auto immune disorders basic information and lab testing

simple parts of testing and identification
some auto immune diseases listed

1. Chapter 28
Autoimmune Disorders

2. Behavioral Objectives
At the end of this lecture, the MLS and MLT student
will be able to:
Define tolerance
Describe mechanisms for autoimmunity
MLS MLT
Describe Proposed
mechanisms of autoimmunity
(Level 1)
Describe proposed
mechanismsof autoimmunity
(Level 1)
1.Release of sequestered
antigens
-
2.Escape of tolerance at the T
cell level
-

3. The MLS and MLT students will be
able to:
Describe the clinical symptoms and lab findings of
classic autoimmune diseases:
Systemic Lupus erythematosus
Graves Disease
Rheumatoid arthitis
Addison’s Disease
Diabetes mellitus

4. What is Autoimmunity?
The breakdown of the immune system’s ability to
discriminate between self and non-self; the body’s
immune system therefore mounts immune reaction
(i.e. produce antibodies) against self antigens with
harmful effects to the individual

5. Self-Recognition (Tolerance)
Tolerance-or self-recognition-is the lack of
immune response to self antigens and is initiated
during fetal development.
This is our normal state of being-our immune system
tolerates proteins and antigens that belong to us
(self).
Central tolerance-develops in thymus during
fetal life-
Peripheral tolerance-a process involving
mature lymphocytes and occurs in circulation.

6. Auto-antibodies and Role
Not all autoantibodies are bad or cause disease
Normal function of Autoab-
binds with certain antigen to rid of dead cells and
defective self-antigens; form complexes which are then rid
of from the body
For autoimmune disorder to occur, autoantibodies must
be present and damage to organ/s.

7. Spectrum of Autoimmune Disorders
Over 80 serious chronic diseases
All characterized by the immune system that
has gone awry or misdirected.
The immune system is always being activated
Unable to recognize the self that it was
supposed to protect-instead it attacks it.
Autoantibody-immunoglobulins in
autoimmune disorders
Autoantigens-specific antigens being attacked

8. Factors Influencing Development of Autoimmunity
Genetic Factors-not well established, but certain
genetic predisposition in some cases-
Autoimmune disorders more likely in women than
men
Presence of certain HLA
Patient Age-60-70 years peak age
Exogenous Factors-drugs, ultraviolet radiation,
chronic infectious disease

9. ImmunopathogenicMechanisms
1. Sequestered antigenor Hidden antigen theory
Certain antigen are hidden within the organ, escapes the
detection by the immune system during fetal
development-(lack of contact with monophagocyte
system, :. No tolerance was developed for it.
However, when the antigen escapes to the circulation (e.g
due to trauma), the immune system now detects this and
sees it as foreign.

10. Mechanisms for Autoimmunity, con’t:
2. Altered antigens-that arise from biological,
chemical or physical processes
3. A foreign antigen-shared or cross-reactive with
self antigens or tissue components
Mutation
Loss of the immunoregulatoryfunctionby the T
lymphs subsets

11. Systemic Lupus Erythematosus (SLE) -antibodies
directed against T lymphs
Grave’s disease-antibodies against thyroid
Rheumatoid Arthritis (RA)-antibodies against
joints
Addison’s disease-antibodies against cortical
elements
Diabetes mellitus-(IDDM)-antibodies against
pancreatic Beta cells

12. Select Autoimmune Disorders we will
study
Organ Specific
Disorders
Thyroid-
Hashimoto’s;
Graves disease
Stomach –Pernicious
anemia
Adrenal-Addison’s
disease
Pancreas-Juvenile
diabetes
Organ-Non-Specific
Disorders
Kidney-Systemic Lupus
erythematosus
Joints-Rheumatoid
arthritis

13. Hashimoto’s Disease
Symptoms Lab Findings
Autoimmune disease of the
thyroid gland
Damage to the thyroid is
mediated b y producing
autoantibodiesagainst the
thyroid proteins –notably the
thryroglobulinsand
thyroperoxidase
Hypothryoidism-dry skin,
intolerance to cold temp.
fatigue, weight gain.
Hypothyroidism with bouts of
hyperthryoidism
Testing for thyroid-stimulating
hormone(TSH)
Free T3, Free T4,
Antibodies against:
a. thyroglobulin anti-Tg)
thyroid peroxidase(anti-TPO)
microsomal antibodies

14. Grave’s Disease
Symptoms Clinical Findings
Too much thyroid hormone
Hyperthryroidism
When TSH receptor antibody
occupies the receptor sites ,
there is no negative feedback
resulting in increased levels of
T3 and T4
Antigens implicated:
Thyrothropin receptor; Thyroid
peroxidase; Thyroglobulin
Due to autoantibodies that
mimic TSH

15. Addison’s Disease
Symptoms
Clinical Findings
Also called chronic adrenal
insufficiency; hypocorticolism,
hypoadrenalism
Adrenal atrophy-idiopathic
autoimmune process
Women-2x more affected than
men
HLA class II antigens DR3 and
DR4
against cortical elements
Antibodies against adrenal
cells
Low serum Cortisol with
elevated corticotropin
Antibodies

16. Diabetes mellitus
Symptoms –
High blood sugar
Clinical Findings
Type 1; Insulin-dependent
diabetes mellitus (IDDM);
juvenile onset diabetes;
diabetes before 30-IDDM
Immune destruction of B cells
in pancreas
Congenital Rubella infection
Associated with HLA-DR3,
DR4, DQ2, DQ8 antigens
Exogenous insulin injections-
to maintain normal blood
sugar level
Antibodies:anti-insulin, anti-
islet cell antigen 2

17. SYSTEMIC LUPUS ERYTHEMATOSUS
(SLE)
symptoms Lab findings
SLE -chronic autoimmune
disorder that may affect the
skin, and other organs
Inflammation and B cell
activation.
Characteristic “butterfly rash”
of the face
Joint pain and swelling
Tests used to diagnose
SLE:
�Antibody tests,
including:
�Antinuclear antibody
(ANA) panel
�Anti-double strand
(ds) DNA
�Antiphospholipid
antibodies
�Anti-Smith antibodies

18. Rheumatoid Arthritis (RA)
symptoms Clinical findings
Chronic Inflammation of the
peripheral joints-
Lab testing-
ESR
RF -IgM marker
ANA-antinuclear antibodies
-
TITERS OF > 1:160 is
indicative of autoimmune
disease

19. Review Questions
1-4