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principles_20190518182821 Flashcards

1
Q

what are the oxidation states of carbon?

A

alkane (fats) > alcohol (carbs) > aldehyde > carboxylic acid > carbon dioxide

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2
Q

what is the first law of thermodynamics?

A

energy neither created or destroyed

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3
Q

what is the second law of thermodynamics?

A

energy converted from one form to another, some becomes unavailable to do work

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4
Q

where is collagen triple helix found?

A

connective tissue

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5
Q

role of smooth ER

A

synthesis of steroid hormones

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6
Q

role of rough ER

A

synthesises polypeptides

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7
Q

role of golgi apparatus

A

receives materials from ER and distributes, can also modify proteins

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8
Q

what is nucleoside

A

base and sugar

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9
Q

what are purines

A

adenine and guanine

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10
Q

what are pyrimidines

A

uracil, thymine and cytosine

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11
Q

what kind of bonds between 3 OH group and 5 triphosphate

A

phosphodiester

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12
Q

what is the leading strand

A

always has free 3’ end (dna always synthesised in 5-3 direction)

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13
Q

role of rRNA

A

combines with proteins to form ribosomes found in nucleolus

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14
Q

role of tRNA

A

carries amino acids to be incorporated into protein anticodon consists of 3 nucleotides

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15
Q

role of mRNA

A

carries genetic information for protein synthesis

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16
Q

what are the three types of RNA which eurkaryotic cells have

A

pol I, II and IIIpol II synthesises all mRNA

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17
Q

what is TFIID

A

general transcription factor required for all Pol II transcribed genes

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18
Q

steps in the initiation of translation

A

GTP provides energy, ribosomal subunit binds to 5’ end, initiator tRNA (located in P site) pairs to start codon and large subunit joins assembly and initiator tRNA

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19
Q

steps in the elongation of translation

A

elongation factor brings aminoacyl-tRNA to A site where second elongation factor regenerates the first to pick up next a-tRNA

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20
Q

what catalyses the peptide bond formation between amino acids in P and A sites

A

peptidyl transferase

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21
Q

steps in termination of translation

A

occurs when A site of ribosome encounters a stop codon (UAA, UAG, UGA)

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22
Q

where are free ribosomes found

A

in cytosol proteins for cytosol, nucleus or mitochondria post translational

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23
Q

where are bound ribosomes found

A

plasma membrane, ER, golgi, secretionco-translational

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24
Q

what are enzymes without cofactor called

A

apoenzymes

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25
Q

what are enzymes with cofactor called

A

holoenzymes

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26
Q

what is vmax?

A

maximal rate of reaction at unlimited substrate concentrationintersect of straight line with Y

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27
Q

what is Km

A

michaelis constant - 50% vmax intersection with X

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28
Q

what happens in competitive inhibition

A

km varies

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29
Q

what happens in non-competitive inhibition

A

vmax varies

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30
Q

what is the difference between haemoglobin and myoglobin

A

haemoglobin shows allosteric regulationmyoglobin - michaelis menten

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31
Q

anabolism

A

requires energy, endergonic and reductive

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32
Q

catabolism

A

breakdown to produce energy, exergonic and oxidative

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33
Q

basic steps in glycolysis

A

hexokinase phosphorylates glucosephosphofructokinase phosphorylates fructose-6-phosphatepyruvate kinase converts phosphoenolpyruvate to pyruvate

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34
Q

what is the fate of NAD

A

reduced to NADH+ H+ in glycolysis regenerated through oxidative metabolism of pyruvate

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35
Q

basic steps in aerobic metabolism of pyruvate

A

enters matrixconverted to acetyl-coA (by PDC)condenses with 4c to form 6c compound this 6c decarboxylated twice - yields CO24 oxidation reaction - yeilds NADH+ H+ and FADH2GTP formed 4c compound recreated

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36
Q

what enzyme of TCA is integrated in inner membrane of mitochondria rather than matrix?

A

succinate dehydrogenase

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37
Q

how many electrons transferred in conversion of NAD+ to NADH+ H+

A

3 pairs

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38
Q

how many electrons needed to reduce FAD to FADH2

A

1 pair

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39
Q

what does TCA cycle generate from each a-coA

A

3 NADH+ H+1 FADH21 GTP2 CO2

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40
Q

what is the first step of oxidative phosphorylation (electron transport)

A

electrons from NADH enter at complex 1, electrons from FADH2 enter at complex II (TCA), electrons handed down from higher to lower redox potentials, transferred onto O2 ti form H2Otransfer of electrons through respiratory chain is coupled to H+ transport 3/4 complexes pump H+ (1, 2 and 4)forms electrochemical gradient - more protons in intermembrane space than matrix, matrix negative so protons attracted

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41
Q

what is second step of oxidative phosphorylation

A

ATP synthesis

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42
Q

what inhibits oxidative phosphorylation

A

cyanide, azide and CO inhibit transfer of electrons to O2 (no proton gradient can be formed)

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43
Q

what is the final balance from respiration

A

glycolysis - 2 ATPTCA cycle - 2 ATP (2 GTP)glycolysis, PDH, TCA cycle - 25 ATP and 10 NADH+ H+TCA cycle - 3 ATP (2 FADH2)

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44
Q

how many ATP molecules does one glucose yeild

A

30-32

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45
Q

what are the stages of cell cycle

A

G1 - S - G2 - M - G1DNA synthesis at S

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46
Q

basics of DNA synthesis

A

DNA helicase unzips DNA, DNA polymerase copies 5-3 strand then the 3-5 strand in okazaki fragments which DNA ligase joins

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47
Q

what causes sequence variations within a gene

A

changes in promotor sequence and change in exon sequence

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48
Q

what causes sequence changes in DNA between genes

A

SNPslarger deletions or duplications

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49
Q

what is chromosome of normal female

A

46 XX

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50
Q

what is aneuploidy

A

whole extra or missing chromosome

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51
Q

47XY + 21

A

down syndrome, trisomy 21

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52
Q

47XY + 14

A

miscarriage, trisomy 14

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53
Q

47 XY + 18

A

edward syndrome, trisomy 18

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54
Q

45 X

A

turners syndrome

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55
Q

47 XXY

A

klinefelters syndrome

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56
Q

what is a roberstonian translocation

A

two acrocentric chromosomes stuck end to end - increases risk of trisomy in pregnancy

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57
Q

what is microarray CGH

A

1st line chromosome test, detects any missing of duplicated piece of chromosomesaCGH - paediatric

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58
Q

what is gonadal mosaicism

A

causes recurrence risk for autosomal dominant condition even if parent unaffected

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59
Q

what is somatic mosaicism

A

all cells suffer mutations as they divide, repair mechanisms exist

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60
Q

what genes start cells dividing when switched on?

A

oncogenes

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61
Q

what is mendelian disorder

A

disease caused by change in single gene umbrella term for autosomal dominant, recessive, x linkedhigh penetrance, small environmental contribution

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62
Q

what is chance of children getting disease in X linked mutations

A

mother carrier - 50% chance daughter is carrier and 50% chance male is affected no male - male transmission

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63
Q

what does mitochondrial DNA contain

A

important genes for mitochondrial metabolic pathways and ribosomal RNAs

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64
Q

what kind of mutations occur in mitochondria

A

point mutations and deletions, inherited almost exclusively materally

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65
Q

symptoms of mitochondrial mutations

A

myopathy, diabetes, deafness, optic atrophy, stroke like episodes and encephalitis

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66
Q

how do mutations cause disease

A

only having one working copy not enough (haploinsufficiency) so abnormal protein interferes with normal (dominant negative) and mutation activates gene resulting in loss of heterozygosity

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67
Q

what is the characteristics of a multifactorial disease

A

genetic change just another risk factor and penetrance for any one mutation is low

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68
Q

what is imprinting (non mendelian)

A

differences in gene expression depending on wether gene is maternally or paternally inherited

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69
Q

angelman syndrome is example of non mendelian inheritance, what symptoms?

A

neurogenetic disorder: developmental delay, intellectual disability, ataxia, epilepsy, happy, frequent laughing eg - chromosome 15

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70
Q

what is heteroplasmy (non mendelian)

A

different daughter cells contain different proportions of mutant mitochondria

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71
Q

what do drug metabolism genes do

A

metabolise carcinogens

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72
Q

what is the mechanism of gene activation

A

duplication of gene, activation of gene promotor and change in amino acid sequence

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73
Q

what is FISH

A

can light up specific bit of chromosome if you know which bit to light up

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74
Q

mutation in what gene can cause breast cancer?

A

BRCA1 - carriers have 80% risk of breast or ovarian

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75
Q

characteristics of rare autosomal forms of breast cancer

A

young age of onset, many cancer and rare tumours

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76
Q

characteristics of multifactorial predisposition breast cancer

A

everyone at same risk anyone with family history at increased risk

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77
Q

what is components of inner cytosol

A

solution of proteins, electrolytes and carbohydrates

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78
Q

what is the components and role of cytoskeleton

A

determines shape and fluidity of cells made from thin, intermediate filaments and microtubules

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79
Q

microfilaments

A

7nm, composed of actin

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80
Q

intermediate filaments

A

> 10nm, composed of proteins

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81
Q

microtubules

A

25nm, composed of tubulin, originate from centrosome, polar and dynein and kinesin attach to them and move them along

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82
Q

what are occluding junctions

A

link cells to form diffusion barrier (tight junctions)

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83
Q

what are anchoring juncitons

A

provide mechanical strength, link submembrane actin bundles of adjacent cells (adherent junctions)

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84
Q

what are the role of desmosomes in anchoring junctions

A

link submembrane intermediate filaments of adjacent cells

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85
Q

what are the role of hemidesmosomes in anchoring junctions

A

link submembrane intermediate filaments of cells to extracellular matrix through transmembrane proteins

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86
Q

what are communicating junctions

A

allow movement of molecules (gap junctions) each junction studded with pores produced by connexion proteins

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87
Q

haematoxylin dye

A

purple, basic dye (affinity for acidic molecules)

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88
Q

eosin dye

A

pink, acidic dye

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89
Q

sqaumous epithelium

A

flattened

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90
Q

cuboidal epithelium

A

cube

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91
Q

columnar epithelium

A

tall and thin

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92
Q

what are the different kinds of glandular epithelia

A

exocrine (product secreted towards basal end of cell, distributed by vascular system, ductless glands) and endocrine (apical end of cell, ducted glands)

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93
Q

what are the three types of cartilage

A

hyaline (articular surface, tracheal rings, costal cartilage, epiphyseal growth plates)elasticfibrocartilage

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94
Q

what is the outer shell of a cortical bone which makes up the shaft

A

diaphysis

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95
Q

what occupies end of cancellous/trabecular bone

A

epiphyses

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96
Q

what is the contents of the extracellular matrix of connective tissue

A

fibres (collagen, reticular and elastic fibres), ground substance and tissue fluid

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97
Q

what are the cells of connective tissue

A

fibroblasts, adipose cells, osteocytes, chondrocytes

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98
Q

characteristics of smooth muscle

A

involuntary and non-striated

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99
Q

characteristics of skeletal muscle

A

voluntary and striated, multinucleated nuclei are elongated and located at periphery, just internal to cell membrane (sarcolemma)

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100
Q

characteristics of cardiac muscle

A

involuntary and striated, have intercalated discs which contain multiple intercellular junctions to maintain mechanical integrity

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101
Q

what is the connective tissue coat surrounding nervous tissue

A

meninges in CNSepineurium in PNS

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102
Q

role of astrocytes (type of glia)

A

support and ion transport

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103
Q

role of oligodendrocytes (type of glia)

A

produce myelin

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104
Q

role of microglia (type of glia)

A

provide immune surveillance

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105
Q

role of schwann cells (PNS) - type of glia

A

produce myelin and support axons

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106
Q

types of salivary glands

A

parotid, submandibular and sublingual

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107
Q

1st layer of GI tract

A

mucosa:epithelium - sits on basal laminalamina propia - loose connective tissue muscularis mucosae - thin layer smooth muscle

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108
Q

2nd layer of GI tract

A

submucosa: loose connective tissue

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109
Q

3rd layer of GI tract

A

muscularis externa: 2 thick layers of smooth muscle, inner circular and outer longitudinal layer

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110
Q

4th layer of GI tract

A

serosa or adventitia: outer layer of connective tissue that either suspends digestive tract or attaches to other organs

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111
Q

characteristics of protective mucosa

A

non-keratinised stratified squamous epithelium

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112
Q

characteristics of absorptive mucosa

A

simple columnar epithelium with villi and tubular glands

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113
Q

characteristics of secretory mucosa

A

simple columnar epithelium with extensive tubular glands

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114
Q

in the large intestine (protective and absorptive) the outer longitudinal smooth muscle is not continuous, what is it?

A

found in 3 muscular strips called teniae coli

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115
Q

what is the nervous tissue in the digestive tract?

A

enteric nervous system - ganglia between 2 muscle layers that make up muscularis externa

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116
Q

product of exocrine gland of pancreas

A

pancreatic digestive enzymes

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117
Q

product of endocrine gland of pancreas

A

islets of langerhans - produce insulin

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118
Q

what does the kidney contain

A

nephrons

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119
Q

what is the different layers of artery

A

tunica intima (endothelial cells)tunica media (smooth muscle)tunica adventitia (supporting connective tissue)

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120
Q

layers of arteriole

A

1 or 2 layers of smooth muscle in tunica media and almost no adventitia

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121
Q

layers of capillaries

A

endothelial cells and basal lamina have pericytes (connective tissue cells with contractile properties)

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122
Q

where are continuous capillaries found

A

muscle, nerve, lung, skin

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123
Q

where are fenestrated capillaries found

A

have poresgut mucosa, endocrine glands and kidney

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124
Q

where are sinusoidal capillaries found

A

large gaps liver, spleen, bone marrow

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125
Q

layers of venules

A

endothelium and pericytes

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126
Q

layers of veins

A

tunica intima, thin continuous tunica media, obvious tunica adventitialarge veins have thick tunica adventitia

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127
Q

definition of variolation

A

exposure of individual to the contents of dried smallpox pustules from infected patient

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128
Q

what is commensal bacteria

A

friendly (barrier to infection) which competes with pathogen for scarce resources

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129
Q

what receptors involved in innate immune system

A

PAMPs : PRRs

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130
Q

what receptors involved in adaptive immune response

A

antigens : antigen receptors

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131
Q

what are phagocytes

A

neutrophils, monocytes, macrophages, dendritic cellsingest and kill bacteria important source of cytokines

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132
Q

what is the role of eosionophils, mast cells and basophils

A

granular cells which release chemicals for acute inflammation

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133
Q

what is the role of complement proteins

A

inflammation and defence

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134
Q

mast cells

A

reside in tissues and protect mucosal surfaces, degranulate and release histamine and tryptasegene expression - TNF, chemokines and leukotrienes

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135
Q

basophils and eosinophils

A

circulate in blood and recruited to sites of infection

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136
Q

by what three mechanisms do neutrophils attack pathogens

A

phagocytosis release of antimicrobial peptides and degradative proteasesgenerate extracellular traps

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137
Q

what do active neutrophils produce

A

TNF (cause cell death)

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138
Q

what do dead and dying neutrophils + tissue cells + microbial debris produce

A

pus

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139
Q

what are monocytes

A

precursor of macrophages - limit inflammation and involved in tissue repair and wound healing

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140
Q

role of macrophages

A

reside in tissues, ingest and kill pathogens, clear debris, inflammation, tissue repair and antigen presentation

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141
Q

role of dendritic cells

A

immature cells in peripheral tissues but when in contact with pathogen, mature and migrate to secondary lymphoid tissue where they stimulate adaptive response

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142
Q

CD4+ cells

A

helper T cellregulator of immune system and activate other immune cells

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143
Q

CD8+ cells

A

cytotoxic T cellskill virally infected body cells

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144
Q

what are interferons

A

type of cytokineanti-viral function

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145
Q

what are TNF

A

type of cytokinepro-inflammatory

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146
Q

what are chemokines

A

type of cytokinecontrol and direct cell migration

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147
Q

what are interleukins

A

type of cytokineIL2 - t cell proliferationIL10 - anti inflammatory

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148
Q

what is the acute phase response

A

result of infection, trauma or infectionliver produces acute phase proteins in response to pro inflammatory cytokines (IL1, IL6 and TNF)

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149
Q

what is the complement system

A

family of proteins produced in liver that circulate in blood which enter infected and inflamed tissues

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150
Q

what are the functions of complement system

A

membrane attack complexopsonisation chemotaxisclearance of immune complexes inflammation

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151
Q

what is opsonisation and what causes it

A

coating of microorganisms by immune proteins (opsonins)caused by C3b, CRP, antibodiesenhances phagocytosis

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152
Q

how does complement mediated lysis work

A

C5b bind to pathogen surfaceC6, C7, C8, C9 and C5b = membrane attack complex

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153
Q

how does complement mediated inflammation and chemotaxis work

A

C3a and C5a bind to receptors on mast cells / basophils and release granules which produce histamine and chemokines

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154
Q

what is a T cell antigen receptor

A

membrane bound protein heterodimer has alpha and beta chain

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155
Q

what is a B cell antigen receptor

A

membrane bound antibody (IgM or IgD)has light and heavy chain and disulphide bridges

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156
Q

how are pathogens activated

A

MHC/HLA proteins display peptide antigens to T cellsclass 1 - expressed on all nucleated cells - present peptide antigens to cytotoxic T cellsclass 2 - only dendritic cells, macrophages and B cells - present peptide antigens to helper T cells

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157
Q

what does each antibody contain

A

each heavy and light chain contains variable region (antigen binding site) and a constant domain

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158
Q

IgG

A

most abundant, actively transported across placenta

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159
Q

IgM

A

surface bound monomer, 1st Ig type produced in immune response

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160
Q

IgD

A

extremely low levels in blood, surface bound

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161
Q

IgE

A

extremely low levels normally, produced in allergic response

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162
Q

IgA

A

2nd most abundant type, monomeric form in blood, dimeric form in breast milk, saliva, tears and mucosal secretions

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163
Q

what types do mothers pass to baby

A

IgG and dimeric IgA

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164
Q

what is the effector function of antibodies

A

clearance mechanisms - mediated interaction of constant region with effector molecules by complement and Fc receptors

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165
Q

what is agglutination

A

immune complex formation

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166
Q

other characteristics of antibodies

A

can function as opsoninscan stimulate NK cellscan trigger allergic response can undergo class switching - b cells switch antibody heavy chain segment

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167
Q

what is the germinal centre reaction

A

b cell proliferation, antibody heavy chain switching, generation of high affinity antibodies and differentiation into plasma cells and memory B cells

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168
Q

what is pathogenicity

A

ability of a microorganism to produce disease

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169
Q

how do bacteria replicate

A

binary fission

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170
Q

what is microaerophilic atmosphere

A

reduced o2 conc and enriched co2

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171
Q

what secretes exotoxin

A

gram positive bacteria, produced inside cell and exported from it

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172
Q

what secretes endotoxin

A

gram negative bacteria, part of gram negative bacterial cell wall

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173
Q

what are moulds

A

type of fungi, produce spores and hyphae eg aspergillus

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174
Q

what are yeasts

A

type of fungi, single cells that reproduce by budding eg candida

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175
Q

characteristics of gram positive streptococcus

A

aerobic cocci chainsalpha haemolysis (partial) - strep pneumoniae (pneumonia, meningitis) and strep viridans (endocarditis)beta haemolysis (complete) - group A strep (throat and skin infection) and group B strep (neonatal meningitis)

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176
Q

characteristics of gram positive enterococcus

A

aerobic, cocci chains, non-haemolytic, normal gut commensal and cause of UTI

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177
Q

characteristics of gram positive staphylococcus

A

cocci clusterscoagulase positive (golden) - staph aureus - wound, skin infection - flucloxacillincoagulase negative (white) - staph epidermis - normal skin commensal, IV line infection

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178
Q

process of fever

A

antigen attacks macrophage, releases cytokines, travel to anterior hypothalamus of brain, stimulates production of prostaglandin E, resets bodys thermal set point and body shivers to conserve heat (slows growth of pathogens)

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179
Q

characteristics of gram negative cocci

A

diplococci, aerobic eg neisseria gonorrhoea and neisseria meningitidis

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180
Q

characteristics of coliforms

A

gram negative bacilli, aerobic (can be anaerobic)gut commensals eg e.coli, klebsiella, proteusgut pathogens eg salmonella, shigella, e.coli O157 gentamicin first line antibiotic

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181
Q

characteristics of strict aerobes

A

gram negative bacillieg pseudomonas aeruginosa and legionella pneumophilia

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182
Q

what are the types of spiral or curved gram negative bacilli

A

campylobacter - food poisoning helicobacter pylori - gastritis

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183
Q

what is haemophilus influenzae

A

small gram negative bacillus, common cause of chest infection (esp in COPD)

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184
Q

characteristics of gram positive anaerobic bacilli

A

CLOSTRIDIUM SPPpart of normal bowel flora, produces spores and exotoxin that cause severe tissue damage

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185
Q

characteristics of gram negative anaerobic bacilli

A

bacteroides sppnormal gut commensals, only pathogenic when found in other sites metronidazole - 1st line treatment for anaerobes

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186
Q

characteristics of mycobacteria

A

thick waxy outer coat acid fast bacilli or ZN stain TB

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187
Q

what is the process of gene transfer by transformation

A

DNA from dead bacteria taken up by living and incorporated in plasmids

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188
Q

what is process of gene transfer by conjugation

A

sex pilus (fimbria) produced by one bacteria through which plasmid DNA can be transferred

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189
Q

what is the process of gene transfer by transduction

A

viruses infecting bacteria can transfer bits of DNA from one bacterium to another

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190
Q

definition of bactericidal

A

kill bacteria

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191
Q

definition of bacteriostatic

A

inhibit bacterial growth

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192
Q

what are antibiotics what work on cell wall

A

penicillin cephalosporins (ceftriaxone)glycopeptides (vancomycin)

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193
Q

how to distinguish between gram positive and gram negative organisms

A

positive - thick peptidoglycan and single phospholipid bilayer negative - think peptidoglycan and two phospholipid bilayers

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194
Q

what are the different kinds and the characteristics of penicillin

A

flucloxacillin, co-amoxiclav and amoxicillininhibit cell wall synthesis by preventing cross linking of PGN subunits bactericidal, narrow spectrumbeta-lactam antibiotic excreted rapidly via kidneystype 1 hypersensitivity

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195
Q

characteristics of cephalosporins

A

inhibit cell wall synthesis bactericidal beta-lactam antibitic may cause c. diff excreted by kidneys

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196
Q

characteristics of glycopeptides

A

binds to end of growing chain, prevents cross linking and weakens cell wallbactericidal only active against gram positive cell wall excreted in urine

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197
Q

what are the antibiotics which inhibit protein synthesis

A

macrolides (erythromycin, clarithromycin, azithromycin) - bacteriostatictetracyclines (doxycycline) - bacteriostaticaminoglycosides (gentamicin) - bactericidal

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198
Q

characteristics of macrolides

A

lipophilic and pass through cell membranes easily (useful for infection where bacteria hides from immune system)excreted via biliary tract

199
Q

characteristics of tetracyclines

A

broad spectrum, can destruct intestinal flora (cause secondary infections)permanently stain teeth of children <12 yearsexcreted via biliary tract

200
Q

characteristics of aminoglycosides

A

mainly active against gram negative aerobic organisms (coliforms and pseudomonas aeruginosa)damage of kidney and CN VIII - vestibulochlearexcreted in urine

201
Q

what are the antibiotics which act on bacterial DNA

A

metronidazoletrimethoprim fluoroquinolones

202
Q

characteristics of metronidazole

A

causes strand breakage of bacterial DNAtreat true anaerobic infectionsinteracts with alcohol

203
Q

characteristics of trimethoprim

A

inhibits bacterial folic acid synthesis some activity against some gram negative and some gram positive

204
Q

examples and characteristics of fluoroquinolones

A

CIPROFLOXACIN (can cause tendonitis) LEVOFLOXACINprevent supercoiling of bacterial DNAbactericidal restricted (c diff)weakens tendons, causes seizuresexcreted in urine

205
Q

which antibiotics are to be avoided in pregnancy

A

trimethoprim and metronidazole avoid in first 3 months gentamicin, tetracycline and fluoroquinolones avoided!!

206
Q

what is the mechanism of antibiotic resistance

A

changes in bacterial DNA cause change in gene product which is target of antibiotic (MRSA)bacteria can code for enzymes which degrade of inactivate antibiotic efflux pumps actively export antibiotics out of bacterial cell - genetic change may result in increased efflux

207
Q

what are the stages of viral replication

A

1) attachment (ligand > receptor)2) entry (endocytosis) 3) uncoating (release nucleic acid from capsid)4) nucleic acid and protein synthesis (host ribosomes and polymerases used)5) assembly (nucleic acid and proteins packaged together)6) release by budding (viral released with host envelope) or lysis (accumulate until cell bursts)

208
Q

how can antibodies be used in prevention of viral infection

A

neutralising antibodies (IgG and IgM) prevent virus binding to cellular receptors

209
Q

how can viruses be detected

A

PCR, antigen detection

210
Q

what is necrosis

A

no energy, death of tissues, pathological, elicits adjacent tissue response

211
Q

what is coagulative necrosis

A

proteins coagulate, preservation of cell outline eg MI

212
Q

what is colliquative necrosis

A

necrotic material becomes softened and liquefied (pus), no cell structure remains eg in brain

213
Q

what is gangrenous necrosis

A

cell death by necrosis then infection on top of it - anaerobic bacteria may grow

214
Q

what is fibrinoid necrosis

A

fibre deposition eg damage to blood vessel in malignant hypertension

215
Q

what is the role of p53 protein

A

if lost, it can lead to development of cancer p53 can be spellchecker at G1, if mistakes are found cell cycle paused and repair attemptedif cant be repaired, p53 stimulates caspases and indices apoptosis

216
Q

what is the role of telomeres

A

cap chromosomes to prevent degradation and fusionadds on TTAGGG after its lost to prevent cells dying

217
Q

how can free radicals (chain reaction leading to lipid peroxidation) be formed?

A

drugs, O2 toxicity, reperfusion injury, inflammation, intracellular killing of bacteria

218
Q

what is phenylketonuria?

A

metabolic disorderaccumulation of phenylalanine caused by deficiency in enzyme which converts phenylalanine to tyrosine guthrie test

219
Q

what is the beneficial effects of acute inflamation

A

toxin dilution, entry of antibodies, fibrin formation, drug transport, oxygen and nutrient delivery and immune response stimulation

220
Q

what are the harmful effects of acute inflammation

A

digestion of normal tissues, swelling and inappropriate inflammatory response - type 1 hypersensitivity

221
Q

what is chronic inflammation

A

subsequent and often prolonged tissue reactions follow initial response cells: plasma, lymphocytes and macrophages

222
Q

what is the fluid exudate in inflammation

A

proteins including immunoglobulins fibrinogen - fibrin on contact with ECM, acutely inflamed organ surfaces commonly covered in fibrin

223
Q

what is margination

A

loss of intravascular fluid and increased plasma viscosity allowed neutrophils into plasma (only occurs in venules)

224
Q

what increases surface adhesion molecule expression

A

complement C5aleukotriene b2TNF

225
Q

what increases endothelial cell expression of adhesion molecules

A

IL1endotoxinsTNF

226
Q

what releases histamine (chemical mediator) which causes vascular dilation

A

released by mast cells, eosinophils, basophils and platelets release stimulated by C3a, C5a and lysosomal proteins (released by neutrophils)

227
Q

what does serotonin (chemical mediator) do and where is its receptors found

A

increased vascular permeability 5HT (receptors) present in high concentration in platelets

228
Q

what is the role of chemokines (chemical mediator)

A

attract various leukocytes to site of inflammation

229
Q

role of leukotrienes (chemical mediator)

A

type 1 hypersensitivity

230
Q

role of prostaglandins (chemical mediator)

A

increase vascular permeability, stimulate platelet aggregation

231
Q

how are micro-organisms recognised

A

when coated in opsonins (Fc fragment of IgG, C3b or collectins)

232
Q

what is suppuration

A

formation of pus - neutrophils, bacteria and cellular debris

233
Q

what is the macroscopic appearances of chronic inflammation

A

chronic ulcer (breach in mucosa, base lined by granulation tissue and fibrous tissue extends through muscle layer)chronic abscess cavity thickening of wall by fibrous tissue granulomatous (crohns, TB)fibrosis

234
Q

what kinds of damage are reversible

A

reduced aerobic respiration / increased anaerobicmembrane pumps failcell swellingaccumulation of lipid

235
Q

what kinds of damage are irreversible

A

severe damage to cell membranes and mitochondrialeakage of enzymes nuclear changes - ATP changes, cell membrane damage

236
Q

what is a granuloma

A

in chronic inflammationcollection of macrophages (response to foreign bodies eg bone, asbestos, TB, parasites, syphilis and malignancy)

237
Q

what causes wound contraction

A

myofibroblasts

238
Q

what is metaplasia

A

one type of cell becomes another form of cell in response to stress (at risk site for cancer)barrett’s oesophagus

239
Q

characteristics of a benign neoplasia

A

no necrosis N:C ratio normal minimal pleomorphism (change in size/shape)eg adenoma and papilloma

240
Q

characteristics of a malignant neoplasia

A

necrosis common N:C ratio increased pleomorphic (alter shape/size)aneuploid eg carcinoma (cancer of epithelial cell), carcinoma in situ (not invading other tissues) or sarcoma (cancer of mesenchymal cell - MALIGNANT)

241
Q

what is dysplasia

A

disordered growth pre-malignant process

242
Q

what is angiogenesis

A

formation of new, abnormal blood vessels (successful tumours)

243
Q

what are the different routes for metastasis

A

lymphatic route - carcinomahaematogenous route - sarcoma

244
Q

what is the double hit hypothesis

A

one faulty gene puts person at increased risk two faulty mutated genes will result in functional problem

245
Q

what are some examples of oncogenes (turn up genes that promote growth) which can be effected by mutations?

A

RAS (GTP binding) eg colon, lung, pancreatic, bladder, renal and melanomaBRAF - 50% melanoma RAF mutated - some colonic malignancies Myc eg lymphoma, neuroblastoma, small cell carcinoma of lungP13K must common mutated kinase in cancer eg haematological malignancies

246
Q

why is the PTEN gene significant

A

without it, p27 cells can proliferate in uncontrolled fashion

247
Q

example of DNA repair genes effected by mutation

A

BRCA 1 + BRCA 2 (breast cancer)

248
Q

what is Bcl2

A

anti apoptotic gene usually switched off for purpose of getting rid of self reactive lymphocytes

249
Q

what is an epithelial cancer called

A

carcinoma

250
Q

what is glandular cancer called

A

adenoma v adenocarcinoma (malignant)

251
Q

what is squamous cancer called

A

papilloma v squamous cell carcinoma (malignant)

252
Q

what is a paraneoplastic syndrome

A

rare disorders that are triggered by an altered immune system response to a neoplasm (new growth)non-metastatic systemic effects that accompany malignant disease

253
Q

what is the biochemical complications of diabetes

A

ketoacidosisnon-enzymatic glycosylationhypoglycaemia lactic acidosis

254
Q

what is the cause of an atheroma

A

response to endothelial injury recruitment of macrophages and platelets lipid accumulation smooth muscle proliferation

255
Q

what are the complications of atheroma

A

thrombosis, aneurysm, dissection, embolism and ischaemia

256
Q

what is the results of left ventricular hypertrophy

A

increased LV loadpoor perfusioninterstitial fibrosismicro-infarcts diastolic dysfunction

257
Q

what is the virchows triad (3 things thought to contribute to thrombus)

A

vessel wall (loss of endothelial surface, inflammation)blood flow (stasis, turbulence)blood constituents (platelets, coagulation proteins, viscosity)

258
Q

what is the difference between thrombus and embolism?

A

thrombus - solid mass of blood constituents formed within blood vesselembolism - mass of material in vascular system moving from its site of origin to lodge in vessels in distant site

259
Q

what is a infarction and how is it caused

A

zonal necrosis due to sudden occlusion of blood supply due to lack of O2 and nutrient supply re-perfusion injury possible due to formation of free radicals

260
Q

what is pharmacodynamics

A

what drug does to body

261
Q

what is pharmacokinetics

A

what body does to drug

262
Q

what is affinity

A

strength of association between ligand and receptor

263
Q

what is efficacy

A

ability of an agonist to evoke cellular response

264
Q

what is the difference between competitive and non competitive antagonism on a graph

A

competitive - cause parallel rightward shift of agonist concentration with no depression in maximal responsenon competitive - depress the slope and maximum response curve - no shiftPICTURE ON DOC

265
Q

how does the degree of ionisation effect the absorption of a drug

A

only unionised forms readily diffuse across bilayer depends on pKa (pH at which 50% of drug is ionised and 50% unionised)

266
Q

what is henderson-hasselbalch equation

A

pH - pKa = log (A-/AH) = acidallows you to determine how active drug may be in body in blood stream or acidic stomach

267
Q

what is the oral availability of a drug

A

fraction that reaches systemic circulation after oral ingestion

268
Q

what is the systemic availability of a drug

A

fraction that reaches systemic circulation after absorption

269
Q

what is the volume of distribution (Vd)

A

apparent volume in which a drug is dissolved (distributed with concentration equal to that of plasma)IV: Vd = dose/plasma concentration

270
Q

what is the therapeutic ratio of a drug

A

MTC/MEC (max tolerated conc and max effective conc)higher the TR, safer drug

271
Q

what is the half life of drug eliminated at first order kinetics

A

half life is inversely proportional to elimination rate constant t1/2 = 0.69/Kel

272
Q

how to work out the rate of elimination of a drug

A

clearance (volume of plasma cleared of drug in unit time) x plasma concentration

273
Q

what is the characteristics of a drug which is eliminated at zero order kinetics

A

initially eliminated at constant rate then return to first order

274
Q

which factors influence drug disposition

A

ADME - absorption, distribution, metabolism and excretion

275
Q

what is the role of drug metabolism

A

converts drugs to more polar metabolites not readily absorbed in renal tubules, facilitating excretionconvert drugs to metabolites that are less active than parent compound

276
Q

what is the first phase of drug metabolism

A

RHS of liver - oxidation, reduction and hydrolysisthis makes drug more polar, adds chemically reactive group permitting conjugation

277
Q

what is the second phase of drug metabolism

A

LHS of liver - conjugationthis adds an endogenous compound, increasing polarity

278
Q

what happens to the membrane potential in depolarisation

A

becomes less negative (opposite for hyperpolarisation)

279
Q

what is the characteristics of sodium channels

A

Na flows inwardly conc 140mm outside cell, 10-15mm insidedriving force - Vm - ENanegative driving force - inward movement of sodium

280
Q

what is the characteristics of potassium channels

A

K flows outwardlydriving force - Vm - Ekwhen positive, outward movement of K

281
Q

what are the ion channels responsible for action potential in neurons

A

voltage activated Na channels - depolarising voltage activated K channels - hyperpolarising

282
Q

what is the effect of the activation of voltage activated Na channel (activated by depolarisation)

A

opening of a few channels causes further depolarisation positive feedback (upstroke of graph)

283
Q

what is the effect of the activation of voltage activated K channel (activated by depolarisation)

A

outward movement of K causes repolarisation which turns off stimulus negative feedback (downstroke of graph and undershoot)

284
Q

what happens during an absolute refractory peroid

A

no stimulus, however strong, can elicit a second action potential

285
Q

what happens during a relative refractory period

A

stronger than normal stimulus may elicit second action potential

286
Q

what is the role of oligodendrocytes

A

produce myelinated cells in CNS (schwann cells do PNS)

287
Q

what is the role of astrocytes

A

star shaped, support homeostasis and maintain BBB

288
Q

what is the role of microglia

A

immune surveillance, macrophages of CNS

289
Q

what are the preganglionic and post ganglionic neurones in sympathetic NS

A

pre - AChpost - usually noradrenaline

290
Q

what are neurones in parasympathetic

A

both pre and post - AChcontrols cranial nerves 3/7/9/10

291
Q

sympathetic and parasympathetic role in male reproduction

A

sympathetic - ejaculationparasympathetic - erection

292
Q

what is the steps in neurochemical transmission

A

1) precursor taken up2) transmitter synthesised and stored3) action potential depolarises4) calcium influx through voltage activated channels5) calcium induced release of transmitter6) receptor activation7) enzyme mediated inactivation of transmitter or reuptake of transmitter

293
Q

characteristics of ligand-gated ion channels

A

consist of separate glycoprotein subunits forming a central, ion conducting channel allow rapid changes in permeability of membrane to certain ionsrapidly alter membrane potential

294
Q

what is the structure of receptor in GPCR

A

integral membrane protein 7 transmembrane spans joined by 3 extracellular and 3 connecting loops

295
Q

what is the structure of G protein in GPCR

A

peripheral membrane protein3 polypeptide subunits (alpha binding site)contains guanine nucleotide binding site which can hold GTP

296
Q

what happens when there is no signalling in GPCR

A

receptor unoccupiedG protein binds GDPeffector not modulated

297
Q

what happens when the signal is turned on in GPCR

A

agonist activates receptorG protein couples with receptorGDP dissociated from and GTP binds to alpha subunitG protein dissociatedalpha subunit combines with and modified activity of effectoragonist may dissociate from receptor, but signal persists

298
Q

what happens when signal is turned off in GPCR

A

alpha subunit acts as enzyme to hydrolyse GTP -> GDPG protein alpha subunit recombines with By subunit completing G protein cycle

299
Q

what are nicotinic acetylcholine receptors (ligand gated)

A

consist of 5 glycoprotein subunitsalpha 1-10, beta 1-4, gamma, delta, epsilonbinding of transmitter opens gate

300
Q

what is role of M1 GPCR muscarinic ACh receptor at parasympathetic neuroeffector junctions

A

Gg - stimulates phospholipase C which increases stomach acid secretion

301
Q

what is role of M2 GPCR muscarinic ACh receptor at parasympathetic neuroeffector junctions

A

Gj - inhibition of adenylyl cyclase and opening of K+ channels which decreases HR

302
Q

what is role of M3 GPCR muscarinic ACh receptor at parasympathetic neuroeffector junctions

A

Gg - stimulates phospholipase C which increases saliva secretion and bronchoconstriction

303
Q

what stimulates the re-uptake of NA at sympathetic neuroeffector junctions

A

transporters U1/U2

304
Q

what stimulates the metabolism of NA at sympathetic neuroeffector junctions

A

MAO and COMT

305
Q

what is the role of B1 GPCR adrenoreceptor at sympathetic neuroeffector junctions

A

Gs - stimulation of adenylyl cyclase which increases HR and force

306
Q

what is the role of B2 GPCR adrenoreceptor at sympathetic neuroeffector junctions

A

Gs - stimulation of adenylyl cyclase which causes relaxation of bronchial and vascular smooth muscle

307
Q

what is the role of A1 GPCR adrenoreceptor at sympathetic neuroeffector junctions

A

Gg - stimulation of phospholipase C which causes contraction of vascular smooth muscle

308
Q

what is the role of A2 GPCR adrenoreceptor at sympathetic neuroeffector junctions

A

Gj - inhibition of adenylyl cyclase which causes the inhibition of NA release

309
Q

how does amphetamine work

A

U1 substrate inhibits MAOdisplaces NA into cytoplasmNA accumulates in synaptic cleft causing increased adrenoceptor stimulation

310
Q

how does prazosin work

A

selective, competitive antagonist of a1vasodilator used as anti-hypertensive

311
Q

how does atenolol work

A

selective, competitive antagonist of B1used as anti-anginal and anti-hypertensive agent

312
Q

how does atropine work

A

competitive antagonist of muscarinic ACh receptors, does not block nicotinic Ach receptorsblocks parasympathetic division of ANSused to reverse bradycardia post MI and in AchE poisoning

313
Q

what is the difference between muscarinic and nicotinic receptors

A

muscarinic - G-protein coupled receptors (GPCRs) that mediate a slow metabolic response via second messenger cascadesnicotinic - ligand-gated ion channels that mediate a fast synaptic transmission of the neurotransmitter

314
Q

what is the role of cholesterol

A

contributes to fluidity and stability stiffens membrane

315
Q

where are docking marker acceptor proteins and where are they found

A

found in inner membrane surfaceinteract with secretory vesicles leading to exocytosis of vesicle contents

316
Q

what is the role of cadherins (cell adhesion molecule)

A

hold cells within tissues together

317
Q

what is the role of integrins (cell adhesion molecule)

A

span membrane acting as link between extra and intra cellular environments

318
Q

what is the function of carbohydrates

A

self-identity markersrole in tissue growth

319
Q

what does the ficks law of diffusion relate to

A

magnitude of conc gradientsurface area of membrane across which diffusion taking placelipid solubility of substancemolecular weight of substancedistance through which diffusion must take place

320
Q

what is osmolarity

A

concentration of osmotically active particles in solution osmoles/litrebody fluids approx 300mOsm

321
Q

what is tonicity

A

effect a solution has on cell volume

322
Q

what is secondary active transport

A

energy not used directly, stored in form of an ion concentration (usually Na+)

323
Q

what are the two mechanisms of secondary active transport

A

symport (co transport) - solute and Na move in same directionantiport (exchange / countertransport) - solute and Na move in opposite direction

324
Q

what mechanism of transport is Na+K+ATPase

A

primary active 3 Na out and 2 K inbut, conc gradient for Na+ is inwards and outward for K+

325
Q

what is the role of Na+K+ ATPase

A

establish Na and K conc gradient across plasma membrane regulate cell volume by controlling conc of solutes inside cellenergy used to drive pump indirectly serves as energy source for secondary active transport

326
Q

what happens in endocytosis

A

membrane pinches off to engulf substance

327
Q

what happens in exocytosis

A

vesicle fuses with membrane, releasing contents to ECF

328
Q

what is membrane potential

A

Emseparation of opposite charges across membraneunits mV

329
Q

at resting potential, the membrane is 100x more permeable to what ion

A

K+

330
Q

what is the equilibrium potential for K+

A

when conc gradient and electrical gradient balance each other membrane potential at Ek is -90mV

331
Q

what is the equilibrium potential for Na+

A

membrane potential at ENa is +61mV

332
Q

what is the Nernst equation

A

Elon = 61log10 [ion]o / [ion]i

333
Q

what is the resting potential for a typical nerve cell

A

-70mVK+ gradient most important factor in setting Em

334
Q

what is the Goldman-hodgkin-katz equation and what is it used for

A

Em = 61log10 Pk+ [K+]o + PNa+ [Na+]o / Pk+ [K+]I + PNa+ [Na+]Icalculates overall membrane potential p is relative permeability

335
Q

what is hyperpolarisation

A

change that makes cell membrane potential more negative

336
Q

what is depolarisation

A

change that makes cell membrane potential more positive

337
Q

what hormones control glucose during starvation

A

cortisol (adrenal gland)growth hormone (pituitary)

338
Q

what are the pancreatic islets of langerhans (endocrine glands)

A

alpha cells - glucagonbeta cells - insulindelta cells - somatostatin

339
Q

what does insulin convert (favours anabolism - build up)

A

glucose -> glycogenfatty acids -> triglyceridesamino acids -> protein

340
Q

what is the effect of insulin

A

lowers glucose by stimulating uptake from blood and activating liver enzymes

341
Q

what is the role of ANS on glucose

A

parasympathetic activity - promoting secretionsympathetic activity - inhibiting secretion

342
Q

what is the effects of glucagon

A

raises glucose by increasing glycogenolysis, inhibiting liver glycogen synthesis, promoting liver gluconeogenesis, lipolysis

343
Q

what is the effect of sympathetic nerve activity on glucagon

A

stimulates release

344
Q

what is the effect of adrenaline

A

raises glucosestimulates glycogenesisstimulates gluconeogenesis(cortisol also does all of above plus lipolysis)released during short term emergencies

345
Q

where is growth hormone located and what is its response to starvation

A

anterior lobe of pituitary decreases glucose uptake by musclemobilises glucose from liverpromotes lipolysis in fat cells

346
Q

what are baroreceptors

A

located in aortic arch and carotid sinussensitive to stretch, firing rate increases when MAP increasesonly respond to acute changes (firing decreases if HBP sustained)

347
Q

what is the systolic pressure

A

when heart is contracting (<140mmHg)

348
Q

what is diastolic pressure

A

when heart is relaxed (<90mmHg)

349
Q

what is MAP

A

average arterial BP during single cardiac cycle (70 - 105mmHg)MAP = [(2xdiastolic) + systolic] divided by 3MAP = cardiac output x total peripheral resistance

350
Q

what is cardiac output

A

stroke volume x heart rate

351
Q

what is feedforward control

A

responses made in anticipation of a change

352
Q

what is negative feedback control

A

primary typeopposes initial change components: sensor, control centre and effectorpromotes stability by regulation of controlled variable through flow information along closed loop

353
Q

what is positive feedback control

A

not as often as negative amplifies initial change

354
Q

how is heat gained in body

A

metabolic heat - increased by hormoneradiation - emission of heat energy in form of electromagnetic waves (1/2 is loss)convection - transfer of heat energy by air currents, combines with conductionconduction - transfer of heat between objects in contact

355
Q

how is heat lost in body

A

convection - air next to skin warmed by conduction so less dense and rises whilst cooler air moves next to skinconductionradiationevaporation - passive (water diffuses from skin etc) or active (sweating by sympathetic NS)

356
Q

How does negative feedback control maintain temperature

A

sensor detects change sends signal to hypothalamuseffectors (skeletal muscles, skin arterioles, sweat glands) triggered and respond to restore variable

357
Q

what does the posterior hypothalamic centre respond to

A

coldvasoconstrictionincreased muscle toneshivering

358
Q

what does the anterior hypothalamus centre respond to

A

warmth vasodilationsweating (sympathetic NS)decreased muscle tone

359
Q

how is a fever caused

A

macrophages release chemicals which act as endogenous pyrogenstimulates hypothalamus to release prostaglandinsthis resets thermostat higherhypothalamus initiates mechanism to heat body thermostat reset to normal if pyrogen release is reduced

360
Q

what is defined as fever

A

38-40 oC

361
Q

what is defined as hyperthermia

A

> 40 oC

362
Q

what is defined as hypothermia

A

35 or below oC

363
Q

vascular smooth muscles are partially constricted at rest (vasomotor tone) - how is this achieved?

A

tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline

364
Q

what is the exception to “there is no parasympathetic innervation of arterial smooth muscle”

A

penis and clitoris

365
Q

what is gametogenesis

A

germ cell formation (oogenesis > oocyte, spermatogenes > spermatozoa)

366
Q

what is cleavage

A

period of rapid cell division which leads to blastomereswhen 8 cells, compaction takes place so zygote becomes blastocyst

367
Q

what is gastrulation

A

formation of germ layerectoderm (outer)mesoderm (middle)endoderm (inner)

368
Q

what is the process in fertilisation

A

sperm binds to zona pellucida glycoprotein acrosomal enzymes released from sperm head digest way into eggegg and sperm plasma membrane fuse and sperm contents enter effect sperm entry triggers completion of meiosis 2 and release of cortical granules by oocyte

369
Q

what is the fate of the ectoderm

A

epidermis of skin, nervous system

370
Q

what is the fate of the mesoderm

A

subdivided into 3 partsparaxial - axial skeleton, voluntary muscle, parts of dermisintermediate - urogenital systemslateral plate - somatic part (lining of body wall) or visceral part (CV system, mesothelial covering of organs etc)

371
Q

what does the incomplete closure of the embryonic foramen oval in the septum lead to

A

atrial septal defect (ASD)orventricular septal defect (VSD)

372
Q

what is a meta-analysis

A

a statistical analysis that combines results of multiple scientific studies

373
Q

what are the phases of clinical trials

A

I - clinical pharmacology (dosage, safety)II - initial clinical assessment (likely effectiveness, common adverse effects)III - randomised controlled trialIV - post marketing surveillance (less common adverse effects)

374
Q

sagittal

A

separated left to right

375
Q

coronal

A

separated front to back

376
Q

axial

A

chopped in half

377
Q

what is the two types of surface of the wrist

A

dorsal or volar

378
Q

what is the two types of surface of hand

A

dorsal or palmar

379
Q

what is the two types of surface of tongue

A

dorsal or ventral

380
Q

what is two types of surface of foot

A

dorsal or plantar

381
Q

what is flexion (opposite is extension)

A

decreasing angle between bones at a joint

382
Q

what is abduction (opposite is adduction)

A

movement away from medial plane

383
Q

what is internal/medial rotation (opposite is lateral rotation)

A

anterior surface rotates towards median plane

384
Q

what is circumduction

A

circular motion at joint

385
Q

what is movements made by foot

A

eversion or inversion

386
Q

what is movement made by forearm

A

pronation (palm down) or supination (palm up)

387
Q

what is pulmonary circulation

A

from right side of heart, to lungs and back to left side

388
Q

what is systemic circulation

A

from left side of heart, to capillary beds of organs etc back to right side

389
Q

where does the heart lie and what is it surrounded by

A

lies deep to costal cartilages and between lungs (in inferior middle mediastinum) and is surrounded by pericardium

390
Q

what is the layers of pericardium

A

visceral serous pericardium covers the heart whilst parietal serous pericardium lines fibrous pericardium

391
Q

what is bicuspid (mitral valve)

A

between left atrium and left ventricle

392
Q

what is tricuspid valve

A

between right atrium and right ventricle

393
Q

what is the crux

A

fibrous cardiac skeleton in septum which acts as electrical insulator

394
Q

what is anastomosis

A

connection between arteries without capillary network - provide alternative route of blood flow called collaterals

395
Q

what is end arteries

A

when there is only arterial blood supply to area - occlusion result in infarction and irreversible cell death

396
Q

what does the arch of the aorta branch into

A

brachiocepallic trunk (bifurcates into right common carotid and right subclavian arteries)left common carotid (bifurcates into external and internal carotid)left subclavian

397
Q

what nerve innervates carotid sinus

A

glossopharyngeal

398
Q

where does the vertebral artery (travels through vertebral foraminae of cervical vertebrae then through foramen magnum to supply brain) branch from

A

subclavian artery

399
Q

where is lymph drained

A

central veins in root of neck at venous angles

400
Q

what is ossification

A

process in which initial, small, hyaline cartilage grows into bone

401
Q

what is the periosteum

A

connective tissue sleeve which is vascularised and well innervated (pain when torn during fracture)

402
Q

what are examples of bony features

A

greater tubercle of humerusstyloid process of radius

403
Q

what are the 33 bones of the vertebrae

A

7 cervical 12 thoracic 5 lumbar 5 sacral (fuse to form 1 sacrum)4 coccygeal (fused to form 1 coccyx)

404
Q

what is the intervertebral foramen

A

between adjacent vertebrae and spinal nerves emerge through here

405
Q

what is the facet joint

A

between articular processes of 2 adjacent vertebrae

406
Q

what is special about C1 atlas

A

does not have body of spinous process

407
Q

what is special about C2 axis

A

has odontoid process

408
Q

what is special about C7

A

first palpable spinous process in 70% of people

409
Q

what bones are in the hand

A

carpal bones (wrist) metacarpals (palm)phalanges (fingers)

410
Q

what bones are in the foot

A

tarsal bones (mid foot)metatarsals (forefoot)phalanges (toes)

411
Q

example of circular muscle

A

orbicularis oculi

412
Q

example of fusiform muscle

A

biceps brachii

413
Q

example of pennate muscle

A

deltoid

414
Q

example of quadrate muscle

A

rectus abdominus

415
Q

what is the role of a tendon

A

attach muscle to bonean aponeurosis is a flattened tendon

416
Q

what is role of posterior fibres of deltoid

A

extension of shoulder

417
Q

what is role of middle fibres of deltoid

A

abduction of shoulder

418
Q

what is role of anterior fibres of deltoid

A

flexion of shoulder

419
Q

what is the role of shallow socket of glenoid fossa of scapula

A

circumduction of shoulder

420
Q

what is paralysis

A

muscle without functioning motor nerve so cannot contract and would have reduced tone

421
Q

what is spasticity

A

muscle has intact motor nerve but descending controls from brain not working - increased tone

422
Q

what is compartment syndrome

A

increased pressure caused by swelling and affects functions of muscles of nerves (fasciotomy to relieve pressure in emergency)

423
Q

what is a fibrous joint

A

limited mobility, stable syndesmoses (unites bone with fibrous sheet)sutures (between bones of skull)fontanelles (wide sutures in neonatal skull)

424
Q

what is a cartilaginous joint

A

fairly limited mobilityprimary - joins bones e.g. epiphyseal growth platesecondary - fibrocartilage e.g. intervertebral disc

425
Q

what are the features of a synovial joint

A

2 or more bones articulating articular surfaces covered in hyaline cartilage a capsule wraps around jointcontains joint cavitysupported by ligamentsassociated with bursae (prevents friction)other special features (articular disc in TMJ joint)

426
Q

what are the types of synovial joint

A

pivot (Atlanto-axial joint - turns neck)ball and socket (hip)plane (acromioclavicular joint)hinge (elbow)biaxial (fingers)

427
Q

what is subluxation

A

reduced area of contact between articular surfaces

428
Q

what is dislocation

A

complete loss of contact between surfaces

429
Q

what happens in the dislocation of TMJ

A

head of condylar process of mandible becomes stuck anterior to articular tubercle of temporal bone

430
Q

what forms the pelvic roof

A

parietal peritoneum (lining of abdominal cavity)

431
Q

what is the most inferior part of the part of the peritoneal cavity in an upright female patient

A

rectouterine pouch

432
Q

what is the three layers of the uterus wall

A

perimetrium, myometrium and endometrium

433
Q

how is an unfertilised ovum expelled

A

contraction of myometrium

434
Q

how is testes developed

A

originate on posterior wall of abdominal cavity then descent into scrotum via inguinal canal

435
Q

what produces sperm

A

seminiferous tubulessperm pass to rete testis into head of epididymis which becomes vas deferens

436
Q

what does the spermatic cord (passes through abdominal wall) contain

A

vas deferens, testicular artery and pampiniform plexus of veins

437
Q

what is the role of the seminal gland

A

produces seminal fluid connects with vas to form ejaculatory duct containing semen (sperm and fluid)

438
Q

how does an erection form

A

3 cylinders of erectile tissue become angorged with blood at arterial pressure

439
Q

which muscle prevents drooling

A

orbicularis oris

440
Q

what is tonsils at back of mouth called

A

palatine tonsils

441
Q

what are the extrinsic muscles of the mouth

A

4 pairs which attach tongue to bony skeleton and moves tongue around during mastication, speech and swallowing

442
Q

what are intrinsic muscles of the mouth

A

4 pairs in various directions which change shape of tongue during friction

443
Q

what are the three major saliva glands

A

parotid (near ear)submandibular (under mandible)sublingual (under tongue)

444
Q

what are the 3 parts of the pharynx

A

nasopharynx, oropharynx and laryngopharynx - last 2 used in resp and GI pathway to risk of aspirating material into respiratory tract

445
Q

what is role of oesophagus and at which vertebrae does It pierce diaphragm

A

transmits food etc from pharynx to stomachgradual transition of skeletal to smooth muscleT10 vertebrae

446
Q

what is role of small intestine and what is the three parts

A

transit, digestion and absorption (proximal to distal) duodenum, jejunum and Ileum

447
Q

what is role of large intestine

A

transit, reabsorption of H2O and electrolytes stool formation

448
Q

what kind of pain does a patient with GI tract obstruction experience

A

colicky pain - comes and goes response is increased peristalsis proximal to site of obstruction

449
Q

what is the role of cricopharyngeal sphincter

A

junction between laryngopharynx and oesophagus - prevent regurgatation

450
Q

what is role of pyloric sphincter

A

junction between stomach and duodenum - control relieve of chyme from stomach

451
Q

what is role of external anal sphincter

A

control release of stool

452
Q

what is components of the foregut and what artery supplies it

A

oesophagus to mid-duodenumliver and gall bladderspleen1/2 of pancreascoeliac trunk of abdominal aorta

453
Q

what is components of midgut and what artery supples it

A

mid duodenum to proximal 2/3rds of transverse colon1/2 of pancreassuperior mesenteric artery

454
Q

what is components of handgun and what artery supplies it

A

distal 1/3 of transverse colon to proximal 1/2 of anal canalinferior mesenteric artery

455
Q

what is a peripheral nerve

A

bunch of axons wrapped in connective tissue

456
Q

CN I and location

A

olfactory nerve - forebrain

457
Q

CN II and location

A

optic nerve - forebrain

458
Q

CN III and location

A

oculomotor nerve - midbrain

459
Q

CN IV and location

A

trochlear nerve - midbrain

460
Q

CN V and location

A

trigeminal nerve - pons

461
Q

CN VI and location

A

abducent nerve - junction (pons and medulla)

462
Q

CN VII and location

A

facial nerve - junction (pons and medulla)

463
Q

CN VIII and location

A

vestibulocochlear nerve - junction (pons and medulla)

464
Q

CN IX and location

A

glossopharyngeal nerve - medulla

465
Q

CN X and location

A

vagus nerve - medulla

466
Q

CN XI and location

A

spinal accessory nerve - spinal cord

467
Q

CN XII and location

A

hypoglossal nerve - medulla

468
Q

how are spinal nerves named

A

according to vertebrae above it except in cervical region when named according to vertebrae below e.g. c8 exists between c7 and t1

469
Q

what is conus medullaris

A

L1/L2 IV disc level where spinal cord ends

470
Q

what is cauda equine

A

lumber and sacral spinal nerve roots descending in vertebral canal to their respective intervertebral foraminae - horse tail

471
Q

what is a dermatome

A

area of skin supplied by both anterior and posterior rami

472
Q

what is at T4 dermatone

A

male nipple

473
Q

what is at T10 dermatone

A

umbilicus

474
Q

what is a nerve plexus

A

network of intertwined anterior rami

475
Q

what nerves are in brachial plexus C5-T1

A

axillary nerve, median nerve, musculocutaneous nerve, radial nerve and ulnar nerve

476
Q

how are sympathetic nerve signals passed

A

originate from brain, exit spinal cord with T1-L2, travel to sympathetic chains, pass into all spinal nerves and hitch a ride to splanchnic nerves where they supply organs

477
Q

how are parasympathetic nerve signals passed

A

leave CNA via cranial nerves III, VII, IX and X via sacral spinal nerves

478
Q

what does vagus nerve supply

A

organs of neck, chest and abdomen

479
Q

what is role of sacral spinal nerves

A

carry parasympathetic axons to hindgut, pelvis and perineum

480
Q

what does the somatic NS supply

A

body wall and external environment

481
Q

what does the autonomic NS supply

A

supplies visceral motor system and internal environment

482
Q

what do mechanoreceptors sense

A

course touch, fine touch, vibration and proprioception

483
Q

what do nociceptors sense

A

pain

484
Q

somatic sensation is linked with posterior nerves and is 3 neurone chain. What are these 3 neurones?

A

primary somatosensory area, sensory homunculus and motor homunculus

485
Q

what is motor innervation associated with

A

anterior nerves before they synapse onto skeletal muscle of lower limb and muscles contract

486
Q

characteristics of upper motor neurone

A

opposite side from movement, axons cross at brainstem, upper motor neurone lesion

487
Q

characteristics of lower motor neurone

A

same side as movement, connect to skeletal muscle, lower motor neurone lesion

488
Q

what is ischaemia

A

problem in which there is reduced blood flow

489
Q

what is cockily pain

A

obstruction, will be dull, achy and poorly localised

490
Q

test sensitivity

A

proportion of those who have disease who are correctly identified with positive test (same as negative predictive value)

491
Q

test specificity

A

proportion of those who do not have disease who are correctly identified by negative test (same as positive predictive value)

492
Q

1-Negative predictive value

A

% of people with negative result who have health problem

493
Q

prevalence

A

number of cases of a disease present in a population at a specific point in time / number of persons at risk of having the disease at that point in time

494
Q

incidence rate

A

number of NEW cases of a disease occurring in population during specific period of time / number of persons exposed to risk of developing disease during that period

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