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CPR Exam 2 > Erythrocyte and Heme Biochemistry - Zaidi > Flashcards

Erythrocyte and Heme Biochemistry - Zaidi Flashcards

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1
Q

RBC live how long

A

120 days

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2
Q

most HB is made where

A

in the Normoblast before it ejects its nucleus and becomes a Reticulocyte

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3
Q

Fetal Hb

Adult Hb

A

F : ag

A : aB and ad

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4
Q

Fe on the porphyrin does what when O2 binds

A

conformational change to line up with heme done on proximal F8 histidine or Hb + globin chain
distal histidine increases affinity for O2 = cooperativity

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5
Q

Myoglobin curve

Hemoglobin curve

A

Hyperbolic

Sigmoid = Cooperativity

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6
Q

what makes Hb curve sigmoid

A

cooperativitry and binding affinity of O2 to Hb (66% delivery)

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7
Q

paO2 of exerse and at rest

A

E: 20 (21% delivery)

R : 40 (+ 45% delivery)

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8
Q 
2,3 -BPG does what to Hb curve
pH does what to Hb curve
CO2 does what to Hb curve
H+ does what to Hb curve
Histidine does what to Hb curve
A 
lower O2 affinity (left shift)
lower O2 affinity
Lower O2 affinity
Lower O2 affinity
Lower O2 affinity
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9
Q

reason H+ releases more O2

A

protons stabilize Hb so it can release O2 more easilty

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10
Q

reason HbF has higher affinity to O2

A

it does not respond to 2,3- BPG as well

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11
Q

Sickle Cell anemia

A

B-globin mutation (Glutamic acid –> Valine)

= research try to make HbF in these people (hydroxyurea right now causes inflammation)

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12
Q

Where is Fe stored

A

liver, BM, Spleen, GI

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13
Q

Ferritin

A

binds to Fe+3

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14
Q

Hemosiderin

A

broken down ferritin

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15
Q

how is Fe absorbed from animal products

A
  1. Fe+2 absorbed into Enterocyte
  2. Fe+2 —-> Fe+3 (Ferroxidase cerruloplasm) (TO BE STORED in ferritin)
  3. Fe+2 absorbed into blood by Ferroportin
  4. Fe+2 —-> Fe+3 (Ferroxidase in blood) + bound to transferrin
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16
Q

how is Fe absorbed from non-animal products

A
  1. Fe+3 —-> Fe+2 (Duodenal Cytocrome B, Dcytb)
  2. Fe+2 absorbed into enterocyte (DMT1)
  3. Fe+2 absorbed into blood by Ferroportin
  4. Fe+2 —-> Fe+3 (Ferroxidase in blood) + bound to transferrin
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17
Q

Ferroportin needs what to function

A

Hephaestin

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18
Q

Ferroportin is degraded by what

A

Hepcidin

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19
Q

what does duodenal cyt b need to function

A

VIT C

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20
Q

how is Transferrin taken up by target tissue that need Fe

A

Transferrin binds to TfR
it i internalized
LOW pH = release of Transferrin from TfR
Mito takes FE and makes heme (DMT1)**

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21
Q

what causes Hepcidin to be made

A
  1. Transferrin
  2. TfR
  3. HFE (Human homeostatic iron regulator protein
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22
Q

what does iron deficiency cause

Tx:

A

Hypochromic microcytic anemia, pale (low Hb) small RBCs
(aspirn overuse, X absorption, X Fe in diet, GI lood loss)
Fe supplements

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23
Q

what does iron overload cause
causes
TX:

A 
Hereditary Hemochromatosis (HH)
Fe can accumulate in heart, liver and pancreas
1. MUTATED HFE
2. upregulated absorption 
Blood letting + Fe chelators
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24
Q

what 2 things are important for making RBCs

A

VIT B12 (cobalamin)
FOLATE
= both make DNA

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25
VIT B12 of folate deficiency causes what
Megaloblastic macrocytic anemia (big and normal color (normal Hb levels) RBCs) = shown in blood smear, BM and has hype-segmented N)
26
Folate metabolism involves what steps
1. Folate 2. Dihydrofolate (DHF) = DHF reductase 3, THF = DHF reductase ****active form
27
what is THF truly activated | + function
what it is methylated (methylyne THF = N5-methyl-THF) = synthesis of purines (Formyl THF) + T (methylyne THF) = other DNA synthesis roles
28
Folic acid in what foods
liver, eggs, milk, legumes, yeast, leafy veggies, citrus fruit
29
Folic Acid is absorbed where and how long it
SI jejunum | 3-6 months in liver
30
how is THF unmethylated
by VIT B12
31
Methotrexate
Antineoplastic agent inhibit DHT reductase = X DNA synthesis in RBCs = for treating cancer patients
32
VIT B12 deficiency causes what to happen
Folate is stuck as N5-methyl- THF (folate trap) | megoloblastic macrocytic anemia
33
vit b 12 reaction on folate
N5-methyl- THF ----> B12-CH3 (methyl cobalamin) + THF
34
most causes of Vit b 12 deficiency
X IF = pernicious anemia
35
how is VIT B12 absorbed
1. VitB12 + protien R go to duodenum 2. Parietal cells make IF that go to duodenum 3. Pancrease make protease that degrades Protein R 4. IF binds to VitB12 and go to ileum 5. IF-VitB12 in blood carried by transcobalamin 2
36
how to test for VIT B12 deficiency
GOLD standard = Schilling Test 1. see if labeled B12 is in urine (then it is absorbed, if present = low B12 in diet) 2. if no, see if labeled b12 is in urine when IF is added (then IF deficiency)
37
Heme structure
porphirin ring with Fe+3 in the middle (4 of them are in Hb)
38
what type of Fe is in activated Heme
Fe+2 , ferrous
39
Biosynthesis of Heme happens where
1. Mitochondria 2. Cytosol 3. Mitochondria
40
Phase 1 Heme synthesis
1. Glycine + Succinyl CoA ----> ALA (ALA synthase)
41
what does ALA synthase need to function
VIT B6
42
Part 2 of heme synthesis
ALA go into ctoplasm 1. 2 ALA ----> Porphobilinogen (PBG) by ALA Dehydrogenase **** 2. Hydroxymethylbilane (PBG deaminase) 3. Uro-porphyrinogen 3 (UP 3 synthase) 4. Coprophorynogen 3 (UP 3 decarboxylase)
43
Part 3 of heme synthesis
Coprophorynogen 3 goes to mito 1. CP 3 ----> Protoprophyrinogen 4 (CP 3oxidase) 2. PPP 4 ----> Protoporphyrin 4 (PPP 4 oxidase) 3. PP 4 ----> HEME **** ( Ferrochelatase)
44
- feedback in heme synthesis
HEME and Hemin ----I ALA synthase
45
Lead poisoning caused by
----I ALA dehydrogenase (ALA buildup) ----I Ferrochelatase (PP4 buildup) = ALA resembles GABA, neurotoxic = microcytic + Hypochromic anemia
46
Porphyrias are what acute hepatic : Erythropoietic :
enzyme in making heme X neuro sx skin and photosensitive sx
47
Acute intermittent porphyria
Hepatic | X PBG deaminase (PBG ----> Hydroxymethylbilane)
48
Congenital Erythropoietic Porphyria
Erythropoietic | X UP 3 synthase (Hydroxymethylbilane ----> UP 3)
49
Porythyria Cutanea Tarda
H and E | X UP 3 decarboxylase (UP3 ----> CP3)
50
Variegate Porphyria
H | X PPP 4 oxidase (PPP4 ----> PP4)
51
Congenital Erythropoietic Porphyria SX
build up of Uropophyrinogen 1 (UPP1) ----> uroporphyrin 1 (UP1) = red urine, teeth, photosensitivity
52
Variegate Porphyria SX
"celebrity porphyrias of King George 3) | = Hallucinate , ABD pain, Convulsions, Delirium
53
Hb degradation to what
Globin and Heme
54
Heme degradation
1. cleave bridge = Biliverdin (HEME OXYGENASE + O2) **** | 2. Biliverdin ----> Bilirubin (Biliverdin Reductase)
55
what is released by heme oxygenase
CO take by Hb needs O2 to function Fe+2 ----> Fe +3
56
how is bilirubin conjugated
1. Bilirubin (insoluable) released in BV) + bound to albumin 2. BR-albumin is taken to liver 3. UDP glucouronyltransferase **** RLS****used to conjugate 4. conjugated bilirubin is soluble and goes to gallbladder
57
UDP glucouronyltransferase
RLS for BR conjugation | 2 Glucocuronates + Bilirubin
58
Conjugated BR becomes what it GI----> feces and Kindey----> pee
GI : urobilinogen ----> Stercobilin | Kidney: Urobilin
59
jaundice is caused by
elevated BR
60
Pre-Hepatic jaundice
high UC-BR = hemolytic anemia = mom-fetus blood incompatibilty = internal hemorrhage
61
Intra-Hepatic jaundice
liver problem to conjugate or uptake BR = Criggler-Najjar Syndrome = Gilbert Syndrome
62
Pre-Hepatic jaundice
``` X BR excretion by bile duct HIGH C-BR (found in urine DARK and stool PALE)**** = Chelstatic jaundice , cholestasis =gall stones = drugs ```
63
Criggler-Najjar Syndrome Type 1 Type 2
X UDP - GT 1 : complete loss 2. mutated so some works = brain damage
64
Criggler-Najjar Syndrome Tx
----I heme oxygenase phototherapy eat Ca and carbonate liver transplant
65
Gilbert Syndrome
lowered UDP - GT from stress or alcohol or fasting
66
Hepatitis
inflammed liver from virus, cirrhosis, or cancer HIGH C-BR, UC-BR (skin and sclera yellow) Dark urine
67
bruise color
Red : heme green : biliverdin orange : bilirubin brown : hemosiderin
68
Neonatal Jaundice
normal due to HIGH UC-BR (X or low UDP- GT (usually during HbF breakdown) TX: 1. phototherapy (blue florescent light) = conjugated BR 2. strong ----I heme oxygenase (no heme breakdown)

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