Science for Medicine Flashcards

1
Q

classification of disease

A

Growth

Unnatural

Degenerative

Developmental

Inflammatory

Circulatory

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2
Q

Feed forward control

A

more sensitive form of negative feedback

sensors are involved so changes can be anticipated e.g. temperature regulation

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3
Q

configuration

A

The fixed arrangement of atoms in a molecule. e.g. cis/trans

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4
Q

Conformation

A

The precise arrangement of atoms in a molecule

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5
Q

role of the cytoskeleton

A

provides strength and support, while also allowing for cell motility

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6
Q

pH means

A

-log[H+]

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7
Q

pH=

A

pKa + log[A-]/[HA]

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8
Q

osmolality

A

The number of osmoles per kilogram of solvent

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9
Q

desmosomes

A

cell-cell junctions provide firm anchorage

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10
Q

Tight/occluding junctions

A

cell-cell junctions seal intercellular spaces

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11
Q

gap junctions

A

cell-cell junctions allow for cell-cell communication

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12
Q

Hemidesmosomes

A

cell-ECM junctions

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13
Q

Hepatocytes

A

epithelial cells of the liver

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14
Q

endocrine

A

secretes into the blood

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15
Q

exocrine

A

secretes to the “surface”

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16
Q

composition of the layers of the skin

A

epidermis - epithelium

dermis - connective tissue

hypodermis - fat

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17
Q

papillary layer

A

top layer of dermis loose connective tissue blood vessels nerve endings

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18
Q

Reticular layer

A

bottom layer of dermis dense irregular connective tissue

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19
Q

composition of bone

A

protein: mostly type I collagen
minerals: Hydroxyapatite

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20
Q

alpha helix bonds

A

H bonds between the N-H group and the C=O group in every 4th amino acid.

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21
Q

beta sheet bonds

A

H bonds between the amide groups of linear polypeptide chains

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22
Q

Tertiary structure interactions

A

van der Waals

ionic interactions

hydrogen bonding

disulphide bridges

hydrophobic interactions

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23
Q

fate of absorbed galactose

A

phosphorylayed to galactose-1-phosphate

converted to gucose-1-phosphate

converted to glucose-6-phosphate

enters glycolysis

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24
Q

fate of absorbed fructose

A

phosphorylated to form fructose-1-phosphate

converted to glyceraldehyde

phosphorylated again to form glyceraldehyde-3-phosphate (G3P) and enters glycolysis

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25
Q

functions of the pentose phosphate pathway

A

produces NADPH

produces pentose sugars needed for nucleic acid synthesis

metabolises any pentose sugars in the diet

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26
Q

phases of the pentose phosphate pathay

A
  1. oxidative, irreversible part
    - generates NADPH
    - converts G-6-P to ribose-5-phosphate
  2. non-oxidative reversible part
    - interconverts between sugars
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27
Q

fluoroscopy

A

obtains moving images using x-ray

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28
Q

carnitine fatty-acyl CoA

A

enzyme that transports carnitine-FA across the inner mitochondrial membrane

inhibited by malonyl CoA so FA synthesis and degradation don’t occur simultaneously

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29
Q

types of membrane receptors

A

receptors that act as ion channels

receptors with intrinsic enzyme activity

receptors that interact with JAK kinases receptors that interact with G-proteins

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30
Q

Andenylyl Cyclase pathway

A

g-protein linked receptor activates adenylyl cyclase.

Adenylyl cyclase is phosphorylated by ATP producing cAMP

cAMP activates cAMP dependent protein kinase A (PKA)

PKA can phosphorylate many proteins to regulate their function.

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31
Q

Phospholipase C pathway

A

g-protein linked receptor activates phospholipase C

phospholipase C converts PIP2 to IP3 and DAG

IP3 stimulates the endoplasmic reticulum to release Ca2+

Ca2+ and DAG activate protein kinase C (PKC)

PKC can phosphorylate many proteins to regulate their function.

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32
Q

laws of thermodynamics

A

energy can be converted between forms but not created or destroyed

all energy transformations lead to an increase in entropy

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33
Q

conduction velocity increases…

A

with fewer Na+ channels (opening them is time consuming)

there can be fewer channels in myelinated and wider axons as charge travels further up them

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34
Q

excitatory CNS neurotransmitters

A

acetylcholine

norepinephrine

dopamine

seratonin

histamine

glutamate

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35
Q

inhibitory CNS neurotransmitters

A

GABA

Glycine

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36
Q

recruitment of motor units

A

As load increases, more motor units are recruited to compensate

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37
Q

Slow oxidative muscle fibres

A

more mitochondria so more oxidative phosphorylation

more vascular so higher delivery of O2 and nutrients

contain myoglobin to help with O2 delivery

fibres are red and of low diameter

Resist fatigue

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38
Q

fast oxidative muscle fibres

A

more mitochondria so more oxidative phosphorylation

more vascular so higher delivery of O2 and nutrients

contain myoglobin to help with O2 delivery

fibres are red and of low diameter

Intermediate resistance to fatigue

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39
Q

fast glycolytic fibres

A

few mitochondria but high concentration of glycolytic enzymes and glycogen.

low blood supply

white fibres with low diameter

Fatigue quickly

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40
Q

ATP

A

a free energy carrier

couples anabolic and catabolic reactions

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41
Q

electron carriers used in redox reactions

A

NAD+

NADP+

FAD+

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42
Q

NAD+ is used…

A

In redox reactions of glycolysis, and the TCA cycle

43
Q

NADP+ is used…

A

in anabolic reactions

e.g. fatty acid synthesis

44
Q

osteoclasts are derived from

A

a haemopoietic lineage

45
Q

osteoblasts are derrived from

A

a mesenchymal lineage

46
Q

fates of glycogen in skeletal muscle and the liver

A

Skeletal muscle:

glycogen –> glucose-1-phosphate –>

glucose-6-phosphate –> glycolysis

(forms ATP for muscle contraction)

Liver:

glycogen –> glucose-1-phosphate –>

glucose-6-phosphate –> glucose

(enters the bloodstream to increase blood glucose concentration)

47
Q

fate of dietary protein

A

1. denaturation of proteins by HCl

2. pancreatic enzymes create a mix of free amino acids and free peptides

3. membrane enzymes break everything down into di-/tri-peptides

4. all is absorbed into intestinal cells and completely broken down into free amino acids by peptidses

5. free amino acids enter the blood stream

48
Q

primary lymphoid organs

A

thymus

bone marrow

foetal liver

where lymphocytes are generated

49
Q

secondary lymphoid organs

A

Lymph nodes

spleen

where immune responses are initiated and lymphocytes maintained

50
Q

digestion of dietary carbohydrates

A
  1. salivary amylases in the mouth
  2. pancreatic amylases in the duodenum
  3. membrane enzymes in the jejenum
51
Q

absorbtion of glucose

A

glucose is transported through glucose symport, driven by the concentration gradient of Na+ created by Na+/K+ ATPase.

glucose then enters the boodstream through glucose uniport, driven by its own concentration gradient.

galactose has a similar mechanism

52
Q

absorption of sucrose

A

moves down its own concentration gradient through the cannel protein GLUT5

53
Q

precursors for gluconeogenesis

A

lactate from excercising muscle.

oxaloacetate from proteins

54
Q

Glutamate

A

only glutamate can obtain its nitrogen directly from NH4+ (ammonium ions). this reaction requires reduction of NADPH and breakdown of ATP.

glutamate can then transfer its amino groups to alpha-keto acids to form other amino acids

55
Q

how is nitrogen transporthed through the blood?

A

as alanine or glutamine

(amino acids that have no charge)

56
Q

reasons for strength of bone

A

minerals (hydroxyapatite) - withstands pressure

collagen - withstands tension (a bit flexible)

57
Q

protective roles of the skin

A

repair

waterproofing

chemical resistance

UV light penetration

termoregulation

immune protection

wear and tear

58
Q

high affinity means

A

smaller concentration is needed to evoke the same response

59
Q

sources of intracellular calcium

A

opening ion channelsto allow calcium to enter.

inhibition of calcium transport out of the cell.

released from internal stores in the endoplasmic reticulum, stimulated by IP3-

60
Q

cutaneous receptors

A

sensory receptors found in the skin

61
Q

purpose of propioceptors: muscle spindle and golgi tendon organ

A

provide sensory info for…

  1. propioception + kinaesthesia
  2. spinal reflexes
  3. to inform voluntary movement from the brain
62
Q

spindle discharge

A

no. of APs fired

decreases with contraction.

increases with relaxation.

63
Q

Golgi tendon organ

A

monitors muscle tension.

muscle contraction = mors APs fired.

muscle relaxation = less APs fired

64
Q

Stretch Reflex

A

stimulus: muscle is stretched

receptor: muscle spindle

response:

1. agonist contracts (monosynaptic reflex)

2. antagonist relaxes (inhibitory interneurones)

  • reciprocal inhibition

3. info ascends to brain in dorsal collumns

65
Q

inverse stretch reflex / clasp knife reflex/ golgi tendon organ reflex

A

stimulus: muscle contacts

receptor: GTO

response:

1. antagonist contracts (excitatory interneurones)

2. agonist relaxes (inhibitory interneurones)

3. info ascends to brain in dorsal collumns

66
Q

flexor withdrawal reflex

A

stimulus: pain

receptor: nociceptors

response:

1. ipsilateral flexors and contralateral flexors contract (excitatory interneurones)

2. ipsilateral extensors and contralateral flexors relax (mixture of interneurones)

3. info ascends to brain in contralateral spinothalmic tract

67
Q

ways in which enzymes catalyse reactions

A

entropy reduction - enzymes force substrate into correct orientation

Desolvation - bonds between enzyme and substrate replace H-bonds between substrate and solution

Induced fit - conformational changes in the enzyme put bonds under pressure

68
Q

V0 (initial rate of reaction)

A

increases with substrate concentration

69
Q

Vmax

A

maximum reaction velocity

occurs when all enzyme active sites are full

70
Q

meaning of Vmax and Km

A

high Km = low affinity

high Vmax = high efficacy

71
Q

competitive inhibition

A

active site is blocked so affinity is decreases = increase in Km

increasing substrate conc. means the same Vmax can still be reached

72
Q

non-competitive inhibition

A

active site is not blocked so Km is unchanged

increasing substrate conc. doesn’t change inhibition so Vmax decreases

73
Q

covalent modification

A

e.g. phosphorylation

regulates many enzymes

74
Q

average circulating volume in a typical adult male

A

5 litres

75
Q

function of plasma proteins

A

Albumin = transport

globulin = transport and immunoglobulins

fibrinogen = clotting

76
Q

erythropoietin

A

a hormone produced in response to hypoxia.

controls and accelerates erythropoietin.

produced in kidneys

77
Q

Leukopoiesis (WBC formation)

A

controlled by a cocktail of cytokines that are released from endothelial cells, fibroblasts and mature WBCs.

cytokines stimulate mitosis and maturation of leukocytes.

78
Q

thrombopoietin

A

regulates platelet formation

79
Q

viscosity of plasma

A

1.8x thicker than water

80
Q

viscosity of whole blood

A

3-4x thicker than water

81
Q

antibody structure

A

light chain (V-shape)

heavy chain (Y-shape):

has a variable (top) region and a constant (bottom) region.constant region is the same in all antibodies from the same class.

82
Q

protein I of electron transport chain

A

oxidises NADH to form NAD+ (2e-s enter protein)

passes 2 e-s to ubiquonone (Q) to from ubiquonol (QH2)

pumps H+ ions into the intermembrane space

83
Q

protein II of electron transport chain

A

oxidises FADH2 to form FAD+

passes electrons to Ubiquinone (Q) forming ubiquinol (QH2)

84
Q

protein III of electron transport chain

A

receives electrons from QH2 from proten I and II.

passes leectrons on to cytochrome C

pumps H+ ions into the inntermembranous space

85
Q

protein IV of electron transport chain

A

receives electrons from cytochrome C.

passes electrons on to O2 forming H2O.

pumps H+ ions throgh to the intermembranous space

86
Q

3 phases of beta oxidation

A

Activation (in cytosol):

FA + CoA –> AcylCoA

(uses breakdown of 2 ATP)

Transport:

carnitine shuttle

Degradation:

dehydrogenation, hydration, dehydrogenation.

AcylCoA –> Acetyl CoA + FA chain (reduced by 2C)

87
Q

FA degradation

A

dehydrogenation: reduction of FAD+

Hydration: H2O added

dehydrogenation: reduction of NAD+

Thiolysis:

product splits into acetylCoA and a FA chain

produces 12 ATP

88
Q

fatty acid synthesis

A

Elongation:

acetylCoA + CO2 –> Malonyl CoA

(involves the breakdown of ATP)

{loss of CO2}

Reduction: oxidation of NADPH

Dehydration: loss of H2O

Reduction: oxidation of NADPH

{loss of CoA}

produces a FA chain, longer by 2 C

89
Q

location of fatty acid synthesis

A

Cytosol

90
Q

TCA cycle

A
91
Q

irreversible steps of glycolysis

A

glucose –> glucose-6-phosphate

fructose-6-phosphate –> fructose-1,6-bisphosphte

PEP –> Pyruvate

* all involve the breakdown or production of ATP

92
Q

Glycogen synthesis

A

1. short chains of glucose are added to glycogenin

2. chains are extended by glycogen synthase

3. long chains are broken and branked by glucose branching enzyme

93
Q

Glycogen degradation/ mobilisation

A

1. terminal glucose molecules removed, phosphorylated and released as glucose-6-phosphate

2. 3 of the 4 remaining molecules are reattched to the main chain

3. the last molecule is released as free glucose

94
Q

1st nitrogen aquiring reaction

A

NH4 –> carbamoyl phosphate

(requires the breakdown of 2ATP)

95
Q

2nd Nitrogen aquiring reaction

A

citrulline + aspartate –> arginosuccinate

(requires breakdown of ATP to AMP)

the aspartate comes from a transamination reaction with glutamate and oxaloacetate (the carbon skeleton for aspartate)

96
Q

Urea formation

A

arginine + H2O –> UREA + ornithine

(arginine and ornithine are part of the urea cycle)

97
Q

glutamine/ glutamate conversion

A

Glutamine + H2O <–> Glutamate + NH4

98
Q

how does nitrogen enter the liver mitochondria

A

all dietary amino acids transfer their amino groups to alpha-ketoglutarate forming glutamate (and their carbon skeletons).

nitrogen enters the mitochondria in glutamate or glutamine (that has come directly from the blood)

99
Q

NMJ activity

A

1. motor neuron AP reaches the presynaptic terminal

  1. voltage gated Ca2+ channels open

3. Ca2+ stimulates Ach vesicles to move towards the synapse

4. Ach is released by exocytosis and diffuses accross the synapse

5. Ach gated Na+/K+ channels open

6. Na+ enters the cell and generates an endplate potential

7. voltage gated Na+channels open

8. Na+ enters the cell and an AP is generated

* Ach is removed by acetylcholinesterase

100
Q

skeletal muscle contraction

A
  1. the AP causes the sarcoplasmic reticulum to release Ca2+ ions
  2. Ca2+ binds to troponin which changes the conformation of tropomyosin
  3. this allows myosin heads to bind to actin binding sites and make the muscle contract
  4. to end contraction, Ca2+ is rapidly taken up into the sarcoplasmic reticulum by an ATPase
101
Q

smooth muscle contraction

A

1. the AP opens voltage gated Ca2+ ion channels so extracellular Ca2+ ions enter the muscle cell

(some Ca2+ is also released from the sarcoplasmic reticulum)

2. Ca2+ binds to calmodulin, activating it

3. activated calmodulin activates myosin light chain kinase

4. activated myosin light chain kinase phosphorylates myosin heads allowing for muscle contraction.

102
Q

Pacinian corpuscle structure

A

a cutaneous mechanoreceptor.

consists of an un myelinated nerve ending surrounded by connective tissue membrane lamellae with fluid in between the lamellae.

103
Q

pacinian corpuscle action

A

1. a mechanical stimulus deforms the capsule

2. the nerve ending is stretched causing ion channels to open

3. Na+ enters the cell generating a receptor potential which generates an action potential.

4. fluid redistributes between the lamellae and APs stop firing until the stimulus is removed (Adaptation)

104
Q

Nociceptors

A

free nerve endings.

detect painful stimuli.

do not adapt.