Vitamins and Minerals Flashcards
In what organs is excess iron stored
Liver, spleen, bone marrow
Pathophysiology of iron poisoning
Causes peroxidation of membrane lipids and free radical generation
symptoms of acute iron poisoning
GI: nausea/vomiting, gastric bleeding (iron settles in the stomach), hematemesis, abdominal pain. If bleeding severe - hypovolemic shock
Symptoms of iron poisoning 6-72 hours after ingestion
Metabolic acidosis
Symptoms of iron poisoning 2-8 weeks after ingestion
Scarring of GI tract, obstruction
Ferritin
Iron-protein complex of ferric acid and apoferritin, is cellular storage protein for iron
An acute phase reactant - take it away from circulation from bacteria who like iron
Transferrin
Protein that binds ferric molecules and transports them through plasma
Made in liver
What are the levels of transferrin in iron deficiency
Increased - cells hungry for iron so looking for transport molecule to bring them more
Half life of transferrin
8 days
Function of Zinc
Essential for 100+ enzymes Important in formation of zinc fingers (transcription factor motif) Healing, immune system Essential for carbonic anhydrase Essential for lactate dehydrogenase
Zinc deficiency
Delayed wound healing Decreased body and facial hair Hypogonadism Anosmia Dysgeusia Decr immune response Rash around eyes, mouth, nose, anus (acrodermatitis) Anorexia and diarrhea Growth retardation Depressed mental function Infertility
What is acrodermatitis
Rash seen in zinc deficiency - around eyes, mouth, nose, and anus
Signs of lead poisoning
Decreased IQ, hearing problems, growth impairment, impaired peripheral nerve function (wrist, foot drop), lead lines in growing bones and teeth (burton’s lines)
With severe: Anemia, colic/abd pain, nephropathy, encephalopathy
What enzymes does lead inhibit
Ferrochelatase and ALA dehydratase –> decreased heme synthesis and increased RBC protoporphyrin
What is basophilic stippling
RBCs retain aggregates of rRNA because lead inhibits rRNA degradation
Treatment of lead poisoning in kids vs adults
Remove exposure
1st line: Dimercaprol (SEVERE) and EDTA
Kids: Succimer
Where does mercury accumulate
Kidney and brain
Side effects of mercury poisoning
Neuropsych effects
Acrodynia - peeling of fingertips
Bluish colored lines on gingivae
Burton’s lines = lead poisoning
Ergocalciferol
D2 - ingested form - from plants
Cholecalciferol
D3 - synthesized in skin
25-OH D3
Made in the liver from D3
1,25 DHCC
Physiologic active form in vitamin D, made in kidneys
FUnction of 1,25 DHCC
- Increases Calcium uptake in intestine by increasing expression of calcium binding protein
- Works in intestine to increase absorption of Mg and P
- Stimulates PTH-dependent reabsorption in distal tubules
- Stimulates bone reabsorption when necessary (with PTH)
Vit D deficiency mechanisms
- Inadequate dietary
- Impaired hydroxylation by liver
- Impaired hydroxylation by kidneys
- End organ insensitivity
Vit D deficiency clinical
Rickets/Osteomalacia
Demineralization problems of bone
Bone tenderness, skeletal deformities, bowing of legs, growth problems, pathologic fractures, dental problems
Pathophysiology of Vit D deficiency
Serum calcium drops so PTH increases which breaks down bone, decreasing serum phosphate and trying to increase serum calcium
Vitamin D toxicity
Too much Vitamin D supplementation
Hypercalcemia
From sarcoidosis - increase conversion to 1,25 from macrophages in granulomas
Vitamin K
Involved in post translational modification of clotting factors
Made in intestinal flora
Clotting factors dependent on K
Protein C and S
Prothrombin
2, 7, 9, X