physician - allows physician to discern a disease status, or monitor the evolution of a disease
- Correct interpretation is key

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16
Q

Inflammation

A

Response characterized by pain, swelling, redness and heat

It starts as a protective response, with the production of defense mediators

inflammation delivers leukocytes and host defense molecules from the circulation to the damaged sites to eliminate it

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17
Q

Steps of inflammation

A
  1. RECOGNITION: Sentinel cells like macrophages recognize pathogens or damaged cells
  2. RECRUITMENT of leukocytes: liberate mediators that trigger a vascular reaction
  3. REMOVAL: Removal of stimulus that triggered the reaction
  4. REGULATION: Regulation of th inflammation reaction
  5. REPAIR: repair of the tissue
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18
Q

Vascular changes due to inflammation

A

During inflammation, there is increased vascular permeability, allowing specific molecules such as leukocytes to reach the site of damage (leukocyte extravasation)

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19
Q

Sepsis

A

Refers to when the inflammatory reaction is system, causing pathological abnormalities

This systemic reaction may involve the hypothalamus (fever), the pituitary gland (cortisol), the liver (producing acute phase proteins), the bone marrow (production of neutrophils), and the immune system.

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20
Q

Acute vs. chronic inflammatory responses

A

Acute: Fast, prominent signs, mainly neutrophils. Its characterized by exudation of fluids and plasma proteins, edema etc.

Chronic: Slow, often severe and progressive, monocytes and lymphocytes, less prominent signs. It is the response to an agent that is more difficult to eradicate, and is therefore a slow reaction associated with fibrosis and tissue destruction

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21
Q

Steps of acute inflammation

A
  1. Change in blood flow and vessel permeability increases (for increased leukocyte extravasation). Vasodilation also occurs
  2. Exudate is formed –> high protein content
  3. Then, the transudate forms –> when the fluid leaks out due to increased hydrostatic pressure and decreased osmotic pressure. Thus, a biomarker is decreased albumin content (which goes into the endothelial tissue)

Leukocytes also accumulate at the site of injury, regulated through cytokines. This process is called chemotaxis

Eventually, there is the termination of the acute inflammatory response (after the offending agents are removed). After this, we undergo a phase of repair.

Anti-inflammatory mediators terminate the acute inflammatory reaction when its no longer needed

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22
Q

Chemotaxis

A

Refers to the migration of cells triggered by a chemical mediator. In the case of acute inflammation, it refers to cytokines recruiting leukocytes at the site of the inflammation.

Both endogenous and exogenous substances act as chemoattractant.

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23
Q

Leukocyte infiltration

A

First 6-24 hours: Predominantly neutrophils at the inflammatory infiltrate. the sis because they respond faster than cytokines, but undergo apoptosis fast

Subsequent 24 hours: Monocytes - high half life, over time they become the dominant population

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24
Q

Outcomes of acute inflammation

A
  1. Complete resolution: normal function, replacement of injured cells
  2. Scarring: Connective tissue replacement, leading to fibrosis (and in some cases loss of function)
  3. Progression of the response to a chronic inflammation (angiogenesis, fibrosis, and permanent mononuclear cell infiltrate)
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25
Chronic inflammation
Coexisting inflammation, tissue injury and attempt to repair scarring Mediated by cytokines Prolonged response to persistent stimuli It can either lead to recovery, or systemic inflammatory response
26
Ebb-phase
First phase of injury Generally short Clinical shock, resulting in reduced tissue perfusion first 12/24 hours All energy is devoted to the repair of damage
27
Flow phase
Can last for weeks or days, follows the ebb phase in metabolic responses to injury Alteration of the metabolism - increased temperature and oxygen consumption, production of stress hormones, increased proteolysis (for the catabolism of amino acids used to produce energy) Ensures energy is made available to repair the damaged tissue
28
Systemic inflammatory response syndrome (SIRS)
1. Temperature higher than 38 degrees 2. Heart rate higher than 90bpm 3. Respiratory rate more than 20 per minute 4. PCO2 less than 32 mmHg 5. Low levels of albumin 6. High white blood cell count
29
In medio stat virtus
An excessive inflammation, the underlying cause being a human disease Also results in increased susceptibility to infections Most common cause = leukocyte deficiency
30
Biomarkers of inflammation
1. Body temperature 2. WBCs count and formula examination 3. Acute phase proteins 4. Erythrocyte sedimentation rate
31
Body temperature
Cytokines act as endogenous pyrogens on the hypothalamus by over regulating the set point for the control of body temperature
32
White blood cells count
To determine is the inflammation is caused by bacteria or viral agents Also used to distinguish between chronic inflammation and an allergic reaction Bacterial agents = increased neutrophils - status of leucocytosis Viral agents = increase in WBCs - status of lymphocytosis Chronic = normal or slightly elevated WBCs Allergic reaction = parasitosis, slight increase in WBCs, and an increase in eosinophils (through formula examination)
33
Acute phase proteins
Functionally and biochemically diverse, but they are all produced by the liver whose plasma concentration increases or decreases by at least 25% during the acute inflammatory phase Can be either: - Positive acute phase proteins if they increase - Negative acute phase proteins
34
Changes in APPs
1. Small - physiological stress and in several psychiatric illnesses 2. Moderate - strenuous exercise, childbirth, heatstroke 3. Substantial - infection, trauma, burn, surgery, tissue infarction etc. (inflammation)
35
Positive APPs
Increase in the plasma in response to disease usually in 1-2 days Can be characterized as: - Major: increase 100-1000 fold, reaching their peak 24-48 hours after insult. An example includes serum amyloid A or CRP - Moderate: increase 5-10 fold - decrease at slower rates - Minor: Increase slightly above resting levels, at a gradual rate OR can also be characterized based on the cytokine they produce (another flashcard)
36
Protease inhibitors
Prevent the spread of tissue necrosis when lysosomal enzymes are released from damaged cells
37
Coagulation factors
Increased coagulation factors prevent excess blood loss
38
CRP and complement proteins
Contain and eliminate infection
39
PAPPs type 1 vs type 2
type 1: - Induced by interleukin-1 and TNFA and B - Prototype is serum amyloid A type 2: - induced by interleukin-6 - prototype is CRP (C-reactive protein)
40
Electrophoretic protein pattern test (QPE)
Used to stratify proteins in the plasma, and measure their concentration in acute inflammation, there is an observed decrease in albumin and increase in alpha, beta and gamma peaks
41
CRP
C reactive protein Synthesized by the liver after stimulation of interleukin 6. Protein of the acute phase of inflammation. Can bind to numerous endogenous and exogenous substances, facilitating their removal from the circulation (opsonization) Normal: 3mg/L Moderate: 3-10mg/L Active inflammation: >10mg/L Peak occurs 72h after the start of the inflammation, and disappears after 7 days Can increase due to states unrelated to inflammation, eg. pregnancy, weight loss, excessive exercise etc.
42
Serum amyloid A - SAA
More specific parameter than CRP in the measurement of acute inflammation Better at distinguishing the minimum response, and is a very sensitive index for transplant rejection
43
Negative APPs
Decrease in plasma concentration greater than 25% in the response to inflammation Reduction either occurs rapidly or gradual The most important are albumin and transferrin (iron status)
44
Albumin
Synthesized by the liver, decreases during acute inflammation Serves as a carrier for many hormones, calcium and fatty acids. Also binds unconjugated bilirubin, and is useful for the absorption of certain drugs. half life of 20 days, 50% of the total hepatic protein output. Can either be - abnormal distribution (capillary permeability - acute inflammation) - reduced synthesis - liver diseases - dilution - overyhydration - abnormal excretion/degradation - nephrosis, burns, catabolic states etc. used to check hepatic functionality and protein production Under physiological conditions it regulates the oncotic pressure in the plasma. Low albumin means more plasma escaping the vessel, resulting in edema. Hypoalbuminemia can be caused by starvation, or over hydration Doesn't effectively indicate protein synthesis in short term conditions
45
Erythrocyte sedimentation rate (ESR)
Non specific test for inflammation Measures how much time it takes for the red blood cells to aggregate and sink towards the base of the tube Rouleaux = typical aggregation of RBCs during inflammation and decreased protein concentration. Factors promoting it is the decrease in plasma proteins, and the increase in immunoglobulins and alpha globulin. Usually used to flow the progression of the inflammation
46
Tests to order during inflammation
1. Serum protein electrophoresis - moderate sensitivity, minimum specificity 2. WBC counts - high sensitivity, moderate specificity 3. EST - high sensitivity, minimum specificity 4. CRP or SAA - high sensitivity and specificity
47
Autoimmunity
refers to a wrong response to self-agents, leading to the production of autoantibodies directed against the cells of our own organism Hallmark: autoantibodies Etiology (causation) is still unknown, but there is genetic and environment susceptibility Affects women more than men (eg. lupus) Can either be systemic or localized (organ specific), depending on the distribution of auto antigens recognized
48
Steps of autoimmnunity
1. Potential phase 2. Subclinical phase 3. Latent phase 4. Clinical phase
49
ANA
Antinuclear antibody eg. anti-DNA, anti-histones, soluble nuclear antigens. This is typical used to diagnose a non organ specific autoimmune disease (like lupus). Can be measured through indirect immunofluorescence, or immunometry (0=negative, +4=ma. positivity). The intensity of the fluoresce indicates the severity of the autoimmune disease Autoimmune diseases are the persistence of this positivity
50
ENA
Other most used test for the detection of systemic antibodies is the extractable nuclear antigen test In general, ENA is requested after a positive ANA test It can react with proteins present at the level of the cell nucleus
51
Organ specific autoantibodies - thyroid gland
1. Peroxidase 2. Thyroglobulin autoantibody (found in Hashimoto's disease) 3. TPO, TRAb and TSI 4. Anti-microsome
52
Celiac disease
Autoimmune disease of GI tract caused by gluten Resultant decrease in absorption 1. Anti-liadin antibodies 2. Anti-transglutaminase antibodies Histological confirmation by gastroscopy
53
Type 1 diabetes
Autoimmune disease against the beta pancreatic cells Fasting blood glucose and urinalysis AntiGAD antibodies: Enzyme that catalyzes the formation of GABA from glutamate (protective function in the beta cells). This is used to distinguish between type 1 and type 2 diabetes
54
Iron
1-2mg per day Ferric (Fe3+) or ferrous (Fe2+) Proteins: - Ferritin = storage - Transferrin = transport
55
Iron absorption
20% is absorbed as heme iron, thanks to the heme carrier protein 1. Its bioavailability is poorly influenced by the nutritional state (decreased by calcium and food processing) remaining 80% is absorbed as a non epic form mediated by the divalent metal transporter 1 (DTM1). Bioavailability is strongly influenced by the acidic environment of the stomach Reduction of ferric to ferrous form in the presence of acid pH
56
Transferrin
liver protein, important to make iron soluble and transport it (binds to two iron molecules. Ferric iron - insoluble at physiological pH and potentially toxic Binds to iron in the intestines and transports it to the storage compartments IN iron deficiencies, TF increases to compensate for the shortage and captures all the available iron Unsaturated transferring (30%), in which one or both binding sites for iron are free, is important because it represents the reserve capacity of transferrin (in case of high iron levels). It minimizes the risk of free iron toxicity Transferring and iron reserves have an inverse relationship
57
Lactoferrin
Absent in the blood but important during inflammation inflammation is characterized by a more acidic pH. Lactoferrin has a higher affinity for Fe at lower pH and thus keeps Fe more stably bounded, limitin its availability for pathogens. Its found in the granules of neutrophils
58
Haptoglobin
Prevents the kidney loss of hemoglobin (prevents the excretion or iron and hemoglobin)
59
Ferritin
Stores iron in a soluble form - indirect measure of iron levels. Works also as a hepatic protein (receptor) Hemosiderin stores iron in an insoluble form. Stores iron in macrophages within the liber and bone marrow
60
Biomarkers of iron homeostasis
1. Serum iron 2. Transferrin, measured directly or indirectly through total iron binding capacity (TIBC) 3. Serum ferritin 4. Hemoglobin
61
Serum iron
Measures the amount of iron in the blood Values change according to chronobiology Useful to asses an iron overload (eg. acute iron poisoning) Should NOT be used for diagnosing iron deficiency these levels decrease only when the reserves no longer compensate for the deficiency
62
Serum ferritin
Measures stored iron levels in the body Highly sensitive to both iron deficiency and accumulation (inflammation or overload) Each monogram of ferritin corresponds to 8-10mg of stored iron Decreases: - Iron deficiency anemia (early indicator) - Vitamin C deficiency Increases: - Excessive serum iron concentration - Destruction of RBCs or hemochromatosis - Inflammation (although this is unrelated to iron levels - ferritin is an APP)
63
Serum transferrin
Primary transporter of iron in the body, keeping iron in a soluble, non toxic form Increase when stored iron is low, and decrease when its high Can be analyzed by estimating the total iron binding protein capacity (TIBC), which is an indirect method of transferrin saturation High saturation = iron overload Low saturation = iron deficiency Decreases during inflammation - they are negative APPs
64
Hemoglobin
Measures the concentration of hemoglobin in the blood To diagnose conditions affecting RBCs and anemia
65
Plasma vs serum
Serum is plasma without the coagulation factors
66
Total protein test
Evaluates the combined amount of protein, including albumin and immunoglobulin High protein - increase in protein synthesis, or fluid loss Decreased total protein - loss of blood or edema, or increased catabolism (or decreased protein synthesis) Determined by the ratio of solute to solvent Can also determine hydration levels of patients
67
Plasma protein electrophoresis
Enables the separation of proteins, facilitating their detection Serum is used, since it lacks fibrinogen Proteins undergo separation under a consistent electric field Albumin has a conc. of 40 --> most abundant protein in our bloodstream, with an average half life of 20 days
68
Oncotic pressure
Osmotic pressure due to the presence of proteins - determines the distribution of the extracellular fluid between intravascular and extravascular compartments Edema = decreased plasma oncotic pressure, leading to an increased capillary permeability
69
Alpha-1 anti-trypsin
Following albumin in protein electrophoresis Inhibitor of proteases Elevated levels indicate inflammation Also contributes to the formation of angiotensin, prompting sodium retention, and amplifying extracellular fluid (ECF), worsening edema.
70
Alpha-2 globulin: hatpglobulin and macroglobulin
Haptoglobulin: binds hemoglobin - diagnoses intravascular hemolysis Macroglobulin: inhibitor of proteases
71
Ceruloplasmin
Protein rich in copper Serves as a ferroxidase and a scavenger for superoxide Elevated levels during pregnancy Decrease is associated with Wilson disease (discoloration of the sclera - yellow)
72
beta-1 globulin: Transferrin and ferritin
Ferritin: Storage of iron - measured to evaluate body iron reserves Transferrin: Primary transporter of iron in the plasma
73
Immunoglobulins
Antibodies uniform composition, cluster together during protein electrophoresis
74
Hypogammaglobulinemia
Decrease in gamma globulins Can be inherited conditions, can occur in hematological diseases, or can be a result of increased catabolism Too small concentration sin blood to be detected by electrophoresis
75
Hypergammaglobulinemia
Elevated concentrations - liver inflammation, diminished albumin levels
76
Paraproteins
B lymphocyte lineage Associated with multiple myeloma Last negative portion of the electrophoretic spectrum
77
procalcitonin
Precursor of calcitonin, which is particularly relevant in sepsis Decrease in inflammation is mirrored by a reduction in the procalcitonin peak
78
Calprotectin
Protein associated with neutrophils, relevant especially in inflammatory bowel disorders. Measured in fecal samples for gastrointestinal inflammation
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Clinical Lab (3 decks)

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