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6 Cards in this Set

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Sickle Cell Disease

Basic Cause: RBC shape is distorted. Val (hydrophobic) substituted for Glu (hydrophilic) & interacts with an exposed hydrophobic pocket, initiating Hb polmerization - braid/clumps. Can occlude blood vessels.


Biochemical Cause: Single point mutation (A to T) in the 7th codon of the beta-globin gene. Changes glutamic acid (Glu, hydrophilic) to valine (Val, hydrophobic). Autosomal recessive inheritance.


Effect: Hemolytic crises &/or vaso-occlusive crises. Every organ system could be affected. Fatigue, dizziness, stroke, headaches, jaundice, priapism, enlarged spleen, acute chest syndrome, acute or chronic pain (esp. in bones and joints), cold extremities.


Treatment: Newborns are screened. Proper hydration, avoid any vaso-constrictive meds or conditions that promote hypoxia, extreme temp changes, treat infection promptly (promotes vaso-occlusive crises), take folid acid (promotes RBC synthesis), Hydroxyurea to stimulate body to make fetal Hb

Methanol Poisoning

Basic Cause: Methanol consumption


Biochemical Cause: Alcohol dehydrogenase converts methanol into formaldehyde & formic acid


Effect: Blindness, death


Treatment: Administer alcohol, which competes with the methanol

HIV Infection

Treatment: Ritonavir & Saquinavir, which resemble Phe-Pro containing peptides cleaved by HIV protease during the HIV life cycle

Coumadin

Basic Cause: "Blood thinner" via competitive inhibition


Mode of action: During gamma-carbxylation, vitamin K is oxidized. Vitamin K reductase reduces vitamin K, which is necessary for each subsequent round of gamma-carboxylation. Coumadin is a competitive inhibitor of this reaction, blocks reformation of reduced vitamin K.


Reason for Administration: To prevent blood clots from forming or growing larger

Aspirin

Basic Cause: "Blood thinner" via irreversible inhibition


Mode of Action: Aspirin irreversibly acetylates a serine residue in cyclooxygenase preventing synthesis of TxA2. Effect is retained for the life of the platelet


Reason for Administration: To prevent propagation of clotting activation

Heavy Metal Poisoning


(Arsenic, Lead, Mercury, Cadmium)

High levels exacerbate porphyric attacks by reaction with, and inhibition of, sulfhydral-containing enzymes involved in heme synthesis.


Basic Cause: Acquired disorder of heme synthesis


Biochemical Cause: Heavy metals bind to free sulfhydryl groups. Most lead poisoning symptoms are thought to occur by interfering with delta-aminolevulinic acid dehydratase (ALAD). Heavy metal toxicity is caused by tight binding of a metal to a sulfhydral groups at the active site of an enzyme or distant to the active site (covalent bond). Irreversible inhibition.


Effects: Irritability, poor appetite, lethargy, abdominal pain (with or without nausea), sleeplessness, headaches, constipation.


Treatment: Remove source of exposure. GI decontamination. Chelation therapy.