Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMS200 > wk 11, lec 2 > Flashcards

wk 11, lec 2 Flashcards

1
Q

what are red blood cells aka

A

erythrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what do RBCs contain

A
  • Carry O2
  • Contain hemoglobin  bind O2 in lungs and release in tissues (for gas transport and exchange)
  • Remove CO2 (bring back to lungs for exhalation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

where are RBCs made

A
  • Made in bone marrow
    o Erythron= proliferating marrow erythroid precursors + circulating RBCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

RBC lifecycle

A

120 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where are RBC recycled

where are made in fetus

A
  • Recycled in liver and spleen
    o Made in spleen and liver in fetus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

shape of RBC

A
  • Biconcave shape; maximize SA for gas exchange and to move through vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when will hemoglobin bind and dissociate at low and high [ ]

A

o Hemoglobin binds oxygen at high [ ]
o Oxygen dissociates from Hb at low [ ]
o Healthy O2 saturation in Hb is 95-99%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

when will Hb bind Co2

A

o HB binds CO2 with low affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what do RBCs have to convert CO2 in bicarbonate HCO3-

A

carbonic anhydrase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what do RBC lack

A

nuclei

o Cant synthesize protein and limit lifespan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are RBC derived from

A

from myeloid progenitor (pronormoblast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

steps to form RBC

A
  • RBCs derived from myeloid progenitor (pronormoblast)
    o Stimulated to divide by GM-CSF and erythropotein (EPO)
    o Before nucleus extruded; RBC accumulate Hb and proteins
    o The late normoblast because anucleate
    o Reticulocyte has remnants of golgi, ER, ribosomes which get extruded to become mature RBC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what 2 things stimulate myeloid progensit to divide and get closer to being RBC

A

GM-CSF and erythropoietin (EPO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how many times does pronormoblast divide to make RBC and via stimulation of what

A
  • Pronormoblast divides to make 16-32 mature RBCs via EPO stimulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

where is EPO erythropoietin made

A

kidneys by epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  • EPO made in kidney by epithelial cells ; what happens in high vs low oxygen conditions
A

o High oxygen conditions= hypoxia inducible factor (HIF) is ubiquinated and degraded by proteasomes

o Low oxygen conditions= HIF binds proteins, is translocated to the nucleus and stimulates EPO production (make more RBCs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

high or low oxygen to make EPO

A

low oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

generation of RBC depends on

A

EPO, bone marrow, adequate iron and amino acids for HB production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

which energy pathway for RBC to get ATP

A
  • RBC need glycolysis for ATP (no oxidative metabolism bc no mitochondria)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what antioxidant to RBC have

A
  • RBC have glutathione stores when in high oxygen and cant make new proteins need to be able to combat free radical production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cytoskeleton in RBC - if absent what disorder does it cause

A
  • Cytoskeletal proteins help RBC maintain shape –> disorder = loss of red cell mass (anemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

subunits in hemoglobin

A

2 alpha and 2 other chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what does each subunit in hemoglobin contain

A

o Each subunit has heme moiety containing iron to bind oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the majority type of hemoglobin and what is less

A
  • 97% is HbA (2 alpha, 2 beta chains)
    o 2% is HbA2 (2 alpha, 2 delta chains)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

fetal hemoglobin

A

o Fetal Hb (2 alpha, 2 gamma) – very high affinity for oxygen bc cant bind 2,3 DPG well

26
Q

what has a higher affinity for hemoglobin that oxygen

A
  • Carbon monoxide has 200x higher affinity for Hb than oxygen
    o Forms carboxyhemoglobin
27
Q

how is heme made

A
  • Heme is made through reactions with glycine and succinyl-CoA precursors
28
Q

what is the hemoglobin dissociation curve

what 4 things decrease hemoglobin affinity for oxygen**

A
  1. increase temp
  2. increase DPG
  3. increase PCO2
  4. decrease pH
29
Q

where are RBCs eliminated

A

by macrophages in spleen red pulp

30
Q

how is hemoglobin metabolized

where does the iron go? where does the heme go? where does the globin go?

A

o Iron recycled and sent back to bone marrow
o Heme eliminated in bile and stool as bilirubin
o Globin is recycled into its component amino acids

31
Q

what happens to senescent (old) erythrocytes/ RBCs

A
  • Senescent (old) erythrocytes are phagocytosed by macrophages and heme degraded into biliverdin then bilirubin and released into blood
32
Q

what is heme degraded into

A

degraded into biliverdin then bilirubin and released into blood
o Unconjugated bilirubin carried to liver bound by albumin

33
Q

what is unconjugated bilirubin carrier to the liver by

A

albumin

34
Q

where is bilirubin conjugated and how

A

in the liver

o Add 1-2 residues of glucuronic acid
o Catalyzed by uridine diphosphate glucanosyltransferase (UDG)

35
Q

how is conjugated bilirubin excreted

A
  • Bilirubin glucuronide excreted into bile
36
Q

where is iron absorbed

A

duodenum

37
Q

what is better absorbed fe2+ or fe3+

A

fe2+

38
Q

how is iron transported

A

o Transported through divalent metal transporter (DMT)

39
Q

what prevents iron overload

A

hepcidin

40
Q

hepcidien function

A

o Excess iron can damage cells so liver transport iron from enterocytes into bloodstream via hepcidin
 Hepcidin prevents iron overload

41
Q

what does hepcidin block

A

ferroportin transporter

42
Q

what is hepcidin stimulated by

A

inflammation IL-6

43
Q

what is hepcidin inhibited by

A

reduced iron stores and erythroferrone (released by developing erythroblasts)

44
Q

what does transferrin transporter accept iron from

A
  • Transferrin transporter transport iron though blood
    o Accepts iron from ferroportin
45
Q

cells with transferring receptors do what

A
  • Cells with transferrin receptors can endocytose transferrin and store it in ferritin protein complex
46
Q

where is iron stored

A
  • Store iron in hepatocytes, spleen, and bone marrow
47
Q

storage form of ferritin is

A

hemosiderin

48
Q

what % of anemia is iron deficiency anemia

A

50%

49
Q

causes of iron deficiency anemia

A
  • Lack of iron in diet, parasites stealing iron, increased iron requirements in childhood or pregnancy, menstruation, trauma, GI bleed
50
Q

iron requirements for male and female

A
  • Male: 15 mg/d with 6% absorption
  • Female: 11 mg/d with 12% absorption
51
Q

what increases the absorptionn of iron and what decreases it

A
  • If iron deficient can increase absorption by 20% if meat, but 5-10% if vegetarian

o Vegetarians; phytates and phosphates reduce iron absorption by 50%

52
Q

symptoms of iron deficiency

A

fatigue, dyspnea, exercise intolerance
o Blood loss: metorrhagia, hematochenzia, melena, hematuria

53
Q

signs of iron deficiency

A

pallor (conjunctiva), tachycardia, flow murmur

54
Q

labs for iron deficiency anemia

A

o labs: abnormal CBC
Low CBC count, reduced Hb [ ], reduced reticulocytes, microcytic and hypochromic RBC, increased red cell distribution width
- Severe: size (anisocytosis) and shape (poikocytosis) changes in microcytic and hypochromic RBC

  • Labs: iron
    o Decreased ferritin and serum iron, increased total iron binding capacity
55
Q

morphology in iron deficiency anemia

A

microcytic and hypochromic

56
Q

what’s impacted in early iron store depletion

A

marrow iron stores, serum ferritin, total iron binding capacity (TIBC)

57
Q

progression of iron deficiency

A
  • Initially: ferritin drops, TIBC increases
  • Then: serum iron and transferrin saturation drop
  • Late: CBC abnormal; hypochromic, microcytic anemia
  • Blood Hb [ ] drop
58
Q

alsolute iron deficiency vs functional iron deficiency

A

Absolute iron deficiency: Reduction of total body iron stores, which may progress to IDA

Functional iron deficiency: Iron is inadequately mobilized from stores to the circulation and erythropoietic tissue.

59
Q

causes of absolute iron deficiency

A

-increased demands
-decreased intake
-decreased absorption
-chronic blood loss

60
Q

causes of functional iron deficiency

A

-chronic inflammation and elevated hepcidin levels (i.e. IBD, kidney disease, autoimmune, infection)
-increased erythropoiesis (ESA therapy or endogenous response to anemia)

61
Q

iron stores in functional iron defieincy

A

could be normal or high

BMS200 (46 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions