MTC Exam III part VI Flashcards
Sodium
(trace mineral)
biochem, deficiency, toxicity, type
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
What are the two major pathways for the first step of alcohol metab?
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
Potassium
(trace mineral)
biochem, deficiency, toxicity, type
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
chloride
(trace mineral)
biochem, deficiency, type
B: primary anion and important for acid-base balance. helps make HCl
Deficiency: growth failure, lethargy, irritability, weakness, GI distress
Type: osmotic/electric
trimethylaminuria
defect in flavin-containing monooxygenase 3. get fishy odor after eating choline, as in soybeans, liver, fish, or egg consumption. autosomal recessive
Magnesium biochem functions
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
What are the two steps of alcohol metab?
EtOH to acetaldehyde to acetate
Mg: sources and absorption
Sources: green leafy veggies: Mg is bound to the chlorophyll molecule
Absorbed passively in large intestine
Mg Deficiency and toxicity
Deficiency: neuromuscular excitability and impaired insulin secretion
toxicity: diarrhea, drowsiness, lethargy, and weakness. often used in antacids and laxatives
What foods have lots of zinc and copper?
shellfish, grains, legumes
Copper: (trace mineral)
biochem
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
copper deficiency
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.
copper toxicity
usually seen with fungicides or contaminated water or very high amts of supplementation
symptoms: GI probs, brain and liver damage
zinc biochemsitry
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
zinc deficiency
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
chromium: (trace mineral)
biochem, deficiency, toxicity, type
biochem: helps with glucose homeostast. part of apo-chromodulin which enhances the effects of insulin.
deficiency: not known
toxicity: cancer
Selenium: (trace mineral)
biochem, deficiency, toxicity, type
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?
glucose-6-phosphate dehydrogenase deficiency
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.
butyrylcholinesterase deficiency
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.
trimethylaminuria
defect in flavin-containing monooxygenase 3. get fishy odor after eating choline, as in soybeans, liver, fish, or egg consumption. autosomal recessive
malignant hyperthermia
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.
marasmus
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
3 major metabolic consequences of excessive alcohol consumption
hypoglycemia, lactic acidosis, ketoacidosis
where is alcohol absorbed?
stomach (slow), upper GI tract (fast)
Kwashiorkor
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
What are the two major pathways for the first step of alcohol metab?
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
what is the 2nd step of alcohol metab?
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)
How do we regenerate NAD after alcohol consumption?
- pyruvate reduction to lactate
- OAA to malate regenrates NAD, but causes hypoglycemia
- Ketone genesis
alpha-1-antitrypsin deficiency
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.
Aminoglycoside-induced deafness
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)
why do we see fatty liver in kwashiorkor?
not enough apolipprotein B-100, so we can’t make VLDLs and triglycerides get stuck in liver.
