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Pathology > Path 1- chapter 6 > Flashcards

Path 1- chapter 6 Flashcards

0
Q

What are point mutations (missense)?

A

a nucleotide base is replaced by another (codes for alternative AA; beta globin: sickle cell disease; nonsense mutation replaces a nucleotide base by a stop codon)

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1
Q

Many congenital disorders are _________. not all hereditary disorders are _________. not all congenital disorders are _________.

A

hereditary; congenital; hereditary

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2
Q

What are frameshift mutations?

A

insertion/deletion of 1 or 2 nucleotides, alters “reading frame” (insertion, deletion, duplication)

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3
Q

What is a trinucleotide repeat?

A

amplification of a sequence of 3 nucleotides (fragile x syndrome)

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4
Q

What is Pleiotropy?

A

single mutation may have a variety of phenotypic effects

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5
Q

What is Li-Fraumeni syndrome?

A

TP53: various CAs

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6
Q

What is genetic heterogeneity?

A

multiple mutations may be expressed as the same trait

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7
Q

What is an autosomal dominant disorder?

A

1 parent is affected; offspring have a 50% chance of manifesting

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8
Q

in an autosomal dominant disorder which is more expressed, homozygous or heterozygous?

A

heterozygous is most common

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9
Q

What are factors associated with autosomal dominant disorders?

A

reduced penetrance (have mutation, but are phenotypically normal) and variable expressivity (same mutation is expressed differently within different individuals)

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10
Q

What are autosomal recessive disorders?

A

largest group of mendelian disorders (most commonly disrupts enzymes; offspring have 25% chance of expressing disease)

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11
Q

in an autosomal recessive disorder which is more expressed, homozygous or heterozygous?

A

homozygous

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12
Q

What are x-linked disorders?

A

Most commonly x-linked recessive; transmitted by heterozygous females transmit; affects male offspring

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13
Q

affected males (x-linked) transmit to daughters what percent of the time?

A

~100% carriers

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14
Q

What is Marfans syndrome?

A

autosomal dominant (fibrillin gene mutation); skeletal, ocular, cardiovascular (pleiotropy); 85% familial, 15% sporadic

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15
Q

What is fibrillin?

A

structural proteins, from fibroblasts

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16
Q

What are the key skeletal, ocular, and cardiovascular problems associated with marfans syndrome?

A

skeletal: long limbs, high-arched palate, joint hypermobility
ocular: bilateral lens subluxation (ectopia lentis)
cardiovascular: ruptured aorta (lethal), mitral valve prolapse (floppy valve syndrome)

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17
Q

What are some signs of marfans syndrome?

A 
Wrist sign: thumb/index fingers overlap
Steinberg sign (thumb sign)
Pes Planovalgus (flatfoot)
Dolichocephaly (elongated face)
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18
Q

What is Ehlers-Danlos syndrome?

A

this is a group of single gene disorders; autosomal dominant or recessive; defective collagen synthesis/structure; collagen lacks tensile strength; hyper-extensible skin, hyper-mobile ligaments; vulnerable to trauma; poor wound healing (vessel fragility)

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19
Q

What is familial hypercholesterolemia?

A

most common mendelian disorder (1:500); autosomal dominant; mutation is LDL receptor (LDLR) gene; hepatocytes: 75% of LDLRs; can be heterozygous or homozygous

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20
Q

Who is likely to get heterozygous familial hypercholesterolemia?

A

adulthood onset (xanthomas; increase LDLs 2-3x); premature atherosclerosis

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21
Q

What are xanthomas?

A

cholesterol deposits on tendons

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22
Q

Who is susceptible to homozygous familial hypercholesterolemia?

A

Childhood onset; LDLs increase 5x; xanthomas

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23
Q

Which is more severe heterozygous or homozygous familial hypercholesterolemia?

A

homozygous: children; more severe/lethal
heterozygous: adults; less severe

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24
Q

What is cystic fibrosis?

A

autosomal recessive; CFTR gene; decrease chloride ion transport; salty kiss; variable features: mild to lethal; chronic pulmonary infections (most common cause of death); GI and exocrine (pancreatic insufficiency- 90%); pseudomonas aeruginosa (80% by age 18)

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25
Q

What happens with the male reproductive system in cystic fibrosis?

A

95% males have azoospermia and male infertility (absent vas deferens)

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26
Q

What happens with the sweat glands in cystic fibrosis?

A

reduced resorption of sodium chloride (salty)

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27
Q

What is phenylketonuria (PKU)?

A

seen in 1:10,000 infants; autosomal recessive, affects homozygotes; severe mental retardation: age 6 months; urine and sweat is musty or mousy odor; decrease pigmentation (skin and hair)

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28
Q

tyrosine is a precursor to _______

A

melanin

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29
Q

What is maternal PKU?

A

Teratogen (crosses placenta)

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30
Q

What is galactosemia?

A

autosomal recessive (1:60,000); mutated galactose-1-phosphate uridyltransferase (GALT); abnormal galactose metabolism; galactose-1-phosphate accumulates; Failure to thrive, 1st week after birth

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31
Q

What is lysosomal storage diseases (LSDs)?

A

autosomal recessive, inherited; lack of lysosomal enzymes; metabolites accumulate (stored); early onset: infants/children

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32
Q

What are the 5 types of LSDs?

A

Tay-sachs disease; Niemann-pick disease, type A and B; Niemann-pick disease, type C; Gaucher disease; mucopolysaccharidosis

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33
Q

What is Tay-Sachs disease?

A

inability to metabolize Gm2 gangliosides; mutated hexosaminidase A enzyme; mental retardation, blindness, motor weakness; normal at birth, weakness by 6 mo.; risks are ashkenazi jews

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34
Q

What is Niemann-Pick disease, type A and B?

A

Acid sphingomyelinase deficiency; accumulation of sphingomyelin; early onset: evident during infancy

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35
Q

What is the difference between type A and type B niemann-pick disease?

A

Type A: most severe, visceromegaly + neuro. damage (fatal by age 3)
Type B: visceromegaly, no neuronal damage (limited to hepatosplenomegaly

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36
Q

What is niemann-pick, type C?

A

more common than type A and B, combined; defective lipid transport (mutated NPC1 or NPC2); cholesterol and Gm1 and Gm2 gangliosides accumulate; childhood onset, ataxia, dystonia (spasm), dysarthria, psychomotor regression

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37
Q

What is Gaucher’s disease?

A

glucocerebrosidase gene mutation (glucocerebrosides accumulate); enlarged phagocytes: “gaucher cells”; severe hepatosplenomegaly; 3 types

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38
Q

What are the differences between the three types of Gaucher’s disease?

A

Type 1= MC (99%), less severe, ashkenazi jews

Type 2-3= more severe, neuro. disturbances

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39
Q

What is mucopolysaccharidosis?

A

group of disorders; deficiency in ECM breakdown enzymes; hepatosplenomegaly, clouding in cornea, course facial features, mucopolysaccharides in urine

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40
Q

What are the types of mucopolysaccharidosis?

A

Hurlers syndrome (type 1) and Hunter syndrome (type 2); both accumulate heparin sulfate and dermatan sulfate

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41
Q

What is Hurler syndrome (mucopolysaccharidosis)?

A

autosomal recessive, alpha-l-iduronidase deficiency; corneal clouding

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42
Q

What is Hunters syndrome (mucopolysaccharidosis)?

A

x-linked; L-iduronate sulfatase deficiency

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43
Q

What are glycogen storage diseases?

A

AKA glycogenoses; group of enzymatic deficiencies; inherited (most commonly autosomal recessive; glycogen accumulates (liver, skeletal muscles, heart

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44
Q

What are the types of glycogen storage diseases?

A

von Gierke disease (hepatic type); McArdle disease (myopathic type); Pompe disease (type II glycogenosis)

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45
Q

What is von Gierke disease (hepatic type)?

A

glucose-6-phosphatase deficiency; impaired liver glycolysis to hepatomegaly and hypoglycemia; failure to thrive

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46
Q

What is McArdle disease (myopathic type)?

A

muscle phosphorylase deficiency; impaired muscle glycolysis to weakness/cramps

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47
Q

What is pompe disease (type II glycogenosis)?

A

lysosomal acid maltase deficiency; every organ, cardiomegaly; lethal by age 2

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48
Q

What are complex multigenic disorders?

A

greater than 2 genes (small effect); environment “unmasks” the genetic trail; type 2 diabetes: obesity + genetic risks

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49
Q

What are features of complex multigenic disorders?

A

increase number of inherited genes = increased risk; identical twins share risk, decrease with non-identical; first degree relative have similar risk; expression in 1 offspring, increase risk in siblings

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50
Q

What are cytogenetic disorders?

A

altered chromosomes have a large influence on bodily structure and function; 50% of 1st trimester spontaneous abortions (1:200 live births); 23 chromosomes (haploid, n)

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51
Q

What are cytogenetic disorder abnormalities?

A

numeric (monosomy 2n-1; aneuploid, trisomy, 2n+1); structural (breaks, deletions)

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52
Q

What is polyploid?

A

3n, 4n

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53
Q

What is a translocation?

A

transfer of a part of 1 chromosome to another chromosome

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54
Q

What is isochromosomes?

A

centromere divides horizontally, not vertically

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55
Q

What is robertsonian translocation?

A

centric fusion, chromosome lost

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56
Q

What are deletions?

A

loss of a portion of a chromosome

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57
Q

What are inversions?

A

2 interstitial breaks in a chromosome and the segment reunites after a complete turnaround

58
Q

What is a ring chromosome?

A

a variant of a deletion after loss of segments from each end of a chromosome, arms unite to form a ring

59
Q

Loss of genetic material is ______ severe

A

more (lethal)

60
Q

Gain of genetic material is ______ severe

A

less

61
Q

What are some examples of a gain in genetic material?

A

entire chromosome is a trisomy; part of a chromosome is robertsonian translocation

62
Q

cyogenetic disorders most commonly result from __________ alterations

A

spontaneous (de novo changes)

63
Q

What is an allosome?

A

sex chromosome; less severe, subtle phenotypic changes, infertility

64
Q

What is trisomy 21?

A

Down syndrome; body and brain (1:700); most common

65
Q

What is trisomy 13?

A

patau syndrome; cardiac and renal 1:15,000; microcephaly, lethal by age 1 (80%)

66
Q

What is Cri du chat syndrome?

A

cat like cry; fragmented 5th chromosome, 1:50,000; cognitive and motor dysfunction, drooling

67
Q

What is Down syndrome?

A

trisomy 21; most common chromosomal disorder (1:700); 95%: meiotic nondisjunction; 47 chromosome; increase maternal age; most common cause of severe mental retardation; cardiac malformations (40%); leukemia (20x)

68
Q

Up to 30% of people with Down syndrome have ____ ______ instability

A

atlanto-axial

69
Q

What is familial Down syndrome?

A

4% of cases; robertsonian translocation

70
Q

What is 22q11.2 deletion syndrome?

A

deletion of hand 11 on chromosome 22

71
Q

What are the two types of deletion syndromes?

A

DiGeorge syndrome and velocardiofacial syndrome

72
Q

What is DiGeorge syndrome?

A

Thymic hypoplasia: decrease T cell immunity (increase infections); parathyroid hypoplsia: hypocalcemia (tetany)

73
Q

What is velocardiofacial syndrome?

A

structural defects: cardiac, facial; mild immunodeficiency

74
Q

What are allosomal cytogenetic disorders?

A

allosome= sex chromosome (n23); more compatible with life; relatively minor

75
Q

What is the relatively minor allosomal cytogenetic disorders?

A

lyonization (x-inactivation: 1 female X chromosomes is inactivated, Barr body); very little info on y

76
Q

What are hallmark conditions for allosomal cytogenetic disorders?

A

Klinefelter syndrome; Turner syndrome

77
Q

What is Klinefelter syndrome?

A

greater than 2 chromosomes, greater than 1 Y (nondisjunction during meiosis); most common cause of male hypogonadism and sterility; 1:1,000 male births; gynecomastia (breast CA, increase 20x); risk is increased maternal age

78
Q

What are Turners syndrome?

A

most common from an absence of 1 X chromosome (45,x); loss of short (p) arm of X (partial or complete); short stature, amenorrhea (streak ovaries), neck webbing, androgynous female appearance; cubitus valgus

79
Q

What are single gene disorders with atypical inheritance?

A

don’t follow mendelian patterns; hallmark examples: triplet-repeat mutations, mutations in mitochondrial genes, genomic imprinting

80
Q

What are triplet repeat mutations?

A

AKA: trinucleotide repeat disorders; subset of microsatellite repeats, neurodegeneration

81
Q

What are mutations in mitochondrial genes?

A

enzymes for oxidative phosphorylation

82
Q

What is genomic imprinting?

A

epigenetic silencing of genes

83
Q

What is fragile x syndrome?

A

triple-repeat mutation (FMR1 mutation); x-linked, primarily affects males; familial mental retardation; macroorchidism (90%); 30-50% female carriers develop fragile x; grandpa to carrier daughter to grandson

84
Q

what is genetic anticipation?

A

features become more aggressive with each generation

85
Q

What are the ratios for fragile x syndrome for men and women?

A

males: 1:1,550; females: 1:8,000

86
Q

diseases caused by mutations in mitochondrial genes?

A

Rare; mitochondrial genes: strict maternal inheritance; hallmark: leber hereditary optic neuropathy; degeneration of retinal ganglia and CN II; loss of central vision, bilateral, progressive

87
Q

What are the types of genomic imprinting diseases?

A

Angelman syndrome and Prader-Willi syndrome

88
Q

What is angelman syndrome?

A

paternal imprinting and maternal deletion of 15q12 (laughter; “happy puppet syndrome”)

89
Q

What is a Prader-Willi syndrome?

A

maternal imprinting and paternal deletion of 15q12; obesity (hyperphagia)

90
Q

What are pediatric diseases?

A

pediatric: birth through age 17 years; infant, child, adolescent

91
Q

What are infant pediatric diseases?

A

birth through 1st year (neonate: birth through 4 weeks- highest risk)

92
Q

What are child pediatric diseases?

A

birth to puberty

93
Q

What are adolescent pediatric diseases?

A

puberty to adulthood

94
Q

What are congenital disorders?

A

3% of neonates: illness, disability, death (features: cosmetic to lethal)

95
Q

What is the leading cause of death in infants?

A

congenital malformations, chromosomal abnormality

96
Q

What is the leading cause of death for 1-14 years?

A

accidents

97
Q

What are features of congenital disorders?

A

polydactyly, cleft lip, tetralogy of fallot; stillbirth

98
Q

What are transcervical perinatal infections?

A

ascending; from vagina to cervix; most common is bacterial (strep)

99
Q

What are transplacental perinatal infections?

A

hematogenous (blood) spread; crosses placenta (mc) or transfusion at birth; TORCH infections

100
Q

What are the TORCH infections?

A

T: toxoplasma; O: other (treponema pallidum, HIV, HBV, TB, plasmodium falciparum); R: rubella virus; C: CMV; H: HSV

101
Q

What is prematurity restrictions?

A

less than 37 weeks gestations, 2nd MC cause of neonatal mortality (number 1 congenital defects)

102
Q

What are the small-for-gestational-age growth restrictions?

A

chromosomal disorders, fetal infection, placental factors, various maternal factors (MC)

103
Q

What are the terms of pregnancy?

A

pre-term: <37 weeks; early term: 37-38 weeks; full term: 39-40 weeks; late term: 41st week; post-term: ≥ 42 weeks

104
Q

What is respiratory distress syndrome?

A

immature lungs: decrease surfactant production; difficulty inflating alveoli (atelectasis); hyaline membrane disease; surfactant: type II pneumocytes, 1st breath

105
Q

What is necrotizing enterocolitis?

A

prematurity, enteral feeding (feeding tube); most common location, ileum, cecum, ascending colon; bloody stool to distention to circulatory collapse

106
Q

What is Sudden infant death syndrome?

A

most common 2-4 months; during sleep; 3rd most common cause of death during infancy; most common after first month

107
Q

What is the SIDS triple risk model?

A

vulnerable infant; critical developmental period for homeostatic control (1 month-1 year); decrease arousal or cardiorespiratory control

108
Q

What is fetal hydrops?

A

accumulation of edema, during gestation; stillborn, die within first few days after birth, complete recovery

109
Q

What is hydrops fetalis?

A

generalized edema, lethal

110
Q

What is cystic hygroma?

A

local edema, may not be lethal

111
Q

What are immune hydrops?

A

antibody induced hemolysis (incompatibility, rare to due Rh antibody prophylaxis)

112
Q

What is nonimmune hydrops?

A

most common; chromosomal abnormalities (45X; trisomies), cardiovascular defects

113
Q

What are pediatric tumors?

A

Cancer; 2nd most common cause of death from 4-14 years; 3 benign pediatric tumors

114
Q

What are the 3 types of benign pediatric tumors?

A

hemangioma, lymphangioma, and sacrococcygeal teratomas

115
Q

What is a hemangioma?

A

most common tumors of infancy; endothelial capillary tumor; infancy, self-resolves by age 7 years

116
Q

What are lymphangiomas?

A

lymphatic counterpart of hemangiomas; most common at neck, trunk, axilla

117
Q

What are sacrococcygeal teratomas?

A

most common germ cell tumors of childhood; 75% benign, ≤4 months old, MC external; 12% malignant, older children, lethal; 13% are “immature teratomas,” increase anaplasia= increase malignant potential

118
Q

What are pediatric malignant tumors?

A

differ from adult CA; teratogens, genetic abnormalities; spontaneously regress; more favorable prognosis

119
Q

What are 3 unique pediatric cancers?

A

neuroblastoma, retinoblastoma, wilms tumor

120
Q

What is a neuroblastoma?

A

malignant tumor, 98% sporadic

121
Q

Infantile malignancy is ______ neuroblastoma

A

50% (7-10% of pediatric CA)

122
Q

Neuroblastomas have homer-wright pseudo-rosettes. what are they?

A

neutrophils surrounded by tumor cells (90% secrete catecholamines)

123
Q

Which age group has a better prognosis for neuroblastoma?

A

younger (<18 months) have better prognosis

124
Q

What are features of neuroblastoma for children <2 years?

A

protuberant abdomen (tumor and edema), fever, cachexia, mets to skin (“blueberry muffin baby”)

125
Q

What are features of neuroblastomas for children >2 years?

A

may go unnoticed, until signs of metastasis; hepatomegaly, osseous pain, ascites (fluid in peritoneal cavity)

126
Q

Neuroblastomas metastasize via _________ and __________ systems

A

lymphoid and hematopoietic (liver, lungs, bone marrow); spontaneous resolution is common

127
Q

Retinoblastoma is malignant and is the MC _______ ___ malignancy

A

pediatric eye (post. retina)

128
Q

Retinoblastoma can be genetic or sporadic. Which is more common?

A

Sporatic (60%): sporadic RB1 mutation; isolated and unilateral tumors
(genetic 40%: inherited RB1 mutation; MC multiple bilateral tumors; Risk: osteosarcoma, other soft tissue tumors

129
Q

Retinoblastoma incidence ______ with age (MC age __ years)

A

decreases; 2

130
Q

What are unique characteristics for retinoblastoma?

A

may be congenital; risk of other primary tumors (RB mutation, TSG); may spontaneously regress

131
Q

the nodular mass for retinoblastomas is on the ____ retina

A

posterior

132
Q

Retinoblastoma mets to _______ _____, via optic nerve

A

subarachnoid space (METS: CNS, calvarium, peripheral osseous structures, lymphatic system)

133
Q

Retinoblastomas have flexner-wintersteiner rossettes. What are they?

A

cuboidal cells surrounding empty lumen

134
Q

Retinoblastomas has a characteristic called the ____ ____ reflex

A

cat eye

135
Q

What is wilms tumor (nephroblastoma)?

A

malignant; MC pediatric kidney tumor, 2-5 years old

136
Q

Wilms tumor is an enormous tumor + other congenital malformations. What are some symptoms of wilms?

A

abdominal pain, fever, hematuria; palpable mass

137
Q

What is WAGR syndrome? (wilms tumor)

A

W= wilms; A= aniridia, G= genitourinary, R= mental retardation

138
Q

What are other syndromes associated with wilms tumor?

A

denys-drash-syndrome (DDS) and beckwith wiedemann syndrome

139
Q

Does wilms tumor have a good or bad prognosis?

A

good prognosis (treatment with nephrectomy and chemotherapy)

140
Q

What are prenatal indications for genetic analysis?

A

any increase risk of chromosomal abnormality; maternal age >34 years, chromosomal abnormality in previous child, carrier of x-linked condition; amniocentesis, umbilical cord blood, or biopsy

141
Q

What are postnatal indications for genetic analysis?

A

congenital anomalies, mental retardation, developmental delay, history of multiple spontaneous abortions, infertile offspring; peripheral blood lymphocytes

142
Q

What are congenital disorders?

A

present at birth (not always inherited)

143
Q

What are hereditary disorders?

A

inherited in germ line; transmitted to offspring; genetic, familial

Pathology (3 decks)

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