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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
succinyl CoA
from Krebs cycle
26
hemoglobin alpha and beta
most common hemoglobin chains
27
Porphyrin
attaches to iron and formed heme made up of pyrrole rings methyne bridges iron porphyrins - animals magnesium-containing porphyrins - chlorophyll
28
Ferrous form
active hemoglobin, Fe2+
29
Transferrin
transfers iron from the intestines (duodenum) to the plasma
30
Ferritin
#1 storage protein for iron
31
Hemosiderin
storage protein for iron, additional storage area
32
spleen
graveyard of RBC
33
bilirubin
poryphyrin is transformed into this when RBC dies
34
cytochrome P450
found in liver, can degrade poison and drugs, contained in heme
35
heme
not only found in hemoglobin but also in other enzymes | mostly synthesized in bone marrow, but the rest in hepatocytes
38
Mast cells
inflammation, histamine and heparin
39
Uroporphyrinogen III and Coproporphyrinogen III pathway
more common than the 1
40
Heme synthesis
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
Uroporphyrinogen decarboxylase
turns uroporphyrinogen into coproporphyrinogen, something about acetyl group
42
Ferrochelatase
Changes protoporphyrinpgen III into protoporphyrin III
43
Porphyrias
abnormalities in heme synthesis pathway need heme, iron symptoms: abdominal pain photosensitivity neuropsychiatric symptoms
44
Porphyria Cutanea Tarda
Photosensitivity, blistering
45
Photosensitivity
abnormalities in late heme synthesis pathway
46
Abdominal pains
Abnormalities in early heme synthesis pathway
47
Sideroblastic anemia with ringed sideroblasts
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
Iron deficiency
not extremely red, RBCs are small.
49
Protoporphyrin 9 / protoporphyrin 3
where iron attaches to, using the enzyme ferrocheletase
50
ALA dehydratase
responsible for ?
51
Lead poisoning
heme not formed basophilic stippling micrositic hypochromic anemia zinc in ALA dehydratase exchanged for lead
52
Bilirubin metabolism
Bilirubin is nonpolar, attaches with albumin. Conjugation happens in liver. Transfer glucoronic acid
53
Conjugated bilirubin
becomes component of bile | goes to small intestines
54
Bile
produced in the liver and stored in the gallbladder | water, cholesterol, bilirubin, bile salts
55
Bile salts
Active component of bile, emulsifies fats
56
Bilirubin
``` comes from dead red blood cells cannot emulsify enter the liver heme is converted into this. bilirubin = basura (in pee or in poop) ```
57
Urobilinogen
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
Urobilin
Product of urobilinogen, gives yellow color to urine
59
Stercobilin
product of urobilinogen, gives brown color to feces
60
Indirect / unconjugated hyperbilibirunemia
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
direct/conjugated hyperbilibirunemia
``` 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
kernicterus
unconjugated bilirubin penetrated the blood brain barrier | yellowing of brain of newborns resulting in encephalopathy
63
Hb Gower 1
Made up of zeta chains and epsilon chains
64
HbF
alpha 2, gamma 2. persists for several weeks and months after birth
65
HbA
Seen 8 months onwards. produced in bone marrow
66
HbA2
bone marrow
67
Taut form of hemoglobin
low oxygen affinity | many salt bridges
68
Relaxed form of hemoglobin
high oxygen affinity | little salt bridges
69
positive cooperativity
once 1 oxygen attaches, it is much easier for the other oxygens to attach why? destruction of salt bridges
70
myoglobin
``` 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
myoglobinuria
following massive crush injury, myoglobin escapes into urine and colors urine dark red (tea colored)
72
hemoglobin
sigmoidal curve
73
allosteric effectors
factors found in hemoglobin that will affect binding of oxygen for hemoglobin only
74
Shifting to the right of the oxy-hemoglobin dissociation curve
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
shifting to the left of oxy-hemoglobin dissociation curve
opposite, increased binding of oxygen to hemoglobin
76
Bohr effect
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
2,3- Biphosphoglycerate
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
Methemoglobin
binds to ferric form affinity to cyanide treatment for cyanide poisoning: induce methemoglobinia and the administer methylene blue so patient urinates cyanide
79
Carboxyhemoglobin
cherry pink patient | high carbon monoxide. shift to the left, oxygen bound tightly to hemoglobin
80
Glycosylated hemoglobin
attachment of glucose to HbA1C
81
Sickle cell disease
glutamate substituted for valine (polar substituted for nonpolar)
82
Alpha thalassemia
``` alpha chain. 4 genes encodes for the chains. 1 affected = silent carrier 2: alpha thalassemia trait 3: Hb H Disease 4: Hydrops fetalis ```
83
Beta Thalassemia
only 2 genes | manifestations only after birth

Hematology-Immunology (5 decks)

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