Week 1 Flashcards
Vitamin B6 deficiency
Associated with microcytic hypochromic anemia. Isoniazid can cause vitamin B6 deficency.
Conjugated “direct” Biliruben
has been processed in the liver so it is soluble in water. It is excreted by the gal bladder, and converted to urobilinogen and makes feces brown.
Unconjugated “indirect” biliruben
Is heme which has been taken from a broken down RBC in the spleen and is not soluble in water, bound to albumin and is sent to the liver.
Porphyrias
Inherited group of disorders from enzyme deficiencies in the pathway for heme biosynthesis. Intermediates of the pathway accumulate and can have toxic effects. Porphiria Tarda is the #1 porpheria and is not life threatening.
Porphyria Cutanea
Can be aquired from “Hepatitis C”. Sx. are bullous dermatois, scarring, hyperpigmentation, and hypertrichosis.
Ferroprotein
is the iron exporter which transports Fe from the enterocyte into the portal plasma
Haephestin
Converts Fe2+ to Fe3+ for transport by transferrin.
Transferrin
Plasma iron transporter, binds 2 molecules of Fe3+
Hepcidin
Is a polypeptide produced in response to inflammation and leads to increased iron stores by preventing Fe release from the cell. Produced by hepatocytes.
Ferretin
is the main source of Fe storage in the cytosol. water soluble and holds up to 4500 atoms of Fe.
Iron deficiency
low ferretin, microcytic anemia. Often due to heavy periods, or a GI bleed in younger individuals. Look for source of blood loss.
hemochromatosis
too much iron in the blood usually treat by phlembotomy
hereditary hemachromatosis
A label for autosomal inherited overload disorders. hereditary conditions affect hepcidin/ ferroportin access. It is genetically heterogenous
Type I hereditary hemachromatosis
Is autosomal recessive, incoplete penetrance. “serum feritin is the reason for increased Iron.” death is from liver cirrhosis, or hepatocellular carcinoma. tx. phembotomy
Oncotic Pressure
In the arterioles, blood pressure forces fluid out. In the venules, oncotic pressure draws fluid back in due to low bp and high protein and solute concentration
Escites
Is a build up of fluid on the belly often due to low albumin levels not drawing fluid back in the venules.
Anemia
When hemoglobin or red blood cells are too low in number.
Metheglobin
Is hemoglobin containing Fe3+. Some NADPH from glycolyisis is used to convert back to hemoglobin using NADPH and glucuronic acid.
Oxidants and the blood
benzocaine, lidocaine nitrites etc. can lead to the oxidation of blood. Treat by the administration of “methylene Blue” or ascorbic acid.
2,3 Bisphosphoglycerate
Allows more o2 release from hemoglobin leading to a shift to the right.
Pentose phosphate pathway
Major source for Reduced NADPH in RBCs, protecting Hb and other stuff from oxidant injury. We need this pathway to regenerate glutathione back to the nonreduced form so it can keep absorbing radicles
Glucose-6-Phosphate Dehydrogenease
Is the enzyme which catalyzes the firs step of the pentose phosphate pathway. erythrocytes cannot make more G6PD. It is the most common enzyme deficiency in the world. It is x-linked. RBCs tend to lyse under conditions of oxidative stress.
Innate immune system
Myleoid precursor, recognizing self from non self
Adaptive immune system
Lymphoid precursor, T and B cells. Ability to recognize and destroy an individual pathogen.