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4BBY1040 > Muscles and Organs > Flashcards

Muscles and Organs Flashcards

L15 L16 L17 L18 L21

1
Q

What are some smooth muscle containing organs?

A

Blood vessels (contorls blood flow and pressure)
GI tract (controls mixing and propulsion of GI contents)
Bladder (Controls uninattion)
Uterus (Responisble for labour)
Respiratory system (Controls diameter of airways)
Corpus cavernosum and Vas deferens (controls ejactuation and erections)
Iris (Controls pupil diameter)

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2
Q

What drugs affect the smooth muscles of the cardiovasulcar system?

A

Vasodilators

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3
Q

What drugs affect the smooth muscles of the GI system?

A

Spasmolytics (anti-muscarinic)

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4
Q

What drugs affect the smooth muscles of the Genitourinary system?

A

Anti-muscarinic and Beta3 agonists to treat lower urinary tract symptoms
PDE inhibitors for erectile dysfunction

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5
Q

What drugs affect the smooth muscles of the respiratory system?

A

Bronchodilators

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6
Q

What are the mechanisms for drugs affecting smooth muscle function?

A

Drugs block or stimulate receptors
or
Drugs act on smooth muscle cell signal transduction

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7
Q

How are smooth muscles stimulated?

A

Calmodulin can bind to up to 4 Ca2+ ions. When [Ca2+] in smooth muscle increases, Ca2+ binds to calmodulin, which then binds to myosin light chain kinase to form an active complex.
The complex phosphorylated myosin, which automatically begins the cross bridge cycle to cause contraction.

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8
Q

What relaxes smooth muscles?

A

Myosin phosphatase activation dephosphorylates myosin which because contraction to cease.

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9
Q

What does rho kinase do to smooth muscle?

A

Inhibits myosin phosphatase which causes Ca2+ sensitisation to promote contraction of smooth muscle

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10
Q

What does NO do to smooth muscles?

A

Actuvates myosin phosphatase to cause Ca2+ desensitisations to promote relaxation of smooth muscle.

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11
Q

What is used to treat hypertension?

+why does this treatment work?

A

Vasodilators
Hypertension is high blood pressure, BP = TR x CO —> so if you decrease TPR by dilating the blood vessels, BP will decrease.

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12
Q

What is stable angina and how is it treated?

A

Pain in the chest during exercise/stress sue to insufficient coronary circulation.
Venodilation or arteriolar dilation. Surgery could also be used to open up arteries

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13
Q

What is vasospastic angina and how is it treated?

A

Coronary artery spasm which causes insufficient blood flow to heart.
Arterial/ arteriolar dilatation. Surgery could also be used to open up arteries

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14
Q

How does [Ca2+] for smooth muscle increase?

A

Noradrenaline/angiotensin II bind to external receptor.
This activates phospholipase C to catalyze PIP2 –> DAG + IP3.
IP3 causes sarcoplasmic reticulum to release Ca2+ (1) and DAG activates receptor gated channel to allow Na+ and Ca2+ (2) to enter the cell via electrochemical gradient.
The influx of Na+ cause depolarisation, which opens voltage gated channel to allow Ca2+ (3) to enter cell. The voltage gated channel is the main cause of [Ca2+] increase.

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15
Q

What releases NO?

A 
Bradykinin
ATP
Histamine
H+
CO2
ACh
Also released by blood flow...
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16
Q

What does NO actually do to smooth muscle?

A

NO activates guanylate cyclase (GC). GC catalyses GTP–> cGMP
cGMP activates protein kinase G (PKG)
PKG causes K+ to be pumped out of the cell to cause membrane hyperpolarisation, which block voltage gated channels.
PKG causes Ca2+ to be pumped back into the sarcoplasmic reticulum and back out of the cellout of the cell.
PKG also causes Ca2+ desensitisation

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17
Q

How is cGMP regulated?

A

Phosphodiesterase (PDE) regulates cGMP

cGMP–> GMP

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18
Q

What activates the renin-angiotensin-aldosterone system?

A

A fall in blood volume, fall in blood Na+ or fall in blood pressure

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19
Q

What is the renin-angiotensin-aldosterone system?

A

Renin is released and bind to angiotensin molecule to form angiotensin I.
Angiotensin converting enzyme converts angiotensin I to Angiotensin II utilising bradykinin.

Angiotensin II is responsible for ADH increase, vasoconstriction, and aldosterone release.

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20
Q

What do ACE inhibitors do?

A

Block production of angiotensin II and inhibit bradykinin breakdown.
Reduced blood pressure, via vasodilation.

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21
Q

What are ARBs?

A

Angiotensin receptor blockers.

ARBs don’t affect bradykinin metabolism, and reduce blood pressure via vasodilation

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22
Q

What are CCBs and what are some examples?

A

Calcium channel blockers
Treats hypertension and angina.

Amlodipine (acts only on blood vessels) inhibits constriction of arterioles by blocking voltage gated Ca2+ channels, causing vasodilation.
Verapamil (acts on heart) reduces heart rate and contractile force by blocking voltage gated Ca2+ channels.

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23
Q

What is minoxidil?

A

K+ channel opener, which causes vadodilation

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24
Q

What is nicorandil?

A

K+ channel opener and a cGMP stimulator, which both cause vasodilation.

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25
Q

What do organic nitrates do to blood vessels?

A

‘a pharmacological endothelium’

An NO group is removed to cause the same effects on the blood vessels as NO –> vasodilation

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26
Q

What is the corpus cavernosum?

A

Network of blood vessels within the penis. When filled, erection occurs.

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27
Q

What does sildenafil do?

A

Blocks PDE5, which means theres more cGMP.
Erection of the penis is stronger/ lasts longer.
Can also treat pulmonary hypertnsion.

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28
Q

What does the pelvic nerve of the urinary tract do?

A

Releases ACh to contract detrusor and releases NO to relax the urethra.
Switches on to cause urination.

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29
Q

What does the hypogastric nerve of the urinary tract do?

A

Releases NA to relax the detrusor via B3 receptor and constricts urethra via a1 receptors.
Keeps bladder relaxed to allow it to fill up when switched on.

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30
Q

What does the pudendal nerve of the urinary tract do?

A

Releases ACh to constrict the external urethral sphincter via nicotinic receptors.
This is a somatic input and switches off to allow urination

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31
Q

What is myocardial infarction?

A

Heart attack due to coronary thrombosis

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32
Q

What are arrhythmias?

A

Lack of normal heart rhythm, leading to a fall in cardiac output

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33
Q

What is heart failure?

A

Insufficient cardiac output to meet body’s needs.

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34
Q

What effect does anticholinesterases have on the heart and why?

A

Slows the heart rate because cholinesterases are inhibited, increasing [ACh]. ACh slows the heart rate down (via the parasympathetic NS).

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35
Q

What is ivabradine?

A

Inhibits the funny current in SA node.

Slows heart rate independently of ACh or the parasympathetic nervous system.

36
Q

Describe how the parasympathetic NS works on the heart.

A

ACh is the neurotransmitter that acts on M2 muscarinic receptors at the SA node.
ACh released from vagus nerve to decrease heart rate by hyperpolarising the cardiac cells.
Does no effect the contractile force.

37
Q

Describe how the sympathetic NS works on the heart.

A

Noradrenaline is the neurotransmitter that acts on B1-adrenoreceptors on heart muscle cells.
Increases both heart rate and contractile force (and therefore increases cardiac output)

38
Q

How does B1-adrenorecptor stimulation lead to increased heart rate?

A

When a B1-agonist binds to the B1-adrenoreceptors in the cardiac cells, protein kinase A is produced (via G-protein pathway), and the production of PKA causes altered function of proteins (via protein phosphorylation).

This includes the proteins responsible for the funny current. There is faster decay of the funny current which increases heart rate.

39
Q

How does B1-adrenorecptor stimulation lead to increased heart contractile force?

A

When a B1-agonist binds to the B1-adrenoreceptors in the cardiac cells, protein kinase A is produced (via G-protein pathway), and the production of PKA causes altered function of proteins (via protein phosphorylation).

This includes the voltaged gated Ca2+ channels, which causes more Ca2+ to enter. Additionally more Ca2+ is taken up into the SR (due to Ca2+-induced Ca2+ release) and more Ca2+ is released from the SR. All of these factors increase how much Ca2+ bind to tropinin which increases contractile force.

40
Q

What does isoprenaline do to the heart?

A

Acts on the B1- and B2- receptors to increase heart rate and contractile force, so cardiac output overall.

41
Q

What does dobutamine do to the heart?

A

Acts on B1-receptors to increase the contractile force of the heart in patients with acute heart failure.

42
Q

What do B-blockers so?

A

Block the effects of sympathetic system on the heart.
Decrease heart rate and contractile force, especially during exercise, decreases arterial blood pressure, decreases cardiac work + O2 demand.

Propranolol is a non-selective B-blocker and bisoprolol is a B1-selective B-blocker

43
Q

What are cardiac glycosides?

What are some examples?

A

They are positively inotropic drugs.

Ouabain, foxgloves and digoxin.

44
Q

What is the mechanism of cardiac glycosides?

A

They decrease Na+ gradient by blocking Na/K ATPase pump PARTIALLY.
The increased [Na+] in cell, less Ca2+ pump is pumped out via Na/Ca exchanger, so there is more Ca2+, more Ca2+ is taken up into SR, more Ca2+ is released SR.

45
Q

What does ranolazine do?

A

The ‘late Na+ current’ causes Na+ to continue to enter the cell, even during contraction, which causes [Na+]i to increase, which causes [Ca2+]i to increase.
This causes diastolic stiffness, which reduces filling of heart during diastole and reduces contraction force, both of which increase cardiac work.
Ranolazine inhibits ‘late Na+ current’.

46
Q

What do anriarrhythmic drugs do?

A

Decrease excitability if tissue, so theres less of a chance that action potentials will be generated to the rest of the heart
or
prolong action potential and therefore refractory period so high frequency action potentials are less likely

47
Q

What is the Vaughan Williams classification for antiarrhythmic drugs?

A

Class I: Interfere with Na+ channels
Class II: B-Blockers
Class III: Block K+ channels
Class IV: Block L-type Ca2+ channels

48
Q

What do class I antiarrhythmic drugs do? Give an example of one

A

Block Na+ channel so reduce excitability in cardiac muscles, not SA or AV nodes
Lidocaine

49
Q

What do class II antiarrhythmic drugs do? Give an example of one

A

B-Blcokers, so reduce arrythmias due to sympathetic over-activity
Metoprolol

50
Q

What do class III antiarrhythmic drugs do? Give an example of one

A

Block repolarising K+ channel, so prolongs action potential and therefore refractory period
Amiodarone

51
Q

What do class IV antiarrhythmic drugs do? Give an example of one

A

Blocks L-type Ca2+ channel, so reduce excitability of SA and AV nodes
Verapamil

52
Q

What is atherosclerosis?

A

The build up of plaque in the arteries underneath the endothelium, which narrows the artery.

Macrophages go into the walls of arteries (from inflammation), forming fatty streaks, which if continual, causes atheroscelerotic plaque.

53
Q

What is angina?

A

Temporary squeezing/crushing sensation or pain in the chest.

54
Q

What is asthma?

What causes it?

A

Disease of the airways, associated with the conducting zone (trachea, bronchi, bronchioles).
Symptoms are induced by allergen cross-linking with the receptors of (mast cells) which cause the cell to release inflammatory mediators (such as histamines, prostaglandins, leukotrienes and cytokines) which causes bronchoconstriction and oedema.

55
Q

What are some anti-inflammatory agents?

A 
Glucocorticosteroids
 Xanthines
Cromones
Leukotriene antagonists
Anti-IgE (Omalizumab)
56
Q

How do B2 agonists work to treat asthma?

A

B2 agonists activate adenylyl cylase which causes ATP to be converted to cAMP. CAMP activates protein kinase A which converts MLCK to phosphorylated MLCK, which causes cell relaxation. This relaxes the airways of an asthma patient

57
Q

What are some B2 agonist examples?

A

Short acting B2 agonists (SABA):
salbutamol, terbutaline, fenoterol

Long acting B2 agonists (LABA):
Saltmererol, formoterol, indacaterol

58
Q

What are the side effects of B2 agonists?

A

Some of the drugs (from inhalers) will enter orally. If the inhaler isnt taken properly;
tremors
increased heart rate
hypokalemia

59
Q

How do muscarinic antagonists work to treat asthma?

A

Inhibiting the post synaptic M3 receptor.
This prevents the smooth muscle contraction and mucus secretion is induced by activation of parasympatheitc nerves.
This relaxes the bronchioles as treats asthma.

60
Q

What are the side effects of using muscarinic antagonists when treating asthma?

A

Not necessarily related to just asthma treatment, but any treatment involving muscarinic antagonists.
Side effects: dry mouth mainly

61
Q

What do glucocortisteroids do?

A

Inhibit leukotriene and cytokine synthesis/release.
They inhibit recruitement of inflammatory cells
Anti-oedema
Increases beta-adrenoceptor function

62
Q

Glucocorticosteroids side effects.

A

Inhaled route:
Fungal infection
Hoarseness, coughing, voice problems

Prolonged high dose/ oral:
Growth retardation
Osteoporosis
Diabetes, weight gain
Water retention, hypertension
63
Q

How do Xanthines work to treat asthma?

A

Relaxes smooth muscle airways through cyclic AMP pathway. They inhibit PDE (which converts cAMP to AMP), which increase cellular cAMP on cell which allows more phosphorylated MLCK to be in the cell.

64
Q

What are some examples of xanthines?

A

Theophylline, Aminophylline and caffine (although this does not have any clincal applications)

65
Q

What are the side effects of xanthines?

A 
Nausea
Vomiting
Arrhythmias
Hypokalemia, 
Hypotension
Seizures
66
Q

What are cromores?

What are some examples?

A

Mast cell stabilisers that reduce inflammatory cell activation and recruitment. Not very effective though.

Sodium Cromoglicate and Nedocromil sodium

67
Q

What does Omalizumab do?

A

Binds to free IgE antibodies to decrease cell-bound IgE. Less IgE is then available to activate immunoglobulin which reduces the allergic inflammation.

Its expensive

68
Q

Glucocorticosteroids mechanisms for asthma treatment.

A

The steroid allows binds to HSP90 protein, and the protein steroid complex dissociates within the cell. The steroid and its receptor engage with the gene in the nucleus. This causes repression of NFkB and AP-1 which are inflammatory genes. This reduces the production of inflammatory proteins.

They can also activate proteins involved in anti-inflammatory.

69
Q

How do diuretics treat hypertension?

A

Diuretics reduce blood volume and cardiac output. They also dilate arteries.

70
Q

How do diuretics work?

A

Inhibits the reabsorption of sodium, which inhibits the reabsorption of water which increases the volume excretes via the urine

71
Q

Which diuretic affects the Loop of Henle?

A

Loop diuretics/ high ceiling diuretics.

72
Q

Which diuretic affects the distal tubule?

A

Thiazide diuretics

73
Q

What diuretics affects the collecting tubules?

A

K+ sparing diuretics

74
Q

Which diuretics affects the Proxiaml tubules?

A

No diuretics affect eh proximal tubule

75
Q

What is the mechanism of high ceiling diuretics?

Give some examples of theses diuretics.

A

Block of the Na+, K+, 2Cl- co-transporter in the thick ascending loop of Henle. Strongly inhibits Na+ reabsorption.

76
Q

What is the mechanism of thiazide-type diuretics?

Give some examples of theses diuretics.

A

Block Na+, Cl- co-transport in the distal convoluted tubule, reduce plasma volume, venous return, cardiac output

77
Q

What is the mechanism of K+ sparing diuretics?

Give some examples of theses diuretics.

A

The diuretics inhibit Na+ uptake and K+ secretion in the collecting tubule, which reduces the loss of K+ from the body.

78
Q

What are side effects of high ceiling diuretics?

A 
Hypokalaemia (low plasma K+)
Metabolic alkalosis
Depletion of plasma Ca2+ and Mg2+
Hypovolaemia
Ototoxicity (deafness, tinnitus, dizziness) can occur if concommitent use of aminoglycoside antibacterial
79
Q

What is the hierarchy of power for the diuretics?

A

Loop diuretics
Thiazide diuretics
K+ sparing diuretics

80
Q

What is thiazide-type diuretics effect of TPR?

A

There is a fall in blood pressure.
Initially the the CO falls, but after a few weeks it returns to normal output.
The TPR decreases, then returns to normal after a short amount of weeks, then gradually decreases over the course of many weeks. This causes the fall in BP

81
Q

What are side effects of K+ sparing diuretics?

A

Hyperkalemia

These drugs aren’t administered alone though, so a bad degree of hyperkalemia doesn’t usually occur.

82
Q

What is spironolactone?

A

It is an aldosterone antagonist. It is used to counteract high aldosterone levels in the body (hyperaldosteronism)

83
Q

Name two ENaC blockers?

A

Amiloride and Triamterene

84
Q

What do ENaC blockers do to the kidneys?

A

Block collecting tubule ENaC to block Na+ reabsorption and K+ secretion.

85
Q

What are the two types of K+ sparing diuretics?

A

Aldosterone receptor antagonists and ENaC blockers

86
Q

Why are K+ sparing diuretics used with other types of diuretics?

A

Thiazide or loop diuretics cause hypokalemia because they work by causing Na+ resorption. The channel that the diuretic works on causes K+ to be released into the ultrafiltrate.

K+ sparing diuretics block K+ from being released into the ultrafiltrate, so normokalemia occurs, as well as diuresis.

4BBY1040 (6 decks)

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