MTC Exam III part VI

Question 1

Sodium
(trace mineral)
biochem, deficiency, toxicity, type

Answer 1

B: Extracellular ion that maintains the electrical and osmotic balance of the cell
D: Primary deficiency rare but leads to hyponatremia. Can cause CNS edema, nausea, vomiting, headache, confusion, irritability, fatigue, hallucinations, muscle weakness.
toxicity: We take in lots of salt, and we can usually excrete lots of salt, though this may eventually lead to hypertension.
type: electric/osmotic

Question 1

What are the two major pathways for the first step of alcohol metab?

Answer 1

ADH in the cytoplasm (ADH=alcohol dehydrogenase). generates NADH from NAD
CYP2E21- cyt p450 system. in ER. this can be upregulated with chronic alcohol use –> tolerance

Question 2

Potassium
(trace mineral)
biochem, deficiency, toxicity, type

Answer 2

biochem: osmotic potential. It is the principle intracellular cation. It can also respond to insulin: enters the cells as a rxn to insulin
Deficiency: primary deficiency can lead to cardiac arrhythmias and muscle weakness and glucose intolerance.
Subclinical deficiency may exacerbate hypertension

Question 3

chloride
(trace mineral)
biochem, deficiency, type

Answer 3

B: primary anion and important for acid-base balance. helps make HCl
Deficiency: growth failure, lethargy, irritability, weakness, GI distress
Type: osmotic/electric

Question 3

trimethylaminuria

Answer 3

defect in flavin-containing monooxygenase 3. get fishy odor after eating choline, as in soybeans, liver, fish, or egg consumption. autosomal recessive

Question 4

Magnesium biochem functions

Answer 4

Biochem: slow, chronic regulator of biological functions. Linked with controll of cell growth ,energy metabolism, and cell death
Very common cofactor/allosteric regulator.
Complexes with ATP and useful in mitochondria.
Mg also helsp bind phosphate in the linkages of DNA and RNA and stabilizes the molecules. Without Mg, we see cell cycle arrest.
Mg blocks Glutamate-NMDA receptors in neural tissue
Helps faciliate the cross-bridge cycle in muscle

Question 4

What are the two steps of alcohol metab?

Answer 4

EtOH to acetaldehyde to acetate

Question 5

Mg: sources and absorption

Answer 5

Sources: green leafy veggies: Mg is bound to the chlorophyll molecule
Absorbed passively in large intestine

Question 6

Mg Deficiency and toxicity

Answer 6

Deficiency: neuromuscular excitability and impaired insulin secretion
toxicity: diarrhea, drowsiness, lethargy, and weakness. often used in antacids and laxatives

Question 7

What foods have lots of zinc and copper?

Answer 7

shellfish, grains, legumes

Question 8

Copper: (trace mineral)

biochem

Answer 8

type: trace mineral
biochem: helps with oxidase enzymes (cytochrome oxidase, super-oxide disumuaste, lysyl oxidase for collagen synthesis, monamine oxidase for neurtransmitter cataboism
ceruloplasmin: reactant in the immune system that mobilizes transport of iron into RBCs

Question 9

copper deficiency

Answer 9

deficiency:
Menkes disease: x linked recessive disorder that alters the distribution of copper. kids have super kinky hair., skeletal abnormalities, failure to thrive, and infections

Dietary probs usually due to gastric bypass surgery or excess zinc consumption. Mostly neuro symptoms like ataxia and neuropathy and anemia.

Question 10

copper toxicity

Answer 10

usually seen with fungicides or contaminated water or very high amts of supplementation
symptoms: GI probs, brain and liver damage

Question 11

zinc biochemsitry

Answer 11

enzyme cofactor. examples include carbonic anhydrase, which converts CO2 and bicarb and DNA/RNA pol
also improtant in TF factors that have zinc finger domains
also in prostate gland functions - Zn regulates m-acontiase: prostates like to secrete citrate in seminal fluids.
Brain function: modutlates synaptic transmission and plasticity

Question 12

zinc deficiency

Answer 12

common in pts with diabetes, alcoholism, or liver disease. problems are hypogonadis, deformed bones, poor wound healing, abnormal hair or nais, loss of taste, and CNS abnormalities
may also be due to autosomal recessive disorder in infants

Question 13

chromium: (trace mineral)

biochem, deficiency, toxicity, type

Answer 13

biochem: helps with glucose homeostast. part of apo-chromodulin which enhances the effects of insulin.
deficiency: not known
toxicity: cancer

Question 14

Selenium: (trace mineral)

biochem, deficiency, toxicity, type

Answer 14

biochem: part of glutathione peroxidase, which is an antioxident
plays a role in thyroid function where it is bound to de-iodinase enzymes
Deficiency: cardiac wasting (Keshan’s disease) and muscular wasting. due to probs with free radicals.
toxicity: maybe slight increase in skin cancer risk?

Question 15

glucose-6-phosphate dehydrogenase deficiency

Answer 15

G6PD is the enzyme used in the first step of NADPH synthesis. NADPH is needed in both pathways employed to detox H2O2.
In this case, G6PD deficiency leads to a loss of reduction ability and we see hemolysis. Crises are triggered by fava beans, sulfa drugs, or anti-malarial drugs. X-linked disorder. Also a problem in factory workers exposed to aniline.

Question 17

butyrylcholinesterase deficiency

Answer 17

metabolizes succinylcholine, which is a short-acting muscle relaxant for induction of anesthesia. If deficient, you must adjust dose and provide more mechanical ventilation. Autosomal recessive.

Question 18

trimethylaminuria

Answer 18

defect in flavin-containing monooxygenase 3. get fishy odor after eating choline, as in soybeans, liver, fish, or egg consumption. autosomal recessive

Question 19

malignant hyperthermia

Answer 19

ryanodine receptor mutation that is autosomal dominant. leads to muscle rigidity, extremely high fever, respiratory and metabolic acidosis, hyperkalemia, myoglobinuria, and consumptive coagulopathy.
treated with dantrolene.

Question 20

marasmus

Answer 20

deficiency in dietary calories. body uses its own energy, leading to wasting, irregular vitals, low weight for height, bradycardia, hypotension, hypothermia, thin hair, weakness, anemia, wrinkled skin, irritability

Question 21

3 major metabolic consequences of excessive alcohol consumption

Answer 21

hypoglycemia, lactic acidosis, ketoacidosis

Question 22

where is alcohol absorbed?

Answer 22

stomach (slow), upper GI tract (fast)

Question 23

Kwashiorkor

Answer 23

deficiency of protein relative to total calorie intake: sickness of weaning. Edema, protuberant abdomen, hair loss, skin lesions, infection susceptibility, hyper/hypopigmentation, apathy, loss of appetite, decreased blood albumin, low BUN, hypokalemia. hypernatremia and hyperchloremia

Question 24

What are the two major pathways for the first step of alcohol metab?

Answer 24

ADH in the cytoplasm (ADH=alcohol dehydrogenase). generates NADH from NAD
CYP2E21- cyt p450 system. in ER. this can be upregulated with chronic alcohol use –> tolerance

Question 25

what is the 2nd step of alcohol metab?

Answer 25

acetaldehyde to acetate in the mitochondria. converted via ALDH (acetaldehyde dehydrogenase). Generates another NADH.
ADLH2*2: polymorphism with incomplete dominance that makes drinking both more unpleasent and more dangerous (common among Asians)

Question 26

How do we regenerate NAD after alcohol consumption?

Answer 26

1. pyruvate reduction to lactate
2. OAA to malate regenrates NAD, but causes hypoglycemia
3. Ketone genesis

Question 27

alpha-1-antitrypsin deficiency

Answer 27

alpha-1-antitrypsin is an inhibitor of proteolytic enzymes. these patients get emphysema and cirrhosis and COPD. Common allele is the Z allele, which as an aa substitution that prevents proper liver secretion (leads to apoptosis). Smoking is very bad for these pts.

Question 29

Aminoglycoside-induced deafness

Answer 29

dose dependent complication. mitochondrial inheritance that has tight binding of aminoglycoside to ribosome leading to lack of protein synthesis. Exp. in ear (irreversible) and kidney (reversible)

Question 29

why do we see fatty liver in kwashiorkor?

Answer 29

not enough apolipprotein B-100, so we can’t make VLDLs and triglycerides get stuck in liver.