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MCM Boxes > Boxes > Flashcards

Boxes Flashcards

1
Q

Reaction speed

A

Standard free energy change (deltaGº’) indicates weather rxn will proceed but not how fast. To go faster, rxn needs enzyme (catalyst)

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2
Q

Acid-Base balance and kidneys

A

Kidneys regulate blood pH (7.37-7.43) by removing protons from the blood in the form of ammonium ion (NH4+) and reabsorbing bicarbonate (HCO3-) into blood.
Low pH –> removal of protons, reabsorption of bicarbonate.
High pH –> fewer protons removed, less bicarbonate reabsorbed.

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3
Q

Respiratory acidosis

A

Hypoventilation leads to an increase in CO2. Carbonic anhydrase converts CO2 into carbonic acid, lowering pH.

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4
Q

Metabolic acidosis

A

When the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. Addition of a strong acid that cannot be metabolized. Excretion of HCO3- via diarrhea, weakened kidney function (reabsorption).

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5
Q

Respiratory alkalosis

A

Hyperventilation leads to dec concentration of CO2 in blood.

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6
Q

Metabolic alkalosis

A

Addition of a strong base, loss of acid.

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7
Q

Gastric proton pump inhibitor

A

H+/K+ ATPase. Parietal cells in gastric lumen pump H+ into lumen, where it forms HCl. When a proton pump inhibitor is prescribed (ex omerprazole), HCL production is decreased. Dec absorption of nutrients (hypochlorhydria), reduced gastric acid efficiency enzymes, and inc susceptibility to food posioning.

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8
Q

Cheleating agents for lead poisoning

A

Lead inhibits ALA, an enzyme involved in the biosynthesis of heme. Heme is a coenzyme of hemoglobin. Lead poisoning symptoms: abdominal pain, anemia, irritability, headache, signs of impaired NS. Administration of EDTA is used bc lead has a higher affinity for EDTA than for calcium. Lead is expelled in urine.

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9
Q

Troponin in MI

A

cTn-1 used as biomarker for detection of MI bc it is usually found in cardiac muscle, but after MI it can be found in serum.

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10
Q

Phosphatidylserine

A

Usually present in the intracellular sheet, but if cell is undergoing apoptosis phosphatidylserine displayed in the extracellular surface of the plasma membrane to attract phagocytes.

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11
Q

Niemann-Pick Disease

A

Enzyme that breaks down sphingomyelin (A-SMase) is deficient, so SM accumulates. Enlargment of liver and spleen, neurological issues, characteristic “cherry red spot” in retina.

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12
Q

Erythroblastosis fetalis

A

If mom is Rh- and first fetus is Rh+, mom produces antibodies during pregnancy. During second pregnancy, if fetus is RH+ antibodies can cross placenta and attack the fetus. Preventable by injecting mother with anti-RhD immunoglobulin.

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13
Q

Spur Cell Anemia

A

Elevated cholesterol levels in RBC causes them to become too rigid and burst as they pass through capillaries of the spleen. Membranes rupture.

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14
Q

Mimantine/Namenda

A

Glutamate is associated with Alzheimers. There are antagonists that act as glutamate inhibitors in the glutamate receptor (ligand gated).

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15
Q

Invocana

A

Medicine that inhibits SGLT1, preventing glucose from being absorbed into the blood and hence lowering blood glucose level. Treatment for diabetes.

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16
Q

Cystic Fibrosis

A

Mutation in CF gene causes mutated CFTR ion channel, which actively pumps Cl- out of the cells. Cl- accumulation inside the cell causes Na+ to flow in (NaCl), followed by water. Results in thicker mucus and susceptibility to illness. In sweat glands, result is very salty sweat. Autosomal recessive.

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17
Q

Cystinuria

A

Defect in dibasic amino acid transporter. Results in accumulation of cystine, arginine, lysine, and ortnithine. Cystine stones form in kidneys, patient presents with renal cholic. Autosomal recessive.

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18
Q

Hartnup

A

Defect in non-polar/neutral amino acid transporte (ex. alanine, valine, threonine, leucine, tryptopham). Tryptophan used as precursor for neurotransmitters and NADH+. Failure to thrive: cerebral ataxia, nystagmus, photodermatitis and photosensitivity.

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19
Q

Ouabain

A

Cardiotonic glycoside drug used to treat congestive heart failure (CHF) by blocking Na+/K+ ATPase. Results in Na+ intracellular accumulation and Ca2+ intracellular accumulation (bc glycoside slows down NCX). Ca2+ in the sarcoplasm results in stronger heart contraction.

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20
Q

Hemolytic anemia

A

A glycolytic disorder of pyruvate kinase (PK) in red blood cells that disrupts their ion gradient due to lack of ATP and causes them to die prematurely.

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21
Q

Starvation and the brain

A

Brain needs glucose for energy bc it is the only fuel molecule that can cross the blood brain barrier (BBB). During starvation, brain gets glucose from liver via gluconeogenesis and uses ketone bodies for fuel (which are acidic).

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22
Q

Diabetes Type 1

A

insulin deficiency due to lack/destruction of beta pancreatic cells

23
Q

Tarui Disease

A

Malfunction in PFK-1. Glycolysis cannot proceed. May lead to hemolytic anemia, muscle cramps and weakness.

24
Q

F1,6 bisphosphatase Deficiency

A

Glycolysis cannot proceed, similar to Tauri disease.

25
Q

Von Gierke disease (GSD1a)

A

Mutation in G6Phosphatase, glucose cannot remain trapped in the cell. Patient presents with hypoglycemia , hepatomegaly due to buildup of glycogen in liver, and lactic acidosis.

26
Q

Fanconi-Bickel syndrome

A

AR. Mutation in GLUT2. Glc. Gal, and Fru cannot move from enterocyte to bloodstream. Hepatomegaly.

27
Q

Sorbitol accumulation

A

In cells that lack sorbitol dehydrogenase (enzyme that converst sorbito (from glucose) to fructose), sorbitol accumulates lading to an influx of water, which causes inflammation. Cataracts, retinopathy, peripheral neuropathy.

28
Q

Hereditary Fructose Intolerance (HFI)

A

Defective aldolase B (enzyme that converts fructose to other things) results in accumulation of fructose, eventually leading to death of liver cells. Patient enforces diet free of fructose. All deaths related to diagnosis.

29
Q

High Fructose Corn Syrup and Obesity

A

Even though the glycemic index of HFCS is lower than that of sucrose, the metabolism of HFCS bypasses PFK (rate limiting step), so it does not use energy. In addition, the fructose is then converted to TAG’s.

30
Q

Galactokinase Deficiency (non-classic galactosemia)

A

AR. Marked by the accumulation of galctose. Cataracts in infancy (within the firs months of life) due to accumulation of galactose in eye lens. Treatable by galactose-free diet.

31
Q

Galactosemia

A

Deficiency in glucose 1P uridyltransferase (GALT) leads to accumulation of GALACITCOL. FAILURE TO THRIVE

32
Q

G6PD Deficiency

A

Enzyme that converts G6P into products for PPP. More likely to affect patients of African descent. Presentation of hemolytic anemia. 2GSH not produced, hydroxyl free radicals remain free.

33
Q

Pompe disease

A

AR. Lysosomal accumulation of glycogen due to accumulation of acid maltase (takes glycogen to glucose). Disorder in children often fatal, leads to accumulation of glycogen in the heart.

34
Q

Carnitine deficiency

A

Derivative of lysine, an essential amino acid. Strict vegetarians may have carnitine deficiency. Mild muscle cramping and weakness. In some cases causes death. Genetic deficiencies in carnitine are more severe.

35
Q

MCAD Deficiency

A

AR. Impaired breakdown of MCFAs. Excessive excretion of MCA in urine secondary carnitine deficiency). Accumulation of fatty acids in liver, interferes with urea cycle, elevated levels of ammonia. Patient relies on glucose. May lead to sudden death by hypoglycemia. Early diagnosis has excellent prognosis with behavior modifications.

36
Q

Physiological Ketoacidosis

A

Mild to moderate increase in KB formation. Occurs during fasting, pregnancy, in babies, after prolonged exercise and ketogenic diet.

37
Q

Pathological Ketoacidosis (Diabetes)

A

Inc in glucagon:insulin ratio induces overproduction of ketone bodies, which lower blood pH. Fruity breath odor.

38
Q

ALT and ASP as diagnostics

A

Normally located in mitochondria and cytoplasm. If found in blood, diagnostic of
ALT- viral hepatitis, liver cell necrosis, circulatory collapse
AST- MI

39
Q

Homocystinuria

A

Methionine –> Homocystine
When homocystine cannot be metabolized, it aggregates creating homocysteine, a toxic substance that primarily affects the eye, skeletal, CNS, and vascular organs.

40
Q

Maple Syrup Disease

A

During exercise, branched chain amino acids are used for energy. Patient cannot metabolize branch chain amino acids, results in branched-chain ketoaciduria. Branched-chains in urine give urine sweet odor. BC in blood has toxic effect, leading to dec in brain function.

41
Q

Phenylketonuria (PKU)

A

Phenylalanine cannot be metabolized, converted to phenylpyruvate (and then to phenyllactate and phenylacetate). These disrupt neurotransmission, a.a. transport in the brain and myelin formation.

42
Q

Ammonia Toxicity

A

Disorder in urea cycle leads to excessive ammonia. Toxic to brain and CNS.

43
Q

High protein diet

A

Study 1964 found that a high protein diet inc urea cycle enzymes (vs high carb diet).

44
Q

Creatine Kinase (CK)

A

Creatine selective to the heart, when found in other places it is diagnostic for MI.

45
Q

Methotrexate

A

Anticancer drug. Inhibits conversion of DHF to THF, needed for the formation of purines.

46
Q

Sulfa drugs

A

Disrups DNA replication selectively in bacteria

47
Q

5-Fluorouracil

A

Anticancer drug. Stops the production of pyrimidine synthesis.

48
Q

Orotic Aciduria

A

Inability to convert orotic acid to UMP. Megaloblastic anemia.

49
Q

Acyclovir

A

Virus infected cells that combine phosphate with nucleoside to form nucleotide inhibited by Acyclovir, which resembles a nucleotide and prevents DNA formation. Used to treat chickenpox and herpes lesions.

50
Q

Adenosine deaminase (ADA)

A

Overproduction- hemolytic anemia

Underproduction- SCID immunodeficiency

51
Q

Gout

A

Uric acid not processed well, crystal induced arthritis in lower joints.

52
Q

Renal lithiasis

A

Kidney stones produced from defect in APRT. (Adenine –> AMP)

53
Q

Lesh-Nyhan Syndrome

A

Overproduction of uric acid due to defect in HGPRT enzyme in the purine salvage pathway. May lead to gout, affects CNS.

MCM Boxes (1 decks)

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