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NPB101 > After MT3 > Flashcards

After MT3 Flashcards

1
Q

Thyroid hormone secretions cells

A

Follicular cells; form spheres that surround an inner lumen that is acellular (contains no cells) that consists of colloid (protein)

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2
Q

Colloid

A

consistsmainlyofthyroglobulin, a large protein where thyroid hormone synthesis takes place.

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3
Q

Thyroid hormone synthesis (IMPORTANT)

A
  1. Thyroid hormone is made of Tyrosine and Iodine (I).
  2. Iodine is an essential nutrient
  3. It is reduced to Iodide (I-) before absorption in the small intestine.
  4. It is taken up and converted into thyroid hormone by the thyroid gland.
  5. There are 2 active forms of Thyroid hormone:
    - Tetra-iodothyronine (Thyroxine, T4)
    - Tri-iodothyronine (T3)
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4
Q

Lower rate of T3 and T4

A

Going to burn fewer calories
Not produce as much heat; put on more weight
Storing nutrients

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5
Q

Major effects of thyroid hormone

A
  1. Metabolism (warm-blooded vertebrates)
    Important determinant of basal metabolic rate (BMR)
    INCR - Rate of O2 consumption
    Calorigenic (heat producing)
  2. INCREASE- Heart rate,strength of contraction (permissive for sympathetic NS)
  3. Growth (permissive for GH)
  4. Development of the CNS
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6
Q

Thyroid hormone is lipophilic so

A

Actions at target cells via nuclear receptor
Target cells regulate deiodinase expression (T4–T3)
[ can remove iodide]

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7
Q

Thyroid disease

A

As many as 1 in 10 will experience a thyroid disorder during their lifetime. Many of these conditions are life-long but treatable.

Many with thyroid problems are unaware of their condition, yet consequences can be serious, e.g. pregnant women with undiagnosed hypothyroidism risk miscarriage and fetal developmental problems.

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8
Q

Hypothyroidism (too little thyroid hormone)

A

-reduced BMR
-poor tolerance of cold
-tends to increase weight (fuels stored, not burned)
-easily fatigued
-diminished alertness, poor memory

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9
Q

Hyperthyroidism (too much thyroid hormone)

A

-elevated BMR
-excessive perspiration, poor tolerance of heat -reduction in body weight (fuels burned, not stored)
Burning fuel to generate heat

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10
Q

Goiter

A

Enlarged thyroid gland
Can occur w BOTH hyper or hypOthyroidism
Develops when thyroid gland is overstimulated

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11
Q

Causes of hypothyroidism

A

Causes:
– Primary failure of thyroid gland:
Autoimmune disease (Hashimoto’s thyroiditis)
– Secondary to a deficiency of TRH, TSH, or both
– Inadequate dietary supply of iodine

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12
Q

Hypothyroidism as an adult

A

Fatigue, weight gain, weak pulse, cold intolerance, mental sluggishness and depression (goiter if due to thyroid hormone synthesis problem)
=>Reversible with thyroid hormone replacement therapy or iodine in diet

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13
Q

Hypothyroidism during perinatal period (infant)

A

“Cretinism”
Short stature, poor motor skills, moderate to severe mental retardation (goiter if due to thyroid hormone synthesis problem)
=>Effects on nervous system irreversible if not corrected shortly after birth

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14
Q

Cause of hyperthyroidism; elevated TH secretion

A

• Most common cause is Graves’ disease
– Autoimmune disease
– Characterized by exopthalmos (bulging eyes), goiter
– Weight loss, heat intolerance, insomnia, rapid heart rate

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15
Q

Treatment for hyperthyroidism

A

Surgical removal of a portion of the over-secreting thyroid
Administration of radioactive iodine
Use of antithyroid drugs

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16
Q

MAIN originate sites for immune system

A

Thymus & bone marrow

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17
Q

Leukocytes

A

Collective name for all the immune cells in our body

Leukocytes fall into 2 broad categories:
-Lymphoid cells (T lymphocytes, B lymphocytes, Natural Killer cells)
-Myeloid cells (Monocytes/macrophages, granulocytes and precursors for red blood cells and platelets.

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18
Q

Macrophage vs monocyte

A

Monocyte = still IN BLOOD
Macrophage= left blood and entered tissues

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19
Q

Where will the immune cells originate from

A

Stromal stem cells !

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20
Q

Myeloid cells

A

Neutrophil
Basophil
Eosinophil
Monocyte/macrophage
Platelets
Red blood cells

21
Q

Lymphoid

A

T lymphocytes
B lymphocytes
Lymphoid progenitor cell
Natural killer cell

22
Q

T lymphocytes (T cells)

A

-originate in the Thymus
-necessary for cell-mediated immunity.
-uses T cell receptors

23
Q

B lymphocytes (B cells)

A

-originate in the Bursa of Fabricius (and the Bone Marrow)
-necessary for humoral immunity.
-uses B cell receptors = antibodies

24
Q

Macrophages (called monocytes in the blood)

A

-professional phagocytic cells
-scavenge our tissues in search of pathogens, dead cells and other debris
Essential for tissue maintenance

25
Q

Granulocytes

A

-different types: neutrophilic, eosinophilic, basophilic, mast cells
-professional phagocytic cells that release the content of their granula as part of specific immune responses (e.g. against large extracellular parasites)

Find pathogens, engulf, die
Degranulate- encapsulate- its contents are so toxic they can overcome a bigger parasite

26
Q

Acquired cells

A

T lymphocytes
B lymphocytes

27
Q

Beta cells (receptors etc)

A
  • Consists of 2 Heavy chain and 2 Light chains
  • Linked by disulfide bonds
  • Constant domain determines antibody properties
  • Tip of the variable domain provide the antigen binding site
    MOST of life they are UNACTIVE
28
Q

1 specific B cell receptor will pertain to

A

Only 1 specific B cell

29
Q

Antigen binding site

A

High affinity
Anything can be bound by B cell receptor (proteins, lipids, fat etc)

30
Q

B cell antibody is

A

Unique and HIGHLY specific
- A B cell makes only kind of 1 antibody
- Each antibody is HIGHLY specific for one particular antigen (usually a part of a protein)

31
Q

How do we generate a near infinite number of antibodies ?

A

Random combination of VDJ gene segments

the combinatorial power of Heavy and Light chains yields > 100 Million possible antibodies!

Many B cells make antibodies that recognize proteins of our own body (’self’). These B cells are killed off in the Bone Marrow = negative selection.

So if you are infected by a new pathogen (e.g. Sars-CoV2), you likely already have a B cell that makes just the right antibody against it.

32
Q

How can single B cell make a difference against a pathogen?

A

Clonal expansion
Binding of antigen and interaction with a helper T cell stimulates the matching B cells to divide and expand the close of selected cells

Most of the new B cell clones differentiate into plasma cells, which secrete antibodies

Few of the clones differentiate into memory B cells, which respond to a later encounter with the same antigen

33
Q

Primary antibody response

A

-in response to first antigen exposure
-takes a few weeks
-moderate concentration of low – medium-strength antibodies

34
Q

Secondary antibody response

A

-in response to subsequent antigen exposure
-takes a few days
-high concentration of high-strength antibodies

35
Q

Why do we vaccinate

A

vaccinate so that we mount a better antibody response faster!!

36
Q

How do antibodies help fight pathogens

A
  • Agglutination (causes antigenic cells to clump together)
  • Activation of the complement pathway, a cascade of biochemical responses that ends with the formation of the Membrane Attack Complex, which kills pathogens
  • Opsonization (coating of the surface of pathogens with Abs), initiating phagocytosis
  • Leads to activation of Natural Killer cells
37
Q

T cells

A
  • Dimer of 2 TCR chains
  • Tip of the variable domain provides the antigen binding site.
  • Each T cell has a unique TCR, a large T cell repertoire is generated similar to B cells.
  • 2 major subtypes:
  • helper T cells
  • cytotoxic T cells
  • Helper T cells provide essential ‘help’ to B cells in mounting a humoral immune response. Without T cell help, most antibody- mediated (humoral responses) cannot take place.
  • Cytotoxic T cells can kill cells via cell-cell contact. Important in the defense against virus-infected cells and cancer.
38
Q

Non self

A

fragment of a pathogen after degradation in the lysosomes

39
Q

Self

A

refers to the Major HistoCompatibility genes (MHC), which encode a protein dimer on the cell surface that ‘presents’ this small fragment

The repertoire of MHC genes is variable between individuals
If we are looking for an organ donor ‘match’ we are looking for a donor with a similar MHC gene repertoire as the transplant recipient.

40
Q

Cytotoxic T cells

A
  • All cells express MHC class I
  • MHC-I + peptide is recognized by TCRs on cytotoxic T cells, along with a CD8 co-receptor.
  • If the peptide is ‘self’ presented in the context of ‘self’, nothing happens.
  • If the peptide is ‘non-self’ (e.g. from a virus that has infected the cells) and is presented in the context of ‘self’, cytotoxic T cells with the right TCR to recognize the peptide will kill the infected cell.
41
Q

Helper T cells

A
  • Specific Antigen Presenting Cells express MHC class II
  • MHC-II + peptide is recognized by TCRs on helper T cells, along with a CD4 co-receptor.
  • If the peptide is ‘non-self’ (e.g. from a bacterium that was phagocytosed) presented in the context of ‘self’
    by an antigen-presenting cells (APC), this activates the helper T cell
  • Activated helper T cells can then provide help to B cells that present ’non-self’ antigen.
  • Help is provided in the form of cytokines, which are soluble signaling molecules released by the helper T cells to promote proliferation (cell division) of those B cells that are activated.
42
Q

How do helper T cells help the B cells

A

Helper T cells assist B cells by recognizing the antigen presented by the B cell and providing essential signals for activation. Upon antigen recognition, helper T cells release cytokines that stimulate B cell proliferation and differentiation into plasma cells, which produce antibodies. They also provide “co-stimulatory signals” through direct cell-to-cell interactions, enhancing B cell activation. In addition, helper T cells help promote the formation of memory B cells, ensuring long-term immunity against the pathogen.

LOOOK AT SLIDES

43
Q

What role does innate immunity play

A
  • Innate immune cells are really efficient Antigen Presenting Cells
  • Without antigen presentation, there will be no acquired immune response
  • Innate immune cells are also very capable of scavenging our bodies for anything damaging (foreign or self!) and clean up.
  • Innate immunity provides a much faster, local response (inflammation) to a threat (damage or a pathogen). This usually takes care of the threat and promotes tissue repair.
44
Q

How does innate immunity know to respond

A
  • Innate immune cells recognize Pathogen-Associated Molecular Patterns (PAMPs) or Danger Signals
  • PAMPs or Danger Signals broadly flag to the innate immune system that something is amiss and requires an immune response. Examples:
  • Lipopolysaccharide (Gram negative bacteria)
  • Unmethylated DNA (virus)
  • Heat shock proteins (self), which normally never occur outside of the cell and are therefore a sign of unusual damage and cell death.
45
Q

Disorders of the innate immune system

A

Genetic mutations in the signaling pathway of the PAMPs or Danger Signals lead to defects of the Innate Immune System.
- Increased susceptibility to severe and recurrent viral and bacterial infections
Over-active innate immune responses lead to auto-inflammatory diseases, usually related to the excess strength of signals that promote inflammation

46
Q

Disorders of the acquired immune system

A

Rare mutations affect the ability to carry out VDJ recombination. No BCRs and TCRs can be made, causing the absence of the acquired immune system
This disorder is called Severe Combined Immuno Deficiency, is hereditary and primarily affects boys (often X-linked).

47
Q

AIDS- acquired immune deficiency syndrome

A

Human immunodeficiency virus (HIV) infects and kills CD4+ helper T cells resulting in lack of B and cytotoxic T activation

48
Q

Innate and acquired arms of immune system work together to

A

provide us with protection against the wide range of pathogens we might encounter over our lifetime.

If either the innate or the acquired immune system are mis- regulated, immune disorders ensue.

NPB101 (7 decks)

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