Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

USMLE 1 > Easily forgettable diseases > Flashcards

Easily forgettable diseases Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

Hartnup disease

A

Auto recessive
deficiency in neutral a.a. transporters in proximal tubule and on enterocytes.
Neutral aminoaciduria (tryptophan) –> niacin deficiency
Pellagra-like symptoms (dementia, diarrhea, dermatitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Osler-Weber-Rendu syndrome

A

Aka hereditary hemorrhagic telangiectasia
auto dom
disorder of BV leading to telangiectasia, reccurent nose bleeds (epistaxis), skin discolration, AV molformations, GI bleeding, hematuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Von recklinghausen’s disease AKA

A

NF1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

tuberous sclerosis

A 
neurocutaneous disorder with multi-organ system involvement. Numerous benign hamartomas. 
angiofibromas
visceral cysts
cutaneous angiofibromas
auto dom
ash leaf spots
rhabdomyomas
shagreen patches
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sturge-Weber syndrome

A

non inherited
congenital
anomaly of neural crest derivatives due to mutation in GNAQ gene. Affects small BV -> port wine stain on face. Ipsilateral leptomeningeal angioma
seizures, epilepsy
intellectual disability
episcleral hemangioma -> increased intraocular pressure -> early onset glaucoma
skull - tram track calcifications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Plummer-Vinson syndrome

A

triad of iron deficiency anemia, esophageal webs, and atrophic glossitis
(webs cause dysphagia, which is often seen in iron deficiency anemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

issue with scurvy

A

no vitamin c to hydroxylate lysine and proline on collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Problem with osteogenesis imperfecta

A

problem with forming the triple helix of collagen during the glycosylation step

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

problem with ehlers danlos syndrome

A

problems with cross linking of collagen outside of the fibroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

menkes disease

A

connective tissue disease
impaired copper absorption and transport
decreased activity of lysyl oxidase (which needs Cu) for collagen synthesis
brittle, kinky hair, growth retardation, hypotonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

defect in marfan

A

defect in fibrillin which forms a sheath around elastin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Signs of Prader willi

A

hyperphagia, obesity, intellectual disability, hypogonadism, hypotonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

signs of angelman syndrome

A

inappropriate laughter, seizures, ataxia, intellectual disability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

gene mutation in familial adenomatous polyposis

auto rec or dom?

A

APC gene

auto dom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hungtington disease - repeat? chromosome number?

A

CAG, chrom 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CHromosome number for FAP

A

chromosome 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

gene association with MEN2A and B

A

Ret

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

NF1 chromosome and symptoms

A

Chrom 17
cafe au lait spots, cutaneous neurofibroms (schwann cells, neural crest)
Auto dom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

NF2, chrom # and symtpoms

A

Chrom 22

bilateral acoustic schwannomas, juvenile cataracts, meningiomas, ependymomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

tuberous sclerosis, inheritance and symptoms

A

auto dom

hamartomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what happens with the mutated protein of CF

A

misfolded protein due to impaired post translational processing –> protein retained in RER, not transported to cell membrane. May got to proteasome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

TYpe of mutation for duchenne

A

x linked recessive, frameshift mutation of dystrophin protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

type of mutation for becker muscular dystrophy

A

x linked recesssive, point mutation in dystrophin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

repeat for mytonic type I MD. SYmptoms and characteristics

A

CTG
expansion of DMPK gene -> abnormal expression of myotonin protein kinase –> myotonia, muscle wasting, frontal balding, cataracts, testicular atrophy, arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Fragile x

mutation, symptoms

A

CGG repeat of FMR1 gene, x linked

post pubertal macroorchidism, long face with large jaw, large everted ears, autism, MVP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cri-du-chat

A

microdeletion of short arm of chrom 5

microcephaly, intellectual disability, high pitched crying, epicanthal folds, cardiac abnormalities (VSD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Williams syndrome

A 
Microdeletion of long arm chrom 7
elfin facies, intellectual disability, hypercalcemia
well developed verbal skills
extreme friendliness with strangers
CV problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

22q11 deletion

A 
catch -22
Cleft palate
abnormal facies
thymic aplasia
cardiac defects
hypocalcemia (parathyroid aplasia)

seen with Digeorge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

CHronic granulomatous disesase enzyme

A

NADPH oxidase (converts O2 to superoxide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are people with CGD more susceptible to?

A

Bacteria with catalase. Patients can still make H2O2 to destory bacteria, unless the bacteria have catalase which can destory H2O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

most common human enzyme deficiency

A

G6PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what types of cells are seen in G6PD deficiency

A

bite cells (phagolytic removal of heinz bodies by splenic macrophages)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how are heinz bodies produced

A

G6PD deficiency -> increased hemolysis and ROS damage –> oxidized Hb in RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

essential fructokinase

A

not as bad as fructose intolerance. Defect in fructokinase -> no conversion of fructose to frucose1P.
Auto recessive
benign, increased fructose in urine and blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

frucotse intolerance

A

no aldolase B -> no conversion of fructose 1P to downstream molecules.
Increased fructose 1p -> wasted phosphates -> less available for gluconeogenesis and glycogenolysis.
hypoglycemia, jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what substance need decreased intake in frucotse intolereance

A

fructose and sucrose (frucoste + glucose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

subunits of lactose

A

galactose + glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

subunits of maltose

A

2 glucose molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

galactokinase deficiency

A 
no conversion of galactose to galctose 1P. Increased levels of galactitol (by aldose reductase). 
fairly benign
infantile cataracts (no social smile or tracking of objects)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Classic galactosemia

A

No galactose 1 phosphage uridyltransferase. No conversion of galactose1p to glucose 1 p.
Accumulation of galactitiol -> cataracts
FTT, jaundice, hepatospleno, intellectual disability.
Increased waste of phosphate -> no gluconeogenesis or glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

treatment for classic galactosemia

A

decreased galactose and lactose (galactose + glucose) from diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Hyperammonemia causes what with the energy cycles?

A

Increased NH4 leadsto depletion of alpha-ketoglutarate -> inhibition of TCA cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Required cofactor for CPSI of the urea cycle

A

N-acetylglutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Ornithine transcarbamylase deficiency

A

Urea cycle enzyme.
X linked recessive
can’t eliminate NH3
carbamoyl gets converted to orotic acid instead of citruiline. Orotic acid part of pyrimidine synthesis pathway.
Increased orotic acid in blood and urine. Decreased BUN, increased NH3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

orotic aciduria

A 
inability to convert orotic acid to UMP (pyrimidine synthesis pathway) due to defect in UMP synthase. 
autosomal recessive
megaloblastic anemia
No hyperammonemia (unlike OTC deficiency)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Phenylketonuria

A

decreased phenylalanine hydroxylase (phenyl -> tyrosine) or due to decreased tetrahydrobiopterin cofactor.
intell. disability, growth retard, seizures, fair skin, eczema, musty body odor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what compound must PKU patients avoid

A

aspartame, artificial sweetener

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

alkpatonuria

A

deficiency in homogentisate oxidase (tyrosine –> homogentisic acid -> maleylacetoacetic acid.
Increased homogentisic acid.
dark connective tissues, brown sclera, black urine
arthralgias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

three ways to get homocystinuria

A
  1. cystathionine synthase deficiency (homocysteine -> cystationine –> cysteine)
  2. Decreased affinity of the synthase for B6
  3. Homocysteine methyltransferase deficiency (homocysteine –> methionine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

symptoms of homocytinuria

A 
intellectual disability
osteoporosis
tall stature
kyphoisis
lens subluxation
thrombosis, atheroslcerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Cystinuria

A

defect in renal PCT and intestinal amino acid transporter for COLA (cysteine, ornithine, lysine, arginine)
excess cysteine in urine -> hexagonal cysine stones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

treatment of cystinuria

A

urinary alkalinization (azetazolamide)
chelating agents to increase solubility of stones.
good hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Lynch syndrome

A

aka HNPCC - hereditary non-polyposis colorectal cancer. Mutation in DNA mismatch repair genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Maple syrup urine disease

A

no degradation of branched amino acids (isoleucine, leucine, valine) due to decreased alpha-ketodehydrogenase or B1.
severe CNS defects and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Von Gierke disease

A

glycogen storage disease -> increased glycogen stores in kidney and liver -> hepatomegaly.
Due to glucose-6-phosphatase deficiency (no degradation of glucose6P to glucose).
hypoglycemia
increased blood lactate
must eat often to avoid hypoglycemia, corn starch before bed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

pompe disease

A

glycogen storage disease. defect in lysosomal alpha-1,4-glucosidase. leads to cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Cori disease

A

milder form of von gierke disease. Hepatomegaly and increased glycogen stores without increased lactate.
due to defect in debranching enzyme (alpha 1,6 glucosidase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

McArdle disease

A

glycogen storage disease. Defect in skeletal muscle glucogen phosphorylase (myophosphorylase). Unable to breakdown glycogen in muscle cells. Painful muscle cramps, esp when exercising. Arrhythmias from electrolyte imbalances.
osmosis draws water into muscle cells -> burst- > increased myoglobin in serum and urine -> myoglobinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

deficient enzyme in fabry disease leading to what accumulation

A

alpha galactosidase A

Ceramide trihexoside accumulation

60
Q

deficient enzyme in Gaucher disease leading to what accumulation

A

glucocerebrosidase (beta glucosidase)

glucocerebroside accumulation

61
Q

deficient enzyme in niemann-pick disease leading to what accumulation

A

sphingomyelinase

sphingomyeline accumulation

62
Q

deficient enzyme in tay-sachs disease leading to what accumulation

A

hexosaminidase A

GM2 ganglioside accumulation

63
Q

deficient enzyme in krabbe disease leading to what accumulation

A

galactocerebrosidase

galactocerebroside, psychosine

64
Q

deficient enzyme in metachromatic leukodystrophy disease leading to what accumulation

A

arylsulfatase A

cerebroside sulfate accumulation

65
Q

deficient enzyme in hurler syndrome leading to what accumulation

A

alpha-L-iduronidase

heparan sulfate and dermatan sulfate accumulation

66
Q

deficient enzyme in hunter syndrome leading to what accumulation

A

iduronate sulfatase

heparan sulfate and dermatan sulfate accumulation

67
Q

Fabry disease

A

x linked recessive lysosomal storage disease with deficiency in alpha-galactosidase A leading to accum of ceramide trihexoside
cv and renal disease, angiokeratomas, peripheral neuropathy of hand and feet

68
Q

Gaucher disease

A

autosomal recessive lysosomal storage disease with deficiency in glucocerebrosidase (beta glucosidase) leading to accumulation in glucocerebroside.
Gaucher cells - crumpled tissue paper (lipid laden macrophages)
hepatosplenometaly, pancytopenia, aspectic necrosis of femur, bone crises

69
Q

Niemann pick disease

A

autosomal recessive lysosomal storage disease with deficiency in sphingomyelinase leading to accumulation of sphingomyeline. causes neurodegeneration, hepatospleno, cherry red spot, foam cells (lipid laden macrophages)

70
Q

tay sachs disease

A

autosomal recessive lysosomal storage disease with deficiency in hexosaminidase A leading to accumulation of GM2 ganglioside.
Progressive neurodegeneration, cherry red, lysosomes with onion skin, no hepatosplen or lipid laden macrophages(like in niemann pick),

71
Q

krabbe disease

A

autosomal recessive lysosomal storage disorder with deficiency in galactocerebrosidease leading to accumulation in galactocerebroside and pyschosine.
peripheral neuropathy, devo delays, optic atrophy, globoid cells

72
Q

metachromatic leukodystrophy

A

autosomal recessive lysosomal storage disorder with deficiency in arylsulfatase A leading to accumulation in cerebroside sulfate
central and peripheral demyelination with ataxia and dementia

73
Q

hurler syndrome

A

autosomal recessive lysosomal storage disease with deficiency in alpha-L-iduronidase and accumulation of heparan sulfate and dermatan sulfate
devo delay, gargoylism, airway obstruction, corneal clouding, hepatospleno

74
Q

hunter syndrome

A

x linked recessive lysosomal storage disease with deficiecny in iduronate sulfatase leading to accumulation of heparan sulfate and dermatan sulfate.
(hurler syndrome + aggressive behavior - corneal clouding)
devo delay, gargoylism, airway obsturcttion, hepatospleno

75
Q

Bernard-soulier syndrome

A

deficiency in GpIb on platelets needed to find to vWF sitting on exposed subendothelial collagen

76
Q

Glanzmann thrombasthenia

A

Deficiency in GpIIb/IIIa on platelets needed to connect two platelets together through fibrinogen

77
Q

HbH

A

Excess beta globin froms Beta 4

seen with three allele deletions of alpha globin in alpha thalassemia

78
Q

Hb Barts

A

tetramer of gamma globin. Due to no alpha globin (4 allele deletion) in alpha thalassemia
incompatable with life

79
Q

Fe, B12 and folate. where are each absorbed?

A

Fe - duodenum
Folate - Jejunum
B12-Ileum

80
Q

Spinal columns affected in B12 deficiency –> subacute combined degeneration of spinal cord

A

Lateral corticalspinal tract -> spasticity
Dorsal column –> vibration/ proprioception
(deficiency also caused peripheral neuropathy and dementia)

81
Q

Paroxysmal nocturnal hemoglobinuria

A

acquired defect in myeloid stem cells against GPI which normally connects DAF (CD%55) and MIRL to mature myeloid cells. Makes cells susceptible to complement.

82
Q

The 5 p’s of acute intermittent porphyria

A 
Painful abdomen
Port wine colored urine
polyneuropathy
pyschological disturbances
precipitated by drugs, alcohol, starvation
83
Q

Deficient enzyme in acute intermittent porphyria

A

porphobilinogen deaminase (porphobilinogen accumulation)

84
Q

deficient enzyme in sideroblastic anemia

A

ALA synthase

85
Q

deficient enzyme in porphyria cutanea tarda

A

uroporphyrinogen decarboxylase

86
Q

symptoms of prophyria cutanea tarda

A

blistering cutaneous photosynsitivity

87
Q

Deficiency in TTP

A

ADAMTS13

88
Q

Factor V leiden

A

mutant factor V leading to less degradation by protein C. Hypercoagulation

89
Q

most common inherited bleeding disorder

A

VWF disease

90
Q

most common inherited hypercoagulable disease

A

Factor V leiden

91
Q

CDs for Hodgkins

A

CD15, CD30 positive

92
Q

Burkitt lymphoma translocation

A

t(8;14) - cmyc and heavy chain Ig

93
Q

CD5 and CD20 positive

A

mantle cell lymphoma

94
Q

translocation for mantle cell

A

t (11;14) cyclin D1 and heavy chain Ig

95
Q

follicular lymphoma translocation

A

t(14;18) heavy chain Ig and bcl-2

96
Q

which lymphoma is associated with chronic inflammatory states?

A

Marginal zone lymphoma (MALToma)

hashimotos, sjogren’s, h. pylori

97
Q

starry sky appearance

A

burkitt lymphoma

98
Q

Lymphoma associated with HTLV

A

adult T cell lymphoma

99
Q

waldenstrom macroglobulinemia

A

b cell lymphoma with monoclonal IgM production. Blood viscosity increases

100
Q

CD10, 19, 20+, TdT+

A

B-ALL

101
Q

t (12,21)

A

good prognosis ALL

102
Q

smudge cells

A

CLL/SLL

103
Q

Dry tap and TRAP lymphoma

A

Hairy cell

104
Q

CD marker for HSC

A

CD34

105
Q

which cell most sensitive to radiation?

A

lymphocytes

106
Q

what IL is increased in hodgkins

A

IL 5 due to eosinophila

107
Q

what cancer has increased basophils

A

CML

108
Q

Auer rod

A

AML

109
Q

t (15, 17)

A

APL

110
Q

Leukemia treated with ATRA (retinoic acid)

A

APL

111
Q

DIC risk increased in which lymphoma

A

APL

112
Q

which lymphoma/leukemia has increased risk of autoimmune hemolytic anemia

A

CLL/SLL

113
Q

which leukemia has splenomegaly of red pulp only

A

hairy cell

114
Q

which has a good response to 2-CDA (adenosine deaminase inhibitor)

A

hairy cell

115
Q

pautrier microabscesses

A

mycosis fungoides

116
Q

cerebriform nuclei - which lymphoma

A

sezary syndrome/mycosis fungoides

117
Q

which type of lymphomas have rashes

A

mature T cell cancers (mycosis fungoides and ATLL)

118
Q

What is the mature B cell lymphoma/leukemia

A

hairy cell, hodgkins and non hogkins, CLL

119
Q

what are the mature T cell lymphomas/leukemias

A

Mycosis fungoides and ATLL

120
Q

myelofibrosis

A

proliferation of mature myeloid cells, especially megakaryocytes

121
Q

S100 and CD1a positive

A

langerhans cell histiocytosis

122
Q

birbeck granules

A

seen on em

langerhands cell histiocytosis

123
Q

Jak2 mutation

A

polycythemia vera esp

can also be in essential thrombocytosis or myelofibrosis

124
Q

complex that ab binds to in heparin induced thrombocytopenia

A

IgG against heparin bound to platelet factor 4 (PF4)

125
Q

Dressler syndrome

A

autoimmune phenomenon resulting in fibrous pericarditis (several weeks after MI)

126
Q

BMPR2 inactivating gene mutation

A

primary pulmonary HTN

normally gene inhibits vascular smooth muscle proliferation -> thickened vessels

127
Q

Kimmelstiel wilson lesion

A

diabetic glomerulonephropathy. nodules are eosinophilic and sclerotic

128
Q

paget disease of bone

A

increase in both blast and clast activity

increased hat size and hearing loss common

129
Q

paget disease has increased risk for

A

osteosarcoma

130
Q

osteopetrosis

A

impaired osteoclast - thick and dense bone

131
Q

The 5p’s of acute intermittent porphyria

A 
Painful abdomen
port wine colored urine
polyneuropathy
psychological distrubances
precipitated by drugs alcohol or starvation
132
Q

what is the enzyme deficiency in acute intermittent porphyria

A

porphobilinogen deaminase (prophobilinogen –> hydroxymethylbilane)

133
Q

What is the enzyme deficiency in porphyria cutanea tarda

A

uroporphyrinogen decarboxylase (uroporphyrinogen –> coproporphyrinogen)

134
Q

Gene mutated in osteogenesis imperfecta

A

COL1A

135
Q

alport syndrome

A

problem with type IV collagen (Basement membrane)

Deafness and kidney problems and possible eye problems (Cataracts)

136
Q

association with chiari type II

A

meningomyelocele

137
Q

association with chiari type I

A

syringomyelia

138
Q

polio affects what area of spinal cord

A

anterior horns -> LMN lesions only -> flaccid paralysis

139
Q

werdnig-hoffmann disease

A

aka spinal muscular atrophy. congenital degeneration of anterior horns of spinal cord -> LMN -> floppy baby

140
Q

friedreich ataxia

repeat?

A

GAA repeat of frataxin (iron binding protein) leading to mito function impairment
degen of multiple spinal cord tracts -> staggering, falling, HCM, kyphosis

141
Q

brown sequard syndrome

A

hemisection of spinal cord.
ipsi umn signs below level of lesion
ipsi loss of tactile vibration and proprioception sense below level of lesion
contra pain and temp loss below lesion level
at level of lesion: ipsi loss of all sensation of LMN signs.

142
Q

aggregate seen in Pick disease

A

spherical tau protein (Pick body)

143
Q

accumulation seen in lewy body dementia

A

alpha-synuclein

144
Q

where are lewy bodies found in parkinsons and LB dementia

A

Parkinsons - substantia nigra

LB - neurons of cortex

145
Q

Charcot-Marie-Tooth disease

A

aka hereditary motor and sensory neuropathy
defective production of proteins needed in structure and function of peripheral nerves or myelin.
have associated scoliosis and foot deformities

146
Q

adrenoleukodystrophy

A

x linked
disruption of very long chain fatty acid metabolism
excess build up in nervous system, adrenal glands and testes

147
Q

where do parital (focal) seizures most commonly originate

A

medial temporal lobe

USMLE 1 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions