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Physiology and pharmacology > Phys and pharm 1 > Flashcards

Phys and pharm 1 Flashcards

1
Q

What is pharmacology?

A

The study of mechanisms by which drugs (biologically active compounds) affect the function of living systems

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2
Q

Define the term receptor

A

A protein that when bound to a ligand transmits a signal which turns on or off a specific biological response

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3
Q

What is an agonist?

A

A drug that binds to a receptor producing a response

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4
Q

What is an antagonist?

A

A drug that binds to a receptor and prevents the agonist from binding

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5
Q

What is a ligand?

A

A general term for a molecule which binds specifically to a receptor and thus has affinity. It may or may not have efficacy

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6
Q

Define affinity

A

A measure of how strongly something binds to a receptor

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7
Q

Define efficacy

A

A measure of the effect on some biological property

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8
Q

Define occupancy

A

The proportion of receptors occupied. (Will vary with the agonist concentration)
Occupancy = (number of receptors occupied)/(total number of receptors)

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9
Q

How can occupancy be measured directly?

A

Radioligand binding

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10
Q

What are the five steps of radioligand binding?

A

1) Prepare cells or membranes - detergent treatment and centrifugation
2) Aliquot out membranes onto filters
3) Add radiolabel at different concentrations and equilibrate
4) When equilibrated remove unbound drug by filtration (bound drug remains attached to filter)
5) Count radioactivity of filter

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11
Q

Define mass action

A

Rate of a reversible chemical reaction is proportional to the product of the concentration of the reactants

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12
Q

What is the equation for the agonist concentration required to occupy 50% of the receptors?

A

Xa = Kd where Kd is the dissociation constant and Xa is the concentration when agonist X is added

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13
Q

What is the Langmuir equation?

A

Pa = (Xa)/(Xa + Kd)

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14
Q

What is the Langmuir equation used for?

A

To fit the experimental binding data

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15
Q

How do you convert occupancy to actual values?

A

Multiply by Bmax Bound = (BmaxXa)/(Xa + Kd)

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16
Q

What does Kd give an estimate of?

A

Affinity, high Kd = low affinity and vica versa

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17
Q

Why may binding and response curves differ?

A

The response is often several steps downstream from the binding

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18
Q

What is EC50?

A

Measure of drug potency, the lower the EC50 value, the higher the potency. Concentration of agonist evoking 50% of the response

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19
Q

Define affintity

A

The probability of a drug molecule binding to a free drug receptor at any given instant

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20
Q

Define efficacy

A

The ability of a drug to evoke a response by binding to a receptor

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21
Q

Antagonism can be divided into 5 different classes, what are these?

A

1) Chemical 2) Pharmacokinetics 3) Physiological 4) Non-competitive 5) Competitive

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22
Q

What is chemical antagonism?

A

Agonist is chemically altered by antagonist

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23
Q

What is pharmacokinetic antagonism?

A

Reduction of the amount of drug absorbed by change in rate of renal excretion of agonist and/or change in drug metabolism

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24
Q

What is physiological antagonism?

A

The interaction of two drugs with opposing actions in the body

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25
Q

What is non-competitive antagonism?

A

Blocks some steps in the process between receptor activation and response. Does not compete with agonist for the receptor site

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26
Q

What is competitive antagonism?

A

Act at the level of the receptor and so compete with the agonist for occupancy of the receptor

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27
Q

Competitive antagonists can be sub divided into?

A

Reversible and irreversible

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28
Q

How does reversible competitive antagonism affect concentration response curves?

A

There is a parallel shift to the right with increasing antagonist concentration, the max is not changed

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29
Q

Define dose ratio

A

How many more times agonist is needed in the presence of an antagonist DR = [agonist in presence of antagonist]/[agonist in presence of antagonist]

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30
Q

Define pA2

A

Minus vlaue of where Schild plot crosses x axis
-log10(molar concentration of antagonist that gives a dose ratio of 2)
antagonists with high pA2 are more potent than those with low pA2 values

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31
Q

Define pharmacokinetics

A

How drugs are processed in the body

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32
Q

What are the four ways drugs are processed?

A

1) absorption 2) distribution 3) excretion 4) metabolism

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33
Q

What factors affect absorption of a drug?

A

Site/method of administration, molecular weight - affects rate of diffusion, lipid solubility - ability to cross lipid membrane by diffusion, pH and ionisation - only uncharged species can cross lipid bilayer, carrier mediated transport - active or facilitated for polar molecules

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34
Q

What are the 3 methods of excretion?

A

1) renal 2) GI 3) lung

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35
Q

What are pharmacokinetic models used for?

A

Predict time course of drug action taking into account absorption, distribution, metabolism and elimination

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36
Q

Define the term drug

A

Any compound that can modify the physiological/biological function of living organisms

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37
Q

How do ion channel blockers work?

A

Drug sits in channel to affect permeation

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38
Q

How do ion channel modulators work?

A

Drug binds to the channel protein to affect gating

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39
Q

Define false substrates

A

Drug used by enzyme to genreate abnormal product (e.g. amphetamines)

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40
Q

Define pro-drugs

A

Molecule first requires modification by enzyme before being active (cocaine)

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41
Q

What are the three main classes of cell surface receptors?

A

1) Ligand-gated ion channels 2) GPCR 3) Enzyme linked receptors

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42
Q

What is the basic structure of a GPCR?

A

Single polypeptide chain, all possess 7TM domains (a helical), ligand binding - extracellular domain or buried within TM2&3, all are glycoproteins, some may function as dimers, 3rd intracellular loop responsible for G-protein interaction

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43
Q

What is the basic structure of heteromeric G-proteins?

A

Made up of 3 subunits, alpha, beta, gamma. Couples the GPCR to an effector protein, has intrinsic GTPase activity

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44
Q

What are the five steps of GPCRs when activated?

A

1) Binding of ligand induces conformational change in receptor
2) Activated receptor binds to Ga subunit (activated ligand bound receptor acts as GEF)
3) Binding induces conformational change in Ga; bound GDP dissociates and is replaced by GTP; Ga dissociates from Gbeta gamma
4) Hormone dissociates from receptor; Ga binds to effector activating it
5) Hydrolysis of GTP to GDP causes Ga to dissociate from effector and reassociate with Gbeta gamma

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45
Q

Define second messengers

A

Small diffusible moelcules that relay signals from an effector protein to target molecules

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46
Q

What is the basic structure of receptor tyrosine kinase?

A

Extracellular ligand binding domain, transmembrane domain, intracellular tyrosine kinase domain

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47
Q

What are the 3 steps in tyrosine kinase activation?

A

1) Ligand binding 2) Dimerisation 3) Tyrosine phosphorylation

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48
Q

What do adrenoceptors do?

A

Mediate the actions of adrenaline and noradrenaline

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49
Q

Distinguish between adrenaline and noradrenaline

A

Adrenaline is a hormone released by chromaffin cells in the adrenal medulla, noradrenaline is a neurotrnasmitter released by noradrenergic neurons in the central and autonomic nervous systems

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50
Q

What do the central noradrenergic systems participate in modulating?

A

Attention, memory/learning and (sexual) arousal

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51
Q

Distinguish between sympathetic activity and parasympathetic activity

A

Sympathetic activity increases at times of stress, parasympathetic brings things back to normal

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52
Q

What are variscosities?

A

Where sympatheric axons terminally branch. They are able to release noradrenaline at the post ganglionic neuroeffector junction

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53
Q

What are the key steps in adrenergic transmission?

A

1) synthesis: NA is synthesised from tyrosine within the nerve terminal. Tyrosine is converted into DOPA and then to dopamine in the cytoplasm. Dopamine is taken up into vesicles where it is converted to NA. Adrenal medulla chromaffin cells express phenylethanolamine N-methyltransferase which converts noradrenaline to adrenaline.
2) Storage: NA terminal vesicles possess a dopamine/NA transporter that allows accumulation of noradrenaline at high concentrations inside vesicles.
3) Release: NA release is triggered by depolarisation of the nerve terminal, calcium influx and vesicle fusion with the pre-synaptic plasma membrane
4) Signal transmission: Released NA can bind to adrenoceptors
5) Signal termination: NA is rapidly removed from the synaptic cleft
6) Metabolism

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54
Q

Define asthma

A

Chronic inflammatory disease associated with smooth muscle hyperresponsiveness

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55
Q

How can difficulty breathing out during an asthma attack be measured?

A

FEV1 (forced expiratory volume in 1 second)

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56
Q

What are the two types of modern treatment for asthmatics?

A

Prophylaxis - prevent/reduce inflammation using anti-inflammatory agents, symtomatic relief - rapid reversal of bronchoconstriction

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57
Q

What is the function of the vascular system?

A

To supply oxygenated blood and nutrients to tissues and to remove waste products

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58
Q

Blood vessels have three layers, what are these?

A

Connective tissue adventitia, smooth muscle layer and endothelium

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59
Q

What is the blood-brain barrier?

A

Endothelium of the cerebral capillaries and the choroids plexus epithelium form tight junctions, drugs cannot pass between cells so must cross membrane. This is a barrier for systematic drugs, only water, CO2 and O2 enter the brain with ease

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60
Q

What is the function of the blood-brain barrier?

A

Helps maintain a constant environment around neurons

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61
Q

What are lympahtics and what do they do?

A

They act as a filter at the lymph nodes and remove foreign particles such as basteria

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62
Q

What is an Oedma?

A

Block of lymph flow

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63
Q

What is the blood pressure of a normal adult at rest?

A

120systolic/70mmHg diastolic

64
Q

What is cardiac output?

A

The volume of blood the heart pumps at a given time (Blood flow at any level of circulation)
CO = HR x SV

65
Q

What is the equation for velocity of blood flow?

A

Velocity = flow rate/cross-sectional area

66
Q

How is hypertension defined?

A

Diastolic arterial BP > 90mmHg

67
Q

What are three different voltage dependent calcium channels?

A

N-type - on neurons involved with transmitter release, T-type - in brain and heart, transient openinf, L-type - on smooth muscle, long lasting

68
Q

Distinguish between primary and secondary hypertension

A

Primary HT - no apparent cause, associated risk factors are genetic predisposition, obesity, alcohol consumption, lack of exercise, smoking
Secondary HT - renovascular disease or endocrine disease

69
Q

Name four factors that regulate blood pressure

A

1) Drugs that affect the sympathetic nervous system/muscle contraction
2) Endothelium/local regulation
3) Renin-angiotensin system
4) Changes in blood volume

70
Q

Where does the biggest drop in blood pressure occur?

A

Arterioles

71
Q

What is the function of baroreceptors?

A

Detect blood pressure in aortic arch and carotid sinus. Increase in pressure increases baroreceptor output - increased baroreceptor output leads to decreased sympathetic activity and vica versa

72
Q

Name 3 sites of action to block artery contraction

A

1) Block NA release
2) Adrenoceptor antagonist
3) Effects on calcium

73
Q

What is Reserpine and what are its effects?

A

It is an adrenergic neuron blocker that affects the storage of NA. It is taken into nerve by uptake 1, binds to storage vesicles and stops them concentrating NA so less NA is available for release.

74
Q

What is the difference between a1 adrenoceptors and a2 adrenoceptors?

A

a1 found in artery smooth muscle, agonists treatment for hypotension and shock, a2 found at nerve terminals, agonists act presynaptically to inhibit transmitter release

75
Q

Describe a-adrenoceptor activation

A

Sympathetic nerve stimulation leads to depolarisation of smooth muscle and activation of voltage dependent calcium channels. a-adrenoceptor activation couples through Gq g proteins to stimulate PLC-B and generate IP3 which releases calcium from calcium stores

76
Q

What are endothelins?

A

Family of peptides, three different types -1, 2 and 3 that cause vasoconstriction in different places. ET-1 in endothelial cells, ET-2 in kidney, ET-3 in brain, lung and adrenal gland

77
Q

What is the function of the kidney?

A

Excretion of waste products such as urea, regulation of salt and electrolyte content and the volume of extracellular fluid

78
Q

What is the renin-angiotensin system?

A

Decrease in NaCl in the filtrate is sensed by the macula densa cells of the distal tubule and stimulates renin release, the release is controlled by renal BP (increases in renal BP locally decreases renin release and vica versa). Human angiotensin is continuously synthesised and secreted by the liver. Circulating renin acts on circulating angiotensin to produce angiotensin 1 in the plasma. A1 is converted by plasma to A2 the active form.

79
Q

What are the actions of angiotensin 2?

A

Angiotensin 2 receptors can be divided in to two subtypes.
subtype 1 - predominantly in vascular and myocardial tissue
subtype 2 - found in adrenal medulla and possibly CNS

80
Q

What are diuretics?

A

Drugs that increase the rate of urine flow

81
Q

What is the basic unit of the kidney?

A

Nephron

82
Q

What makes up the nephron?

A

Glomerulus (filtering apparatus), tubular portion that reabsorbs filtrate

83
Q

What is the difference between filtrate and plasma?

A

Same but filtrate has very little protein

84
Q

What is the function of the cardiovascular system?

A

Major transport system, supplies O2, nutrients to the cells, removes CO2, waste products, regulates pH of ECF, osmotic balance and has a signalling function - hormones, immune function

85
Q

Name four cardiovascular diseases

A

1) myocardial infarction 2) angina 3) heart failure 4) arrhythmias

86
Q

What is the typical resting heart rate?

A

70 beats min^-1

87
Q

What is the typical stroke volume?

A

70ml

88
Q

What is the typical cardiac output?

A

5l min^-1

89
Q

Where does the initiation of the heart beat come from?

A

Initiated and controlled by electrical signals in the cardiac muscle cells. The electrical activity is myogenic, initiated by the muscle itself normally at the sino atrial node. Nerves modulate but do not intiate the heart beat

90
Q

What are intercalated discs?

A

They separate cardiac muscle cells. They have many gap junctions to allow electrical conduction thus action potentila spreads from cell to cell throughout the heart

91
Q

Describe the spread of electrical activity in the heart

A

SA node to atrial AP to AV node (delay) to bundle of his (conducting system) to ventricular AP (apex to base)

92
Q

One action potential spreading through the heart has five phases, describe these

A

Phase 0 - rapid depolarisation - inward Na+ current
Phase 1 - early partial repolaristaion
Phase 2 - plateau - inward Ca2+ current and outward K+ current ~ equal
Phase 3 - repolarisation - outward K+ current predominates
Phase 4 - resting potential - largely inward rectifyer K+ current, keeps potential near Ek

93
Q

Describe how calcium triggers contraction in cardiac muscle

A

Calcium binds to the protein troponin C which acts through the troponin-tropomyosin complex associated with the actin filament to allow myosin head to attach to form cross bridges, followed by cross bridge cycling and contraction

94
Q

Describe the mechanism of rise in calcium

A

Action potential travels over surface membrane and down T-tubules. Depolarisation activates L-type voltage dependent calcium channels causing calcium entry. The rise in calcium concentration activates ryanodine receptors (RyRs) to release further calcium from the sarcoplasmic reticulum, this is called calcium induced calcium release.

95
Q

Describe the baroreceptor reflex

A

Provides negative feedback control system that regulates blood pressure. An increase in aterial pressure stimulates barorecptors increasing actvity in the afferent nerves. In response, the medullary centres decrease sympathetic activity and increase parasympathetic activity. This reduces heart rate and contractility reducing cardiac output and reduces contractile tone in blood vessels to reduce peripheral resistance

96
Q

What effects do the sympathetic nerves have on the heart rate and contractility?

A

Increase in heart rate and contractility

97
Q

What effects do the parasympathetic nerves have on heart rate and contractility?

A

Decrease in heart rate and contractility

98
Q

How does sympathetic stimulation increase contractile force?

A

Increases activity of PKA which phosphorylates L type calcium channels to increase their activity. This leads to increase action potential plateau and calcium entry which leads to increases calcium release (CICR) and therefore increase in contractile force

99
Q

What effects do cardiac glycosides have on the heart?

A

Increase in intracellular calcium and contractile force, decrease in heart rate

100
Q

Define the term arryhthmia

A

Disorder of the normal cardiac rhythm

101
Q

There are two types of arrythmias, what are these?

A

Increased heart rate - tachycardia

Decreases heart rate - bradycardia

102
Q

What are the four mechanisms of arrythmias?

A

1) Re-entry
2) Delay after depolarisation
3) Abnormal pacemaker activity (normally quiescent regions of the heart begin pacemaking)
4) Heart block (damage to nodal tissue causes failure to conduct AP properly through the heart)

103
Q

Define ischaemia

A

Inadequate blood flow

104
Q

Define angina

A

Chest pain

105
Q

What are the three types of angina?

A

1) stable angina - pain on exercise, fixed coronary narrowing
2) Unstable angina - pain with increasingly less exercise than rest, formation of thrombus, high risk of MI
3) Variant angina - much rarer, spasm in coronary arteries

106
Q

How do anti-anginal drugs work?

A

Decrease cardiac workload and O2 demand and improve O2 delivery by dilating coronary arteries

107
Q

Name four anti-anginal drugs and describe their mechanisms of action

A

1) B - receptor antagonists - decrease force of contraction and heart rate and so cardiac workload, increase efficiency, decrease O2 demand
2) Organic nitrates - cause coronary artery vasodilation
3) Calcium channel blockers - block voltage gated L-type calcium channels
4) Potassium channel openers - Hyperpolarise coronary arterial smooth muscle which closes calcium channels reducing calcium entry and so causing relaxation and vasodilation

108
Q

Describe the steps leading to myocardial infarction

A

Underlying atherosclerosis - plaques in coronary arteries, plaque rupture, platelet adhesion to exposed glycoporteins, platelet activation, aggregation to form thrombus, reinforced by fibrin, blocks coronary artery

109
Q

Name four treatments for myocardial infarction and describe how they work

A

1) Nitrovasodilator - dilates collaterals to improve blood supply, reduces pain and load on heart
2) Fibrinolytic agent - dissolves clot
3) Aspirin - prevents further clot formation
4) B-adrenoceptor antagonist - reduces sympathetic drive on B-receptors, decreases cardiac work and ATP usage, decreases calcium entry, decreases likelihood of arrhythmias

110
Q

What is the endocrine system?

A

Collection of glands located throughout the body

111
Q

Define the term autocrine

A

Hormone signal acts back on the cell of origin or adjacent cells of the same type

112
Q

Define the term paracrine

A

Hormone signal acts on adjacent cell over a short distance via interstitial fluid

113
Q

Define the term Endocrine

A

Hormone signal carried to distant target cells via the bloodstream

114
Q

Define the term Neurocrine

A

Hormonal signal originates in a neurone and after axonal transport to the bloodstream is carried to distant target cells

115
Q

Hormones can be classified into two main types, what are these?

A

Water soluble - cannot diffuse through the plasma membrane (bind to cell surface receptors and activate second messengers which produce an effect)
Lipid soluble - can diffuse through the plasma membrane (Bind to specific intracellular raceptors that trnaslocate hormones to the nucleus where specific genes are activated)

116
Q

Hormone levels are determined by three factors, name these

A

1) Rate of production
2) Rate of delivery
3) Rate of degradation

117
Q

Where is the parathyroid gland located?

A

Nape of the neck

118
Q

What is the role of the parathyroid hormone?

A

Increase plasma calcium levels, decrease plasma phosphate levels

119
Q

What are the three main target organs of parathyroid hormone?

A

1) Bones - increases number and activity of osteoclasts
2) Kidneys - slows rate of calcium loss from blood to urine, increases loss of phosphate from blood to urine
3) GI tract - promotes formation of calcitrol which increases the rate of calcium and phosphate absorption from food in the GI tract into the blood

120
Q

What are osteoclasts?

A

Cells that break down bone matrix releasing calcium and phosphate into the blood

121
Q

What are octeoblasts?

A

Cells that lay down new bone

122
Q

Fast and slow exchange of calcium between bone and plasma occur, describe the mechanisms of both

A

Fast exchange - calcium is moved from the labile pool in the bone fluid into the plasma by means of PTH activated calcium pumps located in the osteocytic-osteoblastic bone membrane
Slow exchange - calcium is moved from the stable pool in the mineralised bone into the plasma by means of PTH-induced dissolution of the bone

123
Q

What is calcitonin and what does it do?

A

It is a peptide hormone produced by parafollicular cells of the parathyroid gland. It is secreted in response to GI hormones and decreases plasma calcium and phosphate levels

124
Q

What are eight processes modulated by the hypothalamus and pituitary gland?

A

Body growth, milk secretion, reproduction, lactation, adrenal gland function, thyroid gland function, water metabolism, puberty

125
Q

Describe the neurocrine function of the posterior pituitary

A

Oxytocin and antidiuretic hormone are produced by neurones in the hypothalamus and transported down nerve cell axons to the posterior pituitary where they are stored and released to general circulation to act on distant targets

126
Q

Hormones produced by nerve cells in the hypothalamus act via two neurocrine pathways, describe these

A

Direct effects on distant targets via oxytocin and antidiuretic hormone from the posterior pituitary
Hormones secreted exclusively into hypothalamic blood vessels effect endocrine cells within the anterior pituitary

127
Q

What effect do OT and ADH have on the body?

A

OT - milk let down and uterus contractions

ADH - regulation of body water volume

128
Q

Define trophic hormone

A

Hormone that controls the release of another hormone in a target tissue

129
Q

What is necrosis?

A

Cell death by damage

130
Q

What is atrophy?

A

Decrease in cell size and number

131
Q

What is hyperplasia?

A

Increase in cell number

132
Q

What is hypertrophy?

A

Increase in cell size

133
Q

What is apoptosis?

A

Programmed cell death

134
Q

GH secretion is regulated by long loop and short loop negative feedback mechanisms, describe these

A

Long loop - inhibit release of GHRH and action of GHRH in the anterior pituitary, stimulates the release of somatostatin
Short loop - mediated by GH via stimulation of somatostatin release

135
Q

GH deficiency in children results in…

A

Pituitary dwarfism

136
Q

What does GH excess in children and adults result in?

A

Children - gigantism

Adults - acromegaly (large extremitites)

137
Q

What is the basic structure of the thyroid gland and where is it?

A

It is made up of two lobes joined by isthmus, it is bow tie shape and location

138
Q

What is TSH?

A

Thyroid stimulating hormone which is a glycoprotein hormone composed of two non-covalently bound subunits (alpha and beta)
(the alpha subunit is also present in FSH and LH) and is the trigger for thyroid hormone release

139
Q

Define the term exocrine

A

Relating to a gland that secretes outwardly through a duct or ducts to the outside e.g. the gut

140
Q

The pancreas is made up of both endocrine and exocrine cells, what are the function of these cells?

A

Endocrine - arranged in clusters called Islets of Langerhans and synthesise and secrete hormones into the blood via the pancreatic vein
Exocrine - secrete pancreatic juice into the pancreatic duct

141
Q

In the Islets of Langerhans, what are the different cells and their functions?

A 
a cells secrete glucagon
B cells secrete insulin
gamma cells secrete somatostatin
epsilon cells secrete ghrelin
PP cells secrete pancreatic polypeptide
142
Q

What is the function of insulin?

A

To reduce blood-sugar levels

143
Q

What is the function of glucagon?

A

To increase blodd-sugar levels

144
Q

What are the hypoglycaemic actions of insulin in the liver?

A

Activates: glycogenesis, lipogenesis
Inhibits: glycogenolysis, gluconeogenesis, lipolysis

145
Q

What are the hypoglycaemic actions of insulin in the muscle?

A

Activates: glucose transport, lipogenesis, glycogenesis, protein synthesis, AA transport
Inhibits: lipolysis, protein catabolism

146
Q

What are the hypoglycaemic actions of insulin in the adipose tissue?

A

Activates: glucose transport, lipogenesis
Inhibits: lipolysis

147
Q

Define diabetes

A

Characterised by chronically raised blood-glucose concentration due to lack of the hormone insulin and/or deficiency in insulin action

148
Q

Distinguish between type 1 and 2 diabetes

A

Type 1 - presents in childhood, autoimmune disease caused by loss of beta cells (genetic, environmental)
Type 2 - presents in middle age, insulin deficiency due to beta cell dysfunction

149
Q

How is diabetes diagnosed?

A

OGTT (oral glucose tolerance test) - overnight fast, following morning measure plasma glucose concentration, 75g glucose consumed, measure blood glucose after 2 hours
Diabetic - fasting level >7mmol/l
Diabetic - glucose plasma level exceeds 11.1mmol/l after 2 hours

150
Q

How is type 1 diabetes managed?

A

Insulin injections, islet transplantation

151
Q

How is type 2 diabetes measured?

A

Exercise, diet, oral hypoglycaemic drugs, insulin injections

152
Q

How do oral hypoglycaemic drugs work?

A

Increase insulin secretion and sensitivity, decrease glucose absorption

153
Q

What are the male sex hormones?

A

Androgens - testosterone, DHEA

154
Q

What are the female sex hormones?

A

Estrogens - estradiol

155
Q

What are the functions of sertoli cells?

A

Blood-testes barrier, provide nutrients to the developing germ cells, produces seminal fluid, produces androgen binding protein which binds to testosterone

156
Q

The pituitary gland and hypothalamus are physically connected since the hypothalamus drops down through a structure known as the?

A

Infundibulum

Physiology and pharmacology (1 decks)

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