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

Erythrocyte and Heme Biochemistry - Zaidi Flashcards

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
Q

VIT B12 of folate deficiency causes what

A

Megaloblastic macrocytic anemia (big and normal color (normal Hb levels) RBCs)
= shown in blood smear, BM and has hype-segmented N)

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26
Q

Folate metabolism involves what steps

A
  1. Folate
  2. Dihydrofolate (DHF) = DHF reductase
    3, THF = DHF reductase **active form
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27
Q

what is THF truly activated

+ function

A

what it is methylated (methylyne THF = N5-methyl-THF)
= synthesis of purines (Formyl THF) + T (methylyne THF)
= other DNA synthesis roles

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28
Q

Folic acid in what foods

A

liver, eggs, milk, legumes, yeast, leafy veggies, citrus fruit

29
Q

Folic Acid is absorbed where and how long it

A

SI jejunum

3-6 months in liver

30
Q

how is THF unmethylated

A

by VIT B12

31
Q

Methotrexate

A

Antineoplastic agent
inhibit DHT reductase = X DNA synthesis in RBCs
= for treating cancer patients

32
Q

VIT B12 deficiency causes what to happen

A

Folate is stuck as N5-methyl- THF (folate trap)

megoloblastic macrocytic anemia

33
Q

vit b 12 reaction on folate

A

N5-methyl- THF —-> B12-CH3 (methyl cobalamin) + THF

34
Q

most causes of Vit b 12 deficiency

A

X IF = pernicious anemia

35
Q

how is VIT B12 absorbed

A
  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
Q

how to test for VIT B12 deficiency

A

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
Q

Heme structure

A

porphirin ring with Fe+3 in the middle (4 of them are in Hb)

38
Q

what type of Fe is in activated Heme

A

Fe+2 , ferrous

39
Q

Biosynthesis of Heme happens where

A
  1. Mitochondria
  2. Cytosol
  3. Mitochondria
40
Q

Phase 1 Heme synthesis

A
  1. Glycine + Succinyl CoA —-> ALA (ALA synthase)
41
Q

what does ALA synthase need to function

A

VIT B6

42
Q

Part 2 of heme synthesis

A

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
Q

Part 3 of heme synthesis

A

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
Q
  • feedback in heme synthesis
A

HEME and Hemin —-I ALA synthase

45
Q

Lead poisoning caused by

A

—-I ALA dehydrogenase (ALA buildup)
—-I Ferrochelatase (PP4 buildup)
= ALA resembles GABA, neurotoxic
= microcytic + Hypochromic anemia

46
Q

Porphyrias are what
acute hepatic :
Erythropoietic :

A

enzyme in making heme X
neuro sx
skin and photosensitive sx

47
Q

Acute intermittent porphyria

A

Hepatic

X PBG deaminase (PBG —-> Hydroxymethylbilane)

48
Q

Congenital Erythropoietic Porphyria

A

Erythropoietic

X UP 3 synthase (Hydroxymethylbilane —-> UP 3)

49
Q

Porythyria Cutanea Tarda

A

H and E

X UP 3 decarboxylase (UP3 —-> CP3)

50
Q

Variegate Porphyria

A

H

X PPP 4 oxidase (PPP4 —-> PP4)

51
Q

Congenital Erythropoietic Porphyria SX

A

build up of Uropophyrinogen 1 (UPP1) —-> uroporphyrin 1 (UP1)
= red urine, teeth, photosensitivity

52
Q

Variegate Porphyria SX

A

“celebrity porphyrias of King George 3)

= Hallucinate , ABD pain, Convulsions, Delirium

53
Q

Hb degradation to what

A

Globin and Heme

54
Q

Heme degradation

A
  1. cleave bridge = Biliverdin (HEME OXYGENASE + O2) **

2. Biliverdin —-> Bilirubin (Biliverdin Reductase)

55
Q

what is released by heme oxygenase

A

CO take by Hb
needs O2 to function
Fe+2 —-> Fe +3

56
Q

how is bilirubin conjugated

A
  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
Q

UDP glucouronyltransferase

A

RLS for BR conjugation

2 Glucocuronates + Bilirubin

58
Q

Conjugated BR becomes what it GI—-> feces and Kindey—-> pee

A

GI : urobilinogen —-> Stercobilin

Kidney: Urobilin

59
Q

jaundice is caused by

A

elevated BR

60
Q

Pre-Hepatic jaundice

A

high UC-BR
= hemolytic anemia
= mom-fetus blood incompatibilty
= internal hemorrhage

61
Q

Intra-Hepatic jaundice

A

liver problem to conjugate or uptake BR
= Criggler-Najjar Syndrome
= Gilbert Syndrome

62
Q

Pre-Hepatic jaundice

A 
X BR excretion by bile duct 
HIGH C-BR (found in urine DARK and stool PALE)****
= Chelstatic jaundice , cholestasis
=gall stones
= drugs
63
Q

Criggler-Najjar Syndrome
Type 1
Type 2

A

X UDP - GT
1 : complete loss
2. mutated so some works
= brain damage

64
Q

Criggler-Najjar Syndrome Tx

A

—-I heme oxygenase
phototherapy
eat Ca and carbonate
liver transplant

65
Q

Gilbert Syndrome

A

lowered UDP - GT from stress or alcohol or fasting

66
Q

Hepatitis

A

inflammed liver
from virus, cirrhosis, or cancer
HIGH C-BR, UC-BR (skin and sclera yellow)
Dark urine

67
Q

bruise color

A

Red : heme
green : biliverdin
orange : bilirubin
brown : hemosiderin

68
Q

Neonatal Jaundice

A

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)

CPR Exam 2 (22 decks)

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