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Lysosomal Storage Diseases Mnemonics – YouTube
Lysosomal storage diseases (LSDs) are a group of rare inherited metabolic disorders that result from defects in lysosomal function.
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Date Published: 4/1/2022
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Lysosomal Storage Disease | Easy Mnemonic – YouTube
Lysosomal storage diseases, deficient enzymes, & accumulated substrates are demonstrated as a simple mnemonic in this veo.
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Lysosomal Storage Disorders Made Easy | Epomedicine
Mnemonic: Tay-Sach’s and Niemann-Pick’s both are hyphenated and have cherry red spots as feature. Remember: Cherry red spots is not a feature of …
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Lysosomal Storage Disease Mnemonics – My Notes for USMLE
Lysosomal Storage Disease Mnemonics · “A Fabulous Alpha-Male that breaks the hearts of 3 fragile women by peeing on them” · “It’s gauche to glue …
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Lysosomal Storage Disorders – Biochemistry for Medicine
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Lysosomal storage diseases – Knowledge @ AMBOSS
Lysosomal storage diseases are a group of inherited metabolic disorders caused by a deficiency of specific enzymes.
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Lysosomal Storage Disease – visual aid/mnemonic : r/step1
Lysosomal Storage Disease – visual a/mnemonic. Hello guys,. Would anybody point out way to remember these diseases?
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주제에 대한 기사 평가 lysosomal storage disease mnemonic
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What is the most common lysosomal storage disease?
Gaucher Disease Types I, II, and III: Gaucher disease is the most common type of lysosomal storage disorder. Researchers have identified three distinct types of Gaucher disease based upon the absence (type I) or presence and extent of (types II and III) neurological complications.
What is Fabry disease?
Fabry disease is a rare inherited disorder of glycosphingolipid (fat) metabolism resulting from the absent or markedly deficient activity of the lysosomal enzyme, α-galactosidase A (α-Gal A). This disorder belongs to a group of diseases known as lysosomal storage disorders.
What is GSD disease?
Glycogen storage disease (GSD) is a rare metabolic disorder where the body is not able to properly store or break down glycogen, a form of sugar or glucose. GSD affects the liver, muscles and other areas of the body, depending on the specific type.
What enzyme causes lysosomal storage disease?
Tay-Sachs disease: This is caused by a lack of the enzyme hexosaminidases A (Hex-A). This enzyme breaks down a fatty substance called GM2 ganglioside in brain cells.
What is Tay-Sachs disease specifically?
Overview. Tay-Sachs disease is a rare genetic disorder passed from parents to child. It’s caused by the absence of an enzyme that helps break down fatty substances. These fatty substances, called gangliosides, build up to toxic levels in the brain and spinal cord and affect the function of the nerve cells.
Is PKU a lysosomal storage disease?
The first widely utilized newborn screen for a genetic disease did not detect a lysosomal storage disease; rather, it tested for phenylketonuria (PKU), a genetic disorder caused by the inability to break down an amino acid called phenylalanine. Amino acids are the building blocks of proteins.
What mimics Wilson’s disease?
Primary neurologic disorders that can mimic Wilson disease include essential tremor, young onset Parkinson’s disease, focal and generalized dystonias.
What causes gauchers disease?
Gaucher disease is passed down from parents to children (is inherited). It is caused by a problem with the GBA gene. It is an autosomal recessive disorder. This means that each parent must pass along an abnormal GBA gene for their child to get Gaucher.
What is Lumicin?
Factual errors. Lumicin is not, as stated, an enzyme replacement drug for people with a liver disease, but a class of “bacteriocins”, bacteria-killing proteins (lumicins).
What are the different mucopolysaccharidoses?
Mucopolysaccharidosis type I (MPS I) is a condition that affects many parts of the body. This disorder was once divided into three separate syndromes: Hurler syndrome (MPS I-H), Hurler-Scheie syndrome (MPS I-H/S), and Scheie syndrome (MPS I-S), listed from most to least severe.
What are Sphingolipidoses?
Sphingolipidoses are human metabolic storage disorders characterize]d by the accumulation of harmful quantities of glycosphingolipids and phosphosphingolipids. These lipids have in common a hydrophobic portion of their structure called ceramide.
Is Hunter syndrome fatal?
No cure is available for Hunter syndrome. The most severe cases can be life-threatening, with life expectancy typically between 10 and 20 years. People with mild cases of the disease typically live longer into adulthood.
How do you get Pompe disease?
Pompe disease is inherited in an autosomal recessive pattern. Recessive genetic disorders occur when an individual inherits a non-working gene from each parent. If an individual receives one working gene and one non-working gene for the disease, the person will be a carrier for the disease.
NORD (National Organization for Rare Disorders)
Although the signs and symptoms vary from disease to disease in this group, symptoms occur in each case because of an enzyme deficiency that inhibits the ability of the lysosomes present in each of the body’s cells to perform their normal function. The lysosomes function as the primary digestive units within cells. Their function is to break down complex components into simpler ones. Each cell has hundreds of lysosomes that degrade complex cellular components such as proteins (substrates) into simpler components. When this process does not take place, the substrate begins to accumulate in the cells. That is why these diseases are called “storage diseases”. The symptoms of lysosomal storage disorders are generally progressive over a period of time.
This report gives an overview of lysosomal storage diseases as a group. For more specific information on any particular disease in this group, consult the NORD report on that topic.
Some lysosomal storage diseases and a few of their characteristic signs and symptoms are as follows:
Aspartylglucosaminuria: Patients appear normal for several months after birth and then present with recurrent infections, diarrhea, and hernias. Later, there may be a gradual coarsening of facial features, an enlarged tongue (macroglossia) and enlargement of the liver (hepatomegaly).
Batten Disease: Batten disease is the juvenile form of a group of progressive neurological disorders known as neuronal ceroid lipofuscinoses (NCL). It is characterized by the accumulation of a fatty substance (lipopigment) in the brain, as well as in tissue that does not contain nerve cells. Batten disease is marked by rapidly progressive vision failure (optic atrophy) and neurological disturbances, which may begin before eight years of age. Occurring mostly in families of Northern European Scandinavian ancestry, the disorder affects the brain and may cause deterioration of both intellect and neurological functions.
Cystinosis: The early signs of this disorder typically involve the kidneys and the eyes. Excessive storage of the amino acid cystine in all cells of the body results in impaired kidney function, increased sensitivity to light, and marked growth retardation. There are infantile (the most common and most severe), juvenile, and adult forms, each with associated symptoms.
Fabry Disease: The symptoms of Fabry disease usually begin during early childhood or adolescence but may not become apparent until the second or third decade of life. Early symptoms include episodes of severe burning pain in the hands and feet. Other early signs may include a decrease in sweat production, discomfort in warm temperatures, and the appearance of a reddish to dark blue skin rash, especially in the area between the hips and knees. These skin lesions may be flat or raised, and some people may not have them at all.
Gaucher Disease Types I, II, and III: Gaucher disease is the most common type of lysosomal storage disorder. Researchers have identified three distinct types of Gaucher disease based upon the absence (type I) or presence and extent of (types II and III) neurological complications. Most affected individuals have type I, and they may experience easy bruising, chronic fatigue, and an abnormally enlarged liver and/or spleen (hepatosplenomegaly). Gaucher disease type II occurs in newborns and infants, and is characterized by neurological complications that may include involuntary muscle spasms, difficulty swallowing and the loss of previously acquired motor skills. Gaucher disease type III appears during the first decade of life. Neurological complications may include mental deterioration, an inability to coordinate voluntary movements, and muscle spasms of the arms, legs, or entire body.
Glycogen Storage Disease II (Pompe Disease): Pompe disease has an infantile form and a delayed onset form. The delayed onset form may be further broken down into a childhood form and a juvenile/adult form. Patients with the infantile form are the most severely affected. Although these infants usually appear normal at birth, the disease presents within the first two to three months with rapidly progressive muscle weakness, diminished muscle tone (hypotonia) and a type of heart disease known as hypertrophic cardiomyopathy. Feeding problems and respiratory difficulties are common. The childhood form presents during infancy or early childhood. Motor milestones may be delayed and some symptoms may resemble muscular dystrophy. The cardiac enlargement that is often present in the infantile form is seldom seen in the childhood form. The juvenile/adult form presents between the first and seventh decades as a slowly progressive muscle weakness or with symptoms of respiratory insufficiency. There is no cardiac involvement with this form.
GM2-Gangliosidosis Type I (Tay Sachs Disease): Two main forms of Tay Sachs disease exist: the classic or infantile form and the late-onset form. In individuals with infantile Tay Sachs disease, symptoms typically first appear between three and five months of age. These may include feeding problems, general weakness (lethargy), and an exaggerated startle reflex in response to sudden loud noises. Motor delays and mental deterioration are progressive. In individuals with the late-onset form, symptoms may become apparent anytime from adolescence through the mid-30s. The infantile form often progresses rapidly, resulting in significant mental and physical deterioration. A characteristic symptom of Tay Sachs disease, which occurs in 90 percent of cases, is the development of cherry red spots in the backs of the eyes. Symptoms of late-onset Tay Sachs disease vary widely from case to case. This disorder progresses much more slowly than the infantile form.
GM2-Gangliosidosis Type II (Sandhoff Disease): The first symptoms of Sandhoff disease typically begin between the ages of three and six months. The disease is clinically indistinguishable from GM2-Gangliosidosis Type I.
Metachromatic Leukodystrophy: Early signs and symptoms may be vague and gradual, making this disorder difficult to diagnose. Unsteadiness when walking is often the first symptom observed. Occasionally, the earliest symptom is developmental delay or deteriorating school performance. Over time, symptoms may include marked spasticity, seizures, and profound mental retardation.
Mucolipidosis Types I, II/III and IV: Mucolipidosis I, also known as sialidosis, has juvenile and infantile forms (sialidosis type I and sialidosis type II). Sialidosis type I usually becomes apparent during the second decade of life with the advent of sudden involuntary muscle contactions, the appearance of red sopts (cherry-red macules) in the eyes, and/or other neurological findings. Sialidosis type II may begin during infancy or later and is characterized by the same visual characteristics as sialidosis type I, as well as other symptoms such as mildly coarse facial features, skeletal malformations, and/or mild mental retardation. Symptoms of ML II, also known as I-cell disease, typically become apparent during infancy and include abnormalities of the skull and face, growth failure, and/or mental retardation. Type III, also known as pseudo-Hurler disease, is characterized by stiffness of the hands and shoulders with later development of carpal tunnel syndrome, deterioration of hip joints, scoliosis, and short stature. ML IV is characterized by mental retardation, greatly reduced ability in the acquisition of skills requiring the coordination of muscular and mental activities, corneal clouding, retinal degeneration, and diminished muscle tone.
Mucopolysaccharide Storage Diseases (Hurler Disease and variants, Hunter, Sanfilippo Types A,B,C,D, Morquio Types A and B, Maroteaux-Lamy and Sly diseases): The MPS diseases are caused by disturbances in the normal breakdown of complex carbohydrates known as mucopolysaccharides. All of the MPS diseases have certain characteristics in common, which include deformities of the bones and joints that interfere with mobility and often cause osteoarthritis, especially of the large, weight-bearing joints. All of the MPS diseases except Sanfilippo disease interfere with growth, causing short stature.
Niemann-Pick Disease Types A/B, C1 and C2: Niemann-Pick disease is a group of inherited disorders related to fat metabolism. Certain characteristics common to all types include enlargement of the liver and spleen. Children with Niemann-Pick disease, types A or C, also experience progressive loss of motor skills, feeding difficulties, progressive learning disabilities, and seizures.
Schindler Disease Types I and II: Type I, the classical form, first appears during infancy. Affected individuals appear to develop normally until approximately one year of age, when they begin to lose previously acquired skills that require the coordination of physical and mental activities. Type II is the adult-onset form. Symptoms may include the development of clusters of wart-like discolorations on the skin, permanent widening of groups of blood vessels causing redness of the skin in affected areas, relative coarsening of facial features, and mild intellectual impairment.
Lysosomal Storage Disorders Made Easy
Among the common lysosomal storage disorders:
Two of them are Mucopolysaccharidoses (Hunter and Hurler syndrome) Pompe’s disease is Glycogen Storage Disease. Others are Sphingolipidoses.
Inheritance of Lysosomal Storage Diseases
All are inherited as Autosomal Recessive (AR) condition except:
Hunter syndrome (X-linked recessive) Fabry’s disease (X-linked recessive)
Higher risk in Ashkenazi Jews
Mnemonic: Ashkenazi Jews Drink TaNG
Tay-Sach’s disease Niemann Pick’s disease Gaucher’s disease
Enzyme Defects in Lysosomal Storage Diseases
I couldn’t create any mnemonics that could help me remember the enzymes involved in Lysosomal Storage Disease. I thought, best would be to memorize them:
Lysosomal storage disorders Enzyme deficiency Accumulating substance Tay-Sachs disease Hexosaminidase A GM2 ganglioside Niemann-Pick disease Sphingomyelinase Sphingomyelin Gaucher’s disease Glucocerebrosidase Glucocerebroside Fabry disease Alpha-Galactosidase A Ceramide trihexoside Metachromatic leukodystrophy Arylsulfatase A Sulfatides Krabbe’s disease (Globoid cell leukodystrophy) Beta-Galactocerebrosidase (Galactosylceramidase) Galactocerebroside Hurler syndrome (Type I MPS) Alpha-L-iduronidase Dermatan and Heparan sulfate Hunter syndrome (Type II MPS) Iduronosulfate sulfatase Dermatan and Heparan sulfate
Few mnemonics:
HurLer syndrome: α-L-iduronidase HunTer syndrome: Iduronate sulfaTase Fabry’s disease: alpha-galactosidase A (Fabulous Alpha–Guy) Beta-galactosidase is deficient in GM1 gangliosidosis. Gaucher’s disease: Glucocerebrosidase (G for G) Niemann-Pick’s disease: Sphingomyelinase (Spi–N or No-Man Picks his nose with sPhinger) Metachromatic leukodystrophy: Arylsulfatase (Ar–Med) Krabbe’s disease: Beta-galactocerebrosidase Tay-Sach’s disease: Hexosaminidase A (taysaX lacks heXosaminidase A) Gaucher’s have “U” hence, lacks Glucocerebrosidase and Krabbe’s don’t have “U” hence, lacks Galactocerebrosidase.
Hurler vs Hunter Syndrome
The mode of inheritance and enzymes involved are different as mentioned earlier. Besides, other differences are:
Hunter needs eyes to shoot: Hence, eyes are spared in Hunter syndrome while, corneal clouding is a feature of Hurler’s syndrome. Hunter’s are brainier: Mental retardation is seen in both but is more severe in Hurler syndrome. Gargoyle’s Hurl balls of fire: Gargoylism (Gargoyle facies is a feature of Hurler syndrome).
Hepatosplenomegaly is due to accumulation of dermatan and heparan sulfate and seen in both.
Other important facts: Mental retardation is absent in Morquio’s syndrome (MPS type IV). All mucopolysaccharidosis except San-fillipo syndrome cause growth retardation and short stature. Scheie is the mildest, Hurler-Scheie is intermeidate and Hurler syndrome is the severest form of MPS I.
Cherry-Red Spots in Sphingolipidoses
Tay-Sach’s Disease (GM2 gangliosidsosis type I) Niemann-Pick’s disease Metachromatic leukodystrophy Sandhoff disease (Globose accumulation due to lack of Hexosaminidase A and B preventing conversion of Globose into Ceramide trihexoside; GM2 gangliosidosis type II) Farber’s disease (not Fabry’s disease !!! – lack of Acid ceramidase intervening conversion of ceramide into Sphingosine) GM1 gangliosidosis (deficient beta-galactosidase blocking the conversion of GM1 ganglioside to GM2 ganglioside).
Mnemonic: Tay-Sach’s and Niemann-Pick’s both are hyphenated and have cherry red spots as feature. Remember: Cherry red spots is not a feature of Fabry’s and Gaucher’s disease.
Hepatosplenomegaly in Sphingolipidoses
Hepatosplenomegaly is present in those with cherry-red spots except: Tay-Sach’s disease and Metachromatic leukodystrophy Gaucher’s disease
Remember: Hepatosplenomegaly is not a feature of Tay-Sach’s disease and Fabry’s disease.
CNS involvement in Sphingolipidoses
CNS involvement is not a feature of Gaucher’s disease type I (most common form). However, type II and III do present with CNS involvement.
Hepatosplenomegaly CNS symptoms and Cherry red spot + – + Niemann-Pick’s Gaucher’s – Tay-Sach’s Something else
Macrocephaly and Microcephaly
Macrocephaly: Tay-Sach’s disease Microcephaly and Optic atrophy: Krabbe’s disease (Globoid cell leukodystrophy)
Fabry’s disease
Mnemonic: FABRy
Fabry’s disease cause:
Angiokeratomas on skin and Acroparesthesis Blood vessel: Hypertensoin Renal failure
Cells in Sphingolipidoses
Niemann-Pick’s disease: Zebra bodies (Distended lysosomes containing lamellated figures in Electron Microscopy), Foam cells/macrophages Gaucher’s disease: Gaucher cells/macrophages (crumpled tissue paper appearance) Tay-Sach’s disease: Onion-skin layers of whorled membrane within lysosomes (Electron microscopy) Krabbe’s disease (Globoid cell leukodystrophy): multinucleated Globoid cells Metachromic leukodystrophy: PAS + macrophages, Hirsh-Peiffer reaction (Sulfatides bind to cresyl violet and gives brown color instead of purple, i.e. metachromasia).
He is the section editor of Orthopedics in Epomedicine. He searches for and share simpler ways to make complicated medical topics simple. He also loves writing poetry, listening and playing music.
My Notes for USMLE
highyieldandclassicpresentation:
“A Fabulous Alpha-Male that breaks the hearts of 3 fragile women by peeing on them”
Fabry’s Disease results in cardiovascular (hearts) and renal (peeing) disease, due to a lack of (alpha male), alpha-galactosidase A and accumulation of Ceramide Trihexoside (Three fragile women)
“It’s gauche to glue things into your bones with tissue paper.”
Gaucher’s Disease causes hepatosplenomegaly and aseptic necrosis of femur, bone crises (bones) due to deficiency of Glucocerebrosidase.
I’m also partial to the following mnemonic: “Glucose is so gauche. Carrying a big liver around? That’s really tacky, just get a purse. Go hide and cry into some crumpled tissues.”
Gauche for Gaucher’s, hepatosplenomegaly, macrophages look like crumpled tissue paper, glucocerebroside accumulates.
“I hope No man picks his bloody foaming nose with his sphinger” (Courtesy of First Aid 2013)
Niemann-Pick Disease causing progressive neurodegeneration and hepatosplenomegaly, with both a cherry-red spot on macula (bloody) and foam cells (foaming nose), due to a lack of Sphingomyelinase (Sphinger), causing accumnulated sphingomyelin.
causing progressive neurodegeneration and hepatosplenomegaly, with both a cherry-red spot on macula (bloody) and foam cells (foaming nose), due to a lack of Sphingomyelinase (Sphinger), causing accumnulated sphingomyelin. The ‘I Hope’ prefix is to indicate hepatosplenomegaly, which differentiates from the other cherry-red spot in macula disease, Tay-Sachs.
“I put my sachs of onions and cherries in the back of my GM truck. I sure hope they don’t get hexed.”
Tay Sachs – Lysosomes with onion skin, hexosaminidase A is deficient, GM2 gangloside is what accumulates, and of course – cherry red spot.
“I’m Krabbe because I can’t see the globes in the Galaxy.”
Krabbe’s Disease causes optic atrophy (can’t see), globoid cells and galaxy for galacto
“Aryl had many colorful and cerebral brothers, they made him clumsy and crazy.”
Metachromatic Dystrophy – Arylsulfatase A is messed up, cerebroside sulfate accumulates, it has ataxia and dementia. Colorful is for metachromatic.
“Hurlers ran around in a daze, they couldn’t see or breathe”. “When you run hard hard you hurl, you’re bent over and can’t breathe, and you take off your lid to see.”
Hurler’s Syndrome – Results in developmental delay, gargolyism (bent over), airway obstruction (can’t breathe), corneal clouding (can’t see) and hepatosplenomegaly. Results to a deficiency in a-L-iduronase, accumulating heparan and dermatan sulfate.
“They are aggressive hunters who see clearly and hit the x with their arrows.”
Hunter’s Disease manifests with aggressive behavior, no corneal clouding, and is X-linked Recessive inherited. It’s due to a lack of iduronate sulfase, and an accumulation of heparan and dermatan sulfate.
CREDITS
Lysosomal Storage Disorders in Nutrition & Metabolism
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Lysosomal storage diseases
Mucopolysaccharidoses are a group of metabolic disorders that result in the impaired breakdown of glycosaminoglycans (previously known as mucopolysaccharides), due to mutations in lysosomal enzymes. At least nine different types of mucopolysaccharidosis have been identified. The two most common conditions are Hurler syndrome and Hunter syndrome. [13][14]
“Hunters with good eyesight will catch the aggressive chupacabra active in TeXas:” Hunter syndrome (no corneal clouding, aggressive behavior, carpal tunnel syndrome, hyperactivity, and X-linked recessive inheritance).
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