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Hematology-Immunology > RBC Synthesis and Breakdown, Hemoglobin, Myoglobin > Flashcards

RBC Synthesis and Breakdown, Hemoglobin, Myoglobin Flashcards

0
Q

Macrophages

A

eat bacteria and present them to T helper cells
called the soldier or the marine

presents antigen to T cells using ILE-1 (interleukin 1)

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1
Q

Monocyte

A

called monocyte in the blood, but in the tissue, are called macrophages

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2
Q

Basophils

A

called basophils when in the blood but mast cells if in the tissue

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4
Q

Eosinophils

A

allergies and parasitic infections

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5
Q

Neutrophils

A

bacterial infections, granules that can kill bacteria

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6
Q

B cells

A

comes from the bone marrow

‘Bobo’ cells, do their work once out of the bone marrow

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7
Q

T cells

A

comes from the bone marrow but goes to the thymus for maturation. If does not mature, commits apoptosis. Must not react against the body’s own antigens to ‘pass’. If they do not recognize the body’s antigens, they will commit apoptosis

‘Talino’ cells, thymus university (lol), ‘general’

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8
Q

T helper cells

A

help B cells and T cells mature

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9
Q

cytotoxic T cells

A

specific targets: virally infected cells, tumor cells, transplanted / grafted cells

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10
Q

suppressor T cells

A

‘medic’, makes sure that healthy cells are not attacked

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11
Q

memory T cells and memory B cells

A

records events to make sure that future infection will not happen again

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12
Q

B cell activation by T helper cell

A

ILE-4, 5, 6 are needed to activate B cell by T helper cell

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13
Q

plasma cell

A

transformed B cell upon activation by T helper cells. Produces antibodies / immunoglobulins

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14
Q

Immunoglobulins

A

5 types: GAMED. IgG is the smallest, IgM is the largest, first response. IgE involved in parasitic infections and allergies. IgA in secretions (i.e. mucus)

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15
Q

Complement proteins

A

secreted by the liver, found in places with antigen-antibody complexes. ‘like homing missles’ / dog of war

forms membrane attack complex (MAC), causes rupture and activate inflammation, can also recruit macrophages and neutrophils

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16
Q

bag pliability of RBC

A

means that RBC can compress; they are not permanently in biconcave shape

after 120 days, they lose their bag pliability. Once they go to narrow capillaries, they rupture and die (spleen)

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17
Q

Hemoglobin

A

oxygen transport
acts as an acid-base buffer
contains carbonic anhydrase

RBC does not utilize oxygen

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18
Q

Hematocrit

A

percentage of cells in the blood; 40-45% blood volume

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19
Q

Young liver synthesizes blood

A

most of the 2nd trimester RBC production happens in liver.

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20
Q

Erythropoeitin

A

mostly produced in kidneys in response to hypoxia

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21
Q

Anaerobic glycolysis

A

source of energy for RBCs

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22
Q

Vitamin B12 and Folic acid

A

needed for maturation of RBC. Without it, will have megaloblastic anemia (large, fragile, RBC)

folic acid deficiency causes neural tube disorders (froccoli and cauliFlower)
vitamin B12 deficiency: causes neural deficits (baboy, beef)

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23
Q

Reticulocytes

A

immature RBC released into blood. no nucleus, remnants of golgi, mitochondria, other organelles

hemolytic anemia (higher reticulocytes) because of massive death of RBC

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24
Q

Orthochromatic Erythroblast

A

with nucleus, stage of RBC, ER reabsorbed

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25
Q

succinyl CoA

A

from Krebs cycle

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26
Q

hemoglobin alpha and beta

A

most common hemoglobin chains

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27
Q

Porphyrin

A

attaches to iron and formed heme
made up of pyrrole rings
methyne bridges

iron porphyrins - animals
magnesium-containing porphyrins - chlorophyll

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28
Q

Ferrous form

A

active hemoglobin, Fe2+

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29
Q

Transferrin

A

transfers iron from the intestines (duodenum) to the plasma

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30
Q

Ferritin

A

1 storage protein for iron

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31
Q

Hemosiderin

A

storage protein for iron, additional storage area

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32
Q

spleen

A

graveyard of RBC

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33
Q

bilirubin

A

poryphyrin is transformed into this when RBC dies

34
Q

cytochrome P450

A

found in liver, can degrade poison and drugs, contained in heme

35
Q

heme

A

not only found in hemoglobin but also in other enzymes

mostly synthesized in bone marrow, but the rest in hepatocytes

38
Q

Mast cells

A

inflammation, histamine and heparin

39
Q

Uroporphyrinogen III and Coproporphyrinogen III pathway

A

more common than the 1

40
Q

Heme synthesis

A

begins and ends in mitochondria. Intermediate steps in cytoplasm

  1. Formation of gamma aminolevulinic acid (rate limiting step)
  2. Formation of porphobilinogen
  3. Formation of uroporphyrinogen
  4. Formation of heme
41
Q

Uroporphyrinogen decarboxylase

A

turns uroporphyrinogen into coproporphyrinogen, something about acetyl group

42
Q

Ferrochelatase

A

Changes protoporphyrinpgen III into protoporphyrin III

43
Q

Porphyrias

A

abnormalities in heme synthesis pathway
need heme, iron

symptoms:
abdominal pain
photosensitivity
neuropsychiatric symptoms

44
Q

Porphyria Cutanea Tarda

A

Photosensitivity, blistering

45
Q

Photosensitivity

A

abnormalities in late heme synthesis pathway

46
Q

Abdominal pains

A

Abnormalities in early heme synthesis pathway

47
Q

Sideroblastic anemia with ringed sideroblasts

A

mitochondria that is iron-laden, iron is not utilized. Lacking function in ALA synthase. RBC is not properly developed, iron is in the wrong place

48
Q

Iron deficiency

A

not extremely red, RBCs are small.

49
Q

Protoporphyrin 9 / protoporphyrin 3

A

where iron attaches to, using the enzyme ferrocheletase

50
Q

ALA dehydratase

A

responsible for ?

51
Q

Lead poisoning

A

heme not formed
basophilic stippling
micrositic hypochromic anemia
zinc in ALA dehydratase exchanged for lead

52
Q

Bilirubin metabolism

A

Bilirubin is nonpolar, attaches with albumin. Conjugation happens in liver. Transfer glucoronic acid

53
Q

Conjugated bilirubin

A

becomes component of bile

goes to small intestines

54
Q

Bile

A

produced in the liver and stored in the gallbladder

water, cholesterol, bilirubin, bile salts

55
Q

Bile salts

A

Active component of bile, emulsifies fats

56
Q

Bilirubin

A 
comes from dead red blood cells
cannot emulsify
enter the liver
heme is converted into this. 
bilirubin = basura (in pee or in poop)
57
Q

Urobilinogen

A

can be reabosorbed in the intestines or turns up in feces once converted into stercobilin (gives it the yellow / brown color). some are excreted in urine

turns into urobilin upon exposure to air and gives yellow color to urine

58
Q

Urobilin

A

Product of urobilinogen, gives yellow color to urine

59
Q

Stercobilin

A

product of urobilinogen, gives brown color to feces

60
Q

Indirect / unconjugated hyperbilibirunemia

A

cannot be measured directly
total bilib-direct to get the value
indirect reacting, need to add methanol para makita siya
high rbc destruction (hemolytic anemia)

61
Q

direct/conjugated hyperbilibirunemia

A 
direct reacting
caused by bile duct obstruction
can be seen in the blood
why? because veins are forced open (regurgitated in the veins) because of bile duct obstruction
CDR
62
Q

kernicterus

A

unconjugated bilirubin penetrated the blood brain barrier

yellowing of brain of newborns resulting in encephalopathy

63
Q

Hb Gower 1

A

Made up of zeta chains and epsilon chains

64
Q

HbF

A

alpha 2, gamma 2. persists for several weeks and months after birth

65
Q

HbA

A

Seen 8 months onwards. produced in bone marrow

66
Q

HbA2

A

bone marrow

67
Q

Taut form of hemoglobin

A

low oxygen affinity

many salt bridges

68
Q

Relaxed form of hemoglobin

A

high oxygen affinity

little salt bridges

69
Q

positive cooperativity

A

once 1 oxygen attaches, it is much easier for the other oxygens to attach

why? destruction of salt bridges

70
Q

myoglobin

A 
heart and skeletal muscles
reservoir of oxygen
single chain
oxygen carrier
histidine residues
will only release oxygen if cell is hypoxic already
hyperbolic curve
71
Q

myoglobinuria

A

following massive crush injury, myoglobin escapes into urine and colors urine dark red (tea colored)

72
Q

hemoglobin

A

sigmoidal curve

73
Q

allosteric effectors

A

factors found in hemoglobin that will affect binding of oxygen
for hemoglobin only

74
Q

Shifting to the right of the oxy-hemoglobin dissociation curve

A

increase unloading of oxygen by hemoglobin

CABET face right (increase lahat ng factors)
except for: carbon monoxide, fetal hemoglobin (will cause increase binding of oxygen to hemoglobin)

75
Q

shifting to the left of oxy-hemoglobin dissociation curve

A

opposite, increased binding of oxygen to hemoglobin

76
Q

Bohr effect

A

inc in protons cause oxygen to dissociate (increase in acidity)
transport CO2 out of the body
H+ displacing oxygen

high carbon dioxide levels = high metab rates = high demand for oxygen.

77
Q

2,3- Biphosphoglycerate

A

intermediate of glycolysis
BPG mutase converts 1,3 BPG to 2,3 BPG if there is low oxygen in the peripheral tissues
high 2,3 BPG cause unloading of oxygen
found inside RBC
Hypoxia causes erythropoeitin to be released from kidneys, stimulating increase of RBC production. High BPG mutase, high 2,3 BPG, more unloading of oxygen

78
Q

Methemoglobin

A

binds to ferric form
affinity to cyanide
treatment for cyanide poisoning: induce methemoglobinia and the administer methylene blue so patient urinates cyanide

79
Q

Carboxyhemoglobin

A

cherry pink patient

high carbon monoxide. shift to the left, oxygen bound tightly to hemoglobin

80
Q

Glycosylated hemoglobin

A

attachment of glucose to HbA1C

81
Q

Sickle cell disease

A

glutamate substituted for valine (polar substituted for nonpolar)

82
Q

Alpha thalassemia

A 
alpha chain. 4 genes encodes for the chains. 
1 affected = silent carrier
2: alpha thalassemia trait
3: Hb H Disease
4: Hydrops fetalis
83
Q

Beta Thalassemia

A

only 2 genes

manifestations only after birth

Hematology-Immunology (5 decks)

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