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Genetic Disorders

The document outlines various genetic disorders categorized into autosomal recessive, autosomal dominant, sex-linked, and special categories. Each disorder includes information on the associated gene/locus, pathogenesis, and clinical diagnostic keys. Key examples include Sickle Cell Anemia, Marfan Syndrome, and Duchenne Muscular Dystrophy.
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0% found this document useful (0 votes)
4 views4 pages

Genetic Disorders

The document outlines various genetic disorders categorized into autosomal recessive, autosomal dominant, sex-linked, and special categories. Each disorder includes information on the associated gene/locus, pathogenesis, and clinical diagnostic keys. Key examples include Sickle Cell Anemia, Marfan Syndrome, and Duchenne Muscular Dystrophy.
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

I.

Autosomal Recessive Disorders


General Rule: Often involves "Loss of Function" in enzymes. Onset is usually early in childhood.

Disease Gene/Locus Detailed Pathogenesis Clinical & Diagnostic Keys


$\beta$- HBB (11p15) Point mutations in promoter or splicing sites Target cells, "Crew-cut"
Disease Gene/Locus Detailed Pathogenesis Clinical & Diagnostic Keys
thalassaemia → low $\beta$-globin → unpaired $\alpha$- appearance on skull X-ray,
chains precipitate, damaging RBC membrane. Chipmunk facies.
Howell-Jolly bodies,
Glutamic acid $\rightarrow$ Valine at
Sickle Cell Anemia HBB (11p15) autosplenectomy (by age
position 6. Deoxygenated HbS polymerizes.
5), dactylitis.
Phe508 deletion → misfolded protein Meconium ileus in
Cystic Fibrosis CFTR (7q31) degraded in ER → no $Cl^-$ secretion newborns, Pseudomonas
$\rightarrow$ thick mucus. infections, Nasal polyps.
Kayser-Fleischer rings,
Defect in copper-transporting ATPase →
ATP7B low serum ceruloplasmin,
Wilson’s Disease failure to incorporate copper into
(13q14) basal ganglia
ceruloplasmin.
degeneration.
Prussian blue stain
Mutation (C282Y) → low Hepcidin levels →
Hemochromatosis HFE (6p22) positive in liver, "Bronze
uncontrolled iron absorption.
Diabetes," Arthropathy.
Severe sunburn,
Xeroderma Defective Nucleotide Excision Repair (NER);
XP genes telangiectasia, 1000x
Pigmentosum cannot repair pyrimidine dimers.
increased skin cancer risk.
Ochronosis (blue-black
Homogentisate 1,2-dioxygenase deficiency
Alkaptonuria HGD (3q) cartilage), urine turns
$\rightarrow$ high Homogentisic acid.
black on exposure to air.
Phenylalanine hydroxylase deficiency Musty/Mousy odor,
PKU PAH (12q) $\rightarrow$ Phenylalanine converted to intellectual disability,
phenylketones. microcephaly.

II. Autosomal Dominant Disorders


General Rule: Often involve structural proteins or receptors. Shows "Vertical Inheritance" (every generation
affected).

Disease Gene/Locus Detailed Pathogenesis Clinical & Diagnostic Keys


Familial Two-hit hypothesis; mutation in a tumor 100% progress to colon
APC (5q21)
Adenomatous suppressor gene regulating Wnt signaling. cancer; requires
Disease Gene/Locus Detailed Pathogenesis Clinical & Diagnostic Keys
Polyposis prophylactic colectomy.
Polycystin defect affects primary cilia Bilateral large kidneys,
Adult Polycystic PKD1 (16p) /
sensing $\rightarrow$ overproliferation of Berry aneurysms (Circle
Kidney (ADPKD) PKD2 (4q)
tubular cells. of Willis), Liver cysts.
Mutation in Neurofibromin (a GAP) Lisch nodules (iris), Cafe-
Neurofibromatosis 1 NF1 (17q11) $\rightarrow$ persistent RAS activation au-lait spots, optic
$\rightarrow$ cell growth. gliomas.
Subluxation of lens
Fibrillin-1 defect $\rightarrow$ TGF-
(upward), Aortic
Marfan Syndrome FBN1 (15q21) $\beta$ signaling dysregulation
dissection, Pectus
$\rightarrow$ weak elastic fibers.
excavatum.
Increased MCHC, positive
Hereditary Defect in Ankyrin/Spectrin → loss of
ANK1 (8p) Osmotic Fragility test,
Spherocytosis membrane → RBCs become spheres.
Splenomegaly.
Gain-of-function mutation → inhibits
Short limbs, frontal
Achondroplasia FGFR3 (4p16) chondrocyte proliferation at growth
bossing, trident hand.
plates.
Blue sclera, multiple
fractures, dental
Osteogenesis Qualitative or quantitative defect in Type 1
COL1A1/2 opalescence
Imperfecta Collagen (triple helix).
(Dentinogenesis
imperfecta).

III. Sex-Linked (X-Linked) Disorders


General Rule: Recessive forms affect males (XY). Dominant forms affect both but are often lethal in males.

Disease Type Mechanism Clinical & Diagnostic Keys


Gowers' sign,
Duchenne Muscular X-L Frameshift mutation $\rightarrow$ total
pseudohypertrophy of calves,
Dystrophy Rec. absence of Dystrophin (anchors muscle).
elevated Creatine Kinase.
X-L Factor VIII deficiency Increased PTT, normal
Hemophilia A
Rec. $\rightarrow$ failure of intrinsic PT/Bleeding time. Hemarthrosis.
pathway.
Low NADPH $\rightarrow$ low Reduced
X-L Heinz bodies and Bite cells on
G6PD Deficiency Glutathione $\rightarrow$ RBCs cannot
Rec. peripheral smear.
buffer $H_2O_2$.
Absent B-cells and Tonsils;
Bruton’s X-L Defect in BTK (tyrosine kinase)
recurrent bacterial infections
Agammaglobulinemia Rec. $\rightarrow$ B-cells don't mature.
after age 6mo.
NADPH Oxidase defect Negative Nitroblue Tetrazolium
Chronic Granulomatous X-L
$\rightarrow$ lack of superoxide (NBT) test; catalase (+)
Disease Rec.
radicals. infections.
X-L CGG trinucleotide repeat expansion in Large ears, long face,
Fragile X Syndrome
Rec. FMR1 gene. macroorchidism (large testes).

IV. Special Categories (Codominant & Mitochondrial)


Disease Inheritance Mechanism Clinical Key
$\alpha$ 1- Misfolded protein (PiZ allele)
PAS-positive globules in liver;
antitrypsin Codominant accumulates in ER of
Panacinar emphysema in lungs.
deficiency hepatocytes.
Permanent bilateral loss of central
Leber Hereditary Mutations in NADH
Mitochondrial vision; strictly maternal
Optic Neuropathy dehydrogenase (ETC Complex I).
inheritance.

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