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Gene mutation associated-onset diabetes of the young (MODY) Glucokinase
1st step of BOTH Glycolysis and Glycogen synthesis Phosphorylation of glucose to yield glucose-6-P
NADPH is used in *Anabolic processes (fatty acids and cholesterol synthesis) *Respiratory burst *Cytochrome P-450 system *Glutathione reductase
Universal electron acceptors 1. Nicotinamides (NAD+ from vitamin B3, NADP+) 2. Flavin nucleotides (FAD+ from vitamin B2).
Hexokinase vs. Glucokinase Hexokinase: everywhere, LOW Km, LOW Vmax, NOT induced by insulin Glucokinase: Liver+ Beta cells of Pancres; HIGH Km, HIGH Vmax, induced by insulin
Cofactor for enzymes that participate in the synthesis of Tyrosine, DOPAI and Serotonin as well as NO Tetrahrydrobiopterin (BH4)
Cofactor used in transamination (e.g., ALT and AST), decarboxylation reactions, glycogen phosphorylase. Vitamin 86 (pyridoxine)
Necessary for the synthesis of cystathionine, heme, niacin, histamine, and neurotransmitters including serotonin, epinephrine, norepinephrine, and GABA. Vitamin 86 (pyridoxine)
ONLY purely ketogenic amino acids Lysine and Leucine
Neurologic defects, lactic acidosis, increased serum alanine starting in infancy Pyruvate dehydrogenase complex deficiency
Pyruvate dehydrogenase complex deficiency; TREATMENT Increase intake of KETOGENIC nutrients (e.g high fat content or high LYSINE or LEUCINE)
Metabolic processes that take place in the BOTH; mitochondria and cytoplasm 1. Heme synthesis 2. Urea Cycle 3. Gluconeogenesis
Metabolic processes that take place in the Mitochondria 1. Fatty acid oxidation (Beta-oxidation), 2. Acetyl­ CoA production, 3. TCA cycle, 4. Oxidative phosphorylation.
Metabolic processes that take place in the Cytoplasm 1. Glycolysis, 2. Fatty acid synthesis, 3. HMP shunt, 4. Protein synthesis (RER), 5. Steroid synthesis (SER), 6. Cholesterol synthesis.
Most common inherited blood disorder in the US Sickle Cell anemia (HbS)
Hemoglobin S (HbS) aggregates in the Deoxygenated state
Non polar amino acid Valine replaces the charged amino acid Glutamate at the position 6 of the Beta globin chain Sickle Cell anemia (HbS); nucleotide substitution, changed amino acid= MISSENSE mutation
Is the most common non-nuclear DNA found in the eukaryotic cells and its derived completely from the mother Mitochondrial DNA (mtDNA)
Mitochondrial enzyme complex linking Glycolyisis and TCA cycle Pyruvate dehydrogenase complex
Cofactors required for pyruvate dehydrogenase complex and alpha-ketoglutarate dehydrogenase complex reactions l. Pyrophosphate (B1, thiamine; TPP) 2. FAD (B2, riboflavin) 3. NAD (B3, niacin) 4. CoA (B5, pantothenate) 5. Lipoic acid
Administration of glucose to a thiamine (Vit B1) deficient patient (e.g malnutrition, ALCOHOLICS) results in Wernicke Encephalopathy
Diagnosis of Thiamine (Vit B1) deficiency Increase in RBC transketolase activity following Vit B1 administration
Thiamine pyrophosphate (TPP), is a cofactor for several dehydrogenase enzyme reactions • Pyruvate dehydrogenase (links glycolysis to TCA cycle) • Alpha-ketoglutarate dehydrogenase (TCA cycle) • Transketolase (HMP shunt) • Branched-chain amino acid dehydrogenase
Causes a buildup of PYRUVATE that gets shunted to lactate (via LDH) and alanine (via ALT) Pyruvate dehydrogenase complex deficiency
Function of PDH (Pyruvate dehydrogenase) Convert pyruvate to acetyl-CoA for metabolism in the TCA cycle
Necessary cofactor in the synthesis of alpha-aminolevulonic acid (which is elevated in cases of Lead Poisoning) Pyridoxal phosphate (B6)
To treat cyanide poisoning, use 1) Nitrites to oxidize Hb to methemoglobin, which binds cyanide. 2) Thiosulfate to bind this cyanide, forming thiocyanate, which is renally excreted.
Oxidized form of hemoglobin (ferric, Fe3+) that does not bind 02, but has high affinity for cyanide. Methemoglobin
Iron in hemoglobin is normally in a reduced state (ferrous, Fe2+).
Methemoglobinemia can be treated with Methylene blue
Nitrites cause poisoning by Oxidizing Fe2+ to Fe3+
Autosomal-recessive; defective neutral amino acid (e.g, Tryptophan) transporters on proximal renal tubular cells and on enterocytes. Hartnup disease
Essential amino acid precursor for nicotinic acid, serotonin and melatonin Tryptophan
Cerebellar ataxia, pellagra-like symptoms, photosensitivity, neutral aminoaciduria Hartnup disease
Treatment for Hartnup disease 1) High protein diet 2) Nicotinic acid (Niacin,B3)
Nicotinic acid (Niacin,B3) is synthesized from Tryptophan
Niacin, Vitamin B3; DEFICIENCY 1) Glossitis 2) Pellagra: Diarrhea, Dementia (also hallucinations), Dermatitis (e.g, Casal necklace or hyperpigmentation of sun-exposed limbs)
Niacin, Vitamin B3; CAUSES 1) Hartnup disease (decreased tryptophan absorption) 2) Malignant carcinoid syndrome (increased tryptophan metabolism) 3. Isoniazid (decreased vit B6)
Constituent of NAD+, NADP+ (used in redox reactions). Derived from tryptophan. Synthesis requires vit B2 and B6. Used to treat dyslipidemia; lowers levels of VLDL and raises levels of HDL Niacin, Vitamin B3
Niacin, Vitamin B3; EXCESS 1) Facial flushing (induced by PROSTAGLANDINS, not histamine) 2) Hyperglycemia (Acanthosis nigricans) 3) Hyperuricemia (exacerbates Gout)
The 3 D´s of B3 1) Diarrhea 2) Dementia (also hallucinations) 3) Dermatitis (e.g, Casal necklace or hyperpigmentation of sun-exposed limbs)
Most significant causes of Vitamin A (retinol) deficiency 1) Malnourishment 2) Fat malabsorption (e.g Cystic Fibrosis, Cholestatic liver disease)
Vitamin A (retinol); FUNCTIONS 1) Antioxidant 2) Retinal 3) Normal differentiation of epithelial cells into specialized tissue (pancreatic cells, mucus-secreting cells); prevents squamous metaplasia. 4) Treat measles and AML, subtype M3.
Vitamin used to treat measles and AML, subtype M3 Vitamin A (retinol)
Vitamin that prevents squamous metaplasia Vitamin A (retinol)
Vitamin A (retinol); DEFICIENCY 1) Night blindness (nyctalopia) 2) Dry, scaly skin (xerosis cutis) 3) Alopecia 4) Corneal degeneration (keratomalacia) 5) Immune suppression
Vitamin A (retinol); EXCESS 1) Sore throat 2) Skin changes (e.g, scaliness) 3) Cerebreal edema 4) Pseudotumor cerebri 5) Hepatic abnormalities (hypertriglyceridemia, hyperlipidemia) 6) Teratogenic (cleft palate, cardiac abnormalities)
Swollen gums, bruising, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages ¨corkscrew¨ hair Scurvy; Vitamin C (ascorbic acid) deficiency
Vitamin C deficiency causes scurvy due to Collagen synthesis defect. Hydroxylation of specific proline and lysine residues requires vitamin C
Vitamin C (ascorbic acid); FUNCTIONS 1) Antioxidant. 2) Iron absorption by reducing it to Fe2+ 3. Hydroxylation of proline and lysine in collagen synthesis. 4. Dopamine Beta-hydroxylase, which converts dopamine to NE.
ONLY DNA polymerase that has 5´to 3 exonuclease activity; excises RNA primer and damaged DNA sequences which are identified by endonucleases DNA polymerase I
Cut DNA at very specific DNA sequences within the molecule Endonucleases
Removal of supercoils Topoisomerase II
Unwinding of double helix Helicase
Stabilization of unwound template strands (bind only to ssDNA) Single-stranded binding proteins (SSB)
Synthesis of RNA primer Primase (RNA polymerase)
DNA synthesis: LEADING strand DNA polymerase III
DNA synthesis: LAGGING strand DNA polymerase III
Removal of RNA primer and replacement of RNA with DNA (proof reading) DNA polymerase I (5´-exonuclease)
Joining of Okasaki fragments (lagging strand) DNA ligase
Y-shaped region along DNA template where leading and lagging strands are synthesized. Replication fork
RNA-dependent DNA polymerase Telomerase
Adds DNA to 3´ends of chromosomes to avoid loss of genetic material with every duplication Telomerase (only found in EUKARYOTES)
Thyroid hormones alter gene transcription by binding to receptors situated inside of the NUCLEUS
hyperextensible skin, tendency to bleed (easy bruising), and hypermobile joints Ehlers-Danlos syndrome
Ehlers-Danlos syndrome associated with joint dislocation, berry and aortic aneurysms, organ rupture.
Problems with collagen cross-linking Ehlers-Danlos syndrome
Vitamin B5 (pantothenate) Essential component of CoA (a cofactor for acyl transfers) and fatty acid synthase.
Biologically active form of pantothenic acid Coenzime A
Excess of this vitamin can lead to calcium oxalate nephrolithiasis Vitamin C (ascorbic acid)
Excess of this vitamin can increase iron toxicity in predisposed individuals (e.g,those with transfusions, hereditary hemochromatosis) Vitamin C (ascorbic acid)
Converts glucose to sorbitol Aldose Reductase
Tissues that have both enzymes aldose reductase and sorbitol dehydrogenase Liver, lens, ovaries, and seminal vesicles
Intracellular sorbitol accumulation, can cause Osmotic damage (e.g., cataracts, retinopathy, and peripheral neuropathy seen with chronic hyperglycemia in diabetes).
Tissues that have only aldose reductase. Schwann cells, Retina, Lens, Kidneys
In bacteria, one mRNA codes for several proteins. This is means it´s Bacterial mRNA can be polycistronic
Ensures fast and effective DNA replication in Eukaryotic cells MULTIPLE origins of replication
In Eukaryotic there are 5 major DNA polymerases alpha, beta, delta, gamma and epsilon
Hypoxia-induced lactic acidosis is caused by LOW activity of pyruvate dehydrogenase (oxidative phosphorilation pathway) and a HIGH activity of lactate dehydrogenase
Anaerobic glycolysis produces only 2 net ATP per glucose molecule.
Aerobic metabolism of glucose produces 32 ATP via malate-aspartate shuttle (heart and liver), 30 ATP via glycerol-3-phosphate shuttle (muscle).
End of anaerobic glycolysis Lactate
Anaerobic glycolysis (Cori cycle) is the major pathway in RBCs, leukocytes, kidney medulla, lens, testes, and cornea)
Cofactor for lactic acid dehydrogenase Vitamin B3 (niacin)
Has higher affinity for oxygen due to less avid binding of 2,3 BPG. Fetal hemoglobin (HbF); this allows HbF to extract O2 from (HbA) maternal hemoglobin across the placenta
The most important stimulator of insulin release Glucose
Allows facilitated diffusion of glucose into beta cells GLUT 2 (glucose transporter 2)
Insulin-DEPENDENT glucose transporters GLUT-4: adipose tissue, skeletal muscle
Insulin-INDEPENDENT glucose transporters GLUT-1: RBC´s , brain, cornea GLUT-5 (FRUCTOSE): spermatocytes, GI tract GLUT-2 (BIDIRECTIONAL): beta islet cells, liver, kidney, small intestine
ALWAYS utilize glucose because they lack mitochondria for aerobic metabolism RBC´s
Insulin and C-peptide are INCREASED in Insulinoma; whereas EXOGENOUS insulin LACKS C-peptide
Closes K+ channels in beta cells INCREASE in ATP/ADP ratio generated from glucose metabolism within beta cells
Defects of the KATP channel gene can result in Type II diabetes
Regulatory substance that stimulates KATP channel closure in insulin-producing pancreatic beta cells ATP
Anabolic effects of insulin; INCREASE: • Glucose transport (skeletal muscle, adipose tissue) • Glycogen synthesis/storage • Triglyceride synthesis/storage • Na+ retention (kidneys) • Protein synthesis (muscles, proteins) • Cellular uptake of K+ and amino acids
Anabolic effects of insulin; DECREASE: • Glucagon release
is used by the brain during starvation Ketone bodies
3 polypeptide alpha-chains held together by hydrogen bonds to form a rope-like triple helix Collagen (most abundant protein in the human body)
MOST abundant amino acid in the collagen molecule. It occurs AT LEAST every third amino acid position. GLYCINE
Is derived from amino acids (valine, isoleucine, methionine, threonine), odd chain fatty acids and cholesterol Propionyl-CoA (propionic acid)
Congenital deficiency of propionyl-CoA carboxylase the enzyme responsible for converting propionyl-CoA to methylmalonyl-CoA leads to Propionic acidemia
Variety of hormones that exert their intracellular effects via the IP3 second messenger system GnRH, Oxytocin, ADH (V1 receptor), TRH, Histamine (H1-receptor), Angiotensin II, Gastrin
Hemoglobin carries carbon dioxide as Carbamate
High fidelity replication of DNA is accomplished by 3´to 5´ ¨proofreading¨exonuclease activity of DNA polymerase
The Shine-Dalgarno sequence is UNIQUE to Prokaryotes
Are responsible for accuracy of amino acid selection Aminoacyl-tRNA synthetase and binding of charged tRNA to the codon
40S + 60S --> 80S Eukaryotes
30S + 50S ---> 70S Prokaryotes
Absence of galactose-1-phosphate uridyltransferase. Classic galactosemia
Failure to thrive, jaundice, hepatomegaly, infantile cataracts, mental retardation. Classic galactosemia
Deficiency of galactokinase. Galactokinase deficiency
Treatment: exclude galactose and lactose (galactose + glucose) from diet. Classic galactosemia
Classic galactosemia can lead to E.coli sepsis in neonates
Galactose appears in blood and urine, infantile cataracts. May initially present as failure to track objects or to develop a social smile. Galactokinase deficiency
Most common cause of Homocystinuria Deficiency of cystathionine synthase
Refers to the 1 to 4 residues remaining on a branch after glycogen phosphorylase has already shortened it ¨Limit dextrin¨
Enzime activation responsible for the rapid glycogen degradation in skeletal muscle after the onset of contraction Ca2+
Messenger mRNA is produced from DNA by RNA polymerase II
mRNA is composed of 3 sequential bases known as CODONS
Calls for the termination of synthesis of the polypeptide chain STOP codons: UGA: u go away UAA: u are away UAG: u are gone
mRNA start codon AUG (methionine)
Nucleotide substitution resulting in early stop codon. Nonsense mutation
3 IRREVERSIBLE enzymes of Glycolysis Hexokinase (Glucokinase); Fructokinase; Pyruvate kinase
Activates GLYCOLYSIS by inducing PFK-1 and inhibits GLUCONEOGENESIS by inhibiting Fructose-1,6BP Fructose-2,6-BP
IRREVERSIBLE enzimes, Gluconeogenesis 1) Pyruvate carboxylase 2) Phosphoenolpyruvate carboxykinase 3) Fructose-1,6-biphosphatase 4) Glucose-6-phosphatase
2 important pathophysiologic differences between the 2 forms of bilirubin Direct bilirubin-conjugated with glucuronic acid; water Indirect bilirubin-unconjugated; water insoluble, tightly complexed to serum albumin (cannot be excreted in urine even when blood levels are high)
If energy dependent organic ion transport across hepatocellular membrane is selectively inhibited which is the most likely result Increase bilirubin excretion in the urine
P50 Partial pressure of O2 in the blood at which Hb is 50% saturated; normal: 26mmHg
3 variables affect O2 content of blood: Hb level; % O2 saturation of Hb (SaO2); Dissolved O2 (PaO2)
shift to RIGHT (increase P50); facilitates unloading 1) BPG (2,3-BPG) 2) Altitude 3) Temperature 4) Acid (pH); DECREASED 5) C02 6) Exercise
O2 capacity Maximal amount of O2 that can bind to Hb
O2 content Total O2 in blood (bound+dissolved)= (O2 binding capacity X saturation% ) + dissolved O2
O2 delivery to tissues= O2 delivery to tissues= CO X O2 content of blood
shift to LEFT (increase P50); facilitates loading 1) BPG (2,3-BPG) 2) CO poisoning 3) Temperature 4) Acid (pH); INCREASED 5) Fetal Hb 6) Methemoglobin
CO poisoning (Carboxyhemoglobin) is dangerous for 3 reasons: 1) Left shift; decreasing P50 and O2 unloading in tissues 2) 240x greater affinity than 02 for Hb, decreasing O2 content of blood. 3) Inhibits cytochrome oxidase
Insulin acts via a Tyrosine kinase mechanism
Tyrosine kinase leads to activation of protein phosphatase within cells, and protein phosphatase directly modulates the activity of enzymes in the metabolic pathways regulated by INSULIN
Maintain plasma glucose levels for only a few hours of fasting until glycogen stores are depleted Glycogenolysis
Predominant method used by the body to maintain blood glucose concentrations Gluconeogenesis
Gluconeogenesis. IRREVERSIBLE enzymes 1) Pyruvate carboxylase (mitochondria) 2) Phosphoenolpyruvate carboxykinase (cytosol) 3) Fructose-1,6-biphosphatase (cytosol) 4) Glucose-6-phosphatase (ER)
The activity of pyruvate carboxylase is increased by Acetyl-CoA
Pyruvate carboxylase converts pyruvate to oxaloacetate in the mitochondria in a reaction that requires Biotin + ATP
In cytosol. Fructose-1 ,6-bisphosphate is converted to fructose-6-P by Fructose-1,6-biphosphatase. This reaction is inhibited and activated by (+) Citrate (-) Fructose 2,6-biphosphate
Deficiency of the key gluconeogenic enzymes causes Hypoglycemia.
Muscle cannot participate in gluconeogenesis because it lacks Glucose-6-phosphatase
Membrane-enclosed organelle involved in beta-oxydation of very long fatty acids (VLCFA), branched-chain fatty acids and amino acids. Peroxisomes
Infant suffering from hypotonia and seizures shows and impaired ability to oxidize yew long chain fatty acids (VLCFA) and phytanic acid Peroxisomal diseases (neurologic defects; improper CNS myelination)
Urea´s nitrogen in the urea cycle is derived from NH3 and Aspartate
Rate-limiting enzyme in the urea cycle and is activated by Carbamoyl phosphate synthetase I (CPS I) activated by N-acetylglutamate
required cofactor for Carbamoyl phosphate synthetase I (CPS I) N-acetylglutamate
3 main circulating catecholamines Dopamine, NE, Epi
Phenylethanolamine-N-methyltransferase (PNMT) is responsible for the synthesis of epinephrine in the adrenal medulla, is under control of Cortisol
Enzymes responsible for the metabolism of catecholamines Cathecol-O-methyltransferase (COMT), Monoamine oxidase (MAO)
Fructose is rapidly absorbed in the proximal small bowel by the hexose transporter GLUT 5
Disorders of fructose metabolism Essential fructosuria; Fructose intolerance
Involves a defect in fructokinase Essential fructosuria (defect in fructokinase)
Fructose appears in blood or urine Essential fructosuria (defect in fructokinase)
Hereditary deficiency of aldolase B. Fructose-1-phosphate accumulates, causing a decrease in available phosphate, which results in inhibition of glycogenolysis and gluconeogenesis Fructose intolerance (deficiency of aldolase B)
Infant with hypoglycemia, jaundice, cirrhosis, vomiting. Symptoms presented 20-30mins after fructose consumption Fructose intolerance (deficiency of aldolase B)
Hereditary deficiency of aldolase B Fructose intolerance (deficiency of aldolase B)
Fructose intolerance; TREATMENT decrease intake of both fructose and sucrose (glucose + fructose) .
Receptor proteins are either 1) Extracellular (located on cell surface): majority of receptors 2) Intracellular (located in the cytoplasm or nucleus): Steroid hormones
The majority of receptor proteins are extracellular, which is the intracellular exception Steroid hormones
The steroid resceptor is a Zinc finger protein
Increase in melting temperature of DNA Increase in G-C (3H bonds) content
Uracil found in RNA
Thymine found in DNA
Amino acids necessary for purine synthesis GAG Glycine Aspartate Glutamine
Nucleoside Base+ (deoxy) ribose (Sugar).
Nucleotide base + (deoxy) ribose (Sugar) + phosphate; linked by 3´-5´phosphodiester bond
Carbamoyl phosphate is involved in 2 metabolic pathways: De novo pyrimidine synthesis and the urea cycle.
retardation, self-mutilation, aggression, hyperuricemia, gout, dystonia. Lesch-Nyhan syndrome; X-linked recessive
Defective purine salvage owing to absent HGPRT, which converts hypoxanthine to IMP and guanine to GMP. Results in excess uric acid production and de novo purine synthesis. X-linked recessive. Lesch-Nyhan syndrome; X-linked recessive
Lesch-Nyhan syndrome; TREATMENT Allopurinol or febuxostat (2nd line)
Purine salvage deficiencies 1. Adenosine deaminase deficiency 2. Lesch-Nyhan syndrome
One of the major causes of autosomal recessive SCID Adenosine deaminase deficiency
Deletion or insertion of a number of nucleotides NOT divisible by 3, resulting in misreading of all nucleotides downstream= truncated, nonfunctional protein. Frameshift mutation
Early stop codon Nonsense mutation
Histone octamer 2 copies of H2A, H2B, H3, and H4
Between adjacent nucleosomes Histone H1
Difference between 10nm and 30nm chromatin is presence or absence of Histone H1
Euchromatin • Loose • Accessible • Active
Heterochromatin • Condensed • Inaccessible • Inactive
Telomerase • Inactive in somatic cells (skin, blood, connective tissue) • Prokaryotes have single circular chromosomes, hence no telomerases • Inappropriately present in cancer cells
Nicks the phosphodiester backbone of damaged strand Excision endonuclease
Site where RNA polymerase and multiple other transcription factors bind to DNA upstream from gene locus (AT-rich upstream sequence with TATA and CAAT boxes). Promoter
Promoter mutation commonly results in dramatic decrease in level of Gene transcription
Process that occurs on the NUCLEUS following transcription 1) Capping on 5' end (addition of 7-methylguanosine cap); 2) Polyadenylation of 3' end ("" 200 A´s); 3) Splicing out of introns (non-coding regions)
Capped, tailed and spliced transcript is called mRNA
opens DNA at promotor site RNA polymerase II
most numerous RNA rRNA
RNA polymerase I makes rRNA (most numerous RNA, rampant)
RNA polymerase II makes mRNA (largest RNA, massive)
Largest RNA mRNA
RNA polymerase III makes tRNA (smallest RNA, tiny)
Smallest RNA tRNA
l RNA polymerase (multisubunit complex) makes all 3 kinds of RNA. Prokaryotes
Molecular motor proteins Dynein=RETROGRADE to microtubule (+to -) Kinesin=ANTEROGRADE to microtubule (-to +)
Transport cellular cargo toward opposite ends of microtubule tracks. Molecular motor proteins
Drugs that act on microtubules 1)Mebendazole (antihelminthic) 2)Griseofulvin (antifungal) 3)Vincristine/vinblastine (anti-cancer) 4)Paclitaxel (anti-breast cancer) 5)Colchicine (anti-gout)
Male infertility and decreased female fertility, bronchiectasis, and recurrent sinusitis; associated with situs inversus. Kartagener's syndrome (primary ciliary dyskinesia) - immotile cilia clue to a dynein arm defect.
Dynein arm defect Kartagener's syndrome (primary ciliary dyskinesia)
Created by: heidy39



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