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Clinical Science > "Degenerative" Genetic Diseases > Flashcards

"Degenerative" Genetic Diseases Flashcards

1
Q

What is the name for skills that include self-control, memory, self-monitoring, organization, control of emotions, starting and completing tasks, etc. (tasks of daily living)?

A

executive function

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2
Q

What is it called when someone is using too many words to describe something when fewer would suffice?

A

circumlocution

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3
Q

What may be an indicator of reduced function in Alzheimer’s disease?

A

circumlocution

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4
Q

What is a mutation that arises where there is no family history of the condition (may be a new genetic variant in a family)?

A

De novo mutation

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5
Q

What is the most common cause of dementia in the elderly?

A

Alzheimer’s

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6
Q

Alzheimer’s is typically diagnosed over what age in those affected?

A

65

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7
Q

What does Alzheimer’s disease result in?

A

progressive memory loss and premature death

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8
Q

Alzheimer’s has a ___% mortality per year after diagnosis

A

10

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9
Q

Once diagnosed with advanced dementia, half of the AD patients die within?

A

6 months

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10
Q

Although Alzheimer’s is not a specific cause of death, it increases their vulnerability to what?

A

illness and infection due to:
-injuries from falls
-poor nutrition or dehydration
-aspiration pneumonia due to inherent swallowing difficulties

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11
Q

What is the main common cause of death in Alzheimer’s disease patients?

A

aspiration pneumonia

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12
Q

What are the hallmark pathologic changes of Alzheimer’s Disease?

A
  • amyloid plaques
  • neurofibrillary tangles
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13
Q

What are abnormal deposits of the protein beta amyloid in the space between neurons?

A

amyloid plaques

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14
Q

What is formed by clumps of tau protein, which is part of the structure of the microtubules that support the structure of the neuron (limit communication between neurons)?

A

neurofibrillary tangles

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15
Q

Amyloid plaques and neurofibrillary tangles result in what?

A

-synaptic connections between neurons are lost and many neurons stop functioning and die
-atrophy of the brain occurs
-functioning and memory processes greatly decrease

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16
Q

What are the manifestations of Alzheimer’s disease?

A
  • memory deficits
  • language changes
  • visuospatial skills
  • neurobehavioral effects
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17
Q

What are the memory deficits associated with AD?

A
  • recent: unable to remember many events after AD onset
  • remote: able to remember some events that occurred prior to AD onset
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18
Q

What are the language changes associated with AD?

A
  • verbal disfluency and circumlocution
  • anomia (forgetting words)
  • reduced vocabulary
  • diminished comprehension
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19
Q

What are the visuospatial skills associated with AD disease?

A
  • misplaced items
  • get lost frequently
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20
Q

What are the neurobehavioral effects associated with AD?

A
  • loss of or fragmented sleep
  • depression and/or psychosis
  • loss of executive function
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21
Q

What are the two different types of AD?

A
  • early-onset
  • late-onset
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22
Q

Early-onset AD usually occurs between what ages?

A

30-60, but can occur as young as 20

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23
Q

What percentage of AD cases are related to early-onset genes?

A

1-5%

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24
Q

Early-onset AD is commonly associated with what inheritance pattern?

A

autosomal dominant

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25
Q

What are the genes associated with early-onset Alzheimer’s disease?

A
  • amyloid precursor protein gene (APP)
  • presenilin 1 (PSEN1)
  • presenilin 2 (PSEN2)
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26
Q

Which early-onset AD gene has over 30 mutations associated with early-onset AD and may be involved in early neural development, but exact function is unknown?

A

amyloid precursor protein gene (APP)

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27
Q

Which early-onset AD gene has over 150 million mutations and can lead to an overproduction of a longer and more toxic beta amyloid peptide and plaque formation?

A

presenilin 1 (PSEN1)

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28
Q

Which early-onset AD gene is the rarest of the three mutations and has an unknown mechanism but perhaps increases apoptosis in neurodegeneration?

A

presenilin 2 (PSEN2)

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29
Q

What chromosome is the APP gene located on?

A

chromosome 21

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30
Q

Individuals with Down Syndrome have trisomy 21 and an increased expression of what?

A

the APP protein

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31
Q

What increases the development of neurofibrillary tangles and beta amyloid plaques?

A

down syndrome

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32
Q

Individuals with down syndrome have a higher risk of what?

A

early-onset AD

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33
Q

What is the average lifespan of an individual with Down Syndrome?

A

60 years

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34
Q

Late-onset AD typically occurs after the age of what?

A

65

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35
Q

What percentage of cases of AD are late-onset?

A

over 95%

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36
Q

Genetics of late-onset AD represents what types of influences?

A

genetic and environmental influences

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37
Q

How many genes have been identified that are associated with late-onset AD?

A

20

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38
Q

What is the most firmly identified gene involved in late-onset AD?

A

apolipoprotein E (APOE)

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39
Q

What does the APOE variant allele also increase the risk of?

A

other forms of dementia (including vascular dementia and Lewy Body dementia)

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40
Q

What are the risks for late-onset AD in order?

A
  1. age
  2. family history of affected (1st degree relative)
  3. presence of APOE polymorphism
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41
Q

The APOE allele exists in 3 forms, what are they?

A
  1. APOE epsilon 2
  2. APOE epsilon 3
  3. APOE epsilon 4
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42
Q

Which APOE allele is the least common allele, is found in 5-10% of population, and appears to reduce the risk of late-onset AD?

A

APOE epsilon 2

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43
Q

Which APOE allele is the most common allele, is found in 70-80% of population, and plays a neutral role in risk of late-onset AD?

A

APOE epsilon 3

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44
Q

Which APOE allele is found in 10-15% of population, and appears to increase the risk for AD and is associated with an earlier onset?

A

APOE epsilon 4

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45
Q

What increases risk 3 to 8-fold, depending on whether a person has one or two copies?

A

APOE epsilon 4

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46
Q

APOE is a susceptibility gene, not a what?

A

determinant gene

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47
Q

Having 1-2 copies of APOE epsilon 4 does not mean what?

A

that AD will develop in 100% of cases

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48
Q

What is considered a non-reversible, progressive neurodegenerative disease?

A

Huntington’s Disease

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49
Q

What occurs primarily in Caucasian people of NW European ancestry and most commonly begins in mid-life but can begin earlier or later?

A

Huntington’s Disease

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50
Q

Onset of Huntington’s Disease before the age of 20 is considered what?

A

juvenile HD

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51
Q

What is the inheritance pattern of Huntington’s disease?

A

autosomal dominant

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52
Q

Affected individuals with HD are considered what?

A

heterozygous

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53
Q

What are some of the neuromuscular coordination manifestations of Huntington’s disease?

A
  • chorea
  • gait abnormalities
  • absence of smooth eye movement
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54
Q

What are rapid, involuntary movements of the face, trunk, and limbs?

A

chorea

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55
Q

What are the psychosocial and behavioral manifestations of Huntington’s disease?

A
  • irritability, anxiety, depression, disrupted social relationships, paranoia, aggression, delusions
  • loss of insight, inflexibility, memory loss, impaired judgement
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56
Q

What gene codes for the protein called Huntington?

A

HTT

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57
Q

The mutated form of the HTT gene in HD consists of an expanded what?

A

CAG trinucleotide repeat

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58
Q

What is the codon for glutamine?

A

CAG

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59
Q

The average non-affected individual has how many CAG repeats?

A

17-20

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60
Q

A higher number of CAG repeats correlates to what in HD?

A

earlier onset and greater severity of disease

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61
Q

If inheritance of HTT allele in Huntington’s is from the father, what happens?

A

patients tend to develop disease early by about 3 years (paternal allele is more likely to have more CAG repeats than maternal allele)

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62
Q

In HD genetic testing, less than 35 CAG repeats is considered what type of result?

A

negative test result, so no chance of developing Huntington’s

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63
Q

In HD genetic testing, 36-39 CAG repeats is considered what type of result?

A

uninformative test result, so an individual may or may not develop HD but they are at a risk for it; their children are also at risk due to CAG repeat instability across generations

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64
Q

In HD genetic testing, more than 40 CAG repeats is considered what type of result?

A

positive test result, so they will always develop HD

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65
Q

Due to the instability of the CAG gene in HD, you may have a family that this arises _____

A

de novo

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66
Q

What is the most common lethal inherited disorder among Caucasians in the US?

A

cystic fibrosis

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67
Q

Cystic fibrosis is more common in persons of what descent?

A

Northern European descent

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68
Q

What is the inheritance pattern of Cystic fibrosis?

A

autosomal recessive

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69
Q

What newborn screening test is done that can determine if a newborn has cystic fibrosis?

A

heel stick

70
Q

What gene does the Cystic fibrosis mutation occur on?

A

Cystic fibrosis transmembrane regulator gene (CFTR)

71
Q

What does CF disease severity depend on?

A

how much of the normal CFTR gene is present
(more absences = more presentation)

72
Q

What is the most common variant of the CFTR gene and results in loss of a CTT along the gene which changes the resulting proteins produced?

A

delta F508

73
Q

What encodes for a functional transmembrane conductor of ions, especially sodium, chloride, and bicarbonate?

74
Q

What affects the membranes of the:
- respiratory tract
- pancreas
- liver and gallbladder
- intestinal tract
- sweat glands
- reproductive tract

75
Q

What is the most common place that CF occurs and affects?

A

respiratory tract

76
Q

When both parents pass the variant CFTR gene, what fails to work properly?

A

transmembrane conductor

77
Q

What is the normal function of the CFTR gene?

A
  • chloride is moved from inside the cell to outside via the conductor
  • the amount of sodium is regulated
78
Q

What is the variant function of the CFTR gene?

A
  • chloride cannot exit cell
  • sodium absorption is unchecked and repeatedly absorbed into the cell in excess
  • where sodium goes, water follows, so more water than normal is found intracellularly than along the epithelial/mucus layer
  • results in unchecked sodium and water absorption leaving mucus very sticky
79
Q

What are the manifestations of CF in infancy and adolescence?

A
  • malabsorption and failure to thrive
  • pancreatitis
80
Q

What are the pulmonary manifestations of CF that are common but variable and typically occur later in life?

A
  • chronic cough
  • frequent pulmonary infections (pneumonia)
  • dyspnea and exercise intolerance
81
Q

In patients with CF, what can lead to increased pulmonary pressure or pulmonary hypertension?

A

chronic pulmonary disease

82
Q

The high pressure associated with chronic pulmonary disease in CF patients can lead to?

A

stretching in the right ventricle so the right ventricle becomes less effective as a pump and can lead to right heart failure

83
Q

What is another name for cor pulmonale?

A

right heart failure

84
Q

People with right heart failure can develop what?

A
  • dyspnea with exertion
  • chest pain
  • edema
  • possibly cyanosis
85
Q

How does CF affect the pancreas?

A
  • pancreatic digestive enzymes are impaired
  • poor absorption of food resulting in poor growth rate
  • pancreatic inflammation and pancreatitis
  • diabetes mellitus due to pancreatic insufficiency
86
Q

How does CF affect the GI tract?

A

causes multiple conditions that result from thickened mucus of epithelium

87
Q

How does CF affect the liver?

A

liver damage and portal hypertension

88
Q

How does CF affect the genitourinary system?

A

CF males are 98% infertile due to absence of vas deferens

89
Q

What are the two types of neurofibromatosis?

A
  • neurofibromatosis 1
  • neurofibromatosis 2
90
Q

Which type of neurofibromatosis is more common?

A

Neurofibromatosis 1

91
Q

NF1 is due to mutations in which gene?

92
Q

Normal NF1 gene acts as what?

A

tumor suppressor gene

93
Q

NF1 gene produces what protein?

A

neurfibromin

94
Q

What is the inheritance pattern of both NF1 and NF2?

A

autosomal dominant

95
Q

What percentage of NF1 cases are inherited and what percentage result from new mutations?

A
  • 50% are inherited
  • 50% result from new mutations
96
Q

In NF1 and NF2, the variable presentation and onset is based on what?

A

extent of gene mutations

97
Q

Mutations in what gene is NF2 due to?

98
Q

The normal NF2 gene is what type of gene?

A

tumor suppressor gene

99
Q

What protein does the normal NF2 gene produce?

100
Q

What is the gene penetrance for both NF1 and NF2?

101
Q

What are some of the main manifestations of NF1?

A
  • cafe-au-lait macules
  • freckling
  • lisch nodules
  • cutaneous neurofibromas
  • plexiform neurofibroma
  • optic glioma
102
Q

In NF1 patients, what appears during the first year of birth 6 or more are highly suggestive of NF1?

A

cafe-au-lait macules

103
Q

In NF1 patients, what appears by 3-5 years old, and occurs especially in areas of skin opposition, such as axillary and inguinal regions?

104
Q

In NF1 patients, what are small hamartomas of the iris and are more common in adult NF1 patients and less common prior to age 6?

A

lisch nodules

105
Q

What results from abnormal neurofibromin production?

106
Q

Where is neurofibromin found?

A
  • brain
  • kidneys
  • spleen
  • thymus gland
  • other tissues
107
Q

What results in multiple benign tumors (neurofibromas) composed of schwann cells, which produce the myelin sheath of axons?

108
Q

Large deletions that encompass the entire NF1 gene result in more severe (1) and earlier appearance of (2)?

A
  1. mental disability
  2. neurofibromatomas
109
Q

What are tumors of the optic pathway and occur in 15% of children with NF1 under age 6 and rarely occur in adults?

A

optic gliomas

110
Q

The risk for multiple forms of malignant neoplasms (in the brain, nerve sheath and soft tissue tumors especially) increases for individuals with what?

111
Q

What are these bone abnormalities associated with:
- most commonly, anterolateral bowing of the tibia
- scoliosis
- osteoporosis

112
Q

What are these neuropsychiatric outcomes associated with:
- intellectual disability
- ADD
- neuromotor dysfunction

113
Q

What is associated with the development of noncancerous tumors on the auditory and vestibular nerves of the body (known as schwannomas and typically occur bilaterally)?

114
Q

What are tumors on the nerve sheath or CNS?

A

schwannomas

115
Q

NF2 has fewer manifestations of what than NF1?

A

cutaneous manifestations

116
Q

Symptoms of NF2 present earlier or later in life than NF1?

A

later in life

117
Q

What can also affect vision if schwannomas affect structures of the eye like the retina?

118
Q

What are bilateral vestibular schwannomas (acoustic neuroma) which can lead to hearing loss, tinnitus, headache, and balance dysfunction associated with?

119
Q

What can cause tumors of the spine and meninges of the brain (and tumors can cause peripheral neuropathy)?

120
Q

What are skin lesions such as cutaneous and subcutaneous tumors, and skin plaques associated with?

121
Q

What are more subtle in presentation in NF2 than in NF1?

A

skin lesions

122
Q

What do you need to identify NF?

A
  • family history
  • thorough physical examination
123
Q

Genetic testing for NF1 cannot predict what?

A

the severity of the disease

124
Q

What is the inheritance pattern of polycystic kidney disease (PKD)?

A

autosomal dominant pattern

125
Q

Mutations of PKD can occur in what genes?

A

PKD1 or PKD2 genes

126
Q

If there are mutations of PKD in both PKD1 and PKD2 genes, what can happen?

A

earlier presentation of end-stage-renal-disease (ESRD)

127
Q

Rarely, PKD can follow in what type of inheritance pattern?

A

autosomal recessive

128
Q

When PKD presents in an autosomal recessive, what can present?

A
  • can present at birth and cysts may be seen on prenatal US
  • high mortality rate when found newborn
129
Q

Both ADPKD and ARPKD commonly manifest as?

A

bilateral renal cysts (but is a multi-organ disease)

130
Q

What does PKD1 encode for?

A

polycystin-1

131
Q

What does PKD2 encode for?

A

polycystin-2

132
Q

85% of PKD is due to what gene?

133
Q

Mutations on which PKD gene can have an increased severity of symptoms such as larger kidneys and more cysts?

134
Q

Younger onset of PKD symptoms is associated with which gene mutation?

A

PKD1 mutations

135
Q

Which PKD gene mutations can lead to a faster progression to ESRD?

136
Q

15% of PKD is due to which gene?

137
Q

Mutations on which PKD gene can have decreased severity of symptoms compared to PKD1?

138
Q

Which PKD gene mutations can lead to a later onset of symptoms?

139
Q

What will occur in all patients with PKD but will have varying size and amount?

A

renal cysts

140
Q

Kidney size in patients with PKD is typically increased more than how many times their normal size?

141
Q

What replaces normal structure of kidneys in patients with PKD and has altered normal processes of filtration, reabsorption, and urine concentration?

A

cysts and scarring

142
Q

What may be large and palpable on exam with PKD patients?

143
Q

What are these manifestations associated with:
- hematuria (grossly vissible)
- proteinuria
- flank pain
- bladder/kidney infections
- hypertensions
- progression to ESRD (50% of patients by age 60)

144
Q

What are these manifestations associated with:
- polycystic liver disease
- diverticulosis
- dilation of aortic root and cardiac valvular abnormalities

145
Q

What is the most dangerous clinical manifestation or complication of PKD?

A

Intracranial aneurysm

146
Q

10-20% of people with PKD end up with what complication?

A

intracranial aneurysm

147
Q

What can intracranial aneurysm that rupture rapidly cause?

A
  • intense HA
  • intracranial bleeding
  • can be fatal without surgical intervention
148
Q

In PKD patients, what can easily show cysts once they have formed?

A

US or CT scan

149
Q

What causes increased intestinal absorption of iron?

A

hereditary hemochromatosis

150
Q

Increased iron is stored in many organs and causes end-organ damage in which places?

A
  • liver
  • pancreas
  • skin
  • heart
  • pituitary gland
151
Q

What is the inheritance pattern of hereditary hemochromatosis?

A

autosomal recessive

152
Q

What type of penetrance does hereditary hemochromatosis have?

153
Q

Hereditary hemochromatosis is caused by a mutation in what gene?

154
Q

What does the HFE gene encode for?

A

proteins present in hepatocytes and intestines

155
Q

When functional, what does the HFE gene do?

A

strictly regulates the amount of iron absorbed by the body

156
Q

The two most common point mutations in hemochromatosis exists at what sites?

A

C282Y and H63D

157
Q

In hemochromatosis, the point mutation at C282Y causes what?

A

a single amino acid substitution which results in cysteine changing to tyrosine

158
Q

In humans, GI absorption of iron increases when what happens?

A

when stored iron decreases

159
Q

Iron is lost in what?

A
  • sweat
  • shedding skin
  • GI tract
  • Menstruation
160
Q

In hemochromatosis, what is not regulated by the amount of iron stored, causing a deadly accumulation of iron?

A

absorption of iron

161
Q

Hemochromatosis is expressed 10x more in men due to what?

A
  • women have lower dietary intake and menstruate (sex-induced phenotype)
  • if women develop disease, it is often a later age than men
162
Q

Affected persons of what disease do not usually present until age 40 because it is related to an excess absorption of iron over a period of years?

A

hemochromatosis

163
Q

What are these liver abnormalities associated with?
- hepatomegaly
- elevated liver enzymes
- fibrosis and cirrhosis of liver

A

hemochromatosis

164
Q

An increased risk of hepatocellular carcinoma (20-fold to 200-fold) is associated with what?

A

hemochromatosis

165
Q

What is potentiated by alcoholic liver disease and infectious hepatitis, especially?

A

hemochromatosis

166
Q

In hemochromatosis, what is caused by iron deposition into specific tissues/organs?

A
  • diabetes (pancreas)
  • arthropathy (joints)
  • heart disease (dilated cardiomyopathy, heart failure)
  • pituitary gland (hypogonadism and amenorrhea)
  • increased risk of bacteria infections
167
Q

In hemochromatosis, what can become more virulent in the presence of iron?

A

bacteria
examples include Listeria monocytogenes and Yersinia enterocolitica

168
Q

What leads to hyperpigmented skin (bronze color)?

A

hemochromatosis

169
Q

What leads to hypermelanosis?

A

increased iron in the system

170
Q

It is believed that the increased melanin in hemochromatosis is from an increase in what?

A

hemosiderin (an iron-storage complex)

171
Q

In hemochromatosis, some symptoms can be ________

A

reversible

Clinical Science (18 decks)

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