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Year 1 > Block 4 > Flashcards

Block 4 Flashcards

1
Q

What activates the alternate pathway?

A

Polysaccharides such as gram negative bacteria

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2
Q

What determines the function of the antibody?

A

Heavy chain

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3
Q

What is the role of IgD?

A

Activation of B cells.

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4
Q

What is type 4 hypersensitivity?

A

Cell mediated by T helper cells and CD8+ T cells that occurs days after.

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5
Q

How does class switchcing of antibodies occur?

A

Changes to the constant region of the heavy chain

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6
Q

Which part of the natibody is responsible for antigen affinity?

A

Variable region

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7
Q

Difference between heavy and light chain

A

Heavy chain has four segments and light chain has 2 segments

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8
Q

How is the heavy chains linked togehter?

A

Disulphide bond

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9
Q

How is the heavy chain linked to light chain?

A

Disulphide bond

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10
Q

Where does antigen bind to antibody?

A

Fab of either heavy or light chain

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11
Q

Which antibody destroys parasite and worms?

A

IgE

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12
Q

What is the first antibody to be secreted?

A

IgM

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13
Q

Which immunogoblin is found in the lungs and skin?

A

IgE- this mediates allergic and hypersensitivity reactions

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14
Q

Intrinsic pathway

A

PTT

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15
Q

Which cells kill viruses?

A

Cytotoxic T cells

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16
Q

MHC 1 X8= 8

A

MHC2 X 4=8

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17
Q

Which immunogoblin crosss the placenta and cause neonatal probelms?

A

IgG

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18
Q

Which immunogolbin is found in breast milk?

A

IgA- protection of mucous membranes so it is found in saliva, tears, mucous and breast milk. It travels by transcytosis.

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19
Q

How does glucose enter the blood?

A

Facillitated diffusion using GLUT transporter

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20
Q

When do the intrisnic and extrinsic pathways meet?

A

Factor 10

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21
Q

Which cells control type 4 hypersensitivity?

A

Th1 lymphocytes

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22
Q

Which cells activate humoural process?

A

Th2 lymphcytes that activate B cells

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23
Q

What is hyperacute organ rejection?

A

Occurs a few mins after transplant controlled by B cells. It is a type 2 hypersensitivity.

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24
Q

What is the role of TH1 cells?

A

Activate CD8+ T cells

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25
Q

What is acute organ rejection?

A

Days to months after transplant- controlled by Th2 cells and CD8+ T cells in a type 4 hypersensitivty

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26
Q

What causes chronic organ rejection?

A

Th2 cells and CD8+ T cells in a type 4 hypersensitivity

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27
Q

What is the role of IgM?

A

Involved in type 2 and 3 hypersensitivity. It is the first to be released following infection and has the highest complement activation capacity.

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28
Q

What determinnes class effect of antibodies?

A

Fc region

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29
Q

What is the antigen epitope?

A

The region where the antigen binds to antibody.

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30
Q

How is HIV measured?

A

CD4 cells

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31
Q

Which cells are most commonly associated with IgE?

A

Mast cells

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32
Q

Which cells are part of the inate immune response?

A

NK cells

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33
Q

What causes the oxygen dissoication curve to shift to the right?

A

CADET- CO2, Acidosis, DPG (2,3), Exercise, temperature.

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34
Q

What is mannose?

A

An antigen that is a Pathogen-associatied molecular pattern for indicating microbial activity that binds to carbohydrate lecitn

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35
Q

What is a granuloma?

A

Cluster of WBC produced in type 4 hypersensitivity.

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36
Q

Which antibody is most commonly produced?

A

IgA- its dimeric structure means its mostly found in secretions. It is present on mucosal membranes and deficiency causes increased infection of respiratory and GI tract

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37
Q

What causes the oxygen dissoication curve to shift to the left?

A

Alkalosis, reduced temperature

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38
Q

Which cells are important for class switching?

A

Th2

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39
Q

What is C-reactive protein?

A

Produced by the liver which is elevated during inflammation

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40
Q

Which antibody is responsible for blood agglutination?

A

IgM

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41
Q

Which antibody is highest in the blood serum?

A

IgG

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42
Q

Which T cell is effective against extracellular bacteria and fungi?

A

TH17

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43
Q

Interferons

A

Cytokines released during viral infections

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44
Q

Interferon gamma

A

Produced by NK cells and Th cells for chronic granulomatous disease.

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45
Q

When are lymhpocytes raised?

A

Acute viral infection or chornic inflammation

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46
Q

Where does the antibody bind to antigen?

A

Fab region of the epitope.

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47
Q

Extrinsic pathway

A

PT

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48
Q

Assessing fibrinogen -> fibrin

A

Thrombin time- prolonged by heparin or fibrin/fibrinogen deficiency

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49
Q

Bradykinin

A

Causes vasodilation and hypotension and angioedema (swelling of skin.)

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50
Q

What is the smallest antibody?

A

IgG

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51
Q

What cell surface marker is found on all T cells?

A

CD3 for total T cell count

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52
Q

What triggers the lectin pathway?

A

Pathogen surface carbohydrates like lectin

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53
Q

Anaphylactixis

A

Hypotension, tacycardia, dysoniea, swelling

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54
Q

Which cells are found in caute inflammation?

A

Neutrophils

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55
Q

What helps to protect or fight infection?

A

Antigen presentation

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56
Q

What is important for foetal immunity?

A

IgG

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57
Q

What is important for neonatal immunity?

A

IgA

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58
Q

Dendritic cells

A

both myeloid and lymphid lineage. Theyu are responsible for being antigen presenting cells.

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59
Q

What is ferritin?

A

Iron storage protein

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60
Q

What is transferrin?

A

Transportation of iron to the liver and bone marrow

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61
Q

How is serum CO2 levels controlled?

A

Negative feedback

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62
Q

Which immunogolbiins are secreted as monomers?

A

All immunogoblins

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63
Q

Which immunogoblins are pentamers?

A

IgM

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64
Q

Which WBC are the first to be recruited?

A

Neutrophils which is multilobed

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65
Q

What is the feature of eosinohpils?

A

Bilobed nucleus

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66
Q

Macrophage and mast cells

A

Single ncuelus

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67
Q

How does HIV enter cells?

A

CD4

68
Q

What activates macrophages?

A

Interferon-gamma produced by Th1 cells

69
Q

How is the clotting cascade controlled?

A

Positive feedback

70
Q

Which antibody crosses the placenta?

A

Only IgG

71
Q

What receptor is involved in platelet adhesion?

A

GP1B

72
Q

How do platelets bind in adhesion?

A

vWF is present when the subendothelial layer is exposed. Platelets bind to vWF on the subendothelial layer via GP1b receptor. It then releases ADP to activate more platelets. ADP acts via metabatropic P2Y1 or P2Y12 on platelet receptors and causes a confromational change for activation of GP2b3a. Activation of Gp2b3a causes platelet aggregation to form a clot.

73
Q

How does P2Y12 receptor work?

A

Responds to ADP binding. It is a Gi receptor that reduces cAMP for increase of Ca2+ activation of GP2B3A receptor for platelet aggregation

74
Q

What is the role of integrin?

A

It is a receptor which spans the length of the membrane aka GP2b3a receptor. It binds to vWF and fibrinogen for platelet adhesion and aggregation. Formed via calcium dependent association via ADP acting on PY receptors.

75
Q

What is Glanzmann’s thrombasthenia

A

Defiiency in integrin/GP2b3a that reduces platelet adhesion and aggrefgtion and causes bleeding

76
Q

What is the cause of immune thromboocytopenia purpura?

A

Type 2 hypersensitivity that targets integrin/GP2b3a

77
Q

What is ritixumab?

A

Monoclonal antibody derived from the Fab that causes the depletion of B cells to treat lymphoproliferative disorders. It inhibits integrin and causes excess bleeding

78
Q

What is C3 convertase?

A

C3B

79
Q

What is C5 convertase?

A

C4bC2aC3b

80
Q

What activates alternative pathway?

A

Spontaneuous hydrolysis

81
Q

Where is lectin produced?

A
82
Q

What is the MBL pathway?

A

Mannose binding lectin associated protease (MASP) forms which -> MBL protease. This causes lysis of C4 and C2 to form C4AC2B.

83
Q

What begins the extrinsic pathway?

A
84
Q

What begins intrisnic pathway?

A

FXIIa which activates FXI, FIX and FVIII to activate FX-> FXA

85
Q

What activates fibrinogen?

A

Thromobin

86
Q

What activates throbmin?

A

FVa and Factor Xa to cause prothrombin -> thrombin

87
Q

What is the role of vWF?

A

Carries FVIII and responsible for platelet adhesion and aggregation when exposed in subendothelial layer

88
Q

Structure of platelets

A

Glycoprotein coat of GP1B and GP2B3A receptor. Made up of arachidionic acid. It has a Ca2+ surface canalicular system

89
Q

What do platelets contain?

A

Conrtains PDGF to repair vessels after clot and alpha and dense granules/

90
Q

What are alpha granules?

A

Protein granule which contain factor 13, PDGF, vwF and a store of fibrinogen.

91
Q

What are dense granules?

A

Non protein and contain ADP and Ca2+

92
Q

What is the role of Ca2+

A

For contraction and activation of GP2B3A and binding agent for vitamin K dependent factors.

93
Q

What are vitamin K dependent factors?

A

Factor 2, 7, 9, 10

94
Q

Where are platelets found?

A

Peripheral blood and 1/3 in the spleen

95
Q

Difference between acute and chronic myeloid leukemia

A

Acute has decrease in neutrophils; chronic has increase in neutrophils

96
Q

What is the heavy chain?

A
97
Q

What is the light chain?

A
98
Q

What activates mast cells and basophils?

A

Nerves using substance P, C3a and C5a and IgE

99
Q

What is the cause of haematuria?

A

Breakdown of RBC present in urine due to Classical complement antigen-antibody

100
Q

What is the Fc region?

A

Heavy chain only

101
Q

Where is the variable domain of heavy chain?

A

Fab region

102
Q

What is the effect of splenomegaly?

A

Reduced platelet and RBC count

103
Q

Order of absorption

A

Iron in Duodenum, Folate in jejunum, B12 in ileum

104
Q

How is coblamain metabolised and absorbed?

A

Transcoblamain I allows B12 to be transported from salivary gland in mouth to stomach to protect it from acid. It is taken up and absorbed in jejunum by instrinisc facotr produced by parietal cells. Transcobalamin transports B12 in blood to tissue

105
Q

How is folate absorbed?

A

In jejunum by conjugase enzyme in form of tetrahydrofolate. Transfers methyl group to B12. Both are essential for RBC DNA defiency

106
Q

Folate defiency

A

Occurs in alcoholics, when there is malabsorption, in pregancy, haemlytic anaemia, breast feeding.

107
Q

What is HbS?

A

Hb in sickle cell disease

108
Q

HbC

A

Haemoglobin where glutamic acid is replaced by lysine and asymptomatic

109
Q

HbE

A

Haemoglobin E disease which is a mild anaemia

110
Q

When are iron supplements contraindicated?

A

During infection. It can cause vomiting, haemhorrage, diarrhoea

111
Q

Types of vone marrow tissue

A

Fatty tissue and myeloid

112
Q

What do mesenchymal stem cells produce?

A

Fat, cartilage and bone cells

113
Q

When does yellow marrow become red?

A

During fever or severe blood loss

114
Q

What are the platelet agonists?

A

ADP, adrenaline, collagen

115
Q

What is the form of animal diet iron?

A

Haem iron which is more easily absorbed than non haem iron.

116
Q

Where is pepsinogen produced?

A

Fundus in chief cells

117
Q

What is the precursor to bilirubin?

A

Haem -> biliveridin

118
Q

How does urobilinogen form?

A

Bilirubin -> urobilinogen

119
Q

What facillitates b12 absorption?

A

Pancreatic protease

120
Q

WHat is the effect of gastrectomy?

A

Reduced B12 and iron absorption. Stomach acid causes Fe3+ -> Fe2+ and produces parietal cells. There is also osteoporosis because pareital cells produce Ca2+

121
Q

What is the form of vegeterian based iron?

A

Non haem iron

122
Q

What triggers organ/graft rejection?

A

HLA

123
Q

Where is trypsin activated?

A

In duodenum into trypsin via enterokinase. it activates pacreatic proteases

124
Q

Where do the testes drain?

A

Into the para-aortic lymph nodes

125
Q

What drains into the external iliac lymph nodes in males?

A

Glans penis and prostate

126
Q

Where does scrotum drain?

A

Inginal lymph nodes

126
Q

Where does scrotum drain?

A

Inginal lymph nodes

127
Q

Phrenic nerve

A

Anterior to lung hilum. C3, C4, C5

128
Q

What suppleies the left atrium?

A

Left coronary artery and circumflex.

129
Q

What supplied by the LAD?

A

Left ventircle

130
Q

What is supplied by posterior descending artery?

A

Posterior third of interventricular septum

131
Q

What is supplied by left marginal?

A

left ventircle

132
Q

Where is the vasa vasorum located?

A

Tunica advetitia- contains fibroblast, collagen, vasa vasorum in outermost layer

133
Q

Where does superior mesenteric vein drain?

A

Portal vein

134
Q

What is the cause of Goodpasture’s syndrome?

A

Type 2 hypersensitivity against type 4 collagen in basement membrane of kidneys that reduces kidney function for urine

135
Q

What is thiamine?

A

Vitamin B1

136
Q

What is riboflavin?

A

Vitamin B6/FOLATE

137
Q

Aspirin

A

Irreversibly blocks thromboxane A2 formation

138
Q

Role of vitamin K

A

Carboxylation of factor 2, 7, 9 and 10

139
Q

Role of lipoxygenase

A

Converts arachidionic acid to leukotrienes

140
Q

Role of prostaglandin?

A

Decreases platelet aggregation

141
Q

Where is the amjoirty of iron found in the body?

A

Bound to haemoglobin. Plasma iron is the lowest store.

142
Q

Where is oxygen stored in muscles?

A

Myoglobin- monomeric protein found in muscle tissue. This contains iron.

143
Q

Action of heparin

A

Activates anti thrombin which inhibits thrombin and Factor Xa

144
Q

Effect of thromboxane?

A

Derived from prostaglandin and causes vasoconstriction, hypertension and platelet aggregation

145
Q

Haemophilia

A

Factor 8 deficiency

146
Q

Role of B12

A

Regenerate folic acid

147
Q

What reduces uterine tone?

A

Prostacyclin

148
Q

Which clotting factor reduces first in vitamin K deficiency?

A

Factor VII

149
Q

How do inflmamatory mediators form?

A

Phospholipids are freed by phospholipase A2 and form arachiodionic acid. Arachidionic acid forms prostaglandin via COX-1/2. Prostaglandin becomes thromboxane A2 by COX-1 enzyme or propstacyclin by COX-1 or COX-2.

150
Q

WHat do prostaglandins form in vascualr
endothelium?

A

Prostacyclin that causes vasodilation and reduces platelet aggregation via COX-2 or COX-1.

151
Q

What do prostaglandins form in platelets?

A

Thromboxane A2 that causes vasoconstriction and increases platelet aggregation via COX-1 only.

152
Q

Role of COX-2?

A

Formation of prostacyclin from prostaglanidn and activated by inflammation.

153
Q

Role of COX-1

A

Always active and causes formation of prostacyclin or thrombooxane.

154
Q

Role of steroids?

A

Inhibit phospholipase A2 for arachidionic acid -> prostaglandin.

155
Q

Role of NSAIDS?

A

Inhibit COX-1 or COX-2 for inflammatory mediators.

156
Q

Effect of leukotrienes?

A

Produced from arachidionic acid by 5-lipooxygenase (LOX) Causes chemotaxis of neutrophils adn bronchoconstriction of airways.

157
Q

Effect of COX-2 selective inhibitors?

A

Reduces risk of peptic ulcers because prostaglandin is not inhibited but increases bleeding.

158
Q

What medication should not be given after surgery?

A

Aspirin because it is a COX-1 ihibtior which prevents wound healing via clotting throug thromboxane A2.

159
Q

What is transcyotsis?

A

Uptake of substance by forming a vesicle, stabilised with clathrin protein. Clathrin transcytosis is used by epithelial cells for pathogen defenese and passive immunity for IgG upake

160
Q

Where do continuous capillaries not have gaps?

A

Brain

161
Q

Location of continuous capillaries?

A

Lungs, skin, blood-brain barrier

162
Q

Location of fenestrated capillaries?

A

Kidneys and small intestine

163
Q

Effect of folate

A

MAY REDUCE b12

164
Q

Effect of corticosteroids

A

Increase BP and stimulate sodium retenion and water

164
Q

Effect of corticosteroids

A

Increase BP and stimulate sodium retenion and water

Year 1 (191 decks)

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