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101 Bio > Professor Mohankumar’s Lectures > Flashcards

Professor Mohankumar’s Lectures Flashcards

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1
Q

What is blood made up of?

A

Plasma
Buffy coat
Erythrocytes

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2
Q

What is plasma made up of?

A

90% water
10% soluble components e.g
-Plasma proteins
-Nutrients - glucose, cholesterol
-Gases - CO2, O2
-Electrolytes

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3
Q

What is the process of forming blood cells

A

Haematopoiesis

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4
Q

Where does haematopoiesis occur?

A

In red bone marrow

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5
Q

What does the buffy coat contain?

A

White blood cells
Leukocytes
Thrombocytes

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6
Q

What is the term for deficiency?

A

Penia

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7
Q

What is the term for excess?

A

Philia

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8
Q

How is erythropoiesis regulated

A

Negative feedback loop:
The kidney senses low O2 in renal artery triggering the release of erythropoietin (EPO) which stimulates bone marrow to produce erythrocytes. Erythrocytes increase O2 resulting in the decrease of EPO

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9
Q

What are the symptoms of dwarfism

A

Anxiety, depression, poor muscle tone, impaired hair growth, increase adipose tissue, decreased lean body mass

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10
Q

What are the symptoms of Gigantism/acromegaly

A

Enlarged hands/feet, headaches, blurred vision, glucose intolerance (diabetes), hypertension, coarsening of face

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11
Q

What are the symptoms of Graves’ disease (hyperthyroidism)

A

Weight loss, sweating, heat intolerance, goitre, nervousness

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12
Q

What are the symptoms of Primary hyperaldosteronism (Conn’s syndrome)

A

Hyper secretion of aldosterone, low blood potassium levels, high blood sodium levels

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13
Q

What are the symptoms of excess cortisol (cushing’s syndrome)

A

Buffalo hump, obesity, high blood pressure/sugar, cognitive difficulties, stretch marks

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14
Q

What is grave’s disease?

A

Hyperthyroidism - over production of thyroid hormones

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15
Q

What is conn’s syndrome?

A

Hyperaldosteronism - too much aldosterone

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16
Q

What is Cushing’s syndrome?

A

Hypersecretion of cortisol

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17
Q

What are the symptoms of low ADH

A

Diabetes insipidus - polyuria and polydipsia, inadequate release of ADH

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18
Q

What is Addison’s disease

A

Hyposecretion of cortisol

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19
Q

What are the effects of Hyposecretion of cortisol (Addison’s)

A

Darkening of skin, hair loss, decreased appetite, weight loss

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20
Q

A drug is something that…

A

Has a defined chemical structure

Prompts physiological response

Is specific

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21
Q

Pharmacodynamics is…

A

What the drug does to the body

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22
Q

Pharmacokinetics is…

A

What the body does to the drug

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23
Q

What barriers do drugs experience

A

ADME:

Absorption in the GI tract

Distribution, may not get past blood brain barrier

Metabolism

Excretion

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24
Q

What does adrenaline do to the heart

A

Activates the sympathetic NS and increases heart rate as well as force of contraction (beta 1 receptor)

25
Q

What does adrenaline do to the lungs?

A

Relaxes airway and dilates smooth muscles, higher gas exchange (beta 2)

26
Q

The drug must act on the right target and the target gives the right site for it to bind and release the drugs effect

A
27
Q

Drugs targeting enzymes can be inhibitors or substrates

A
28
Q

What is the difference between competitive and non competitive enzymes?

A

Competitive directly compete for the space in the active site

Non-competitive binds to another part of the enzyme and changes the shape of the actual active site

29
Q

What do the transporters on synapses do?

A

They recycle the neurotransmitters by putting them back into the presynaptic cleft

30
Q

What does cocaine do?

A

They block the transporters on the membrane which stops the neurotransmitters from being recycled back into the pre synaptic cleft which means more neurotransmitters bind to the receptors

31
Q

What are the key types of receptors

A

Nuclear receptor
Ligand gated ion channels
Catalytic receptors
G-protein coupled receptors

32
Q

What is an agonist in pharmacology?

A

A drug which acts on the same binding site which prompts a similar response to a neurotransmitter

33
Q

What is an antagonist in pharmacology?

A

A drug which acts on the same binding site, which stops more neurotransmitters and agonists from binding to the receptor which decreases the response

34
Q

What is affinity in pharmacology?

A

How well the drug/ligand binds to it’s receptor

35
Q

What is efficacy in pharmacology?

A

Once something is bound, it’s how well a drug/ligand activates the receptors, or how much of a conformational change there is

36
Q

What must agonists have in a pharmacological sense, to be good drugs?

A

Good affinity and efficacy

37
Q

What would make a good antagonist drug in a pharmacological way?

A

It only has good affinity, does not prompt a response from the receptor. Antagonist blocks the agonist response

38
Q

Equilibrium dissociation constant is the empirical measurement of affinity measure

A
39
Q

What dies kD defined as

A

The concentration of drug required to occupy 50% of receptors (measure of drug affinity)

40
Q

Lower kD means the drug has…

A

A stronger affinity to receptors

41
Q

10-3 milimolar 10-6 micromolar 10-9 nanomolar

A
42
Q

Potency is…

A

The strength of the biological response

43
Q

Efficacy is…

A

How well a drug can activate a receptors

44
Q

Full agonists are…

A

Agonists which produce a 100% response in a receptor

45
Q

Partial agonists are

A

Agonists which produce less than 100% response

46
Q

Non competitive agonists can be either…

A

Allo - different
Steric - Binding site

47
Q

If the antagonist is reversible and competitive, by increasing the agonist the effect of the antagonist is minimised

A
48
Q

A full agonist is when it gets a maximum response (Rmax/100%)

A
49
Q

What is occupancy?

A

The binding of an agonist/antagonist to a receptor

50
Q

Ligands are often

A

Peptides or proteins

51
Q

A drug has to be unionised because…

A

It must be neutral to pass through a plasma membrane

52
Q

The liver is the metabolic hub, but how does it help in association with the GI?

A

It acts as the area which separates bacteria, toxins, drugs and food as the GI just absorbs everything. The liver acts as the barrier. When it goes through the liver this is known as the first pass.

53
Q

Oral drug route

A

Gut -> liver -> Kidney -> site of action

54
Q

Drug metabolising enzymes in the liver include…

A

Cytochromes P450
Alcohol dehydrogenase
Esterases

The liver and the enzymes in it turn drug molecules to polar molecules so they can be excreted

55
Q

If you increase the metabolic activity of an enzyme the drug will be metabolised quicker so the drug isn’t available for as long in the body

A
56
Q

Drug metabolism is a two step process

A

Phase 1 - oxidation, reduction, hydrolysis
(NADPH + O2 required)
Phase 2 - Conjugation, adding polar groups
(OH, NH2, COOH)

57
Q

The higher the concentration of drug the higher the elimination

A
58
Q

What are the layers of the GI tract?

A

Lumen - epithelial tissue
Mucosa - thin layer epithelial tissue, secretes enzymes, mucus and hormones
Submucosa - thick layer connective tissue, has blood cells, lymphatic vessels, nerves and glands which aid in peristalsis
Circular muscle layer - blood vessels and nerves for innervation
Longitudinal muscle layer - Peristalsis (involuntary)
Serosa - thin connective tissue with blood + lymphatic vessels. Secretes serous fluid which grant lubricated sliding movement between surfaces

101 Bio (4 decks)

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