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Mechanisms of Disease > Week 2 Lecture- Genetic Disorders > Flashcards

Week 2 Lecture- Genetic Disorders Flashcards

1
Q

What are the 3 types of genetic diseases discussed?

A
  1. Mendelian disorders
  2. Chromosomal abnormalities
  3. Complex multigenic disorders
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2
Q

What are Mendelian disorders?

A
  • Monogenic disorders
  • Usually rare
  • Single gene defect causes the disorder
  • Has to be a survivable defect
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3
Q

What are chromosomal abnormalities?

A
  • Extra chromosomal material or structural defect in a chromosome
  • Uncommon
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4
Q

What are complex multigenic disorders?

A
  • Complex interaction of multiple genetic defects with environmental factors (predisposition)
  • Genetic defect predisposes you, then an initiating event causes the disease
  • Far more common
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5
Q

What does autosomal mean?

A

Located on chromosomes 1-22 rather than X or Y

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6
Q

What is nondisjunction?

A

Failure of 2 homologous chromosomes (or 2 sister chromatids) to separate at metaphase of meiosis I (or meiosis II/mitosis)
- Problem with separation

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7
Q

What is penetrance?

A

Whether or not the variant genotype can be inferred on the basis of defined phenotypic criteria
- Likelihood that we can determine the patient has the genetic abnormality based on appearance of the phenotype (symptoms)
- Another way to think about it is–> How likely is the altered genetic pattern to cause symptoms

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8
Q

Overview Mendelian disorders

A
  • Single mutation (monogenic) so follow Mendelian inheritance
  • High penetrance
  • Contribute to understanding of physiology- ex: chloride channel function in the lung
  • Rare unless selective pressure- ex: Malaria
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9
Q

List the Mendelian disorders we are focusing on

A
  1. Neurofibromatosis
  2. Ehlers-Danlos Syndrome
  3. Phenylketonuria
  4. Sickle Cell Anemia
  5. Fragile X Syndrome
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10
Q

What specific type of monogenic disorder is neurofibromatosis?

A

Autosomal dominant disorder- genes are located on chromosomes 1-22, one mutation in one gene copy produces disease

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11
Q

How many types of neurofibromatosis are there and what are the differences?

A
  1. Type I (mutation in neurofibromin)- common (1:4000), Highly variable course
  2. Type II (mutation in merlin)- Rare (1:40,0000/50,000), range of tumors

Both are involved in the formation of growths/tumors

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12
Q

How does neurofibromatosis present?

A
  • Neurofibromas
    *Peripheral nerve myelin sheath tumors- overgrowth of cells in myelin sheath
    *Plexiform- infiltration in towards nerve fivers themselves; can produce disruptions in nerve transmissioin
    AND ALSO
    *Solitary- growing out and do not infiltrate
  • Optic nerve gliomas
  • Lisch nodules- pigmented nodules of the irus
  • Cutaneous hyperpigmented macules (spots on skin)- very dark; not freckles or moles
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13
Q

What protein is mutated in type I neurofibromatosis?

A

Neurofibromin I (NF1)

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14
Q

Describe the effect of NF1.

A
  • Mutated in neurofibromatosis I
  • Higher expression in nerve cells with low expression in all other cell types
  • GTPase that inhibits Ras–> responsible for regulation of growth and differentiation
  • Loss of neurofibromin results in unregulated cell growth
    -Absence of NF1= excessive Ras activity
    *Signaling to Ras is associated with increased proliferation or survival of cells, even in the presence of death signals
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15
Q

Why is Ehlers-Danlos Syndrome called a syndrome?

A

There are multiple types

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16
Q

Overview of Ehlers-Danlos Syndrome

A
  • Multiple types- still considered monogenic because each type is associated with a different mutation
  • Defect in fibrillar collagen in CT
  • Synthesis or Structure
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17
Q

What are the symptoms of Ehlers-Danlos Syndrome?

A
  • Elastic skin
  • Bruises easily
  • Overly flexible joints
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18
Q

Mutations in which types of collagen are known?

A

I, III, and v

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19
Q

Name 2 proteins that are required for processing of collagen into fibrillar form that have known mutations.

A
  1. Lysyl Hydroxylase (Kyphoscoliosis- deformities in spinal cord)
  2. Procollagen N- Peptidase (Dermatosparaxis- excessively loose skin)
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20
Q

What is fibrillar collagen?

A
  • Collagen that undergoes structural modification to become a fibrillar collagen, which gives it greater tensile strength
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21
Q

Fibrillar collagen is a major component of what areas of the body?

A
  • Bone
  • Tendon
  • Cartilage
  • Skin
  • Blood vessels
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22
Q

Fibrillar cartilage is important for….

A
  • Wound healing
  • Scar formation
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23
Q

What are some of the complications of Ehlers-Danlos Syndrome?

A
  • Skin is stretchable, fragile, and more vulnerable to trauma–> compromised wound healing
  • Lack of tensile strength leaves gaping wounds
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24
Q

What are the serious internal complications of Ehlers-Danlos?

A
  • Colon rupture
  • Large blood vessel rupture
  • Ocular (cornea rupture, retinal detachment)
  • Diaphragmatic hernia
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25
Q

What is phenylketonuria?

A
  • Metabolic disorder
  • Autosomal recessive
  • Produces severe intellectual disability due to accumulation of phenylalanine, which happens because there is a failure in amino acid catabolism
    *Patients cannot break down phenylalanine
  • Detected in urine using iron compound–> add ferric chloride to urine and it turns olive green
  • Infants are tested shortly after birth because early dietary intervention is important
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26
Q

Describe phenylalanine catabolism.

A
  • Phenylalanine is converted to tyrosine by phenylalanine hydroxylase (PAH)
  • Mutation in the PAH enzyme causes PKU
  • Absence of PAH causes tyrosine (Tyr) to become an essential aa
  • Normal patients can break down Phe themselves to make Tyr
  • Patients with PKU do NOT have a functional PAH and need to get tyrosine from the diet
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27
Q

How many disease- associated PAH alleles have been discovered worldwide?

A

500

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28
Q

What is the most severe phenotype of PKU associated with?

A

Null mutations
- Patients don’t express any PAH
- They get massive accumulation of Phe because they cannot process it at all except to use it in making proteins or excrete it through urine
-

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29
Q

What are the 2 types of mutations associated with PKU?

A
  1. Null mutations
  2. Missense mutations
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30
Q

How can missense mutations in PKU be treated?

A
  • Treated with chaperones that prevent degradation of misfolded enzyme
  • Patients can make the protein, but it does not fold or work quite right
  • For these patients, you can increase the likelihood that the misfolded protein will be degraded
  • Symptoms not as severe
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31
Q

Describe the clinical presentation of PKU.

A
  • Postnatal growth retardation
  • Moderate-severe intellectual disability
  • Recurrent seizures
    * CNS symptoms due to Phe accumulation
    * Inhibits AA transpor across the blood-brain barrier
    * Secondary effects- protein synthesis, energy production, neurotransmitter homeostasis
  • Hypopigmentation (pale)
    * Product of Phe catabolism is a melanin substrate
  • Eczematous skin rashes
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32
Q

What is the current treatment for PKU?

A
  • Dietary–> reduce Phe intake
  • Alternatives include gene therapy
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33
Q

Can an infant suffer symptoms of PKU even if they do not possess the genetic mutation?

A

YES
- If the mother has PKU, the infant is getting excessive Phe from the mother’s blood during pregnancy
- The fetus will suffer symptoms at birth even though it does not have the disease itself
- Discourage breastfeeding after birth (formula)

34
Q

What is the clinical presentation of sickle cell anemia?

A
  • Hemolytic anemia
  • Chronic hypoxia
    * Generalized impairment of growth and development
    * Spleen, heart, kidney, and lung damage
  • Vaso-occlusive crisis
    * Hypoxic injury and infarcts
  • Increased susceptibility to infection (has to do with damage to the spleen)
35
Q

What is hemolytic anemia?

A

Decrease in RBCs because RBCs are being lysed

36
Q

What is the major issue caused by anemia?

A

Decreased O2 in the blood

37
Q

What protein is affected by sickle cell anemia?

A

Hemoglobin
- Mutation in the beta subunit of the protein

38
Q

How do we go from a mutation in the beta2 subunit to hemolytic anemia?

A
  • Mutation produces a sticky patch
    * Mutation goes from serine to a valine, producing a hydrophobic (sticky) patch on HbS that wants to bind to things so it is not exposed to aqueous environment
  • Binds to deoxygenation site (aggregation)–> polymerization of Hb
  • Normal HbA will terminate aggregation–> stops polymerization
  • The amount of deoxygenated sickled hemoglobin is what determines the severity of disease
39
Q

How does sickle cell disease cause hemolysis?

A
  • HbS aggregates are insoluble
  • Form long, helical fibrils (longer than the RBCs are wide)
  • Twist RBC into characteristic sickle shape
  • More fragile and likely to rupture, especially if moving at high rates through smaller blood vessels–> hemolytic anemia
    * In the spleen
    * In small blood vessels
  • More likely to adhere to endothelial surface and one another due to change in expression of adhesion molecules
    * Possible vaso-occulusion
40
Q

Name the primary effects of sickling.

A
  1. Chronic hypoxia
  2. Hemolytic anemia
  3. Bone marrow hyperproliferation to compensate for loss of RBCs
    - Affects bone growth (characteristic deformation)
  4. Decreased nitric oxide (NO), a vascular dilator
    - Released Hb binds to NO, thereby depleting it
    - Decreases NO levels in blood, causing vasoconstriction
41
Q

Describe the mechanism of vaso-occlusion.

A
  • Sickled RBCs block microvasculature
  • Reduced NO causes constriction of blood vessels–> increases risk of blockage (occlusion)
  • Increased expression of adhesion molecules produces aggregates of RBCs
  • Vicious cycle
    * Blockage causes localized hypoxia
    * Hypoxia induces HbS aggregation, more hemolysis, and more blockages
    * Vaso-occlusive crisis results from the vicious cycle because the first blockage induces more blockages
42
Q

What causes pain crisis in sickle cell?

A
  • Pain associated with hypoxic injury
  • Local infarct–> tissue will signal damage to nervous system, which we detect as pain
  • Young children–> can be masked as an osteomyelitis (bone infection)
  • Sickle cell patients are also prone to certain types of infections
43
Q

Why are sickle cell patients at increase risk of bacterial infections?

A
  • Specific to encapsulated bacteria–> host phagocytes do not recognize encapsulated bacteria
  • Immune tissue in spleen participates in opsonization
    * Opsonization: binding antibodies and complement molecules to allow recognition by phagocytes
  • Damage to spleen from injury or sickle cell may cause compromised ability to opsonize bacteria= more prone to infections by certain encapsulated bacteria
44
Q

Why is splenic injury more of an issue in children and not so much in adults?

A
  • Children have not fully developed their immune systems yet
  • If there is a splenic injury in adulthood, the body can still handle most immunological issues because the immune system is fully mature.
45
Q

Can someone who is heterozygous for HbS still have symptoms?

A

Yes, less severe

46
Q

What is the benefit of being heterozygous for HbS?

A
  • 70-90% protection against severe malaria
  • 50% protection against uncomplicated malaria–> 50% less likely to develop the disease
  • Precise mechanism unknown
    * Protected against establishment of parasitemia
    * Protected against progression to symptomatic disease
47
Q

What is the phenotype of fragile X syndrome?

A

Intellectual disability
- Characteristic physical appearance is not always present
* Can be subtle
* Long face, large jaw
- Frequency:
* Males: 1 in 1550
* Females: 1 in 8000
- 30-50% of carrier females are affected, which is a high percentage

48
Q

What is the name of the mutated gene that is associated with Fragile X Syndrome?

A

FMR1- familial mental retardation 1
- Mutation not actually in the coding region of the gene
- When this protein is expressed, the protein produced is normal
- Mutation is in the untranslated region upstream of the coding region in 5’ UTR
* Multiple tandem CGG repeats in the 5’ UTR
- Normal population: 6-55 CGG repeats, avg. 29
- Carriers: 50-200
- Affected: 200-400
- CGG repeats promote DNA methylation

49
Q

What does DNA methylation do?

A

Represses DNA expression by reducing availability for transcription
- If you get methylation in CpG island, it increases the likelihood of histone deacetylase (HDAC) attaching to the area
* This then increases the likelihood of chromatin packaging of the gene
- Because of the high # of CpG islands in this region of this gene, this gene is very likely to be wrapped around a histone
* This restricts the ability to transcribe the gene
- When FMR protein is made, it is normal, but made at much lower levels

50
Q

Why is it called Fragile X?

A

The chromosome is physically fragile in the area with so many CGG repeats
- The chromosome may break
- Cytogenetic abnormality is constriction of the long arm of the X chromosome
* Cleavage of the long arm

51
Q

What is FMRP and how does it result in intellectual disability?

A

FMR1 product is FMRP (FMR protein)
- FMRP is cytoplasmic protein highly expressed in brain and testes
- RNA binding protein associated with polysomes
* Neurons produce lots of protein, have lots of ER and ribosomes (polysomes) to make protein–> specifically at synapses
- Regulates protein synthesis at synapses
- Excessive methylation represses FMRP expression
* Reduced expression of FMRP affects ability to synthesize proteins at synapses
- Altered synaptic function leads to intellectual disability

52
Q

Which diseases did we discuss under the category of chromosomal abnormalities?

A
  1. Trisomy 21 (Down Syndrome)
  2. DiGeorge Syndrome
53
Q

Describe chromosomal abnormalities as a whole.

A
  • Structural or numerical alteration in the chromosomes
  • Rare
  • High penetrance
  • Karyotyping to analyze chromosomes
54
Q

What is karyotyping?

A
  • Take cells that have chromatin condensed into chromosomes
  • Take chromosomes and stain with Gimsa–> histological stain with methylene blue and eosin
    * This stains chromosomes in a nice banding pattern (G-bands)
  • Map genes on chromosomes using G-banding patterns
55
Q

What is the phenotype of Trisomy 21?

A

Down Syndrome
- Intellectual disability
- Characteristic appearance
* short stature relative to family members
* Epicanthal fold- fold of skin on inner eyelid
* Short broad hands
* Protruding tongue

56
Q

What causes Trisomy 21/ Down syndrome?

A

Meiotic Non-disjunction
- Depending on where you get non-disjunction, you get different types of gametes
* Happens during meiosis I= 2 gametes with 2 copies and 2 gametes with no copies–> likely that gametes with no copies are not viable
* Happens during meiosis II= 2 gametes with 1 copy (normal), 1 gamete with 2 copies, and 1 gamete with no copies
[Note: gametes normally have 1 copy of each chromosome]
- This process may cause reduced fertility

57
Q

What are the lesser known symptoms of Down syndrome?

A
  • Congenital heart disease (40%)
  • Digestive problems–> need special diets
  • 10x-20x increased risk of leukemia
  • Abnormal immune responses of unknown etiology
    * Thyroid autoimmunity
    * Lung infections
  • Degenerative neurological disorder similar to Alzheimer’s disease
58
Q

Describe the molecular basis of Down syndrome.

A

Chromosome 21 has 430 genes
- Overexpression of genes is variable–> may explain why 40% have heart disease
Comparing 2 individuals with partial trisomy:
- Down syndrome critical region
- APP (associated with Alzheimer’s), SOD1 (associated with Parkinson’s), Ets transcription factor, et al.
Gene dosage: if someone has more copies of a gene, they are more likely to express more of the protein product because you signal for production of that protein product
- You now have 3 genes that can be activated instead of 2

59
Q

What is DiGeorge syndrome?

A
  • Part of a spectrum of disorders associated with chromosomal deletion
    * Chromosome 22q11.2
    * Other disorder is velocardiofacial syndrome
60
Q

What are the symptoms of DiGeorge syndrome?

A
  • T-cell immunodeficiency, hypocalcemia, cardiac malformations, mild facial anomalies
  • Cardiac malformation and facial dysmorphology are also found in velocardiofacial syndrome
  • This particular deletion also increases risk of:
    * Schizophrenia
    * Bipolar disorder
    * ADHD
61
Q

What are additional symptoms and physical changes associated with DiGeorge syndrome?

A
  • Thymic hypoplasia
    * T-cell development
    * T-cell immunodeficiency
  • Parathyroid hypoplasia
    * Calcium mobilization by parathyroid hormone
    * Hypocalcemia
  • Cardiac malformations
    * Different structures impacted
    * Generally affect outflow tract (transient developmental structure; connects embryonic ventricles with aortic sac)
    * Associated with multiple congenital heart defects
  • Alterations to facial development
    * Mild facial abnormalities
62
Q

What are the characteristics of the deleted region involved in DiGeorge syndrome?

A
  • Very large: 1.5 megabases (1.5 million bases)
  • Different borders for deleted region for 2 different outcomes
  • Many genes present; no specific associations yet
    * 30 candidate genes
    * Transcription factor TBX1 is closely associated with phenotypic features
    * TBX1 targets a gene called PAX9, which is associated with the palate, parathyroid, and thrymus
63
Q

What are complex multigenic disorders?

A
  • Basically a catch-all for diseases that do not fit monogenic or chromosomal criteria
  • Determining if a disease qualifies:
    * Familial clustering
    * Not monogenic or chromosomal
  • Polymorphisms present in the general population
  • Most phenotypical characteristics are the result of the interaction of multiple polymorphisms (ex: eye color)
  • These diseases have multiple polymorphisms and it depends on the combination of polymorphisms–> some cases you have disease, in other cases you do not
64
Q

Are polymorphisms disease specific?

A
  • Some are unique to a specific disease
    * Ex: Bruton’s agammaglobulinemia- mutation in a specific tyrosine kinase that prevents B cell maturation
  • Some are found in multiple diseases
    * Ex: hypersensitivity (allergies) involve HLA components; so does type 1 diabetes
  • Also, some diseases associate with multiple polymorphisms
65
Q

What is a polymorphism?

A
  • Refers to the presence of two or more variant forms of a specific DNA sequence that can occur among different individuals or populations
66
Q

How many genes are implicated in T1 diabetes?

A

20-30

67
Q

Which of the 20-30 genes associated with T1D are important?

A
  • Insulin (Chr11
  • HLA region on Chr6p21
  • PTPN22 (lymphoid protein Tyr phosphatase
  • IL2 receptor alpha (IL2RA)- T cell activation
  • Cytotoxic T-lymphocyte associated protein 4 (CTLA4)- negative reg. of immune response
  • Consistent with autoimmune disease*
68
Q

What contributes to the pathogenesis of type 1 diabetes?

A

Genetic susceptibility + environmental triggers

69
Q

Explain environmental influences

A
  • Polymorphisms may result in predisposition to disease
  • Environmental exposure required for pathogenesis of disease
    * Hypersensitivity reactions
    * Certain autoimmune diseases
    * Type 1 diabetes
70
Q

What are the common characteristics of T1D and T2D?

A
  • High blood glucose
  • Symptoms–> excessive thirst/urination/hunger
  • Insufficient insulin function
71
Q

What is the difference between T1D and T2D?

A

Why the patient has a high BG level
- T2D: insulin resistance
- T1D: reduced insulin production due to autoimmune destruction of pancreatic beta cells

72
Q

Why is there a link between people suffering infection and showing signs of T1D?

A
  • When exposed to bacteria/viruses, immune system is activated
  • If system is not working right because of polymorphisms, this could also mean you activate the cells that attack the pancreatic beta cells.
  • Other possibility is that they are attacking/directed against proteins that have something in common with the protein expressed on the surface of pancreatic beta cell
    -Viruses–> no direct evidence for specific virus
    -Bacteria–> linked but causation unknown
73
Q

What are environmental triggers of T1D?

A
  • Virus
  • Bacteria
  • Nutrition
  • Chemicals
74
Q

Describe the controversial concept of T1D and antigen exposure.

A
  • T1D might be like an allergy gone haywire
    * Some polymorphisms predispose people to allergies; the same polymorphisms might be what predisposes them to T1D
  • Cow’s milk–> cross-reactivity between antibodies to bovine albumin and beta cell surface protein
  • Wheat proteins (specifically gluten)–> overlap between T1D and celiac; insufficient evidence that gluten Ab’s initiate T1D
    * Genetic susceptibility?
75
Q

What is amyloidosis?

A
  • Progressive degenerative disease characterized by fibrillar protein deposits (amyloid deposits)
  • Deposits are improperly folded proteins
    * Type of protein determines type of disease
    * Mutations determine what type of protein you find in the deposit (multiple variants of amyloidosis)
    * Will impinge on neighboring structures–> interfere with function= symptoms
76
Q

What is amyloid?

A
  • Deposit that stains with iodine, which stains starches
  • Have uniform, straight, unbranched fibrils
  • 5-10 % of protein in deposits is serum amyloid P (SAP)–> found in all amyloid deposits; not the protein that is overexpressed
    * Binds to motifs common to all amyloid proteins
    * Calcium dependent function
    * May protect amyloid from proteolysis or phagocytosis
77
Q

What is the common mechanism of amyloidosis?

A
  • Excessive production of precursor or production of mutated precursor
  • Specific type of tertiary protein structure
    * No alpha strands; form beta sheets only
    * Unfortunately, no common structural feature in the protein itself has been linked to amyloidogenicity
    * Thousands auto-aggregate into beta-sheet protofilaments (long fibers)
78
Q

How do you diagnose amyloidosis?

A
  • Amyloid is a very specific structure with specific chemical properties, which allows us to identify them on pathological samples
  • Birefringent crystals diagnostic for amyloidosis
    * Congo Red staining- red= protein, but not necessarily amyloid
    * Polarized light microscopy- apple green= amyloid deposits
79
Q

What are the 2 mechanisms of genetics of amyloidosis?

A
  1. Mutation in amyloid protein
  2. Mutation in non-amyloid protein
    - Therefore, mutation is not always predictive
    - Amyloid typing is usually based on immunohistochemistry for proteins we think are likely to be in that deposit
80
Q

Describe variants in amyloidosis.

A

Nomenclature
- A for amyloid
- Second part for protein type
* AL from Ig light chain
* AFib from fibrinogen–> amyloidosis with fibrinogen in deposits
Clinically–> Systemic vs Localized
- Some specific variants will be localized to specific areas, but many variants can be either systemic or localized

81
Q

Why do we want to ID the protein source in a patient with amyloidosis?

A

Treatment is based on eliminating the source- ex: AL is the most frequent type of systemic amyloidosis
- Target underlying plasma cell issue–> making excessive amounts of Ig light chain
- Chemotherapy–> to destroy plasma cells or the B cells that will differentiate into plasma cells
- Stem cell rescue–> put stem cells into bone marrow so you are no longer making the B cells that become the plasma cells that make the Ig light chain

Mechanisms of Disease (10 decks)

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