Week 1 Flashcards Preview

IHO > Week 1 > Flashcards

Flashcards in Week 1 Deck (41):
1

Vitamin B6 deficiency

Associated with microcytic hypochromic anemia. Isoniazid can cause vitamin B6 deficency.

2

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.

3

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.

4

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.

5

Porphyria Cutanea

Can be aquired from "Hepatitis C". Sx. are bullous dermatois, scarring, hyperpigmentation, and hypertrichosis.

6

Ferroprotein

is the iron exporter which transports Fe from the enterocyte into the portal plasma

7

Haephestin

Converts Fe2+ to Fe3+ for transport by transferrin.

8

Transferrin

Plasma iron transporter, binds 2 molecules of Fe3+

9

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.

10

Ferretin

is the main source of Fe storage in the cytosol. water soluble and holds up to 4500 atoms of Fe.

11

Iron deficiency

low ferretin, microcytic anemia. Often due to heavy periods, or a GI bleed in younger individuals. Look for source of blood loss.

12

hemochromatosis

too much iron in the blood usually treat by phlembotomy

13

hereditary hemachromatosis

A label for autosomal inherited overload disorders. hereditary conditions affect hepcidin/ ferroportin access. It is genetically heterogenous

14

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

15

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

16

Escites

Is a build up of fluid on the belly often due to low albumin levels not drawing fluid back in the venules.

17

Anemia

When hemoglobin or red blood cells are too low in number.

18

Metheglobin

Is hemoglobin containing Fe3+. Some NADPH from glycolyisis is used to convert back to hemoglobin using NADPH and glucuronic acid.

19

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.

20

2,3 Bisphosphoglycerate

Allows more o2 release from hemoglobin leading to a shift to the right.

21

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

22

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.

23

Innate immune system

Myleoid precursor, recognizing self from non self

24

Adaptive immune system

Lymphoid precursor, T and B cells. Ability to recognize and destroy an individual pathogen.

25

Interferons

are cytokines that limit the spread of viral infections

26

Type 1 interferons

INFalpha and INFBeta produced by cells infected with a virus

27

Type 2 interferons

INF gamma. Released by activated T helper cells to initiate a response in an area of viral infection

28

Toll- like receptors

One family of PAMPs (pathogen associated molecular patterns)

29

TLR3

Recognizes dsRNA and leads to signal transduction of phosphoylation cascade, degradation of IkB releasing NFkB acting as atranscription factor to make INF-B which is secreted out ot the cell to neighboring cells leading to activation of antiviral genes.

30

Epitope

The specific location of an antigen that an antibody binds.

31

Pluripotent stem cell differentiation

IL3 leads to lymphoid progenitor
IL3 and GM-CSF (granulocyte monocyte colony stimulating factor) are present, it will become a myeloid progenitor.

32

Chemokines

Are cytokines which attract cells into inflammed tissues.

33

Diapedesis

The process in which neutrophils, and monocytes and probally others leave the blood stream into the tissues.

34

Erythrocyte series steps

Proerythroblast (blast)
Basophilic erythroblast
Polychromatophilic erythroblast
Orthochromic erythroblast
Reticulocyte
RBC

35

Granulocyte series Steps

Myeloblast
Promyelocyte
Myelocyte
Metamyelocyte
Band
Mature

36

MCV

Mean corpuscular Volume, how much volume the RBC has. How big is it and is useful for assessing anemia.

37

Direct Antiglobulin Test

Antihuman-antibody antibodies added to blood sample. If red blood cells link together and precipitate out (positive test), it means our own body is attacking the RBCs and is an autoimmune disorder.

38

Hereditary Spherocytosis

Anemia, Jaundice, splenomegaly. Due to defect in spectrin, leading to spherical RBCs which get taken out by the spleen. tx is splenectomy or transfusions.

39

Leukoerythroblastotic Reaction

Is when immature erythrocytes and lymphocytes are present in the blood. May be malignant or benign.
Low hemoglobin= physiologic
High hemoglobin= likely marrow tumor

40

Lymphocytosis

high white count. If it is all one type of cell, then it is likely malignant. Mature= lots of mature lymphocytes. Reactive= lots of funny looking or not normal lymphocyte precursors. Often caused by infectious MONO

41

Benign vs malignant Lymphocytosis

Benign= toxic changes, fewer immature cells, no basophillia, LAP normal/ increased
Malignant= very high WBC, lots of immature cells, basophillia, LAP decreased. LAP- enzyme not present in malignant cells