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COM MCM > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Composition of blood

A
  1. Plasma

2. Formed elements (WBCs, platelets, RBCs)

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2
Q

Functions of blood

A
  1. Delivery of nutrients and oxygen
  2. Waste removal
  3. Homeostasis
  4. Immune function
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3
Q

Function of erythrocytes

A

CARRY OXYGEN

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4
Q

Hematocrit

A

Percentage of blood that is cells

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5
Q

What stimulates erythropoiesis?

A

Tissue hypoxia, espeically low O2 delivery to kidney

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6
Q

HIF

A

Accumulates in kidney during hypoxic conditions; ubiquitinated with normal oxygenation

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7
Q

How does erythropoietin act on erythroid lineage?

A
  1. Increase stem cell differentation to erythroid lineage

2. Increase rate of RBC maturation

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8
Q

Role of Iron in RBC production?
Cause of deficiency?
Consequence of deficiency?

A
  1. formation of heme
  2. blood loss
  3. microcytic anemia
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9
Q

Role of Vitamin B12 in RBC production?
Cause of deficiency?
Consequence of deficiency?

A
  1. DNA synthesis
  2. Loss of intrinsic factor (pernicious anemia)
  3. macrocytic anemia
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10
Q

Role of Folate in RBC production?
Cause of deficiency?
Consequence of deficiency?

A
  1. DNA synthesis
  2. High heat cooking, alcohol consumption
  3. macrocytic anemia
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11
Q

Oxygen capacity

A

How much O2 can be carried by heme

Calculation: 1.34 mL O2/g Hb x [Hb]

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12
Q

Oxygen content

A

How much O2 is being carried by heme

Calculation: O2 capacity x O2 saturation

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13
Q

Oxygen saturation

A

% available spots on heme with O2 bound; given by pulse oximetry

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14
Q

How is ATP gained and used by RBCs?

A

Anaerobic glycolysis; membrane flexibility, ion transport, maintenance of ferrous iron, prevention of Hb oxidation

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15
Q

Consequence of RBC not getting enough ATP?

A

Hemolysis; RBC lifespan of ~120 days

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16
Q

Fate of “old” RBCs

A

filtered out (hemolysis) by spleen

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17
Q

Fate of “old” Hb

A

Peptide chains broken down to AAs, Heme broken down by bilirubin, Iron recycled for new heme

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18
Q

Anemia

A

Too few RBCs; O2 capacity and content reduced, blood viscosity reduced, heart workload increased

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19
Q

Polycythemia

A

Too many RBCs; O2 capacity and content increased, blood viscosity increased, heart workload increased

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20
Q

Primary polycythemia

A

Due to abnormally high activity of bone marrow in RBC production; low EPO levels

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21
Q

Secondary polycythemia

A

O2 low due to altitude or lung/heart disease; EPO levels high, heart or lungs may be abnormal

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22
Q

Physiologic polycythemia

A

Due to altitude change in environment; EPO levels high

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23
Q

Porphyrin ring structure of heme

A

four 5-membered rings with Fe2+ present

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24
Q

Phase I of Heme biosynthesis

A

In mitochondria; Succinyl CoA + Glycine = ALA

Enzyme: ALA synthase

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25
Q

Phase II of Heme biosynthesis

A

In cytosol; ALA becomes Porphobilinogen, porphobilinogen becomes hydroxymethylbilane
Enzymes: ALA dehydratase, phorphobilinogen deaminase

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26
Q

Phase III of Heme biosynthesis

A

In mitochondria; Protoporphrinogen IX becomes Protoporphyin IX, Protoporphyrin IX becomes heme
Enzymes: Protoporphyrinogen oxidase, Ferrochelatase

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27
Q

Acute Intermittent porphyria

A

Hepatic; defect in porphobilinogen deaminase

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28
Q

Congenital erythropoietic porphyria

A

Erythropoietic; defect in uroporphyrinogen III synthase

Red color in urine, teeth, skin photosensitivity

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29
Q

Porphyria cutanea tarda

A

Hepatoerythropoietic; defect in Uroporpyinogen decarboxylase

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30
Q

Variegate porphyria

A

Hepatic; defect in protoporphyinogen IX oxidase

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31
Q

Heme oxygenase

A

Removes bridge between pyrrole rings of heme; O2 required; Biliverdin synthesized

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32
Q

Biliverdin reductase

A

Removes double bond from Biliverdin and adds H; NADPH required; Bilirubin synthesized

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33
Q

Bilirubin transport to liver

A

Bound to albumin as it is insoluble/indirect/unconjugated

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34
Q

UDP glucuronyl transferase

A

Conjugates free bilirubin 2x in liver

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35
Q

Urobilinogen

A

Either absorbed in kidney and oxidized to urobilin or moved to colon and metabolized to stercobilin

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36
Q

Pre-hepatic jaundice

A

Due to increased production of unconjugated BR; elevated levels of unconjugated/direct BR in blood; direct BR absent in urine

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37
Q

Intra-hepatic jaundice

A

Impaired hepatic uptake, conjugation, or secretion of conjugated BR; hepatic dysfunction; increased unconjugated and conjugated BR, increase in ALT, AST, conjugated BR in urine

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38
Q

Post-hepatic jaundice

A

Problem with BR excretion; elevated blood levels of conjugated BR; conjugated BR in urine (dark), no stercobilin in feces (pale)

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39
Q

Neonatal jaundice

A

Physiological; due to breakdown of HbF as it is replaced with HbA or immature hepatic metabolic pathway/UDP-GT enzyme deficiency

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40
Q

Criggler-Najjar Syndrome

A

Type I: complete absence of UDP-GT gene; causes kernicturus and brain damage-BR accumulates in brain
Type II: benign, mutation in UDP-GT gene; enzyme has less activity

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41
Q

Gilbert Syndrome

A

Relatively common, benign disorder - reduced activity of UDP-GT

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42
Q

Hepatitis

A

Inflammation of liver leading to dysfunction; caused by viral infections (A, B, C); increased levels of direct and indirect BR in blood; yellow discoloration, dark urine

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43
Q

Hereditary Spherocytosis

A

Autosomal dominant disorder where RBCs are spherical, not biconcave; more fragile - results in hemolytic anemia

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44
Q

General structure of Hb

A

Tetramer with 2 alpha and 2 beta globin chains; 8 helical segments; contains heme with ferrous Fe

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45
Q

HbF

A

Fetal hemoglobin; alpha2, gamma2 chains; 0.5% expression

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46
Q

HbA, HbA2

A

Adult hemoglobin; alpha2,beta2 (97% expressed) or alpha2, delta2 (3% expressed)

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47
Q

Sickle Cell Anemia

A

HbS occurs at AA #6 on beta-globin chain; substitution of valine for glutamic acid; causes Hb polymerization and sickle shaped RBCs - hemolytic anemia

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48
Q

B-Thalassemia

A

Underproduction of B chain; relatively common

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49
Q

2,3-BPG effect on ODC

A

Signal to Hb to let go of O2; reduces O2 affinity so Hb gives up more O2 to tissues; shifts curve RIGHT

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50
Q

pH decrease effect on O2 affinity

A

Decreases as pH decreases; favors release of O2; shifts curve RIGHT

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51
Q

HbF vs. HbA ODC

A

HbF will be shifted to the left due to HbF having higher affinity for O2

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52
Q

Pyruvate Kinase Deficiency

A

Build up of 2,3 BPG - problems with ODC and production of ATP; causes anemia

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53
Q

Ferritin

A

Responsible for storage of iron in liver

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54
Q

Transferrin

A

Carries iron to tissues where needed; 30% transferrin usually bound to iron

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55
Q

TIBC

A

Total Iron Binding Capacity; equivalent to transferrin levels; elevated in iron deficiency

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56
Q

Hereditary Hemochromatosis

A

Iron overload leading to organ dysfunction; shows up in 60s or later

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57
Q

Megaloblastic macrocytic anemia

A

Large erythrocytes; can be caused by B12 and folate deficiency, result of decreased DNA synthesis

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58
Q

Folate trap

A

Vitamin B12 required for demethylation of N-methyl-THF/DNA synthesis to occur

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59
Q

B12 Deficiency

A

Leads to macrocytic anemia; due to prevention of appropriate DNA synthesis

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60
Q

Intrinsic factor

A

Carries B12 to ileum where receptors can bring it into body; deficiency can result in pernicious anemia

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61
Q

Hematopoiesis in yolk sac

A

Weeks 3-8

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62
Q

Hematopoiesis in liver

A

Weeks 6-30

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63
Q

Hematopoiesis in spleen

A

Weeks 9-28

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64
Q

Hematopoiesis in bone marrow

A

Weeks 28-birth and into adulthood

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65
Q

Hematopoietic cell compartment

A

Vascular, contains hematopoietic stem cells

66
Q

Marrow stromal compartment

A

Contains growth factors and source of energy to support hematopoietic stem cells

67
Q

Hematopoietic stem cell

A

Capable of self-renewal; pluripotent - differentiate into myeloid or lymphoid lineages

68
Q

Stem cell factor

A

Weak stimulator of hematopoiesis and makes stem cells responsive to other cytokines

69
Q

Flt3 ligand

A

Stimilar to SCF, acts with other growth factors to commit to certain lineage

70
Q

IL-3

A

Give rise to myeloid lineages

71
Q

IL-1 and IL-4

A

Give rise to lymphoid lineages

72
Q

IL-2

A

T cell growth factor

73
Q

IL-2 and IL-6

A

B cell growth factor

74
Q

GM-CSF

A

Stimulates formation of leukocytes and reticulocytes

75
Q

G-CSF

A

Stimulates increase in neutrophils

76
Q

M-CSF

A

Stimulates increase in monocytes

77
Q

EPO

A

Produced in kidneys; causes formation of RBCs

78
Q

TPO

A

Produced in liver; causes formation of platelets

79
Q

Myeloid stem cells

A

Give rise to Monocytes, Neutrophils, Basophils, Eosinophils

80
Q

Lymphoid stem cells

A

Give rise to lymphocytes

81
Q

Granulopoeisis

A

Chromatin condenses, granules form, lobulated nucleus, cell size decreases

82
Q

Agranulopoeisis

A

Heterochromatin increases, no granule formation, no lobulation of nucleus, cell size decreases

83
Q

Neutrophils

A

Phagocytize bacteria, release antimicrobial chemicals

84
Q

Eosinophils

A

Phagocytize Ag-Ab complexes, allergens, inflammatory chemicals; antiparasidic and bactericidal activity

85
Q

Basophils

A

Secrete histamine, heparin; inflammatory reactions

86
Q

Monocytes

A

Differentiate into macrophages, phagocytize pathogens, APCs

87
Q

Self-renewal

A

Ability to reproduce self

88
Q

Immortal Strand (hypothesis)

A

One daughter stem cell retains DNA preserved through generation; other daughter stem cell has newly synthesized DNA strand

89
Q

Totipotency

A

Ability of cell to give rise to all cells of organism (embryonic and extraembryonic tissues); ZYGOTE

90
Q

Pluripotency

A

Ability of cell to give rise to all cells of embryo and subsequently adult tissues; ES CELLS

91
Q

Multipotency

A

Ability of cell to give rise to different cell types of a given lineage; ADULT STEM CELLS

92
Q

Founder Stem Cell

A

Fixed number of cells programmed for a specific lineage with a fixed number of divisions; define size of large final structures; TRUE stem cell

93
Q

Transit Amplifying Cell

A

Transition from cell with stem cell characteristics to a differentiated cell; programmed to divide a limited number of times

94
Q

Asymmetrical division of stem cells

A

One cell has stem cell characteristics, another cell has the ability to differentiate

95
Q

Independent choice (stem cell maintenance)

A

Fate of daughter cells as stem cells or terminally differentiated cells is determined stochastically and/or by environment

96
Q

Derivation of embryonic stem cells

A

From ICM of blastocyst and cultured; capable of indefinite proliferation with unrestricted developmental potential

97
Q

Teratomas

A

Tumors resulting from proliferation of embryonic stem cells into many different types of tissues (lack of axial or segmental organization)

98
Q

Effect of retinoic acid on ES cells

A

Induces differentiation into neurons

99
Q

Somatic cell nuclear transfer (SCNT)

A

Nucleus taken from somatic cell of patient and injected into oocyte of donor (replaces oocyte nucleus); ES cells can be generated from new blastocyst

100
Q

Gene regulatory proteins for ES cells

A

Oct3/4, Sox2, Myc, Klf4

101
Q

Transcription factors for maintenance of pluripotency in ES cells

A

Nanog, Oct4, Sox2, FoxD3

102
Q

Adipose derived MSCs

A

Have ability to self-renew and can be differentiated into many different lineages when manipulated; but can be problematic in real world

103
Q

Bone marrow derived MSCs

A

Ability to regenerate neuronal-like cells and many others

104
Q

iPS cells

A

Somatic cells can be reprogrammed to iPS cells by defined, limited sets of transcription factors; cells are “tricked” into becoming pluripotent from multipotent cells - BEST OPTION FOR SC MANIPULATION

105
Q

Anchoring junctions

A

Cell-cell and cell-matrix adhesions; connected to cytoskeletal elements inside cell

106
Q

Cadherins

A

Mediate cell-cell connection; connected to ACTIN filaments; homophilic

107
Q

Desmosome

A

Mediate cell-cell connection; connected to INTERMEDIATE filaments-mechanical strength; homophilic

108
Q

Integrins

A

Mediate cell-matrix attachment; connected to ACTIN filaments; heterophilic

109
Q

Occluding junctions

A

Seal gaps between epithelial cells to make an impermeable barrier

110
Q

Channel-forming junctions

A

Create passageways for small molecules and ions to pass from cell to cell

111
Q

Signal-relaying junctions

A

Allow signals to be relayed from cell-cell across plasma membranes at cell-cell contact

112
Q

B-catenin role in adhesion and development

A

Adhesion: intracellular anchor protein on tail of cadherin
Development: signaling molecule that works with Wnt signaling

113
Q

Cortial actin ring

A

Contraction affects permeability, gastrulation

114
Q

ARVC relation to desmosomes

A

Missense mutation in Desmocollin-2 is associated

115
Q

Auto-immune, blistering disorders

A

Due to defects in Desmocollins/desmogleins

116
Q

Tight junction

A

Forms seal between cells; claudin and occludin proteins form seal - homotypic adhesions

117
Q

Establishing epithelial cell polarity

A

Full polarization requires separation of apical and basolateral surfaces via tight junction formation; polarity complex controls (Par, Crumbs, Scribble)

118
Q

Gap junctions

A

Spanned by channel forming proteins including CONNEXINS; pore formed so that SMALL molecules can pass through (up to 1000 MW/glucose)

119
Q

Basal lamina

A

Separates cells from underlying/surrounding tissue; selective filter, determines cell polarity; usually consists of laminin, collagen, fibronectin

120
Q

Src/FAK complex

A

Signals downstream of integrins; activates ERK/JNK to regulate cell survival/proliferation/differentiation

121
Q

Glysaminoglycans (GAGs)

A

Covalently linked to protein in the form of proteoglycans

122
Q

Fibrous proteins

A

Collagen, fibronectin; structural and adhesive functions

123
Q

Proteoglycans

A

Hydrated, “ground substance” embeds fibrous proteins; contains repeated GAGs

124
Q

Hyaluronic acid

A

Repeated disaccharides-glucaronic acid and acetylglucosamine, highly hydrated; ability to withstand compressive forces

125
Q

Collagen

A

Triple-stranded helical structure rich in proline and glycine; allows stability of helical formation and tight packing

126
Q

Enzymes affecting hydroxylation of collagen

A

Prolyl and Lysyl hydroxylases

127
Q

Where collagen synthesis occurs

A

Lumen of ER (of fibroblast)

128
Q

Scurvy

A

Inability to make collagen - can’t hydroxylate proline (defect in prolyl or lysyl hydroxylase)

129
Q

Ehlers Danlos

A

Defects in prolyl/lysyl hydroxylase causes super flexible skin

130
Q

Elastin

A

Cross-linked protein via lysyl oxidase; “elastic” - lines up hydrophobic units and decrease of entropy of H2O

131
Q

Marfan’s syndrome

A

Defect in elastin, fibrillin

132
Q

Keratin filaments in epidermis

A

Attached to DESMOSOMES

133
Q

Olfaction

A

Olfactory receptor (GPCR) binds to odorant and activates AC, cAMP; action potential relayed to glomeruli in olfactory bulb

134
Q

Actin filaments

A

Least stable, small, control cell behavior such as shape, locomotion; requires ARP for nucleation

135
Q

ARP

A

Causes local nucleation of actin filaments; growing filaments drive “push” through cytoplasm; creates polarity

136
Q

Microtubules

A

Stable; polar (+/- ends); made of tubulin subunits; contain microtubule-organizing center/centrosome

137
Q

Gamma-TuRC

A

Responsible for nucleation of microtubule growth; nucleated from MTOC

138
Q

Intermediate filaments

A

Rope-like, large fibers; provide mechanical strength; no nucleotide binding/polarity

139
Q

Endocrine signaling

A

Long distance signaling; transport to target molecule via blood stream, such as hormones

140
Q

Paracrine signaling

A

Local signaling affecting nearby cells, such as neurotransmitters

141
Q

Autocrine signaling

A

Cells respond to their own signals; bind to own receptors, such as growth factor

142
Q

Juxtacrine signaling

A

Membrane bound signal attaches to target cell, such as immune cells

143
Q

Lipophilic molecules

A

Lipid soluble molecules that diffuse across plasma membrane and bind to intracellular receptors; ex: steroid hormones

144
Q

Hydrophilic molecules

A

Require cell-surface receptors to trigger signaling events (water soluble); ex: growth factors

145
Q

GPCR

A

Seven pass transmembrane protein

146
Q

Heterotrimeric G-proteins

A

Contain alpha, beta, and gamma subunits; change conformation when bound by a ligand (no catalytic activity)

147
Q

GAP

A

Inactivates G-protein; accelerates hydrolysis of GTP to GDP (G protein complex comes together)

148
Q

GEF

A

Changes conformation to release GDP and activate G protein (release alpha subunit with GTP bound)

149
Q

B-arrestin role in GPCR

A

Shuts off signal relay

150
Q

Adenylate Cyclase

A

Activated by G-alpha/GTP; activates cAMP; cAMP activates PKA which phoshphorylates other proteins

151
Q

PLC

A

Activated by G-alpha/GTP; activates DAG and IP3

152
Q

GRK

A

Phosphorylates GPCR; arrestin binds and prevents conversion of G-alpha/GDP to G-alpha/GTP

153
Q

Gi/o-alpha G proteins

A

Inhibit AC

154
Q

Gq-alpha G proteins

A

Activate PLC instead of AC

155
Q

IP3

A

Release Ca2+ from ER

156
Q

DAG

A

Activates PKC which phorhphoylates proteins

157
Q

Ras-dependent signaling

A

Binds Grb2 in signaling process; leads to (slow) alterations in gene transcription

158
Q

Ras-independent singaling

A

Binds PI3K in signaling process; leads to (fast) alterations in protein/enzymatic activity

159
Q

JAK-STAT Receptors

A

Most direct rout for impacting transcription; STAT translocates to nucleus

160
Q

Ser/Thr Receptors (Smads)

A

More direct signaling route; R-Smad/Co-Smad migrate to nucleus

COM MCM (2 decks)

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