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Medicine UOB > CEP > Flashcards

CEP Flashcards

1
Q

Endocrine signalling

A

Secreting hormone into blood to reach target cell

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2
Q

Paracrine signalling

A

Hormones secreted to reach nearby cells

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3
Q

Autocrine signalling

A

Hormones to a local effect (target sites on the same cell)

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4
Q

How is the response to a drug/hormone measured?

A

Radio ligand binding assay
Amount of radioactivity is proportional to number of receptors

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5
Q

EC50

A

Effective concentration 50%
The concentration required to make 50% response (effect)

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6
Q

Kd (dissociation constant)

A

50% of receptors occupied (binding)

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7
Q

Affinity equation

A

1/Kd (low Kd = high affinity)

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8
Q

Why measure ligand binding?

A

To see affinity of drug

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9
Q

Endocrinology

A

The study of hormones

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10
Q

What are the four types of hormone?

A

Protein (insulin)
Steroid (cholesterol)
Amine/small peptide (tyrosine)
Amino acid derivatives

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11
Q

How are hormones measured?

A

Bioassays
Immunoassays
Mass spectrometry

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12
Q

What are the anterior pituitary hormones?

A

ACTH
TSH
GH
LH/FSH
PRL

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13
Q

What are the posterior pituitary hormones?

A

Vasopressin
Oxytocin

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14
Q

How to treat underactive glands?

A

Hormone replacement
Can be due to autoimmune
Primary/secondary can effect later on down the line and not appear until then

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15
Q

How to treat over active glands?

A

Block receptors
Often caused by tumours (surgery)

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16
Q

What are the 4 main types of receptors?

A

Ligand-gated ion channels (ionotropic)
G-proteins coupled receptors
Kinase-linked receptors
Nuclear receptors (not on plasma membrane)

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17
Q

What is the mechanism of ionotropic/ligand-gated ion channels?

A

Ion channels open when ligand binds
Causes change in membrane potential as +/- ve charges change
Can cause depolarisation/hyperpolarisation

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18
Q

What is the mechanism of GPCRs?

A

Ligand binds
G protein activates/changes conformation
Has a postage or negative effect
Causes ions channels to open or enzymes to produce second messenger
Resulting in a signalling cascade

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19
Q

What is the mechanism of kinase-linked receptors?

A

Ligand bonds directly to enzyme
Conformation change
Phosphorylation cascade occurs
Gene transcription
Protein synthesis

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20
Q

What is the mechanism of nuclear receptors?

A

Ligand diffuses directly across the membrane
Binds in nucleus to transcriptional factor
Gene transcription
Protein synthesis

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21
Q

What is the fastest receptor?

A

Fastest: l-g ion channels
GPCRs
Kinase-linked receptors
Nuclear receptors

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22
Q

How does Adenylyl cyclase work?

A

AC is an effector enzyme activated by a g-protein
It converts ATP into cyclic AMP which is a second messenger

Signal is stopped by cAMP phosphodiesterase

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23
Q

How does phospholipase C work?

A

It has 2 second messengers
Gq activates PLC
Causes PIP2 to convert to DAG and InsP3
Causes Ca2+ to be released from ER

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24
Q

What does a protein kinase do?

A

Adds phosphate

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25
Q

What does a proteins phosphatase do?

A

Removes phosphate

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26
Q

What can mutations in receptor genes lead to?

A

Inactive (no function or under)
Or over active (tumour/hyper function)

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27
Q

What is the thyroid pathway?

A

Hypothalamus released TRH
Anterior pituitary TSH
Thyroid released T3, T4
Increases metabolism

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28
Q

TSH resistance

A

Hypothyroidism
Not enough thyroid activity
Treated by more TSH

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29
Q

Cushing’s syndrome

A

Adrenal tumor
Benign adenoma

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30
Q

What is the endocrine system?

A

A system of ductless glands and cells that secrete hormones
Regulates metabolism, homeostasis, reproduction

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31
Q

Exocrine glands

A

Realise their secretions outside of the body
May be ducted
Not part of endocrine system

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32
Q

Intercrine signalling

A

Acting within the same cell

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33
Q

Hormones are controlled by…

A

Feedback (usually negative)

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34
Q

How does negative feedback work?

A

Senses the change and activated the mechanism to reduce it
The final product of an endocrine cascade acts to inhibit the release of hormones

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35
Q

Axis

A

How glands communicate

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36
Q

Peptide/protein hormones

A

Mainly from pituitary
Made from chains of amino acids
Hydrophilic
No carrier needed in blood
Stored in membrane bound vesicles (to be released via exocytosis)
Produce on RER as pre-prohormone which is broken by proteolysis

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37
Q

Steroid hormones

A

Made from cholesterol
Converted to pregnenolone via CYP11A
This then can differentiate using other enzymes
Hydrophobic (won’t travel in blood)
Can’t store in vesicles so synthesised as required

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38
Q

Where is aldosterone made?

A

Adrenal cortex
Zona glomerulosa

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39
Q

Where is cortisol made?

A

Adrenal cortex
Zona fasciculata

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40
Q

Where is adrenal androgens made?

A

Adrenal cortex
Zona reticularis

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41
Q

How are steroid hormone signals stopped?

A

Inactivated metabolism transformations
Excretion in urine/bile

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42
Q

Amine hormones

A

From thyroid gland
T4 Contains 4 iodine atoms
T3 contains 3 iodine atoms
Small, non polar -> hydrophobic
Soluble in plasma membrane
Require carrier proteins

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43
Q

What do carrier proteins do?

A

Increase solubility
Increase half life
Reservoir in blood

Can have specific and non-specific (looser binding) kinds

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44
Q

Where to hormones bind?

A

Protein- cell surface receptors
Steroid- intracellular receptors

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45
Q

What’s HRE?

A

Hormone response element
Specific areas for hormones to bind in DNA

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46
Q

Exogenous

A

Come from sources outside of living things

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47
Q

Endogenous

A

Come from sources within a living thing

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48
Q

Potency

A

the strength of an intoxicant or drug, as measured by the amount needed to produce a certain response.

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49
Q

Pharmacology

A

The study of mechanism or drug action

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50
Q

Drug

A

Active ingredient in a medicine

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51
Q

What drugs produce an effect by not binding to a receptor? (Physicochemical properties)

A

Antacids
Laxatives
Heavy metal antidotes (EDTA)
Osmotic diuretics
General anaesthetics
Alcohol

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52
Q

Most drugs have ___ potency

A

High
So effect at very low concentrations

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53
Q

Biological specifity

A

Receptor wise
Natural, biological, endogenous receptor/target

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54
Q

Chemical specifity

A

Drug wise
Artificial, chemical, exogenous ligand/drug/agonist

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55
Q

Stereo selectivity

A

In vivo razemisation (equilibrate back to both isomers)
So always both forms appear

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56
Q

What can drugs be classified by?

A

Chemical nature
Symptoms/disease
Organ system effected
Receptor
Duration of action
Generations
Route of administration

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57
Q

Affinity

A

The binding strength of the drug receptor interaction
Or
Likelihood of binding

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58
Q

Receptor in pharmacology

A

Anything that causes a physiological effect when interacting with a drug

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59
Q

Law of Mass action

A

Le chantelier’s principle

A + R <-> AR

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60
Q

E max

A

Maximum response

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61
Q

Relationship between drug conc and response

A

Continuous
Saturation
Exhibits threshold

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62
Q

Kd equation

A

Kd = [A][R] / [AR]
Mol/litre

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63
Q

Langmuir isotherm

A

P= [A] / (Kd + [A])

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64
Q

Kd vs EC 50

A

EC 50 is model free equivalent to Kd (has to be the classic curve)

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65
Q

Agonist

A

Bind to receptor to produce response

Can be endogenous (given from outside also) and exogenous

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66
Q

Antagonist

A

Binds to receptor but no response
Prevent agonist binding so inhibits

Has affinity but no efficacy

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67
Q

Antagonist vs inhibitor

A

Inhibitor - enzymes
Antagonist -receptors

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68
Q

Types of antagonists

A

Competitive- unbind and rebind

Irreversible- covalent binding, same site

Allosteric- alternative site

Channel blockers- plug channel

Physiological- no binding

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69
Q

ADME

A

Absorption, distribution (drug to target)
Metabolism, Excretion (remove drug)

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70
Q

Effective concentration

A

The lowest concentration needed to make an effect

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71
Q

Therapeutic window

A

The concentration window between the toxic and effective concentration

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72
Q

Where can the drug be lost when administered?

A

Not dissolved
Broken down by stomach acid/intestine
Not absorbed
Secreted into bike
Metabolised
Bound to plasma proteins
Excreted
Tissue bound

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73
Q

Routes of administration

A

Enteral (oral, rectal)

Parenteral (subcutaneous, intra-muscular, intra-venous)

Percutaneous (inhalation, sublingual, topical, transdermal)

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74
Q

Absorption depends on…

A

Route
Blood flow at site
Dose
Active vs passive diffusion
Solubility
Chemical nature
Molecular weight
Partition coefficient
Gastric mobility
pH at site
Area of absorbing site
Presystemic elimination
Ingestion with/without food

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75
Q

Bioavailability

A

The fraction of the total dose administered that reaches the plasma

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76
Q

Factors that affect absorption in GI tract

A

Dispersal/solubility of drug in gut
Stability in acid/alkali
Lipid solubility
Time available for absorption
Concentration of drug
Blood flow
Interaction with food
Effect of drug (irritant)
Effect of meals
First pass metabolism

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77
Q

Pharmaceutical interventions that effect absorption

A

Particle size
Dry-powder inhaler
Enteric coated tablets
Slow release

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78
Q

Factors effecting transdermal absorption

A

Lipid solubility
Formulation
Skin thickness
Hydration
Blood flow

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79
Q

Pinocytosis

A

Endocytosis of fluid and dissolved molecules (opposite of exocytosis)

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80
Q

Lipophilicity

A

Likes lipids

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81
Q

Distribution of drugs depend on

A

Lipid solubility
Diffusion barriers
Tissue binding
Plasma protein binding

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82
Q

Albumin

A

Family of soluble globular proteins that transport small molecules in the blood

Decreased levels in liver and kidney disease

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83
Q

Alpha-acid glycoprotein

A

A carrier of basic and neutral lipophilic compounds
Increased in inflammatory conditions

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84
Q

Process of pharmokinetics when drug testing

A

Lipophilic/hydrophilic
pH value
Active perfusion
Large surface area
Diffusion barriers
Any inactivating enzymes

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85
Q

Diffusion barriers

A

Block diffusion across membranes

Main types- BBB, placenta

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86
Q

Apparent volume distribution

A

The notional volume of fluid required to dilute the absorbed dose to the concentration found in plasma

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87
Q

AVD equation

A

AVD = dose / plasma concentration

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88
Q

High AVD

A

Tissue bound
Lipophilic and basic

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89
Q

Low AVD

A

Heavily plasma protein bound

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90
Q

Ion trapping

A

Passive, semipermeable membrane

Only the unionised molecule will travel across the membrane

So a high concentration of an acidic drug will be concentrated in a compartment with high pH

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91
Q

Metabolism

A

Mainly liver (first pass), kidney, skin, lungs, microbiome

Basically anything in can do chemically with a drug
Mainly oxidation and conjunction
Unusually inactivated but not always

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92
Q

Oxidation via

A

Cytochrome p450 enzymes

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93
Q

Conjunction via…

A

Sulfation pathways

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94
Q

Portal vein

A

Something that vascularises twice

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95
Q

First pass metabolism

A

Phase 1- oxidation via cytochrome p450 enzymes
-hydroxyl groups -> more hydrophilic

Phase 11- conjunction reactions
- charged groups are conjugated -> more hydrophilic

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96
Q

Excretion

A

Kidney
-into urine

Liver
-into bile (enterohepatic circulation)

Lungs

Fluids
-salvia, sweat, milk

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97
Q

Performing a PK study

A

Dose
Collect samples (blood, urine etc)
Analysed drug
PK data analysis

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98
Q

How to quantitatively measure drugs in excretion?

A

Mass spec
Liquid chromatography
LC-MS

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99
Q

Dose interval dependent on…

A

Plasma half life

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100
Q

Hormones in anterior lobe

A

ACTH (Adrenocorticotropic hormone)
TSH (thyroid stimulating hormone)
GH (growth hormone)
FSH/LH (follicle-stimulating hormone/ luteinising hormone)
PRL (prolactin)

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101
Q

Hormones in posterior lobe

A

Vasopressin (ADH)
Oxytocin

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102
Q

What is the hypothalamus regulated by?

A

Hormone mediated signals
Neural inputs

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103
Q

Uses of hypothalamus…

A

Final common pathway to anterior pituitary
Non-endocrine function (thirst etc)
Sends signals to other parts of nervous system

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104
Q

Posterior pituitary communication

A

Only through nerves
Secretory granules migrate down axons (supraopyicohypopophyseal)
No hormones produced here only secreted

105
Q

What does the hypothalamus secrete?

A

corticotrophin-releasing hormone
dopamine
growth hormone-releasing hormone
somatostatin
gonadotrophin-releasing hormone
thyrotrophin-releasing hormone

106
Q

What does GHRH stimulate?

A

Growth hormone

107
Q

What does somatostatin do?

A

Inhibit growth hormone

108
Q

What does GnRH stimulate?

A

Follicle-stimulating hormone
Luteinizing hormone

109
Q

What does CRH stimulate?

A

ACTH

110
Q

What does TRH stimulate?

A

TSH

111
Q

What does dopamine stimulate?

A

Inhibits prolactin

112
Q

Growth hormone release

A

Stimulated by hypoglycaemia, exercise and sleep

Suppressed by hyperglycaemia

Released in pulses throughout the day

113
Q

What is GH mediated by?

A

Effects mediated by IGF-1

114
Q

What does GH stimulate?

A

Protein synthesis
Lipolysis
Glucose metabolism
Acquisition of bone mass
Regulation of body composition
Well-being

115
Q

What does FSH and LH trigger?

A

LH- testosterone production in tested

FSH- oestrogen production in ovaries

116
Q

What is the secondary effect of FSH?

A

Estrogen -> breasts, hips broaden, pubic hair, folliculogenesis

117
Q

What is the secondary effect of LH?

A

Testosterone ->
penis/scrotum grow
facial hair grows
larynx elongates
shoulders broaden
hair grows
muscle increases in body
spermatogenesis

118
Q

What does prolactin do?

A

Lactation
But also inhibits GnRH (less FSH/LH)

119
Q

What does ACTH do?

A

Stimulates cortisol production in adrenal gland
-> regulates blood sugar, increases fat, help defends body against infection, respond to stress

120
Q

What does TSH do?

A

Stimulates the thyroid
-> that produces T3 and T4

121
Q

Where is vasopressin synthesised?

A

Supraoptic and paraventricular nuclei of hypothalamus

122
Q

What does vasopressin do?

A

Determines the rate of free water excretion
By changing the permeability of the luminal membrane of cortisol and medullary collecting tubes

123
Q

What stimulates ADH?

A

Hyperosmolality (too much water)
Effective circulating volume depletion (blood loss)

124
Q

What does oxytocin do?

A

Stimulates contraction of smooth muscle in Breast and uterus

-> milk ejection reflex
-> parturition (birth)

125
Q

Pituitary disease manifestations

A

Neurological
Visual
Hypopituitarism
Hormone hypersecretion from adenoma

126
Q

Lesion

A

Damage to tissue

127
Q

Mass neurological effects of pituitary lesions

A

Headaches
Brain damage/hypothalamic damage
Nerve damage
Optic nerve damage
CFS leak

128
Q

Hypopituitarism causes

A

Tumours
Radiotherapy
Pituitary infarction (Sheehan’s syndrome)
Infiltration of pituitary
Trauma
Isolated hypothalamic hormone deficiency (Kallmann’s)

129
Q

What is apoplexy?

A

Bleeding into an organ / loss of blood flow to an organ

130
Q

Infiltration of pituitary

A

Lymphatic infiltration causes inflammation

131
Q

GH deficiency manifestation

A

Children- poor growth
Adults- more abdominal fat, less muscle strength, impaired cardiac function, decreased bone mineral density

132
Q

How to diagnose GH deficiency?

A

ITT
glucagon
GHRH+arginine IGF-1 (blood test)

133
Q

GH deficiency treatment

A

Hormone replacement

134
Q

FSH/LH deficiency manifestations

A

Delayed puberty
Osteoporosis
Anaemia

Men- libido decreased, infertility, less muscle mass, less mood
Women- libido decreased, infertility m, dyspareunia

135
Q

FSH/LH deficiency diagnosis

A

Blood test of hormones
Oestradiol
Menstrual history
Morning testosterone

136
Q

FSH/LH treatment

A

Hormone replacement

137
Q

ACTH deficiency manifestations

A

Fatigue
Weakness
Nausea/vomiting
Anorexia
Hypoglycaemia
Hypotension
Anaemia

138
Q

ACTH diagnosis deficiency

A

9am serum cortisol and ACTH

Dynamic: short synacthen test, ITT, glucagon test

139
Q

Alpha sub units on G proteins

A

Ga s
Ga io
Ga q11

140
Q

ACTH deficiency treatment

A

Replace what is missing (steroids)
Approximate to the natural rhythm

141
Q

TSH Deficiency manifestations

A

Fatigue, weakness
Cold intolerance
Bradycardia
Inability to lose weight
Puffiness
Pale/dry skin
Constipation

142
Q

TSH deficiency diagnosis

A

TSH, fT3, fT4 tests

143
Q

Treatment for TSH deficiency

A

Hormone replacement (levothyroxine)

144
Q

Diabetes insipidus

A

Deficient secretion of ADH

145
Q

Diabetes insipidus causes

A

Idiopathic (autoimmune)

Familial (autosomal dominant mutations, Wolfram syndrome)

Tumours
Neurosurgery
Infiltration disorders
Infections
Hypoxic encephalopathy

146
Q

Hypoxic encephalopathy

A

When blood doesn’t receive enough oxygen for a period of time

147
Q

ADH deficiency manifestations

A

Polyuria (lots of urine)

148
Q

Causes of polyuria

A

Osmotic diuresis (DM, renal failure)
Primary polydipsia
Diabetes insipidus

149
Q

ADH deficiency diagnosis

A

Urine output
Blood (electrolytes, glucose, urea, creatinine)
Water deprivation test

150
Q

ADH deficiency treatment

A

ADH analogues (replacements)

151
Q

Functioning vs non-functioning pituitary adenomas

A

Functioning- secrete hormones from tumours

Non- no secretion

152
Q

GH hypersecretion causes…

A

Acromegaly

153
Q

Acromegaly symptoms

A

Gigantism
Arthritis
Hypertrophy of frontal bones
Hyperhidrosis
Etc

154
Q

Acromegaly diagnosis

A

Oral glucose tolerance test
IGF-1
Pituitary Imaging

155
Q

Acromegaly treatment

A

Pituitary surgery
Dopamine agonists
Somatostatin analogues
GH receptor antagonists
Radiotherapy

156
Q

High prolactin causes

A

Stress, pregnancy, lactation, sex, sleep
Antipsychotics, antidepressants, opiates
Hypothalamic tumours

157
Q

Prolactinoma manifestation

A

Hypogonadism (lack of sex hormones)
Galactorrhoea
Mass effects

158
Q

Prolactionoma diagnosis

A

Pituitary imaging

159
Q

Prolactinoma treatment

A

Dopamine agonists
Surgery
Radiotherapy

160
Q

Cushing’s syndrome

A

Too much cortisol

Could be due to too much ACTH or adrenal disease/steroids

161
Q

Cushing’s disease

A

Excess ACTH from corticotroph adenoma

162
Q

Cushing’s syndrome symptoms

A

Weight gain
Slow healing of cuts
Fatigue
High risk of infections
Glucose intolerance
Moon face/ buffalo hump
Red marks (striae)

163
Q

Cushing’s diagnosis

A

24hr UFC (cortisol in urine)
Midnight serum cortisol
Overnight/low dose dexamethazone suppression test
9am ACTH
Imagining

164
Q

Cushings treatment

A

Pituitary surgery
Radiotherapy
Drugs
Bilateral adrenalectomy

165
Q

TSHoma (mani, diag and treat)

A

Mani-
Thyrotoxicosis

Diag-
Hormonal tests
Imaging

Treat-
Surgery/meds/radiotherapy

166
Q

FSHoma

A

Mani-
Menstrual irregularities
Ovarian hyper stimulation
Testicular enlargement
Infertility

Diag-
hormonal tests
Imaging

Treat-
Surgery
Radiotherapy

167
Q

What protein hormones made up of?

A

An alpha and beta subunit

168
Q

What do TSH, LH, FSH and hCG all share?

A

The same type of alpha subunit

169
Q

Thyroid gland embryology

A

Proliferation on pharyngeal floor (foramen caecum)

Descends through thyroglossal duct then duct obliterates (or becomes thyroglossal cyst)

170
Q

Thyroid gland location

A

Anteriorly: strap muscles
Sternohyoid, sternothyroid

Laterally: sternocleidomastoid muscle

Can only palpate isthmus

171
Q

Thyroid blood supply

A

Superior thyroid artery (first brand of external carotid artery)
Inferior thyroid artery (from thyrocervical trunk)

Superior (into jugular vein)
Middle (into jugular vein)
Inferior thyroid veins (into brachiocephalic vein)
All together- venous plexus

172
Q

The aortic arch extends to…

A

Left subclavian artery
Left common carotid artery

Brachiocephalic artery-> right subclavian and right common carotid

173
Q

Parathyroid glands secrete… and their functions

A

PTH - regulator of serum calcium
Targets kidneys intestine and bone

174
Q

Describe parathyroid glands

A

Small, flattened oval shaped glands
Normally 4 glands
On POSTERIOR of thyroid gland

175
Q

Parathyroid gland embryology

A

Superior parathyroid derived from 4th pharyngeal pouch

Inferior derived from 3rd pharyngeal pouch

Glands descend with thymus but stop earlier

176
Q

Parathyroid glands blood supply

A

inferior thyroid artery

Superior/middle/inferior veins

177
Q

Adrenal glands location

A

Superomedial aspect of kidneys
Retroperitoneal
Level t11-12
Surrounded by Perirenal fat
Separated from kidneys by fascia

178
Q

Retroperitoneal

A

anatomical space located behind the abdominal or peritoneal cavity

179
Q

Adrenal glands structure and secretions

A

Distinct inner medulla (noradrenaline and adrenaline) and outer cortex (cortisol)

180
Q

Adrenal glands blood supply

A

Superior adrenal artery (branch of inferior phrenic)
Middle adrenal artery (branch of abdominal aorta)
Inferior adrenal artery (branch of renal artery)

Right adrenal vein (into inferior vena cava)
Left adrenal vein (into left renal vein then IVC)

181
Q

Adrenal gland innervation

A

Directly by preganglionic sympathetic fibres (from mostly greater splanchnic nerve)

Adrenal medulla acts as a specialised sympathetic ganglion

182
Q

Endocrine pancreas function

A

Islets of langerhans
Release insulin and glucagon

183
Q

Exocrine function of pancreas

A

Acinar cells
Digestive enzymes

184
Q

Endocrine pancreas embryology

A

Begins as two buds that develop rotate and fuse (=2 ducts)

185
Q

Endocrine pancreas location

A

Head -attached to duodenum to the right
anterior to IVC, right renal artery and vein and left renal vein
Bile duct is embedded in its posterior surface

Neck- overlies superior mesenteric vessels
Formation of portal vein occurs posteriorly

Body- left of superior mesenteric vessels
Posterior surface in contact with aorta, SMA left Kidney and adrenal

Tail- enters lienorenal ligament
Related to splenic hiking and left colic flexure

186
Q

mesentery

A

Fold in membrane that attaches the intestine to the abdominal wall

187
Q

Dirty drugs

A

Bind to more than one receptor
Side effects

188
Q

The nature of drug receptors

A

Enzymes
Ion channels
Transports
Physiological receptors
DNA/RNA
Substrates, metabolites and proteins
Monoclonal antibodies

189
Q

Efficacy relative to endogenous agonist scale=

A

Full inverse agonist
Partial inverse agonist
Silent antagonist
Partial agonist
Full agonist
Super agonist

190
Q

Ways to regulate cell function

A

Alter membrane potential
Alter enzyme activity
Alter gene expression

191
Q

GABA a receptor

A

Ligand gated choride ion channel
Benzodiazepine binds to allosteric site and increased affinity of binding

192
Q

Glutamate gated chloride receptors

A

Common channels in nervous system
Important targets for anti parasitic drugs

193
Q

Spare receptors/super agonists

A

Some ‘super agonists’ can produce maximal response without binding to all available receptors

Emax > 100%

194
Q

Partial agonists

A

Low efficacy, cannot produce maximal response even when bound to all receptors

195
Q

Competitive antagonist

A

Bind reversible

Parallel shift of dose/response curve

196
Q

Irreversible antagonist

A

Being covalently
Decrease the maximal response

Can still produce max response -> evidence for spare receptors

197
Q

Allosteric antagonism

A

Being reversibly at different site to agonist
Decrease agonist affinity
Reduced likelihood of agonist binding

198
Q

Channel blockers

A

Bind inside and prevent passage of ions
Tend to be enhanced by receptor activation

199
Q

Physiological antagonist

A

Not binding to receptor

200
Q

Desensitisation

A

Prolonged exposure can reduce response to drug

201
Q

Allosteric effects on receptors

A

Change shape for good or bad

202
Q

Two types of acetyl choline receptors

A

Nicotinic
Muscarinic (GPCR)

203
Q

How to get drugs/signals across a membrane?

A

Integral ion channels
Integral tyrosine kinases
Steroid receptors/nuclear receptors
GPCRs
Cytokine receptors

204
Q

Nuclear receptors location

A

Act In nucleus
But mostly located in the cytoplasm
When steroid bound then conformational change

205
Q

DBD

A

DNA binding domain mediates binding of nuclear receptors

206
Q

Types of G subunit

A

Gs stimulating cAMP pathway
Gi inhibiting
Gq stimulating PLC pathway

207
Q

Diabetes diagnosis

A

Random >11.1mmol/l

Fasting glucose >7mmol/l

HbA1c >48mmol/mol

Need to repeat test if no symptoms

208
Q

HbA1c

A

Reflects previous 10 weeks of ambient circulating glucose

65% or 48mmol/mol

Can be to diagnose
Or measure how well diabetes is being treated

209
Q

Oral glucose tolerance test

A

Gold standard
Fasting state
Measure glucose (>7)
Drink 75g of glucose
Wait 2 hours then measure glucose (>11.1)

210
Q

Cause of diabetes

A

Insulin deficiency or resistance

211
Q

Insulin anabolic function

A

Maintain supply of glucose to tissues
Regulates metabolism in muscles
Promotes protein synthesis
Inhibits breakdown of fat

212
Q

Symptoms of diabetes

A

None
Weight loss
Tiredness
Infection
Candidiasis
Urine
Osmotic symptoms
Polyuria
Thirst
Blurred vision
Coma

213
Q

Proinsulin

A

Cleaved by proteases
Can be measured as is always produced with each insulin molecule
Urinated out

214
Q

Types of diabetes

A

Type 1 immune system attacks and destroys the cells that produce insulin

Type 2 cells don’t respond to insulin

Gestational
Monogenic

215
Q

Cause of type 1

A

T cells attack insulin beta cells in islets of langerhan

216
Q

Treatment of type 1

A

Lifestyle- lower glucose levels when they are exercising
Insulin

217
Q

Insulin delivery system (midlands hybrid closed loop pilot outcomes)

A

Glucose level sensing
Sends signals to machine
Diffuses insulin into body

218
Q

Treatment of type 2

A

Lifestyle
Give drugs that Reduce insulin resistance (metformin, sitagliptin, liraglutide)
Give insulin (gliclazide, insulin injections)
Give something that will Increase glucose excretion (SGLT2 inhibitors: dapagliflozin)

219
Q

Diabetes treatment not for glucose

A

Blood pressure- ACE, beta blockers, ca channel blockers, diuretics

Lipids- statins, fibrates

220
Q

Uncontrolled diabetes

A

Hypoglycaemia- shaky, sweaty, dizzy, hungry, nervous, upset, tired, weak

Hyperglycaemia- dry mouth, thirst, weakness, headache, blurred vision, urination

Long term-
Mental health
Vascular
Cancer

221
Q

Lack of insulin on fat

A

Triglycerides to glycerol/fatty acids
Fatty acids to acetoacetate

To urine ketones/blood ketones/ hydroxybutyrate
Or to acetone (smell in breath)

222
Q

Why lower blood glucose?

A

Irritates endothelial cells
Causes furring
Blocking

223
Q

Complications of diabetes

A

Micro vascular:
Eye
Kidneys
Neuropathy

Macro vascular:
Brain
Heart
Extremities

224
Q

Why does t2 causes more cancer?

A

High levels of insulin
Causes increased growth as stimulates to all cells

225
Q

Care of diabetic patient

A

Lifestyle advice
Glucose control
BP
cholesterol after 40, 4mmol/l
Regular screening
Empathy and engagement

226
Q

Apparent volume of distribution

A

The notional volume of fluid required to dilute the absorbed dose into the concentration found in the plasma

227
Q

Bio transformation of drugs

A

Phase 1
Oxidation/ hydroxylation/ dealkylation/ deamination/ hydrolysis

Phase 2
Conjugation

228
Q

Endocrine cells 3 distinct anatomical distributions are:

A

Grouped into an endocrine gland
Forming discrete clusters
Dispersed singly among other cells known as diffuse neuroendocrine system

229
Q

What are endocrine cells? (Types)

A

Epithelial cells mainly
But some are neuroendocrine cells

230
Q

Neuroendocrine cells

A

Secrete amines that are decarboxylated
Form a secure link with the ANS

Neural crest cell derivative

231
Q

APUD cells

A

Amine precursor uptake and decarboxylation
= neuroendocrine

232
Q

Chromogranin

A

Core protein expressed by neuroendocrine (associated with hormone)

233
Q

Synaptophysin

A

Membrane glycoprotein found in neuroendocrine vesicles

234
Q

How to see if neuroendocrine cells are present?

A

Stain chromogranin or synaptophysin
Or directly stain their specific hormone

235
Q

Where are Neuroendocrine cells normally found?

A

Respiratory
GI Tract
However not readily seen as scattered

236
Q

Larger endocrine glands composed of neuroendocrine cells…

A

Adrenal medulla
Pancreatic uslets

237
Q

Thyroid gland anatomy

A

Thin fibrous capsule of connective tissue
Made up of follicles

238
Q

Follicles are made of..

A

Thyroid epithelial
C-cells
Colloid

239
Q

Use of thyroid hormones

A

Control of metabolism
Regulation of growth
Multiple roles in development

240
Q

What is the active thyroid hormone?

A

T3

241
Q

What’s the difference between t3 and t4?

A

T4 has 4 iodines
T3 has 3

242
Q

What cells produces thyroid hormones?

A

Follicular thyroid cells

243
Q

What are thyroid hormones synthesised from?

A

Thyroglobulin precursor
Tyrosine

244
Q

Thyroperoxidase function

A

Binds iodine to tyrosine residues in thyroglobulin molecules

Forms MIT + DIT

245
Q

T3 is made of…

A

MIT
DIT

246
Q

T4 is made of…

A

DIT x2

247
Q

Thyroid hormone synthesis mechanism

A
  1. TSH binds to TSHR
  2. I- uptake by Na/I symporter
  3. Iodisation of Tg tyrosyl residues by thyroperoxidase
  4. Coupling of iodotyrosyl residues by thyroperoxidase
  5. Export of mature Tg to colloid where it is stored
248
Q

Which thyroid hormone is more abundant?

A

T4

249
Q

How is t3 converted from t4?

A

By deiodinase enzymes

250
Q

Tests of thyroid function

A

Serum TSH (best)
Serum free T4
Serum free T3

251
Q

Hormone levels of hyperthyroidism

A

Low serum TSH
High serum free T4 and free T3

252
Q

Hormone levels of hypothyroidism

A

High serum TSH
Low free t4
Low free t3

253
Q

Main causes of hyperthyroidism

A

Graves hyperthyroidism
Toxic nodular goitre
Thyroiditis

Others:
Exogenous iodine
Factitious
TSH secreting pituitary adenoma
Neonatal hyperthyroidism

254
Q

Distribution of drugs into the CNS depends on?

A

Lipid diffusion

255
Q

What are the different method of elimination?

A
256
Q

Toxicology is the study of…

A

Unwanted or deleterious effects of drugs or chemicals in the body

257
Q

Diabetes is a metabolic disease that is characterised by…

A

High blood glucose concentration

258
Q

People with diabetes are at a greater risk of what conditions?

A

Neuropathy
Nephropathy
Cardiovascular disease
Stroke
Retinopathy
Hearing impairments

259
Q

Polyphagia is…

A

Increased hunger

Medicine UOB (8 decks)

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