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MCM > Diseases > Flashcards

Diseases Flashcards

1
Q

Gallstones

A

Helps to emulsify lipids. Cholesterol in this needs bile salts to stay in solution. Cholesterol hardens if the bile salt concentration is too low.
Oral chenodeoxycholic acid is a replacement therapy to dissolve gallstones

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2
Q

Non polar amino acids

A

Alanine, Glycine, Isoleucine, Leucine, Methionine, Phenylalanine, Proline, Tryptophan, Valine

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3
Q

Neutral Amino Acids

A

Asparagine, Cysteine, Glutamine, Serine, Threonine, Tyrosine

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4
Q

Acidic Amino Acids

A

Aspartic Acid, Glutamic Acid

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5
Q

Basic Amino Acids

A

Arginine, Histidine, Lysine

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6
Q

Diabetic Ketoacidosis (DKA)

A

Hyperglycemia and low blood pH that afflicts individuals with uncontrolled diabetes. Stops glucose from being used. B-oxidation of fatty acids makes ketone bodies. Dehydration, vomiting, confusion
Administer insulin to treat hyperglycemia and fluids to treat dehydration

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7
Q

Enzyme classes

A

Oxireductases, transferases, Isomerases, lyases, Ligases, hydrolases

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8
Q

Apoenzyme

A

Enzyme without it’s cofactor

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9
Q

Haloenzyme

A

Enzyme with it’s cofactors that is activated

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10
Q

Scurvy

A

Vitamin C deficiency. Spongy gums. Skin hemorrhaging

Due to the inability of the cell to make collagen

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11
Q

Ariboflavinosis

A

Riboflavin required for FAD synthesis
Reduced glutathione reductase activity
UV sensitive. Lesions in corners of mouth

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12
Q

Competitive inhibitor

A

Km decreased

Vmax stays the same

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13
Q

Uncompetitive inhibitor

A

Both Km and Vmax reduced by the same factor

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14
Q

Noncompetitive inhibitor

A

Vmax lowered

Km uninhibited

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15
Q

Lead Poisoning

A

Inhibits ALA dehydratase. Necessary for the creation of heme
S/S: abdominal pain, anemia, irritability headaches and encephalopathy.
Treat with Ca-EDTA. LEad has a higher affinity for EDTA than Ca2+. Then can be excreted through the urine.

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16
Q

Glut1

A

Ubiquitous transporter in RBC, brain
Unregulated
1 mM Km

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17
Q

Glut2

A

Liver
High capacity, low affinity Km 10 mM

Also found in B cells of the pancreas. To sense levels to release insulin

Rise in ATP close K+ channels. Opens Ca2+ channels. Causes rapid release of insulin. Activates CaM kinase letting out a slow release of insulin.

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18
Q

Glut3

A

Neurons
Km 1mM
Brain depends greatly on glucose. During extreme starvation however will use ketone bodies.

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19
Q

Glut4

A

Skeletal muscle, adipose tissue, heart
Dependent upon insulin. In microvesicles in the cytosol. When insulin binds, these microvesicles containing the Glut4 move to the surface.
Insulin binds to a receptor on the membrane. Km 5mM

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20
Q

SGLT 1

A

Small intestine. Needs a sodium ion in order to pass the glucose.

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21
Q

Fanconi-Bickel Syndrome`

A

inherited deficiency in GLUT2 transporters in the liver, pancreatic B cells, and proximal tubules.
Can’t transport glucose, galactose, and fructose.
Failure to thrive, hepatomegaly, hypoglycemia and hyperglycemia due to the inability to detect glucose in the bloodstream.
Administer Vitamin D and phosphate to treat rickets.
Uncooked corn starch to provide a sustained supply of glucose

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22
Q

Drug induced lupus erythematosus

A

Body metabolizes drugs by acetylating them. This detoxifies drugs. This is seen in individuals who have genetic mutations in enzymes that carry out these reactions. Makes them have a longer half life. Makes the by-products toxic to the body.
Present with muscle and bone pain, rashes, inflammation of the lungs and heart, fever and fatigue

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23
Q

Mannose-6 Phosphate

A

Proteins that are labelled to be broken down are marked with Mannose 6 phosphate. Leaving the trans golgi they then go to lysosomes in order to be denatured.
In I Cell disease, these GlcNac-PT is defective. Instead of being targeted for lysosomes they are secreted and can be detected in the blood.

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24
Q

Outer sheet membrane lipids

A

Phosphatidylchlorine
Sphingomyelin
Glycolipids

25
Q

Inner sheet membrane lipids

A

Phosphatidylositol
Phosphatidylserine
Phosphatidylethanolamine

26
Q

Phosphatidylserine

A

Usually found on the inside of the cell membrane. In cells that are ready to apoptosis it is on the outside.

27
Q

Niemann-Pick Disease

A

Hereditary disease caused by deficiency in sphingomyelinase. Thus sphingomyelin accumulates in the lysosomes of the liver, spleen, CNS, and bone marrow.
Hepatomegaly, Cherry red macula, seizures, ataxia, spasticity.

28
Q

Spur Cell Anemia

A

Hemolytic anemia.
Characterized by too much cholesterol in the erythrocyte membrane. Causes the cells to have a spiked texture. Cells lyse in the spleen.
Associated with beta lipoproteinanemia and with advanced stages of alcoholic cirrhosis.

29
Q

Cystinuria

A

Autosomal recessive disease caused by a defect in the transport system for Cystine, ARg, Lys, and ornithine.
Causes cystine crystals to form in the kidneys.
Present with renal colic

30
Q

Hartnup disease

A

Autosomal recessive
Defect in transporter for nonpolar or neutral amino acids (e.g. tryptophan)
Primarily found in kidneys and intenstine.
Failure to thrive, rapid repetitive eye movement, intermittent ataxia, tremor and photosensitivity.
Body can’t produce the proteins that are responsible for these actions

31
Q

Cardiotonic drugs

A

Cardiac Glycosides- ouabain and digoxin
they inhibit the Na+/K+ ATPase pump. This increases intracellular Na+ and then intracellular Ca2+.
Results in a strong contraction

32
Q

Cystic Fibrosis

A

Autosomal recessive.
Mutations in the CFTR gene. This is an ion channel that mediates active transport of Cl- ions from inside cells to outside in the airways using ATP. CFTR mediates the uptake of Cl- into the cells.
A defective CFTR causes a salt buildup inside the epithelial cells. Water and Na+ follow it into the cells.
Decreased water content of the mucous layer makes it thicker and harder to breathe

33
Q

COP I

A

Vesicles travelling from one layer of the golgi to another

34
Q

COP II

A

Vesicles travelling from the ER to the Golgi

35
Q

Clathrin coated vesicles

A

Either from the Golgi to the vesicles

Or from endosomes to the Golgi

36
Q

Dynamin

A

Used in order to pinch off the clathrin coated vesicles that are coming into the cell. They are what pinches it off at the very end.

37
Q

Adaptins

A

Mediate the clathrin coating of the vesicles

38
Q

Charcot-Marie-Tooth disease

A

A disease that has to do with lacking in dynamin 2. Affects myelination and cell nerve conduction

39
Q

Centronuclear myopathy

A

Progressive atrophy of skeletal muscles due to a malformation of dynamin 2
Abnormalities of the nervous system

40
Q

Lysosome pH

A

5.5

41
Q

Familial Hypercholesterolnemia

A

Cholesterol uptake is disrupted
Elevated LDL
1.LDL receptors incapable of binding cholesterol
2. LDL receptors binding at reduced capacity
3. LDL receptors bind normally but cannot bring the cholesterol into the cells

42
Q

Zellweger spectrum disorders

A

peroxisome biogenesis disorders
12 genes responsible for this production
Zellweger syndrome is characterized by a reduced number or complete absence of peroxisomes.
No treatment. Death generally within the first year of life.

43
Q

ALT

A

Increased in viral hepatitis, liver cell necrosis, prolonged circulatory collapse.
More specific than AST

44
Q

AST

A

Aminotransferase
Increased 6 to 8 hours after heart attack.
Biliary cirrhosis, liver cancer, pancreatitis, alcohol cirrhosis.
Liver, kidney, intestine and muscle

45
Q

GSH

A

levels decrease in acetaminophen overdose.

46
Q

Consequences of hyperhomocysteinuria and homocystinuria

A

Result from defective metabolism of homocysteine due to Vitamin B6, B12, and folic acid deficiencies.
Or from inherited defects in cystathionine B synthase

Comes from the inability to create THF

47
Q

S-Adenosylmethionine (SAM)

A

Activated methyl donor for many biological methylation reactions
`

48
Q

Ketogenic Amino Acids

A

Lysine and Leucine

49
Q

Ketogenic and Glucogenic Amino Acids

A

Ile, Trp, Phe, Tyr, Thr

50
Q

Maple Syrup urine Disease (MSUD)

A

Autosomal disease
Deficiency of branched chain alpha keto acid dehydrogenase (BCKD)
Presence of branched chain amino acids and derivatives in the urine of patients. They also accumulate in the blood causing toxic effects on the brain.
Some can be regulated by thiamine supplementation
Leucine, isoleucine and valine breakdown.

51
Q

Phenylketonuria (PKU)

A

Defects in phenylalanine hydroxylase activity causes PKU
Phe is converted to phenylpyruvate instead of Tyr
This effects myelin formation resulting in severe brain impairment.
Patient’s urine has a musty odor
1. Need to limit Phe intake.
2. Secondary PKU is caused by deficiency in THB. Essential cofactor of phenylalanine hydroxylase. (The enzyme that is necessary to convert Phe to Tyr)

52
Q

Sulfa Drugs

A

Antibacterial agents
Act as a competitive inhibitor of the bacterial enzyme PABA. This creates folate in bacteria but humans take it in through their diet.

53
Q

Methotrexate

A

Targets Dihydrofoate reductase. converts dietary folate into THF.
Disrupts rapidly dividing cancer cells

54
Q

Ribonucleotide Reductase

A

Takes nucleotides and makes them deoxynucleotides

55
Q

SCID

A

Genetic disorder where the B and T cells are crippled.
Males
ADA deficiency (enzyme that converts Adenosine to Inosine) highly pronounced in the lymphocytes.
Adenosine converted to AMP and ADP by kinases and ultimately to dADP and dATP. Inhibits the active site of ribonucleotide reductase. the low levels of dNDP impairs DNA synthesis.

56
Q

Gout

A

High uric acid levels in the blood. Either from being overproduced or underexcreted.
Sodium urate deposits as crystals into the joints.
Colchicine decreases the movement of granulocytes to the affected areas
Allopurinol inhibits xanthine oxidase raising the levels of more soluble purines hypoxanthine and guanine.

57
Q

Lesch-Nyhan Syndrome

A

Defect in the HGPRT enzyme in the purine salvage pathway.
Hyperuricemia.
Gout. poor muscle control, mental retardation, and a tendency for self mutilation
1. Circulating levels of hypoxanthine and guanine that aren’t used in the salvage pathway are higher than normal making hyperuricemia.
2. Purine biosynthesis also proceeds at levels 200 times that in normal situations. PRPP that normally is used in the salvage pathway is abailable for purine synthesis.

58
Q

Acyclovir

A

Anti-viral agent. resembles guanine and undergoes phosphorylation by viral thymidine kinase faster than the intended product dTMP. It lacks the 3’ hydroxyl group thus stopping DNA replication.
Chicken pox, shingles, and herpes

59
Q

Respiratory Distress Syndrome (RDS)

A

Lecithin, sphingomyelin, and phosphatidylglycerol make surfactant. A deficiency of lecithin causes this

MCM (1 decks)

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