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Biochemistry Flashcards

1
Q

What is the type of cell that makes all types of blood cells?

A

Pluripotent stem cells

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2
Q

What are the 3 dereivatives from the pluripotent stem cells?

A

CFU-GEMM (mixed myeloid progenitor cell)
Lymphoid stem cell
NK-precursor

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3
Q

What type of cell does the NK-precursor make?

A

Nk-cells lol

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4
Q

What are the 2 types of cells that the lymphoid stem cells make?

A

B- and T-lymphocytes

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5
Q

What are the 2 eventual cells make from the BFU-E cells fom the CFU-GEMM?

A

RBC’s (using erythrocyte pathway)

Platelets (using megakaryocyte pathway)

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6
Q

What are the 3 eventual cells make from the CFU-GMEo pathway?

A

Neutrophils (using CFU-GM)
Monocytes (–> macrophages, using CFU-GM)
Eosinophils (using CFU-Eo)

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7
Q

Since RBCs dont have nuclei or mitrochondria, what energy pathway does it use exclusively?

A

Glycolysis

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8
Q

Since RBC’s cant make proteins, is depends on what enzyme that determines its lifespan?

A

G6PD

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9
Q

What is the intermediate of the glycolysis pathway that is used in the HMP shunt (PPP)?

A

G6P

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10
Q

What is the intermediate of the glycolysis pathway that is used in the Rapoport Luberin shunt?

A

1,3-BPG

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11
Q

What is the structure of heme?

A

Porphyrin ring with a Fe at its center

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12
Q

What are the 2 components in teh first step of heme synthesis?

A

Succinyl CoA + Glycine

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13
Q

What is the first enzyme in the heme synthesis pathway to make δ-ALA?

A

δ-ALA synthase

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14
Q

What is the last enzyme in the heme synthesis pathway to put a Fe++ molecule in Protoporphyrin IX?

A

Ferrocheletase

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15
Q

What is the condition where there is a defect in any enzyme in the heme synthesis?

A

Porphyria

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16
Q

Why do vampire and werewolf stories come from people with porphyrias?

A

Cuz the heme intermediates are toxic to the nervous system –> photosensitivity, hallucinations, and seizures

laso, pt have scarring and increased facial hair

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17
Q

When hemoglobin is first degredated, what is the product?

A

Heme

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18
Q

What is teh like span of a RBC?

A

120 days

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19
Q

What is the produce of degredation of heme, which gibes off Fe++ and CO as biproducts?

A

Bilirubin

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20
Q

What does bilirubin bind to in the blood once formed?

A

Albumin

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21
Q

What molecule binds to bilirubin on the albumin, thus kicking off the albumin and forming bilirubin diglucononide?

A

UDP-glucuronate

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22
Q

Where does Bilirubin diglucuronide then put?

A

Bile

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23
Q

What is the term for Hb with Fe in the ferric (3+) state?

A

MetHb

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24
Q

For congenital MetHbemia, what enzyme is missing, which normally reduces ferric Fe to the ferrous state?

A

Cytochrome B5 reductase

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25
Q

What for of Hb can pts also inherit for congential metHbemia?

A

Hb M

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26
Q

Ingestion of what things can cause acquired metHbemia?

A

Certian oxidants like nitrite, quinones, aniline,a nd sulfonamides

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27
Q

What is the treatment for acquried metHbemia?

A

Administering reducing agents like ascorbic acid or methylene blue

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28
Q

What is oxidices by ROS in the RBC so they dont dmg the cell? What pathway keeps this molecule reduced?

A

Glutathione

PPP/HMPshunt

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29
Q

What are the components of the RBC cytoskeleton?

A

Specrin, actin, bands 4.1 and 4.2

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30
Q

Which races are at risk for G6PD deficiencies?

A

Africans and Mediterraneans

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31
Q

What is the inheritance for G6PD deficiencies?

A

X-linked

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32
Q

What medications can cause problems in G6PD deficiencies?

A

Anti-malarials

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33
Q

What 2 cells might u see on blewd smares for G6PD deficiencies?

A

Bite cells

Heinz bodies

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34
Q

This is a set of disorders common from defect in cytoskeletal proteins, notably ankyrin, spectrin, and Band 3.

A

Hereditary spherocytosis

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35
Q

What happens when RBC’s pass through capallaries and the spleen in hereditary sphreocytosis?

A

they’re inflexible (like my time for studying public health) –> change shape to spheres –> hemolysis

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36
Q

In blood typing, what Ab’s will be present in my blood since I’m type O-?

A

Ab’s to A antigen, B antigen, and Rh antigen

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37
Q

What is the universal donor and acceptor?

A

Donor: O- (like me cuz I’m so giving)
Acceptor: AB+ (like brent cuz hes greedy)

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38
Q

What is the suffix to describe the size of RBC’s?

A

-cytic

micro and macro- are the prefixes

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39
Q

What is the suffix to describe the [Hb] in RBC’s?

A

-chromic

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40
Q

Iron deficiency, thalassemia mutation, and lead poisoning may lead to impaired synthesis of what molecule?

A

Hb

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41
Q

What is the RBC morphology with impaired hemoglobin synthesis?

A

Microcytic, hypochromic

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42
Q

What 3 things can cause impaired DNA synthesis?

A

B12 or folic acid deficiency

Erythroleukemia

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43
Q

Impaired DNA synthesis may lead to what RBC morphology?

A

Macrocytic, normochromic

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44
Q

Red cell loss (like from bleeding or hemolysis) may lead to what morphology of RBC’s?

A

NO CHANGE

Normocytic, normochromic

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45
Q

Why does B6 deficiency cause the synthesis of heme production to slow?

Hint: molecule

A

Cuz it requires puridoxal phosphate

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46
Q

What is the RBC morphology in B6 deficiency?

A

Microcytic, hypochromic

pale and small, like a little old lady that isnt getting her B6 vitamins because she was once a student of a geriatrics class and is now showing students the repercussions of elder neglect as she has lost interest in other daily activities over the years and finds that experimental testing keeps her young and happy despite the fact that this experimental testing is deleterious to her health overall.

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47
Q

What is the manifestation of pyruvate kinase deficiency?

A

hemolytic anemia

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48
Q

What is the problem if there is inadquate iron intake or excessive loss of iron?

A

Iron deficiency.

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49
Q

What is the problem if there is a squence of codon 6 of the B chain changed from GAG to GTG, which substitutes Val for Glu?

A

Sicle cell

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50
Q

What is the problem if there are mutations in the alpha gene?

A

alpha thallasemia

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51
Q

What is the disorder if there is decreased absorption of B12 or lack of intrinsic factor?

A

Megalblastic anemia

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52
Q

What is the problem if there are deficiencies in the amt or in the structure of alpha or beta spectrin, ankyrin, band 3 or band 4.1?

A

Hereditary spherocytosis

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53
Q

What is the disorder when there are mitations in the PIG-A gene, affecting synthesis of GPI-anchored proteins?

A

Paroxysmal nocturnal hemoglobinuria

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54
Q

How many alpha globin genes are there?

A

4

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55
Q

How many deletions of alpha globin genes do u need to when u start to see microcytic hypochrmic RBC’s?

A

2

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56
Q

In addition to severe microcytic hypochromic anemia, what is the other manifestation of 3 alpha globin genes missing?

A

Splenomegaly

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57
Q

Do u die as a hydrops fetalis with 4 missing alpha globin genes?

A

Um, yes.

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58
Q

What is the homotetramer called of excess b chains?

A

HbH

like HGH. WHERES THE PROTEIN, MA? I TOLD YOU TO GET ME SOME PROTEIN.

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59
Q

Which coag pathway requires factors already present in the blood?

A

Intrinsic pathway

60
Q

What factor does the intrinsic pathway start with?

A

XII (Hagemann factor)

61
Q

What induces XII to be activated?

A

A negatively charged surface

62
Q

What must XIIa have the presence of to proteolytically cleave XI?

63
Q

What does XI activate?

64
Q

Which factor is activated in the final step of the intrinsic pathway, once VIII is precipitated?

65
Q

What disorder is present in a deficiency of factor VIII?

A

Hemophilia A

66
Q

What factor is deficient in hemophilia B?

67
Q

What activates factor VII to start the extrinsic pathway?

68
Q

What helps VII activate factor X?

A

factor III

69
Q

What are the 4 phases of homeostasis?

A
  1. vasoconstriction of the injured vessel
  2. formation of the platelet plug (1o hemostasis)
  3. formation of the fibirin mesh (2o hemostasis)
  4. dissolution of the clot
70
Q

After endothelial cell injury, what is the molecule that platelets adhere to to start primary hemostasis?

71
Q

In addition to platelet adhesion, what is vWF’s role on factor VIII?

A

stabilizes it in the circulation

72
Q

After platelets bind to vWF via Gp1b receptors, what happens?

A

They change shape and degranulate.

73
Q

What are the 2 molecules released from platelts that promote further platelet activation?

A

ADP and TXA2

74
Q

What is the substance released by platelets that promotes vasoconstriciton?

75
Q

What is the substance released by platelets that stimulates repair of damaged tissue?

76
Q

For platelet aggregation to occur, what is the molecule that binds inbetween the GpIIa/IIIb receptors of the platelets?

A

fibrinogen

77
Q

Which factors are vit K dependent for their synthesis?

A

II, VII, IX, X, C, and S

78
Q

What class of drugs work by inhibiting the regeneration of vitamin K to its active form?

A

Coumarin anticoagulants

dicumarol and warfarin

79
Q

The inhibition of COX by ASA cause the inability to synthesize which molecule, which is required for activation and aggregation of platelets?

80
Q

What do platelets lack which cause the permanent effects of ASA inhbiting COX?

81
Q

What does ASA also inhibit, which normally opposes platelet aggregation, but typically is regenerated within a few hours?

A

Prostacyclin

82
Q

What is the molecule that turns plasminogen –> plasmin?

83
Q

What does plasmin break apart in blood clots?

A

fibrin and fibrinogen

84
Q

What is the requirement for t-PA to work on plasminogen?

A

plasminogen has to be bound to fibrin (trapped in the clot)

85
Q

What is the molecule that binds to free plasmin and inactivates it?

A

a2-antipalsmin

86
Q

What would be the general problem if you lacked a2-antiplasmin?

A

Tendency to bleed

cant inhibit plasmin –> constant breakdown of fibrin and fibirinogen –> no clot formation –> bleeeeeeed

87
Q

What 2 enzymes can bind to free plasminogen and activate it?

A

Urokinase (54kD enzyme form the kidney)

Streptokinase (45kD bacterial protein, which activates plasminogen w/o cleavage)

88
Q

What do urokinase and streptokinase not require to activate plasminogen, unlike t-PA?

89
Q

What molecule is on the surface of the endothelail cells that ↓ blood clotting by binding thrombin?

A

Thrombomodulin

90
Q

What 2 factors do proteins C and S inhibit?

A

Va and VIIIa

91
Q

What molecule on the endothelial cell surface inhibit ATIII?

A

heparan sulfate

92
Q

What is the inheritance of hemophilia A?

93
Q

Where does the bleeding occur in hemophilia A?

A

deep tissues and joints.

94
Q

What is the treatment for hemophilia A?

A

recombinant FVIII

95
Q

What is the inheritance for hemophilia B?

96
Q

Despite lacking IX (a different factor than hemophilia A), why do hemophilia A and B have basically the same problems?

A

Cuz both VIII and IX are in the intrinsice pathway and if either arent there then the intrinsic pathway doesnt work

97
Q

So how do u distinguish hemophilia A from B?

A

protein electrophoresis or DNA analysis

98
Q

What is the inheritance for vW disease?

99
Q

True or False: vW disease is the most common bleeding disorder.

100
Q

Where do u bleed in vW disease?

A

mucous membranes (nose, menorrhegia, eyes)

101
Q

What is the treatment for vW disease?

A

FFP and platelets

102
Q

This is a disorder of very low platelet levels in the blood (<50,000/ul).

A

thrombocytopenia

103
Q

What is normal levels of platelets in the blood?

104
Q

Where does the bleeding occur in thrombocytopenia?

A

capillaries and small venules

105
Q

What is the treatment for thrombocytopenia?

A

whole blood, platelet packs, and splenectomy

106
Q

What are newborns injected with to prevent a deficiency, as their gut flora arent proficient yet?

107
Q

This is a diffuse, itnravascular activation of the clotting cascade and fibrinolysis, resulting in a consuption of coagulation factors.

108
Q

What happens to the PTT and PT in DIC?

A

prolonged

u use up ur coag factors

109
Q

What are the causes of DIC?

A 
Obstetric complication
Sepsis
Adenocarcinoma
Acute promyelocytic leukenia
Rattlesnake bite
110
Q

What do u add to a blood sample in a PTT to activate the intrinsic pathway?

A

koalin clay

111
Q

What do u treat the blood with in a PT to activate the extrinsic pathway?

A

thromboplastin (tissue factor, which activates VII)

112
Q

This is the test where u mix 50:50 of the pts blood and a standard sample, where lengthened showes a circulating anticoagulant and a normal may correct a deficiency.

A

Mixing test

113
Q

This is the test where u stab the pt and see how good platelets are at forming the primary plug.

A

Bleeding time

114
Q

What is the function of the following plamsa proteins?

antichymotrypsin, a1-antitrypsin, a2-macroglobulin, and antithrombin

A

Antiproteases

115
Q

What is the function of the following plasma proteins?

Various coagulation factors, fibrinogen

A

blood clotting

116
Q

What is the function of the following plasma proteins?

immunoglobulins, complement proteins, and B2-microglobulin

A

Immunne defense

117
Q

What is the function of the following plasma proteins?

CRP, a1-acid glycoprotein

A

Inflammation

118
Q

What is the function of the following plasma proteins?

AFP

119
Q

What is the function of the following plasma proteins?

Albumin, ceruloplasmin (Cu), cotricosteroid-binding globulin (cortisol), Haptoglobin lipoproteins, hemopexin, retinol-binding protein, sex-hormon-binding globulin, thyroid-binding globulin, transferrin and transthyretin

A

Transport or binding proteins

120
Q

What is the major protein of the human plasma (60%)?

121
Q

What is the condition when serum albumin levels fall?

A

Edema (Kwashiorkor)

122
Q

This is the molecule that binds to free Hb in a tight noncovalent bond and prevents loss of free Hb, and therefore iron, through the kidneys.

A

Haptoglobulin (Hp)

123
Q

What is the main component of Hp?

A

a2-globulin fraction

124
Q

In what condition do Hp levels drop?

A

hemolytic anemia

125
Q

This molecule inhibits serum proteases (esp elastase) and protects against degeneration of alveolar tissue.

A

a1-antitrypsin

126
Q

What are the clinical manifestations of A1AT deficiency?

go back to respiratory..

A

Emphysema and cirrhosis (the ZZ form)

127
Q

What is the plasma protein that binds to copper and decreased in Wilson’s disease?

A

Ceruloplasmin

128
Q

Which vitamin promotes iron absorption in the GI?

129
Q

If Fe isnt stored in Hb and Mb, how is it stored?

A

Ferritin and Hemosiderin

130
Q

This is the condition where there is an iron overload in the tissues.

A

hemosiderosis

131
Q

Is there usually a high or low amount of fettirin in the tissues?

132
Q

This is a B1-globulin synthsized in the liver that transports Fe through the blood.

A

Transferrin

133
Q

How many ferric ions can tranferrin carry?

134
Q

What is the test to see the transferrin concentration?

135
Q

What are pre-menopausal women prone to because of menses?

A

Iron deficiency anemia

136
Q

What are the RBC characteristics of iron deficiency anemia?

A

hypochromatic microcytic anemia

137
Q

What are the pt Sx of iron deficiency anemia?

A

fatigue, pallor, and reduced exercise capacity

138
Q

What cells are increased in iron deficiency anemia, which reflexts the imapired ferrochelatase-catalyzed incorportation of iron into the protoporphyrin IX ring?

A

Red-cell protoporphyrin

139
Q

What is the most common inherited metabolic disorder in the white population, which is characterized by excessive storage of iron in tissues?

A

Hemochromatosis

140
Q

In primary hemochromatosis, what gene is mutated, which the normal product is a glycoprotein that binds transferrin receptor?

141
Q

What is the typical etiology for secondary hemochromatosis?

A

multiple blood transfusions

142
Q

This is an X-linked diorders that is fatal in infance, where there is a decrease in activity of copper-dependent enzymes?

A

Menkes disease

143
Q

What is the mutation in Menkes disease?

A

extra-hepatic Cu++-binding ATPase

144
Q

This is an AR condition where there is defective excretion of Cu2+ into bile and consequent accumulation of Cu in liver, brain, and other organs.

A

Wilsons disease

145
Q

Levels of what protein is decreased on labs in Wilsons?

A

Ceruloplasmin

146
Q

What is the treatment for Wilsons disease?

A

Penicillamine

147
Q

CRP, A1AT, Hp, alpha1-acid hlycoprotein, and fibrinogen are all markers of what?

A

Acute phase proteins for inflammatory states.

Hem/Onc (5 decks)

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