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Year 1 Intro to Pharmacology and Physiology > ANS clinical cases > Flashcards

ANS clinical cases Flashcards

1
Q

What is asthma?

A

Long term inflammatory disorder of the lungs in which the air ways are hypersensitive and thus can undergo variable, revisable airflow obstructions.

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2
Q

List Asthma triggers.

A 
Infection 
Allergen 
Air pollution 
Cold Air
Exercise
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3
Q

What is the pathophysiology of asthma?

A

Eosinophils accumulate in bronchial smooth muscle. Mucosal oedema follows.
Cytotoxic mediators damage epithelium.
Sensory nerves exposes- hyper responsive bronchial smooth muscle.
Smoot muscle spasms- airway narrows.
Hyper secretion of mucous from inflammation.

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4
Q

What are the symptoms of asthma?

A 
Wheeze
Nocturnal cough 
Chronic cough 
Chest tightness 
Acute attacks of dyspnea
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5
Q

What is the predominant ANS stimuli to humans airways?

A

Parasympathetic

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6
Q

What do M3 receptor stimulation in respiratory smooth muscle cause?

A

Bronchoconstriction

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7
Q

What adrenoreceptor type is found abundantly in lung tissue?

A

beta 2 receptors

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8
Q

What is the arrangement of beta 2 receptor in lung smooth muscle?

A

As are way diameter gets smaller the density of bet 2 receptors gets higher

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9
Q

What physiologically activates beta 2 receptors?

A

circulating NA and Adrenaline

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10
Q

Bronchodilation is caused by stimulation of what receptor in the lungs?

A

beta 2 adreno-receptor

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11
Q

What GPCR is a beta-adrenoreceptor and how does it cause bronchodilation?

A

Gs type, activates adenylyl cyclase
catalases ATP–> cAMP
aAMP binds PKA and allows it to phosphorylate
The phosphyrlation decreases calcium influx into cell from SER and ECM.
Less intracellular calcium means less interaction between actin and myosin.

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12
Q

What are the three subclassed of bronchodilators used to relieve asthma?

A

Beta2 agonist s
Anti-cholinergics
Xantines

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13
Q

Glucocorticoids, Leukotriene receptor antagonsist and inhibitors of mediator release are …….. and can be used to prevent ….

A

anti-inflammatorys

asthma

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14
Q

How do glucocorticoids work as anti-inflammatories?

A

Down regulate the genes involved in the inflammatory response and thus suppress the immune system.

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15
Q

Why are adrenoreceptor agonist generally better than antimuscarinics for treating asthma?

A

The adrenoreceptor agonist will cause bronchodilation irrespective of the cause.
Anti-muscarincs can only dampen parasympathetic control- which often isn’t the primary cause of an asthma attack.

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16
Q

What effect does stimulation of beta 1 receptors have?

A

Heart increases chronotropy and isotropy

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17
Q

Where do you find alpha 1 receptors and what receptor type are they?

A

Vascular smooth muscle

Gq type

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18
Q

What effect does sympathetic innervation have on the kidney?

A

Renin released

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19
Q

Sympathetic innervation of smooth muscle has what effect on TPR?

A

Increases

20
Q

Outline the RAAS.

A

Renin released from kidney. Renin converts angiotensinogen to angiotensin I.

ACE is made in the lung epithelia and convert angiotensin 1 to angiotensin II. Angiotensin II is a vasoconstrictor.

The adrenal cortex is stimulated by angiotensin II to make aldosterone a mineralocorticoid. This causes increase sodium reabsorption in the kidney. Water follows sodium so you retain water which increases blood volume.

Net effect: Increase TPR, Increase blood volume = increase arterial BP

21
Q

Above what BP is someone considered hypertensive?

A

140/90

22
Q

What percentage of hypertension is referred to as primary or essential?

A

95%

23
Q

What rare conditions cause secondary HTN?

A

Conns or phaeochromocytoma

24
Q

Which organ failing could cause HTN?

A

Kidney

25
Q

How do calcium channel blockers work to reduce BP?

A

Internal stores of calcium not released in smooth muscle. Calcium cannot bind actin myosin so reduced contraction and less vaso-constriction.

26
Q

Which ion is principally reabsorbed when a diuretic is used?

A

Sodium

27
Q

What is the action of beta adreno-receptor antagonists on cardiac out put?

A

Reduced CO because of reduced heart rate and reduced force of contraction

28
Q

What effect do beta blockers have on the kidney?

A

Inhibit renin release and so stop the RAAS system

29
Q

Alpha adrenoreceptor antagonists are sometimes used to treat hypertension, outline their mechanism of action.

A

Vasodilation

Reduced TPR - reduced arterial BP

30
Q

What patient group with primary HTN is given ACE inhibitors first line rather than a calcium channel blocker?

A

Under 55s

31
Q

The prominent adrenoreceptor in vascular smooth muscle is alpha 1 but what other subtype can be seen?

A

Beta 2

32
Q

List side effects of adreno-receptor antagonist in treating HTN

A

Postural hypotension
Impotence
Diarrhoea
Arrhythmia

33
Q

List side effects of beta adreno-receptor antagonists

A

Bronchoconstriction is asthmatics
Cardiac failure in CHD patients
Bradycardia
Fatigue (lower CO and higher TPR when muscles need more O2)
Hypoglycaemia (Beta blockers inhibit bodies ability to sense a hypo)
Impotence

34
Q

Why does hypertension treatment have poor compliance?

A

HTN is asymptomatic generally.

Treatments carry side effects

35
Q

What is thyrotoxicosis?

A

High levels of thyroid hormone in the blood.

36
Q

What is thyroxine also known as?

A

T4

37
Q

What stimulates the thyroid gland?

A

TSH from the ant pituitary

38
Q

What is released from the hypothalamus to tell the ant pituitary to release TSH?

A

Thryrotropin releasing hormone

39
Q

What stimulates TRH release?

A

Low T3 or T4

40
Q

High T3 and T4 inhibit release of …. and …. from …. and ….. respectively

A

TRH from hypothalamus

TSH from ant pituitary

41
Q

What are the symptoms of thyrotoxicosis?

A 
Sweating 
Intolerance to heat 
Anxiety 
Tachycardia 
Diarrhoea
Amenorrhea 
Tiredness
Irratibility 
Weight loss
Increased appetite
42
Q

What symptoms distinguish anxiety from thryortoxicosis?

A

Goitre and proptosis in thyrotoxicosis
Increase appetite and weight loss not associated with anxiety
Vasodilation in thyrotoxicoses - they are warm and sweaty. Vasoconstriction in anxiety- they are cold and clammy.

43
Q

What do thyroid hormones do to adrenoreceptors?

A

up regulate their presentation

44
Q

How do you treat thyrotoxicosis?

A

Non specific beta blocker - propranolol (IV)

45
Q

How do you treat thyrotoxicosis?

A

Non specific beta blocker - propranolol (IV)

Iodide blocks T3 and T4 release and stops T4 conversion to T3.

Thiomides inhibit Thyroid hormone synthesis. Inhibit iodination of TH.

46
Q

If at 18 months of hyperthyroidism medication it hasn’t settled, what long term treatments may be considered?

A

COntinuing Thiomides
Radio iodine treatment
Surgery to remove the thyroid- long term TH medication needed

Year 1 Intro to Pharmacology and Physiology (8 decks)

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