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Medicine > IMS > Flashcards

IMS Flashcards

1
Q

Pataus

A

Trisomy 14 - affects midline structures, cleft lip, incomplete brain, congenital heart disease

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2
Q

Klinefelters

A

47XXY

Infertility and poorly developed secondary characteristics as lacks testosterone

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3
Q

Turners

A

45XO

99% Still born

Short in stature, primary amenorrhea, congenital heart disease, puffy feet, redundant skin at back of neck

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4
Q

William Beurens

A

26 genes deleted from q arm of chromosome 7

Bright eyes, wide mouth, upturned nose, heart defect

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5
Q

Digeorge/Velocardiofacial Syndrome

A

Section deleted from chromosome 22

Small mouth, prominent nose, heart defects

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6
Q

Edward’s Syndrome

A

Trisomy 18 - clenched hands, overlapping fingers, multiple malformations

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7
Q

Duchenne Muscular Dystrophy

A

X-linked recessive

Absence of dystrophin, invasion of fibrous tissue

Stands using Gavet’s manoeuvre

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8
Q

Lever Hereditary Optic Neuropathy

A

Reduced vision and hyperarray of disc

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9
Q

Genetic Imprinting

A

Marks on chromosomes show if maternal or paternal

Change in message doesn’t show the origin hence can cause problems

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10
Q

Familial Hyperchilesterolaemia

A

Austomal Dominant

Can be caused by over 150 different mutations

If cholesterol is over 7.5mmol suspect the disease

Lipoprotein A may also be raised

Treat with lifestyle and statins

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11
Q

Macrophages release…

A

TNF and IL-2

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12
Q

MHC Class I are on…

A

All cells

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13
Q

Th helper cell cytokines

A

Th1 - IL-2, IL-5

Th2 - IL-13, IL-16

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14
Q

Myasthenia Gravis

A

May be due to thyroid tumour causing excess antibodies attacking receptors

Blurred vision, fatigue, decline in fitness

Relieved by edrophoneum, neostigme treats it

CMAP decreases each time due to muscle fatigue!

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15
Q

What chiefly carries cholesterol in ester form

A

LDL

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16
Q

Statins are…

A

HMG CoA Reductase Inhibitors

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17
Q

Prenylation

A

Adds small lipid tail to small G proteins to anchor them to the membrane

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18
Q

Rho

A

Prenylated by… regulates the cell cytoskeleton

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19
Q

MRSA

A

Chlorineepexidene wash , isolate for 5 days

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20
Q

Downs Syndrome

A

Trisomy 21 is the most common

Suspect Robertsonoan if high number of miscarriages in family history

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21
Q

Differences between transcription in prokaryotes and eukaryotes

A

1) nucleus in eukaryotes
2) modification in eukaryotes
3) more than one RNA polymerase in eukaryotes

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22
Q

Post transcriptional modifications

A

5’ end capped with 7 methyl guanine - looks like functional 3’ end

3’ end cleaved and polyA tail added

Splicing

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23
Q

RNA transcription error rate

A

10^4

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24
Q

Similarities/differences between DNA and RNA polymerase

A

Similarities: both form chain in 5’ to 3’, both form phosphidesater bonds, both use template strand

Differences: DNA polymerase needs a primer, need a free OH group for DNA, DNA adds deoxy nucleotides

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25
Q

DNA primate

A

makes RNA primers for DNA replication

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26
Q

Base/nucleotide excision

A

Repairs to 10^9!

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27
Q

Sickle Cell Anaemi

A

GAG->GAT 17th nucleotide Glutamic acid –> Hydrophobic valine

sickle cell crisis lasts 5 to 7 days

RBCS die after about 10/20 days

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28
Q

Creative

A

CKMM in muscle, CKMB in heart

CK peaks 12 hours after myocardial infarction

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29
Q

ADH and AldDh

A

Japanese people have efficient ADH, inefficient ALDH due to inactivity of mitochondrial and toxic enYmes of this

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30
Q

Ecstasy

A

Reverts the serotonin SERR transporter to work in the opposite directions!

Often hyponytraemia, hypokalkuraemia, low chloride due to over drinking

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31
Q

Hyponytraemia

A

Low blood sodium, can cause swelling due to uptake of water by tissues

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32
Q

Erections

A

NO stimulates guanyl Cyclase

cGMP, stimulates PKG, causes smooth muscles relaxation and dilation, causes erection

Viagra inhibits PDE5

Ginseng stimulates Nos to make NO

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33
Q

Therapeutic Index

A

Toxic drug dosage:Therapeutic dose

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34
Q

penicillin stable in acid

A

G unstable

V stable

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35
Q

migraine

A

gastric stasis

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36
Q

Gentamicin

A

confined to body fluids whereas vancomycin treats c. diff as not absorbed by G proteins

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37
Q

Digoxin and erythromycin interact

A

gut bacteria usually inactivate digoxin, erythromycin kills this bacteria, less digoxin inactivated hence more drug absorbed

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38
Q

Ethinylesteadiol hepatic re circulation

A

Liver to vile to gut to liver, causes two 2 peaks so the antibiotics can prevent the ethinylestradiol from working

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39
Q

Cockcroft Gault equation

A

Estimates creative clearance = (140-age) x kg x constant all divided by serum creative

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40
Q

Enzyme inducing drug

A

phenytoin

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41
Q

enzyme inhibiting drug

A

erythromycin

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42
Q

H1 receptors

A

Mainly in mucous membranes
If you block causes drowsiness
Most H1 antagonists have anti cholinergic properties

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43
Q

H2 receptors

A

cause acid production

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44
Q

alpha adrenergic receptors

A

In blood vessels

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45
Q

Beta adrenergic receptors

A

beta 1 in heart

beta 2 in bronchioles

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46
Q

Propanol ok

A

blocks beta 1 and 2 equally

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47
Q

Atenolol

A

Blocks beta 1 more than beta 2 but avoid in asthma

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48
Q

Insulin mechanism

A

binds to alpha subunit, enters cell insulin destroyed, beta subunit activates the tyrosine kinase

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49
Q

NSAIDS

A

Aspirin and ibuprofen are non specific

It is COX 2 that causes inflammation

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50
Q

Ramipril

A

ACE inhibitor

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51
Q

MAOIs

A

prevent breakdown of neurotransmitters in synaptic cleft hence treats depression

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52
Q

Local anaesthetics information

A

Charged hydrophilic amine group and lipid soluble hydrophilic aromatic group

Either Amide or Esther bond between them

Amide more common, stable, hypersensitive rare, more likely to be toxic, metabolised by lived, ionised at physiological ph

Ester rapidly hydrolysed by plasma esterases, produce PABA causing hypersensitivity!

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53
Q

Local anaesthetics mode of action

A

1) diffuser through lipophilic nerve membrane unionised
2) low pH in cell ionises them, they then blocks Na channels and then impulses can’t pass

Can also cause myocardial depression and vasodilation

Cocaine causes vasoconstriction

Adrenaline given to cause vasoconstriction to prolong effect as it lessens distribution but don’t use in extremities

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54
Q

beta lactam antibiotics

A

inhibit cell wall synthesis, eg penicillin

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55
Q

macrolides

A

inhibit bacterial cell wall synthesis e.g. erythromycin

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56
Q

anti fungal a

A

Inhibited ergesterole in fungal cell membrane e.g. nyastin

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57
Q

Antihelminths

A

Ascarides treat worms by paralysing effect on the CNS

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58
Q

Nicotinic receptors

A

post synaptically at all autonomic ganglia and neuromuscular junctions

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59
Q

muscarinic

A

post synaptically at parasympathetic neuroeffector junction and at sympathetic sweat glands

5 Types
M1,3,5 activate phospholipase C
M2 in heart to reduce cAMP and reduce heart rate
M4 reduces cAMP this and M2 are negatively couples to adenyl Cyclase

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60
Q

Tyrosine forms

A

NA and ACh

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61
Q

Alpha adrenergic receptors

A

NA>Adrenaline>Isoprenaline

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62
Q

Beta adrenergic receptors

A

Isoprenaline>Adrenaline>Noradrenaline

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63
Q

Alpha 1 adrenergic receptor

A

vasoconstriction, activates phospholipase C

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64
Q

alpha 2 adrenergic receptor

A

inhibits adenylate Cyclase, inhibits neurotransmitter release

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65
Q

beta 1 adrenergic receptor

A

increases cardiac rate and force

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66
Q

beta 2 adrenergic receptor

A

bronchodilator and vasodilator

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67
Q

beta 3 adrenergic receptor

A

lipolysis

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68
Q

Alpha 1 antagonist

A

phenylenephrine

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69
Q

alpha 2 antagonist

A

clonindine

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70
Q

beta 1 agonist

A

dobutamine

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71
Q

beta 2 agonist

A

salbutamol

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72
Q

beta 1/2 antagonist

A

propnalol and atenolol (atenolol blocks 1 more than 2)

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73
Q

Beta blocker effects

A

cold extremities, bronchoconstriction, depression, bradychardia

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74
Q

A2B3 Platelet receptor

A

Aggregation

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75
Q

A2B1, GPV1

A

Adhesion –> binds collagen

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76
Q

CP1b/IX/V, PAR-1, TP, P2Y12

A

Activation –> binds thrombin

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77
Q

Thrombaxane in platelets

A

Used for auto activation, made by COX-1 and TX Synthase

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78
Q

Platelet alpha granules contain

A

fibrinogen, FV, vWF

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79
Q

Dense granules

A

Release ADP - an autocrine molecule, thromboxane is also an autocrine molecule

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80
Q

Sequence of blood clotting with platelets

A

Endothelial damage –> collagen exposed so binds to A2B1 and GPV1

Activated platelets release ADP and thromboxane, binds to P2Y12 and TP to activate others

A2B3 binds fibrinogen along with vWF holding the clot together

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81
Q

Clopidogrel, trigrelor, prasugel

A

ADP receptor inhibitors on platelets

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82
Q

Vitamin K Dependent clotting factors

A

II, VII, IX, X

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83
Q

Serine Proteases

A

VII, IX, X XI, thrombin

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84
Q

Extrinsic Pathway

A

Triggered by trauma, causes the initial coagulation

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85
Q

Intrinsic pathway

A

Consolidates thrombin generation, due to damaged surfaces

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86
Q

Platelet life span

A

5-9 days

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87
Q

Main trigger for coagulation

A

Tissue factor is the main trigger for coagulation, it is found on the surface of all perivascular cells and auto activates FVII when bound

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88
Q

Thrombin helps to activate which other factors

A

FXI, VIII, XIII (shows FXII has an almost irrelevant part in the clotting cascade as thrombin can activate FXI anyway)

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89
Q

T-lymphotrophic virus HTLV1 is associated with what disease

A

leukaemia

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90
Q

Leaukaemia

A

WBC’s accumulate in blood causing bone marrow failure

Initially decreased RBC’s and platelets but high WBCs, then WBC’s also decrease

Hyper viscosity of blood due to high WBC count causes respiratory, neurological problems, tiredness, bleeding and bone pain.

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91
Q

Reed-Sternberg cells characterise what

A

Originate from B lymphocytes in Hodgkins lymphoma

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92
Q

Iron defeciency anaemia

A

Microcytic anaemia, reduced Hb production

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93
Q

Vit B12/folate defeciency

A

Macrocytic anaemia, macroavolocytes also form which causes hyperhsegmented neutrophils

It is also needed for DNA replication

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94
Q

Normocytic Anaemia

A

Caused due to blood loss

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95
Q

Kidney Failure Anaemia

A

Expo (erythropoeitin) is secreted by kidneys and needed for erythropoiesis, treat with rEPO

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96
Q

Haemolytic Anaemia

A

Reduces RBC lifespan from 120 days to just 20

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97
Q

Acquired Anaemias

A

Immune –> haemolytic disease of the newborn

Non-immune –> snake bites, malaria, septicaemia, drugs, mechanical e.g. heart valves

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98
Q

Inherited Anaemias

A

Virtually all inherited anaemias are haemolytic

Spherocytosis –> mutation in alpha or beta spectrin in cell cytokskeleton

RBC enzyme defects –> e.g. glucose-6-dehydrogenase deficiency meaning the RBC lacks NADH

Haemoglobin defects

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99
Q

Sickle Cell Anaemia

A

Glutamic acid –> Hydrophobic Valine, causes sickling of RBC that can block microvasculature

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100
Q

Thalassaemias

A

Deletion of large sections of the alpha globin in haemoglobin

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101
Q

Beta thalassaemia

A

Point mutation in the beta globin gene, if both genes are affected then the patient has HbF and thalassaemia major

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102
Q

What is blood serum

A

Plasma without the clotting factors

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103
Q

Blood and plasma donors

A

O is the universal blood donor, AB is the universal plasma donor

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104
Q

Rhesus blood group

A

Based on a D antigen on transmembrane proteins in RBCs

Haemolytic disease of the newborn –> Rh- mother and Rh+ baby sensitisation occurs if previous pregnancy occurred

Treated with RhIgG at 28, 34 week and within 72 hours of delivery!

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105
Q

Hormones causing vasoconstriction

A

Thromboxane (from activated platelets)
Serotonin (from activated platelets)
Angiotensin (from liver precursor)
Vasopressin/ADH (from pituitary gland)

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106
Q

Primary haemostasis

A

Platelet aggregation and activation

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107
Q

Secondary haemostasis

A

Clotting cascade producing the fibrin clot

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108
Q

Abdominal Aortic Aneurysm

A

Normal aorta is 2-3cm, anything over 5cm is inoperable

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109
Q

Disseminated Intravascular Conjugation

A

Infection which leads to Sepsis

TF is expressed by WBC’s activating factor 7 leading to systemic coagulation causing clots

Clotting factors are all used up hence bleeding occurs

Clotting and bleeding occurring at the same time causing multiple organ failure

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110
Q

Vitamin K Dependent Factos

A

Factors 2, 7, 9, 10, proteins C & S

These undergo a post transcriptional modification of glutamic acid to gamma-carboxyglutamic acid - Gla then binds to -vely charged phospholipids provided by activated platelets via Ca2+

Vitamin K–> KH2–>Epoxide (KO) it is this last step which converts Glu to Gla

KO then converted back to vitamin K

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111
Q

VKOR Inhibitors

A

E.g. Warfarin, prevent the conversion of epoxide back to vitamin K hence prevents clotting as vitamin K dependent clotting factors aren’t produced

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112
Q

Vitamin K Defeciency due to…

A

Malbsorption, liver disease, drugs, bleeding

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113
Q

Haemophilia A

A

Factor VIII defeciency
X-linked recessive
No consolidation of blood clot –> may need treatment with recombinant or plasma concentrates.

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114
Q

Haemophilia B

A

Factor IX Defeciency, Christmas Disease

For treatment of both haemophilias need recombinant or plasma concentrates of FVIII/FIX, but may develop immune resistance to them hence give immunosuppressants

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115
Q

Prothrombin Time

A

TF trigger, measure the extrinsic pathway! Prolonged clotting time in FVII defeciency

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116
Q

Activated Portal Thrombo-plastin (APPT)

A

Prolonged clotting time if deficiency in intrinsic pathway i.e. Factors XII, XI, IX, VII defeciency

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117
Q

PT Normal, Prolonged APTT

A

Haemophilia

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118
Q

vWF

A

vWF multiglomeric protein produced by Weibel Palade bodies in endothelial cells and alpha granules in platelets

Stabilises FVII and involved in platelet adhesion and aggregation

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119
Q

vWF Disease

A

Type 1 - heterozygous - autosomal dominant - mild
Type 2 - functionl - autosomal recessive - mild
Type 3 - complete deficiency - autsomal recessive - severe
Platelet Type - mutation in GPVI affects adhesion/aggregation

Symptoms: menorhaggia, nose bleeds, GI bleeds, petechia, joint or muscular pain

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120
Q

Thrombocytopaenia/thrombobasthenia

A

Acquired: Leukaemia, DIC, Immume thomobcytopenic Propura

Inherited: Congentital amegakaryotic thrombocytopoenia, Farconis Anaemia, Glanzmann (A2B3 mutation) or Bernard Souilleir (GPVI defeciecny)

Symptoms:Haemophilia symptoms but milder

Treatment: Underlying cause, steroids for ITP, platelet transfusion

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121
Q

Bernard Souillier

A

GPVI defeciency

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122
Q

Glanzmann

A

A2B3 mutation

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123
Q

DVT

A

Low blood flow and pressure, in valves of legs –> can cause PE

Thrombus is fibrin and erythrocyte rich!

Risk factors: immobilisation, genetics, pregnancy, cancer (cells express TF), surgery

Treatment: IV Unfractioned Heparin (helps antithrombin)
Slow onset: Warfarin and coumarins, direct thrombin inhibitors e.g. Dabigatran

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124
Q

Virchows Traingle

A

1) Change in endothelial state/injury
2) Hypercoagulative state
3) Circulatory status

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125
Q

Dabigatran

A

Direct thrombin inhibitor

Oral tablet that doesnt need monitoring!

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126
Q

Antithrombin

A

Natural anti-coagulant
Inhibits FIX and X
Stimulated by Heparin

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127
Q

TF Pathway Inhibitor

A

Natural anti-coagulant

Inhibits FXII/TF & X

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128
Q

Protein C

A

Natural anti-coagulant

Proteolytically activates FVa and VIIIa

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129
Q

Protein S

A

Natural anti-coagulant

Cofactor for protein C

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130
Q

Factor V Leiden

A

Arg-Glu mutation. activated Protein C usually cleaves FVa at 3 peptide bonds to inactivate

Mutation stops the cleavage, coagulation can still occur

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131
Q

Fibrolysis

A

Fibrin enhances plasminogen to be converted to plasmin. Plasmin degrades the fibrin clot

tPA and UPA activate plasminogen

PAI-I blocks the tPA and UPA active sites
TAF1 blocks enhancement

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132
Q

Atherosclerosis

A

Inflammation of vessel wall –> macrophages either the subintimal space and turned into foam cells, black rupture, collagen exposed binds A2B1 and GPV1, clotting occurs

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133
Q

Lysophosphatidic Acid (LPA)

A

Activates platelets via P2Y12

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134
Q

Arterial clotting

A

Thrombus is platelet rich

Treatment: Antiplatelets
Aspirin
Statins - lower cholesterol
Abciximab, tirofiban - anti A2B3
Clopidogrel - anti P2Y12
Fibrinolytic  tPA and UPA
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135
Q

Aspirin

A

COX Inhibitor –> Stops inflammation but also stops production of thromboxane hence prevent platelet activation

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136
Q

Abciximab and tirofiban

A

Anti A2B3

137
Q

Heparin

A

Inhibits Thrombin and FXa
Used in surgery and angioplasties
Heparin found in lungs or small intestine!

138
Q

Clopidogrel

A

Anti P2Y12

139
Q

Formalin Fixer

A

Pros: Common, forms covalent bonds between proteins

Cons: Not good for cytoplasmic structure or nucleic acid
Irritant.toxic

140
Q

Glutaraldehyde fixer

A

Pros: Good for sub microscopic structures & EM

Cons: Poor tissue penetration

141
Q

Ethanol

A

Pros: Nucleic Acid

Cons: Poor Morphology

142
Q

Freeze

A

Pros: Nucleic acid and protein

Cons: Poor morphology, uses up lots of space and energy!

143
Q

Wax impregnation of samples

A

Wax is only soluble in benzene hydrocarbons, dehydrate the sample in alcohol, replace alcohol with xylene, samples then used for staining!

144
Q

histological stains Haemoxylin & Eosin

A

H - basic and purple, stains acidic structures purple e.g. DNA

E - acidic and pink, stains basic structures pink e.g. protein

CONS: Fat not stained, can’t tell the difference between collagen and elastin!

145
Q

Massons Trichrome

A

Haemoxylin + Acid Fuschin + Methyl Blue

Collagen - Blue
Muscle, cytoplasm, RBC - red
Nuclei - Black

Good for collagen and connective tissue, shows liver fibrosis. Stains Mucis

146
Q

Periodic Acid Schiffer Stain

A

Picks up mucin (but also glycogen hence use diastase enzyme to remove glycogen)
Can highlight tumours that produce mucin

147
Q

Perls Prussian Blue

A

Detects iron, shows asbestos as iron binds to it

148
Q

Ocein

A

Used in liver pathology, shows asbestos as iron binds to it and Hepatitis B stains copper proteins

149
Q

Gram stain

A

Used for bacteria

150
Q

Grocoh/PASD

A

Used for fungi

151
Q

Ziehl Neelson

A

used for mycobacteria e.g. TB

152
Q

Foci Formation

A

when cancer cells just begin to grow onto of each other

153
Q

Hereditary cancer disease patterns seen in…

A

Li Fraumeni Syndrome and Eroderma Pigmentosam (mutation in DNA repair gene)

154
Q

Hep B Causes

A

Liver cancer

155
Q

H. Pylori

A

Causes stomach cancer

156
Q

Heterocycln amines in cooked meats

A

Causes stomach cancer

157
Q

UV and skin cancer

A

UV rays cause adjacent thymines to pair up forming covalent bonds and thymine dimers, problems for DNA replication hence cancer

158
Q

Alfatoxin

A

Toxin produced by fungi, metabolised in liver to form a reactive intermediate and DNA adduct causing liver cancer.
Common in developing countries

159
Q

DNA Adducts

A

make things more reactive

e.g. benzopyrene binds to deoxyguanine

160
Q

Tight Junctions

A

Occludin/Claudin seals at the apical of cell

161
Q

Adherens Junctions

A

Transmembrane proteins connect across the cell cytoskeleton using actin filaments below the TJ’s

162
Q

Gap junctions

A

small ion channels allowing intracellular exchange

163
Q

Desmosomes

A

TM proteins attach to other proteins on other cells

164
Q

Hemi-desmosomes

A

attach to the underlying basement lamina

165
Q

Exocrine/endocrine glands

A

Exocrine glands open onto surface of epithelial cells, can be simple glands with no ducts e.g. sweat
Endocrine glands are ductless glands that secrete directly into the circulation
Pancreas is both an exo and endoxrine gland!

166
Q

Methods of Secretion

A

Merorcrine - mainly watery, secrete substances out of intact cells e.g. pancreas and sweat glands

Apocrine - portion of cell pinched off containing substances e.g. mammary glands used for proteins and fats

Halocrine - cell disintegrates releasing contents e.g. sebaceous glands most oily secretions

167
Q

Epidermolysis Bullosa Simplex

A

Skin - congenital disease, affects keratin intermediate assembly causing bullae in areas of stress

168
Q

Harlequin Ichthyosis

A

Skin - congenital hyperkeratinisation, fatal due to dehydration, thermoregulation and sepsis

169
Q

Epithelilal Basement Dystrophy

A

In 2% of the population, causes corneal erosions, visual disturbances and material deposition

170
Q

Autosomal Dominant PKD

A

Congenital, afects Ca2+ transport. Increased renal tube proliferation causing nephron cystic degradation, parenchymal compression and renal failure

171
Q

Kartageners Syndrome

A

Congenital cilia dyskinesia with situs inversus. Causes chronic sinusitis, bronchiectasis and subfertilty!

172
Q

Components of connective tissues

A

Extracellular matrix - a gel called ground substances containing proteins and elastic and collagen fibres

Cells - fibroblasts, adipocytes etc

173
Q

Marfans Syndrome

A

Lack of fibrin causes joint laxity, cataracts, aortic dissection and valvular heart diseases

174
Q

Neutrophils

A

Phagocytose bacteria, contain enzyme granules

175
Q

Basophils

A

Rarely seen act like mast cells

176
Q

Eosonopils

A

Bilobed uncles, tomato wearing sunglasses

177
Q

Bone formation

A

Osteoblasts make osteoid in the extracellular matrix, mineralised with calcium to make bone, woven is immature bone which is then replaced by lamella

178
Q

Cartilage formation

A

Chrondoplasts make ground substance and collagen fibres in the extracellular matrix and then become trapped as chondrocytes
Hyaline cartilage - nose, trachea, joints
Elastic - ears
Fibrocartilaed - pubic syphis and intervertebral discs!

179
Q

C3a, C4a & C5a

A

Anaphylatoxins - trigger the degranulation of endothelial cells, mast cell and phagocytes
Cause smooth muscle contraction and enhance vascular permeability
C3a and C5a also attract other neutrophils!

180
Q

MAC

A

C5b, C6,7,8,9 perforate the cell forming a pore in the membrane of the infected cell

181
Q

C3b

A

For opsonisation, binds to the surface of bacteria and is cleaved to iC3b to bind macrophages causing phagocytosis!

182
Q

3 Ways to activate the complement system (all involved C3 & C5)

A

1) Classical Way - C1 binds to an antigen/antibody complex –> cascade triggered however not usually the 1st way to trigger the cascade as takes time to produce antibodies
2) Lectin/mannose binding - mannose-binding lectin binds mannose then Masp1&2, complex then cleaves c2& 4
3) Alternative pathway - auto activation of C3 - occurs constantly at a low rate, but upon contact with bacteria C3b binds factor B & properdin, rapidly activates C3 and C5

183
Q

Pathogens with Mannose Sugar

A

Yeasts - Candida Albicans
Viruses - HIV/Influenza
Bacteria - Salmonela & steptococci
Parasites - Leishmania

184
Q

Macrophages - Residing In Tissues - Activation

A

Resting - collect debris, phagocytose and eliminate apoptic cells, express little MHC Class II

Primed (IFN from NK Cells and T helper cells)
Express more MHC II and take up larger objects by phagocytosis!

Hyperactive (IFN & LPS from gram -ve bacteria)
Macrophages stop proliferating, expand and increase rate of phagocytosis

Produce TNF & IL-1 when hyperactive!!

185
Q

What cytokines do hyperactive macrophages produce

A

TNF & IL-1

186
Q

Neutrophhils - reside in blood

A

Life span 5-9 days
1) Selectin/Ligand binding - SLIG always expressed on neutrophil
IL-1 & TNF from macrophages causes endothelium to express selectin

2) ICAM always on endothelium
LPS and C5a cause neutrophil to express integrin

These stop the neutrophil rolling!

187
Q

What form of methionine do bacteria have?

A

bacteria have f-met, neutrophils track this f-met secreted by bacteria.
C5a and f-met allow the neutrophils to infiltrate the endothelium and surrounding vessels, they become extremely phagocytic

188
Q

What cytokine do neutrophils produce?

A

TNF

189
Q

What cytokines do natural killer cells produce?

A

IFN & IL-2

190
Q

Natural killer cells

A

Produced in bone marrow, found in blood!
Fas ligand binds to Fas on infected cells, causes apoptosis
Perforin protein injects granzyme B, the suicide protein into the cell

191
Q

Innate and viral infections

A

Opsonisation with C3b
MAC produced
TNF and IFN reduce viral production
NK cells cause apoptosis of infected cells

192
Q

Which regions of gene segments change in antibodies?

A

V, D & J gene segments are mixed and matched

193
Q

Which antibody is released first?

A

IgM - pentameric structure of the Fc region can bind up to 5 C1 complexes at a time hence activates lots of complement system! shows innate and adaptive immune repsonse working together!

194
Q

Where does class switching occur

A

In the germinal centres of lymphoid tissues (germinal centres in secondary follicles of cortex of lymph nodes), t helper cells direct the type of antibody the B cells should produce!

195
Q

Where are inactive B cells exposed to antigens?

A

in the lymph nodes - proliferating B cells causes swollen lymph nodes! B cells in both primary and secondary follicles of cortex!

196
Q

Somatic hypermutation

A

High mutation rate in V, D & J segments upto 1 in 1000! Can increase/decrease affinity of antibody! Higher affinity, more likely to bind hence stimulated more so proliferates more

197
Q

Through what processes do the Fc and Fab region of the antibodies change?

A 
Fc - class switching
Fab - somatic hypermutation!
198
Q

T cell tolerance

A

+ve selection - cells must recognise MHC molecules

-ve selection - cells stop expressing CD4 or CD8, if cells recognise self-antigens they are triggered to die!

but no all cells may encounter self antigen, but anergy still occurs if they meet self antigen later due to absence of second signal!

199
Q

B Cell tolerance

A

Become tolerant in bone marrow
Clonal Deletion - if they recognise self antigens they die
Receptor tolerance - daily exposure to the same antigen creates a tolerance
Undergo anergy if they encounter an engine with no help from T cells!

200
Q

Types of APC

A

1) Dendritic cells - in periheral tissues, travel to nearest lymph node to activate T cells
2) Macrophages - in tissues, stay in tissue to fight infection and continue to stimulate T cells when they reach the tissue!
3) B cells - only experienced B cells load antigens onto MHC class II cells, responsible for activating T cells when they encounter the antigen a second time!

201
Q

B cell activation

A

Requires binding antigen

Requires 2nd Signnal from T cells of non T-cells

202
Q

How many antigen binding sites on the antibody?

A

2 antigen binding sites in the fab regions

203
Q

IgM

A

initial response, in the blood stream, kills bacteria, activates complement system

204
Q

IgG

A

Later response, blood ad interstial tissues, prepares the bacteria to be killed. For bacteria and viruses

205
Q

IgE

A

Allergic reactions, parasites and causes most cells to release contents

206
Q

IgA

A

Protects potential pathogen entry routes/ mucosal surfaces! Binds and removes viruses

207
Q

IgD

A

in the B cell membrane to help divisoin

208
Q

Hepatitis Antigens

A

HBsAg detected in the active disease

HBcAb detected in current and previous infections! the vaccination uses only the surface antigen!

209
Q

Graves disease

A

Autoimmune condition, produces antibodies mimicking TSH causing uncontrolled hyperthyroidism

210
Q

T Helper cells have

A

CD4

211
Q

T Cytotoxic cells have

A

CD8

212
Q

T Cell Activation

A 
Antigen presented with an MHC protein (class I or II)
Also second signal from CD28 on T cell interacting with CD80 on the APC
213
Q

T Helper cells

A

release cytokines, chemoattraction, inflammation, stimulate antibody production and make phagocytes work better!

214
Q

Cytotoxic cells

A

virus proteins loaded onto MHC class I molecules in ER and transported to the cell surface

215
Q

Cytokines

A

Produced mainly by T helper cells

216
Q

T helper 1 cells

A

Il-2, IL-5 activates cell mediated & cytotoxic T cells

217
Q

T helper 2 cells

A

IL-4, IL-10, IL-13, act on B cells to control antibody production!

218
Q

Th1 Disease

A

Tuberculoid Leprosry (cytotoxic)

219
Q

Th2 Disease

A

Lepromatour leprosy (helper)

220
Q

HIV

A

Has p120 surface antigen, binds CD4 on T helper cells causing cell death!

221
Q

T & B Cell interaction

A

B cells are APC with MHC Class II and bind with CD4 receptor on T helper cells
Also CD28 and CD80 interaction
T helper cells they produce cytokines to stimulate antibody production

222
Q

Pernicious anaemia

A

autoimmune disease attacking cells in the stomach needed for B12 absorption

223
Q

Non organ specific autoimmune disease

A

Can attack any part of the body e.g. systemic lupus erythematous!

224
Q

Cytoplasm

A

Cytosol + organelles

225
Q

Microtubules

A

2 globular alpha and beta proteins polymerised into proto filaments

13 protofilaments form a tube, can then be doubled or tripled

Provides tracks for organelles to move on and axonal transport occurs

Anterograde transport - transport can occur in both directions on the same microtubule

226
Q

Microtubule assosciated proteins

A

These proteins cross-link the microtubules, one of these proteins in tau which accumulates in alzheimers disease

227
Q

Cilia and flagella are composed of what?

A

Microtubules

228
Q

Nucleus double membrane

A

Inner membrane is smooth, the outer membrane is continuous with the ER

229
Q

Golgi apparatus

A

Flattened containers in the cytosol, proteins are transferred here from the ER in vesicles.
Modifies proteins and lipids by adding carbs, etc. and distributing them and packaging them.

230
Q

Proteosomes

A

Specialised structures to degrade cytosolic proteins.
Enzyme has four rings around a central core
Proteins to be degraded are marked with ubiquitin, this directs them to the core of the proteasome where they are degraded!

231
Q

Gram Staining Bacteria

A

Gram +ve bacteria have a second outer membrane of peptidoglycan hence retain the crystal vile stain and are purple
Grab -ve bacteria take up the counter stain as only have one membrane of peptidoglycan hence giving them a pink colour

232
Q

Nucleoli

A

An assembly of ribosomes, stains darkly, contains RNA and proteins

233
Q

Grifftiths DNA

A

Heat killed virulent and non-virulent. When heat killed virulent mixed with non-virulent - kills mice, shows protein or DNA responsible

234
Q

Avery

A

Only DNA changes non-virulent to virulent

235
Q

Hershey & Chase

A

Grew phages with radioactive P & S, only P found in infected bacteria hence DNA carrier or genetic material

236
Q

Watson & Crick

A

Double helix structure, sugar/phosphate backbone, A+T = 2 bonds

237
Q

Semi-conservative replication

A

Shown by meselsohn & Stahl
DNA replicates at replication fork (where DNA is unwound by DNA Helicase
Single stranded binding proteins bind to stabilise the strand and prevent them recombining
Terminator polymerase sequence produces unstable RNA sequence causing the polymerase to release the RNA

238
Q

What polymerase is used for DNA replication

A

DNA Polymerase III

239
Q

DNA Replication the lagging strand -

A

DNA can only replicate in 5’ to 3’ direction. On the lagging strand DNA is laid down is Okazaki segments, DNA primes lays down regular primers, DNA polymerase I removes primers and DNA ligase seals the gaps

240
Q

What provides the energy to form new phosphodiester bonds?

A

The hydrolysis of dNTPS as new nucleotides are added

241
Q

Uracil-n-glycosylase

A

used to repair DNA, cutes out uracil and DNA polymerase repairs damage

242
Q

Which strand of DNA is copied in transcription?

A

The antisense strand - this means mRNA is that same as the sense strand but with thiamine instead of uracil.

243
Q

What direction does RNA polymerase II move in>

A

3’ to 5’, mRNA is sythesised in a 5’ to 3’

244
Q

What promoter regions in genes are there?

A

TATA box - 25bp away from transcription site
CAAAT box
CpG islands
Allows the binding of transcriptional factors and RNA polymerase to bind and position correctly

245
Q

Types of RNA Polymerase

A

1 type in bacteria
3 Types in eukaryotes
RNA Polymerase I & III = tRNA and rRNA
RNA Polymerase II = mRNA

246
Q

Modification of RNA

A

Splicing - splice some (collection of small RNA and protein) removes introns from pre-mRNA

7-methyl-guanine to 5’ end of mRNA - occurs by 3 enzymes, makes the 5’ end look like the functional 3’ end to avoid degradation

Poly-A Tail added - 200 adenine nucleotides added to the 3’ end, helps transport mRNA out of the nucleus and direct protein synthesis

247
Q

tRNA

A

80 nucleotides, amino acid on the 3’ end, anticodon complimentary to mRNA codon

248
Q

What added amino acids to tRNA

A

tRNA synthetases

249
Q

What are the 3 sites on tRNA

A

A - arrival
P - tRNA already in place
E - tRNA binding

250
Q

What forms the peptide bonds between amino acids

A

RIbosomes

251
Q

Terminator mRNA sequences

A

UAA, UAG, UGA produce release factors

252
Q

Wobble-base pairing

A

Where as long as the first 2 bases on the tRNA anticodon are correct the 3rd base can bind to several bases!
Allows folding a tertiary structure to form
Limits numbers of tRNA required!

253
Q

Purine–>Pyrimidine change

A

Transversion
Transition if same type of base is kept
2

254
Q

2 Pathways of protein assemble

A

1) 20 hydrophobic amino acids added, then incorporated into the lipid bilayer and the rest is synthesised in the cytosol
2) Protein entirely synthesised in cytosol, carboxyl terminal cleaved, fatty acid chain linked to Cys and anchored to the membrane via a G protein (Ras/Rho)

255
Q

BRCA1 Gene

A

Increases the chance of breastcancer

256
Q

Polymorphism

A

A mutation in at least 1% of the population

257
Q

Epigenetics

A

The control of gene expression or cell phenotype by means other than genetic variation! (basically the same DNA but expresssed differently)
e.g. cytosine methylated at CpG sites affects gene expression

258
Q

Menstrual Age

A

Day of last period, starts at day 0, 3 equal trimesters

259
Q

Fertilisation Age

A

Starts at point of fertilisation, 3 unequal periods

1) 0-2 weeks - Early development
2) 3-8 weeks - Embryonic - organogenesis
3) 8 weeks+ - growth and maturation of organs

260
Q

Teratogens

A

Environmental causes of birth defects, body most susceptible in weeks 3-8, week 5 the highest as this is when organogenesis is occurring. CNS and heart have longest critical time in organogenesis hence increased risk of defects

261
Q

Toxiplasmosis

A

1/3 of the population have it, only infectious if caught weeks 3-8 in cat faeces/undercooked meet
Microcephaly, hydrocephaly, microopthalmia

262
Q

Rubella

A

Virus, only harmful if caught weeks 3 to 8

Microcephaly, cataracts, deafness, heart defects

263
Q

Cytomegalovirus

A

Bodily fluids, asymptomatic only causes problems if caught weeks 3 to 8
Causes cereberal calcifcation, intrauterine growth retardation (small at birth), microcephaly, microopthalmia

264
Q

HSV (Type 1 - cold sore, type 2 - gential herpes)

A

Rarely transmitted in utero, usually at delivery

Causes skin lesions, scars, microcephaly, seizures, vision problems!

265
Q

Thalidomide

A

Shortened limbs etc

Treats leprosy.

266
Q

Where does fertilisation occur?

A

At the ampulla

267
Q

Day 4 embryology

A

Morula which is 16-32 cells, differentiates into inner embryo blast cells and outer trophoblast cells

268
Q

Day 5 embryology

A

Blastocyst hatching into uterus, leaves zone pellucida and implants, usually on the posterior endometrial wall

269
Q

Day 7 embryology

A

further differentiation: Trophoblast into the cytotrophoblast and syncytiotrophoblasts
Embryo blast into hypoblast (ventral) and epiblast (dorsal)

270
Q

Day 8 embryology

A

The amniotic cavity develops in the epiblast! syncytiotrophoblasts secreting enzymes to prevent immune response, only nutrients from diffusion via the uterine gland

271
Q

Day 9 embryology

A

Full implantation, yolk sac and trophoblastic lacuna from

272
Q

Day 10/11 embryology

A

Trophoblastic lacune and extramebryonic mesoderm form

273
Q

Day 12/13 embryology

A

chorionic cavity forms in the extra embryonic mesoderm!

274
Q

Day 14

A

Secondary yolk sac forms. A secondary wave of hypoblast cells migrate to form the secondary yolk sac!
Embryo and amniotic cavity are suspended in the chorionic cavity by the connecting stalk!

275
Q

Pregnancy Tests

A

Test for Human Chorionic Gonadotrophin hormone ( HcG_

276
Q

Placenta pruvia

A

Implantation occurs near the cervix, baby can damage placenta during delivery causing haemorrhage. Spot on ultrasounds and consider caesarean

277
Q

Tubal (ectopic)

A

80% of ectopic pregancy, uterine tubes can rupture, extreme pain often mistaken for appendicitis

278
Q

Abdominal

A

Occurs in the rectouterine pouch, if placenta attaches to other organs it can sometimes suvive e.g. the liver

279
Q

Lithapaedion

A

Abdominal implantation of the egg, becomes calcified as too large to be reabsorbed by then boy and the mother needs to be protected from nephrotic tissues

280
Q

Hydatidiform Mole

A

When an empty egg is fertilised, trophoblasts still form showing paternal genes favour this

281
Q

Day 15 embryology

A

Primitive steak forms on dorsal surface establishing the body axis
Definitive endoderm also forms

282
Q

Day 16 embryology

A

Formation of the mesoderm and ectoderm
Ectoderm - Skin, NS
Mesoderm - bones, muscle ,cartilage, kidneys, reproductive system
Endoderm - lungs, glands or liver and pancreas, GI tract lining

283
Q

Day 17 embryology

A

Mesoderm becomes highly organised! divides into:
Paraxial - Skeleton, skeletal muscle, skin
Intermediate - Reproductive system and kidneys
Lateral Plate -linings of the body cavities

284
Q

Day 20 embryology

A

Paraxial mesoderm becomes highly organised, splits into 3/4 somites a day, can estimate the age of an embryo from this, goes cranial to caudal

285
Q

Ectoderm

A

Forms skin and nervous system

286
Q

Mesoderm

A

Forms muscle, bone, cardio, kidneys and reproductive system

287
Q

Endoderm

A

Forms lungs, GI linings, glands of liver and pancrease

288
Q

Paraxial mesoderm

A

Forms skeleton, skeletal muscle, skin

289
Q

Intermediate mesoderm

A

Reproductive trace and kidneys

290
Q

Lateral plate mesoderm

A

Forms the lining of the body cavities.

291
Q

Sirenomella

A

Abnormal gastrulation, as the primitive streak regresses it disappears to early. Insufficient mesoderm in the caudal region hence limbs fuse and abnormalities of the urogenital system

292
Q

Sarcococcygeal Teratoma

A

Primitive streak persists - tumours form as too much mesoderm but good prognosis. 80% females!

293
Q

Day 19

A

Notochord initiates neuralation. Notochord causes the overlying ectoderm to thicken in induction forming the normal plate

294
Q

Notochord organises the Paraxial mesoderm further

A

Sclerotome - forms bone and cartilage
Myotome - Forms skeletal muscle
Dermatome - Form dermis
This means the notochord organises vertebrae formation from somites!

295
Q

Vertebrae formation

A

Organised by the notochord! Sclerotome cells surround the notochord forming the vertebral body and surround the neural tube forming the vertebral arch
Majority of notochord degenerates, remounts as nucleus pulposus in the intervertebral discs!

296
Q

Spina Bifida Occulta

A

Vertebral arch doesn’t form properly, only skin and fat protect the spinal cord, marked by dimpling of skin and tuft of hair

297
Q

Meningocele

A

Meninges sac containing only CSF protrudes through vertebral defect covered by skin

298
Q

Myelomeningocele

A

Meninges sac and spinal cord protrude through defect, not covered by skin. Usually occurs in lower back, easy to damage in birth causing lower limb, continence and reproductive problems.

299
Q

Day 22

A

Fusion of neural folds in the midline - cranially and cardially, as neural folds fuse they detach from the ectoderm and can then be covered by skin

300
Q

Day 25

A

Anterior Neuropore fuses

301
Q

Day 28

A

Posterior Neuroporse fuses

302
Q

Anencephaly

A

Failure of anterior neuropore to fuse - forebrain doesn’t form, only have brainstem, cause premature birth

303
Q

Rachischisis

A

Failure of posterior neuropore to fuse, neural tissue remains fused to the ectoderm, spinal cord doesn’t form properly causing paralysis. Open neural tube prevent vertebrae formation ( a from of spin bifida) and flap plate neural tube exposed at birth!

304
Q

Neurofibromatosis

A

genetic mutation in the NF1 gene (a tumour suppressor gene), gene switched causing benign tumours of nervous system, skin and cranial bones. It is an abnormality in neural crest cell development

305
Q

Week 4 embryology

A

Folding of the embryo! Lateral plate mesoderm splits into parietal (with ectoderm) and visceral (with endoderm and organs)

306
Q

Ectopia Cordis

A

Lateral folds fail to fuse in the thoracic region leaving the heart outside the body

307
Q

Gastroschisis

A

Lateral folds fail to fuse in the abdominal region, investing left outside the body

308
Q

Anterior pituitary

A

Produces hormones

309
Q

Posterior pituitary

A

Stores hormones from the hypothalamus

310
Q

Prolactin secretion

A

Under inhibitory effects from the hypothalamus

311
Q

Glands not controlled by the pituitary gland

A

Parathyroid glands
Adrenal medulla (produces adrenalin)
Pancreas
Gut Hormones

312
Q

How many lobes of the thyroid gland

A

2 lobes

313
Q

What does the parathyroid gland control?

A

Controls calcium levels, secretes PTH to increase absorption of calcium from kidneys and gut and release calcium from bones

314
Q

What do the adrenal glands produce?

A

Cortex 10% of gland - corticosteroids, androgens and mineral corticoid (aldosterone but this isn’t controlled by the pituitary)
Medulla 10% of gland - Catecholamines (adrenaline etc.) - not controlled by the pituitary

315
Q

Testes cells

A

Intersitial/leydig cells - produce testosterone
Seminiferous tubules - contain germ cells to produce sperm
Sertoli cells - produce inhibit

316
Q

Classification of gland abnormalities

A

Primary - affects gland itself
Secondary - affects pituitary
Tertiary - affects hypothalamus

317
Q

Static tests used for

A

Thyroid and Sex hormones

318
Q

Synacthen Test

A

Used for adrenal failure, give ACTH expect to see cortisol rise, if not then fails!

319
Q

Insulin Stress Test

A

Give insulin to reduce BGL, causes stress, body should produce cortisol and cause glucose to be released. If not shows pituitary problem! (glucagon stimulation test is an alternative)

320
Q

Steroid suppression test

A

Give steroids, measure endogenous production should decrease in normal

321
Q

GH Test

A

Give glucose, should switch off growth horome

322
Q

Prolactin oversecretion Causes

A

Prolactinoma - a prolactin secreting pituitary tumour. Micro tumours are less than 1cm in diameter
Non-functioning pituitary tumour - compressing the hypothalamus and stops the inhibiting effect

323
Q

Prolactin oversecretion symptoms

A

Galactorrhea, amenorrhea, sexual dysfunction in men (as it lowers testosterone), headaches and visual problems (tumours can compress the optic chasm)

Diagnose with spot test, MRI of pituitary

324
Q

Prolactin oversecretion Treatment

A

Generally a higher prolactin means a prolactinoma. Prolactinomas are the only tumour that can be traced medically - rarely require surgical intervention

325
Q

Growth Hormone Oversecretion Causes & Symptoms

A

Causes: Tumour

Symptoms: In children - excessive growth, large hands and feet, gigantism
In adults - acrogmegalic face, large hands/feet, sweating

326
Q

Growth Hormone Oversecretion Diagnosis & Treatment

A

Diagnosis: Glucose suppression test, imaging to see if tumour
Treatment: Surgery to remove the tumour, radiotherapy/medical therapy

327
Q

Steroid Under Secretion Causes & Symptoms

A

Causes: Adrenal and pituitary failure

Symptoms: Growth arrest in children, tiredness, dizzy due to low blood pressure, abdominal pain, low aldosterone

328
Q

Steroid Undersecretion Diagnosis and Treatment

A

Diagnosis: Synacthen test - give ACTH expect steroids to rise, detects primary adrenal failure!

IF HYPOTENSION THEN INJECT STEROID STRAIGHTAWAY AS STEROID DEFECIENCY CAN BE FATAL

Treatment: Tablets to replace hormone

329
Q

Hypothyroidism Causes and Symtpoms

A

Causes: Primary - thyroid failure, usually autoimmune
Secondary - pituitary failure, usually complete

Symptoms: Often older women, weak, dry skin, cold, decreased sweating, impaired memory, constipation, weight gain, hair loss

330
Q

Hypothyroidism Diagnosis and Treatment

A

Diagnosis: Static Test, high TSH in primary failure, low TSH in secondary

Treatment: Thyroid replacement tablets ( contain the inactive T4)

331
Q

Sex hormone defeciency causes and symptoms

A

Causes: Primary and secondary gland failure

Symptoms: ED, reduced libido, menstrual problems

332
Q

Sex hormone deficiency tests and treatment

A

Tests: Static test

Treatment: Hormone replacement, generally replace the sex hormones and pituitary hormones are difficult to replace

333
Q

Causes of Amenorrhea

A

Uterine problems
Ovarian problems (hypogonadism, polycystic disease, ovarian failure)
Pituitary or hypothalamus problems (common in athletes)
Prolactinomas

334
Q

Pituitary failure

A

Causes: Large tumours, often high growth hormone levels
Diagnosis: Usually involve multiple hormones

335
Q

Increased parathyroidism

A

Causes: Cancers produce a similar thing to PTH, Drugs

Tests: High calcium and high PTH = primary failure
High calcium and lowP PTH = not parathyroid problem, potentially cancer

336
Q

Cushing Syndrome (High Cortisol) Causes and Symptoms

A

Causes: Pituitary tumour secreting ACTH
Adrenal tumour secreting cortisol
Cancers producing cortisol

Symptoms: Growth arrest in children, round face, truncal obesity, acne, thin extremities, think skin, easy brushing, hypertension, diabetes, higher risk of infection

337
Q

Cushings syndrome diagnosis and treatment

A

Dexamethasone suppression test - should reduce cortisol
High ACTH is secondary cushings, low is

Treatment: Surgery to remove tumours and radiotherapy etc.

338
Q

Hyperthroyidism causes (primary is common, secondary rare)

A

Graves Disease - autoimmune disease attacks thyroid, causes enlarged smooth thyroid (80%) of cases

Toxic nodules - multinodular thryoid

Thyroiditis - inflammation of thyroid, causes initial release of hormones then cells die and it decreases. Tender enlarged thyroid

Drug induced e.g. amiodarone, TSH secreting tumours or iatrogenic

Medicine (22 decks)

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