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Cell and molecular extras > Lecture 11 Cell communication > Flashcards

Lecture 11 Cell communication Flashcards

1
Q

Adrenaline secreted form, binds to, for the

A

Adrenal glands, adrenergic receptors, fight or flight

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2
Q

How is adrenaline transported

A

Blood

every cell exposed yet only some have correct receptors

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3
Q

Describe endocrine signalling

A
  • Long distance: a cell signals to cells distributed widely in body
  • A Hormone is a chemical mediator that is released in one part of the body but regulates the activity of cells in other parts of the body
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4
Q

What drug is specific for beta 1 adrenergic receptors

A

Bisoprolol

This is only expressed in the heart so the it is less responsive to adrenaline, yet the rest of the body is unaffected.

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5
Q

Result of hormones being present in low concentrations

A

Receptor specific and sensitive to change

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6
Q

Synaptic signalling

A

Physical linkage

Target determined by neurones that synapse onto them

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7
Q

Gateway between neuronal and endocrinological systems

A

Hypothalamus/pituitary gland

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8
Q

What makes up cholesterol

A

Lipid - hydrophobic

Alcohol - hydrophilic

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9
Q

Structure of cholesterol allows it to

A

travel through PM and dissolve in aq solution

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10
Q

% of PM made up by cholesterol

A

30

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11
Q

How much cholesterol is synthesised per day

A

10g in 37 step biosynthetic pathway

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12
Q

Cholesterol is the precursor for

A

Steroid hormone

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13
Q

4 examples of steroid hormones

A

Vit D3
Testosterone
Cortisol
Estradiol

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14
Q

Steroid hormone structure allows it to

A

pass through BBB and CM as alcohol/lipid

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15
Q

Structure of nuclear receptors

A 
A/B C terminus
C  DNA BD
D Hinge
E Ligand BD
F C terminus
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16
Q

DNA binding domain encodes

A

ZInc fingers that contain 4 cysteine residues that coordinate with a zinc atom to formed a looped structure allowing it to access a major groove of DNA double helix

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17
Q

All nuclear receptors share

A

The same primary structure

C term - DNA BD - N term

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18
Q

2 forms of nuclear receptors

A

Inactive - inhibitory proteins present
Active - ligand binds, coactivator proteins, C terminus locks ligand in, high affinity –> conf change –> DNA BD –> transcription

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19
Q

Name 2 transcriptional responses of nuclear receptors

A
  1. primary response

2. secondary response

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20
Q

Primary response of steroid hormones

A

Proteins made by R itself

R-steroid hormone activates primary response genes to form primary response hormones

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21
Q

Secondary response of steroid hormones

A

DELAYED response

Primary response proteins shut off primary response genes + turn on 2nd response genes to form 2nd response proteins

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22
Q

Example of nuclear receptor

A

Glucocorticoid receptor

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23
Q

Glucocorticoid receptor detects

A

Dexamethasone - cortisol

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24
Q

Glucocorticoid receptor location

A

IC receptor as dexamethasone diffuses through PM

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25
Q

Dexamethasone complex translocates to..

A

Nucleus

26
Q

Dexamethasone complex mostly expresses

A

TF

Consistent with primary/secondary responses

27
Q

Dexamethasone pathway

A

GR + HSP70 + FKBP52
+
Dex
–> GR + Dex + DNA + tran machinery

28
Q

Glucocorticoid receptor mainly target

A

Metabolism
Catabolism
Biosynthetic pathways

29
Q

When is Dex/cortisol released

A

stress

decreased blood glucose

30
Q

4 main points about glucorticoids

A
  1. for medical therapy
  2. immunosuppression/antiinflamm
  3. broad effects, different organ systems
  4. debilitating side effects = bone loss/glucose dysregulation
31
Q

Describe hypothalamus- pituitary-adrenal axis

A
  1. The hypothalamus produce a 41 aa peptide called corticotropin-releasing hormone (CRH).
  2. This travels to the pituitary gland that releases ACTH which is a peptide hormone. 3. This stimulates the adrenal glands which then release cortisol/dexamethasone
32
Q

What does cortisol effect

A
  1. metabolism
  2. immune system
  3. Memory
  4. electroyltes
33
Q

Disease of too little cortisol + symptoms

A

Addison’s disease

• Depression, flu-like symptoms, nausea, weight loss

34
Q

Types of disease from too little cortisol

A
  • Primary adrenal insufficiency – damage to the adrenal glands so cortisol is not made
  • Secondary adrenal insufficiency – lack of ACTH due to lack of activity or damage to pituitary gland so adrenal glands can’t be stimulated
35
Q

Disease of too much cortisol + symptoms

A

Cushing’s syndrome

Puffy face, weight gain, increase BP, facial growth

36
Q

Causes of too much cortisol

A

Benign adenoma pituitary increases ATCH

LT steroid abuse and use

37
Q

Insulin controls

A

Blood glucose levels

38
Q

Insulin released from

A

Beta cells, Islets of Langerhans - stimulated after meal

39
Q

Type 1 diabetes

A

Destruction of β cells – often as a result of auto-immune attack. This results in high levels of plasma glucose

40
Q

Prevalence type 1 diabetes

A

1:300, age 18

41
Q

Insulin receptor structure

A

Heterotetramer linked by disulfide bonds

Tyrosine kinase activity

42
Q

Conformation changes when ligand binds to IR

A

2 kinases domains closer
Kinase domains trans-phosphorylate
Docking domain, insulin substrate 1 becomes tyrosine phosphorylated

43
Q

3 major biochemical steps in insulin signalling

A
  1. tyrosine phos of R and its substrate IRS
  2. activation lipid kinase P13K
  3. activation multiple serine/threonine kinases = AKT
44
Q

6 step pathway of insulin signalling - more detail

A
  1. Insulin binds to IR
  2. IR tyrosine activated
  3. Tyrosine phos of IR and IR substrate (IRS)
  4. P-tyrosine sites on IRS allows binding of lipid kinase P13K which synthesises PIP3 at PM
  5. PIP3 recrutis PDK and directly phos AKT
    and other serine/threonine kinases
  6. AKT phos ser/thr residues substrates
45
Q

What are the effectors of AKT

A

FOXO –> glucose production
TSC2 –> mTORC1 –> S6K –> protein synth + –> SREBP1c –> lipid synth
GSK3beta –> glycogen sytnh
TBC1D4 –> glucose uptake

46
Q

Types of insulin

A

long acting background insulin replacement

Fast acting bolus for meals

47
Q

Excess insulin disease and symptoms

A

Hypoglycaemia - too little blood sugar, brain only metabolisrs glucose, live muscles take up glucose –> unconscious/death

48
Q

Type 2 diabetes

A

dysreg lipid,carb,protein metab

impaired insulin sercretion/resistance

49
Q

Prevalence type 2

A

1: 17

3. 8m UK

50
Q

Correlation type 2 diabetes

A

There is a strong correlation between body mass index and risk of type 2 diabetes

51
Q

Type 2 diabetes symptoms

A 
Thirsty 
excess glucose in urine as kidneys cant reabsorb all
increased urination 
weight/muscle loss
slow heal cuts/ulcers
thrush 
blurred vision
52
Q

REmission trial

A

High intensity weight loss

46% remission 12m, 36% 24m

53
Q

Summary Remission results

A

Increase QOL, decrease systolic BP/triglycerides/SAEs 12-24m

54
Q

Medication type 2

A

Metformin - antihyperglycameic agent of the biguanide class

55
Q

Mechanism metformin

A

Insulin sensitiser - decrease insulin resistance - reduces plasma fasting insulin levels - weight loss

56
Q

Where and why does metformin accumulate

A

Positively charged - in cells and mitochondria

57
Q

Metformin inhibits

A

Mitochondria complex 1 preventing production of mito ATP –> increased cytoplasmic ADP:ATP and AMP:ATP ratio –> activated AMP-activated protein kinase which regulates glucose metabolism

58
Q

2 classes of steroid hormones

A

corticosteroids - cortex adrenal gland

sex steroids - placenta/gonads

59
Q

corticosteroids e.g. x2

A

gluco/mineralcorticoids

60
Q

sex steroids

A

oestrogen, testosterone, progesterones

Cell and molecular extras (16 decks)

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