Past paper learning Flashcards

1
Q

Causes of hypothyroidism

A

Autoimmune

Post surgery or drugs such as amiodarone

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2
Q

Autoimmune hypothyroidism and antibody involved

A

Hashimotos

Anti thyroperoxidase

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3
Q

Phases of addisonian crisis

A

Vomiting and diarrorhoea
Decreased consciousness and collapse
Cardiac arrest

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4
Q

Clinical features addisonian crisis

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

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5
Q

Why are there no anti-aggregatory effects in other NSAIDS to aspirin

A

They inhibit COX 2

Aspirin binds covalently irreversibly

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6
Q

Why isnt paracetamol a NSAID

A

Has no anti-inflammatory effects

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7
Q

Paracetamol OD

A
  • Paracetamol forms the electrophile NAPQI, which is removed by glutathione conjugation, which is inactive.
  • Paracetamol overdose – too much NAPQI, therefore binding to -SH groups on hepatocyte enzymes, leading to enzyme failure and thus liver failure
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8
Q

3 ways beta blockers reduce BP

A
  • Decrease CO – by decrease HR and contractility
  • Decrease renin release therefore less angiotensin II formed, therefore less vasoconstriction via AT1 receptor
  • Block presynaptic B1 therefore decreasing NA release from presynaptic neurone
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9
Q

How do pre junctional beta adrenoceptors lead to reduced TPR

A

Vasodilation at andrenoceptors in peripheral vasculature

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10
Q

In angina how do beta blockers reduce myocardial oxygen demand

A

Decrease heart rate and contractility
Decrease venous return therefore decrease preload – due to less venous constriction
Less TPR therefore causing decreased afterload

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11
Q

How and where do cholinomimetics control glaucoma

A

At the short ciliary ganglion to cause pupil constriction therefore increased drainage – increased angle between the cornea and iris

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12
Q

How do beta antagonists control glaucoma

A

on ciliary bodies to decrease carbonic anhydrase activity therefore decrease aqueous humour production

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13
Q

How are anticholinesterases a problem at NMJ

A

Cause increase Ach which leads to depolarising block, causing the muscle to be unable to contract

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14
Q

2 drugs with a low therapeutic windown

A

Warfarin

Phenylbarbitol

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15
Q

Difference in where parkinson drugs act

A

i) Carbidopa – Peripheral – acts on DOPA decarboxylase
ii) Entacapone – COMT inhibitor. Acts centrally and peripherally
iii) Domperidone – Dopamine receptor antagonist – more central
iv) Bromocriptine – Ergot derivative Dopamine D2 receptor antagonist - central

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16
Q

How does selegiline cause hallucinations

A

Affects mesolimbic pathway

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17
Q

How does chlorpromazine cause breast enlargement

A

Hyperprolactinaemia due to decreased activity of the tuberoinfundibular pathway therefore less inihibtion of prolactorophs to release prolactin

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18
Q

Enzyme responsible for various metabolism rates of Isonizad

A

Acetyl transferase

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19
Q

Why does do peoples metabolism of fat vary

A

Polymorphism in acetyl transferase

Liver damage

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20
Q

How to prevent overdose of oral anti-anticoagulant

A
  • Give fresh frozen plasma/cryoprecipitate to increase factor concentration
  • Stop taking the drug
  • Supplement vit K, especially if warfarin
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21
Q

D2 antagonist extre-pyramidal side effects

A

Jerky movements

Torticollis

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22
Q

Problems with azothioprine metabolism

A
  • Xanthine oxidase normally metabolises azathioprine into 6-TU which is inactive
  • If treating gout with allopurinol, this blocks xanthine oxidase activity, causing the azathioprine to be metabolised into 6-MeMP (cause hepatotoxicity) and 6-thioguanine (cause myelosuppression)
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23
Q

What do excipients do

A

• Increase the chemical and physical stability of the drug, thus increasing the acceptability for the patient

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24
Q

d) How do anticholinesterases lead to respiratory depression? Explain in terms of its effects on the CNS, the lungs, and voluntary muscles

A
  • CNS: increase levels of Ach in synapses, thus increase the activity of parasympathetic outflow – increased impact of post-ganglionic transmission. Also caused increased sweating and increase secretions. The increased secretions would result in the size of the lumen decreasing leading to less air reaching the lungs
  • Lungs – binds to M3 receptors to cause bronchial smooth muscle to constrict. This would lead to less air traveling through the lungs, with less air reaching the bloodstream, thus causing respiratory depression
  • Voluntary muscle – cause contraction and possibly resulting in a depolarising block, causing decreased activity. This would decrease respiratory muscle activity causing less air to reach the lungs
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25
Q

Alcohol leading to hepatitis

A

During metabolism it produces oxygen free radicals, which damage mitochondria and result in inflammation

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26
Q

How does GABA work

A

GABA receptor protein on the GABA-A receptor, which causes benzodiazepine and GABA receptor proteins to be linked by the GABA modulin protein, causing opening of the chloride channel

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27
Q

Benzodiazpeine used today

A

Diazepam

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28
Q

Uses of diazepam

A

• Used to treat Status Epilepticus
• Anxiolytic
Anti convulsant

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29
Q

How do you reverse the effects of benzodiazepines

A

Competitive receptor

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30
Q

Drugs interacting with benzodiazepines

A

Barbiturates

Alcohol

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31
Q

Man comes in with bacterial infection after MI

A

ECG

Sepsis screening

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32
Q

what is a rebound reaction

A

A condition where the pathology returns after removal of treatment, to a worse degree than before treatment. E.g. clonidine and hypertension

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33
Q

Who is in charge of yellow card scheme

A

MHRA (Medical Healthcare Products Regulatory Agency)

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34
Q

Best anti-hypertensive drug used for diabetics

A

ACE inhibitors

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35
Q

Clopidogrel MOA

A

P2Y12 receptor antagonist, which are found on platelet surface. Prevents ADP binding, thus preventing platelet activation and aggregation

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36
Q

Why is GTN given sublingually

A

Increase systemic absorption

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37
Q

Why are Benzodiazepines better than barbiturates

A

Larger window of safety
Less potent withdrawal effect
Mild effect on REM sleep
Doesn’t induce liver microsomal enzyme

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38
Q

MOA flumezanil

A

Competitive benzodiazepine receptor protein antagonist so prevent benzodiazepine from bind and having a subsequent effect

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39
Q

Drugs with anxiolytic effects

A
TCA
SSRI
Antipsychotics
Antiepileptic
Propranolol (symptom treatment)
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40
Q

4 routes of administration and their speed of action

A
  • Smoke – absorbed through the mucosal membrane of the nose. Relatively fast speed of onset, but would still slightly longer to have an effect on the brain as it needs to pass through the mucosal layer and then through the venous system before it can enter the arterial system to reach the brain
  • Orally – absorbed through the GI tract. Very slow onset as absorption would take a while, and there would be hepatic first pass metabolism which would decrease the concentration available to have an effect and thus it would take longer for an effect to occur
  • IV – injected straight into the venous system. Speed of onset would be very fast, but not the fastest to reach the brain, as it would need to pass through the venous system, and then enter the arterial system before it reaches the brain
  • Inhaled – via the alveoli of the lungs. Causes fastest onset of action for most drugs as it returns directly to the heart via the pulmonary vein before entering the systemic arterial circulation in order to reach the brain and have an effect
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41
Q

Reason for long half life of cannabis

A
  • Cannabinoids are stores in poorly vascularised tissue and fat, and thus the cannabinoids would not easily be removed from the tissue, leading to the cannabis having a long half-life
  • Cannabis is excreted mainly in the bile. However, in the GI tract it may be reabsorbed and thus this would allow it to re-enter circulation, thus prolonging its clearance from the body. This is known as enterohepatic cycling
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42
Q

What to consider before administering antiepileptics

A
  • Type of seizure which they are having – is it partial or general and subtype of these categories
  • Other medication which they may be on which may interact with the medication
  • Duration and frequency of the seizures
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43
Q

MOA phenytoin

A

Phenytoin (not a drug which we have covered) acts on the VGSC to either inactivate them or to keep them in the inactive phase for longer

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44
Q

How does phenytoin influence aspirin, warfarin and amiodarone concentration

A
  • Amiodarone – increased risk of peripheral neuropathy and increased levels of phenytoin. Decrease levels of amiodarone as there would be increased metabolism
  • Aspirin – may displace phenytoin from plasma protein binding and thus increase levels of phenytoin
  • Warfarin – Phenytoin increases levels of isozyme of p450 and thus this would lead to increased metabolism of phenytoin
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45
Q

What is cavulanic acid

A

Beta lactamase inhibitor

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46
Q

If patient is allergic to penicillin what 2 other drugs cant be given

A

Cephalasorins

Carbapenems

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47
Q

Effect of physostigmine on cholinoceptor agonist

A

Physostigmine: Curve would shift left and possibly down. The curve would shift left as physostigmine is a reversible anticholinesterase. As a result, by blocking acetylcholinesterase, it would cause less methacholine to be broken down, leading to a smaller concentration having a greater effect, causing the curve to shift to the left. However, the peak of the curve may be lower and by the muscarinic receptor constantly being opened, it would lead to a depolarising block forming, therefore leading to no more tissue response, and as a result, the maximum tissue response being lower

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48
Q

Effect of atropine on cholinoceptor agonist

A

Curve would shift to the right but remain at the same height. Atropine is a muscarinic receptor antagonist. This would mean that it would compete with the methacholine for the muscarinic receptor, causing the curve to shift to the right. However, by increasing the concentration of methacholine, it would outcompete the atropine for the binding site of the muscarinic receptor. As a result, the maximum tissue response would be reached but a greater concentration of methacholine would be required

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49
Q

Why would brain receive more General Anaesthetic than adipose tissue

A

Brain recieves much more CO

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50
Q

Why is heroin a stronger analgesiac than morphine

A

Heroin (Diacetylmorphine) – has 2 added acetyl groups, replacing the hydroxyl groups. As a result, it is more lipophilic leading to it entering the brain more. As a result, it would have a greater action within the brain due to more accumulating within the brain, thus leading to a stronger analgesic effect

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51
Q

When does GnRH release begin

A

8

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52
Q

3 stages to birth

A
  • Dilation Phase – cervix undergoes effacement and widening with fundally dominant contractions of the myometrium
  • Expulsion Phase – birth of the child
  • Placental phase – where placenta is delivered within 30min of the expulsion
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53
Q

Where do contractions begin and end

A

Fundally dominant, starting from the fundus and ending at the cervix

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54
Q

What is effacement

A

Thinning of cervix

55
Q

What is syntometrine

A

Extra oxytocin given to stimulare contractions

56
Q

What changes do cells in cervix undergo

A

• Goes from Simple Columnar to Stratified Squamous Epithelium as exposed to acidic Uterine Fluids when Cervix opens up in Pregnancy.

57
Q

Things looked for in past medical history of a short presenting child

A
  • Any significant illness in their past
  • Previous growth measurements and growth charts
  • Birth history
  • Chronic Paediatric disease, e.g. CF
  • Any signs of psychosocial deprivation
  • Endocrine conditions
  • Chromosomal abnormalities like Turners having previously been diagnosed
  • Any skeletal conditions, like achondroplasia
58
Q

Things looked for in family history

A
  • Mid parental height
  • Parent marriage issues leading to psychosocial deprivation
  • Any medical conditions of the parents which may have been inherited
59
Q

Things looked for in examination of short child

A
  • Leg length
  • Total height
  • BMI
  • Weight
  • Skin
  • Genitals
  • Hearing and vision
60
Q

How to work out mid parental heigh

A

Male: (Dad + Mum / 2) +7; Female: (Dad + Mum/2 -7)

61
Q

Disadvantages of mid parental height

A

Disadvantages – Due to random gene rearrangement, children may end up taller or shorter than the middle height for the parent, not the best indicator of change in height but better at showing final likely height, not appropriate if either parent is not of normal stature thus only useable for a limited population, the greater the difference in height between the parents causes the mid-parental height to not be accurate

62
Q

Factors affecting height measurements

A
  • Child wearing something like shoes or helmets which may increase height
  • Measured by same person
  • Stand straight and feet against the wall
  • Measuring equipment due to equipment error
  • Equipment should be accurate and maintained
  • Plot correctly on the chart
63
Q

Advantages of MMSE

A
  • Quick to administer
  • Can provide monitoring method for deteriation
  • No additional equipment
64
Q

Disadvantages of MMSE

A
  • Language affects results
  • Floor and ceiling effect
  • Poorly administered
  • Priming effect/training effect
  • Education may affect results
  • Culture may also affect results
65
Q

Problems of giving elderly cognitive tests

A
  • Can’t tell if the decline in cognition is due to ageing or due to pathology, as ageing can cause in decreasing brain function, like slower reaction time
  • Hearing and visual impairments may limit testing
  • Physical impairments, such as arthritis may impact activity tests
66
Q

Advantages of mid parental height

A
  • May indicate abnormal growth if they don’t meet the predicted height
  • Differentiate normal growth but small stature and abnormal growth
  • Easy to calculate
67
Q

Define preeclampsia

A

A multisystem condition arising de novo at 20 weeks’ gestation and finishing by 6 weeks’ post-partum, characterised by hypertension and proteinuria.

68
Q

Risk factors for pre eclampsia

A

Previous history of pre-eclampsia, multiple gestations, first pregnancy, maternal obesity, maternal conditions like hypertension, diabetes or kidney disease, over 35 or 16, family history, polycystic ovarian syndrome, sickle cell

69
Q

Clinical features pre eclampsia

A

Hypertension, proteinuria and oedema

70
Q

Treatment for re-eclampsia

A

Monitor foetus, try aim to deliver after 28 weeks, unless there is a risk to the foetus, corticosteroids to help with surfactant release

71
Q

Theory behind pre-eclampsia

A

Failed remodelling of the spiral arteries so they still have a thick muscular wall, resulting in them responding to the high blood flow by constricting, leading to less blood for the foetus

72
Q

Detection of FGR

A
  • US scans to measure biparietal diameter, femur length, abdominal circumference and head circumference
  • Foetal Doppler flow to detect high resistance blood flow
  • Foetal movement counting – should be >10
73
Q

Differentiate between FGR and low birth weight

A
  • FGR is a broad term for any baby that fails to reach genetic potential
  • LBW is a baby born less than 2.5Kg. It can be normal or abnormal. Abnormal means that it is a FGR
74
Q

What can pre eclampsia cause

A

IUGR
Early delivery
Still birth

75
Q

Best way to deal with FGR

A
  • Monitor foetus and mother
  • Try deliver after 28 weeks, but deliver early if needed
  • Corticosteroids if less than 36 weeks
76
Q

Disorders of neural tube embryology

A
  • Spina Bifida Occulta – Hair by the spina bifida lesion
  • Meningocele – Meninges filled with CSF protruding through the back
  • Myelomeningocele – Contains the neural fibres and tissue protruding through the lesion and out the back
  • Anencephaly – Failure to have the vault of the skull
77
Q

What is a conceptus and name everything that comes from it

A

Everything derived from the fertilised egg. Includes the foetus, placenta, foetal membrane and the umbilical cord

78
Q

When has embryological development finished and when is it defined to have finished?

A
  • By 8 weeks post fertilisation/ 10 weeks gestation age

* Fully recognised as being a human foetus

79
Q

When does luteo-placental shift occur

A

6-9 weeks post gestation

80
Q

What is the name of the steroid producing tissue pre-implant of the embryo

A

Corpus luteum

81
Q

How does luteo placental shift occur

A

HCG stimulates the corpus luteum to initially produce progesterone. However at 6 weeks gestation, the corpus luteum starts to form less progesterone gradually, with progesterone produced by the placenta increasing gradually. By 9 weeks gestation, the corpus luteum has regressed and the placenta is now providing all the progesterone

82
Q

Successful signs of first trimester

A
  • Attachment of the trophoblast cells of the blastocysts to the uterine wall
  • Adequate nutrition, e.g. folic acids
  • Formation of the placenta
  • Spiral arteries remodelling and opening to allow blood to the placenta
83
Q

Symptoms of pre-eclampsia

A
  • Headache
  • Dizziness
  • Blurred vision
  • Swelling of feet/hands (oedema)
84
Q

Long term effect of pre-eclampsia on mother

A

Stroke

CVD

85
Q

What cells produce glucagon

A

Alpha cells

86
Q

Ways to monitor childs height growth

A

Mid parental height

Centiles

87
Q

Physical barriers to sperm

A

Cumula cells
Zona pellucida
Acidic cervix

88
Q

Why is our understanding of pharmacokinetics so important

A

to determine dose used

89
Q

Best drug to give if seizing for long time

A

Diazepam, fastest onset

90
Q

What produces oestrogen in first trimester of pregnanct

A

Ovaries

91
Q

3 oestrogens produced

A

Oestrone
Oestadiol 17
Oestriol

92
Q

Main oestrogen of pregnancy

A

Oestriol

93
Q

What happens to hormones during PCOS

A

High testosterone, gonadotrophin releasing hormone, LH and FSH. Low levels of oestrogen and progesterone

94
Q

4 key features cushings

A

Centripetal obesity, easy bruising, striae and intrascapular fat pad.

95
Q

3 non iatrogenic causes of cushings

A

Ectopic ACTH from lung tumour, pituitary tumour and adrenal adenoma

96
Q

Why can ketoconazole work in primary hyperaldosteronism but not metyrapone?

A

Metyrapone inhibits the conversion of 11-deoxycorticosterone into corticosterone, as this requires 11-beta hydroxylase. 11-deoxycorticosterone does not have negative feedback to hypothalamus or pituitary, therefore it will not inhibit further ACTH release. Furthermore, 11-deoxycorticosterone acts like a mineralocorticoid and so has aldosterone-like effects causing hypertension. Ketoconazole inhibits production of pregnenolone which is the precursor for 11-deoxycorticosterone and aldosterone.

97
Q

Why difficult to measure height of new born baby

A

They are not standing upright, and they may have their legs flexed so it is difficult to measure their true height.

98
Q

Why diffuclt to measure 2 year old

A

Move about a lot

99
Q

Why is it diffiult to measure 5 yo whos ill

A

They are ill, so may be too tired. Also, their pain might prevent them from being able to stand upright for measurement.

100
Q

Parents are concerned their child may be undergoing his pubertal growth spurt – he is 8 years old – you look at clinical findings, height measurements and medical history. What else could you use to see if he is undergoing a growth spurt?

A

You can look at whether they are started hair growth in underarms, chin and upper lip. Also, you can see if their voice is lower and if they have started genital development. Furthermore, growth hormone and testosterone levels can be measured.

101
Q

Why to not give beta blockers to diabetics

A

They can block beta-2 receptors which are in the liver. Beta-2 stimulates glycogenolysis and gluconeogenesis. This means less glucose would be produced, and so this can cause hypoglycemia.

102
Q

Why is promethazine not that effetive at treating peptic ulcers

A

Promethazine is non-selective and is a mixed receptor antagonist, so it also inhibits dopamine and muscarinic receptors. It does not localise in the mucosa, therefore will have low pharmacological effect in the stomach.

103
Q

2 uses of promethazine

A

Promethazine is used in motion sickness and hyperemesis gravidarum, as it inhibits transmission of information between the vestibular system to the chemotactic trigger zone and vomiting centre in the medulla.

104
Q

Why is Vit25(OH)D used to measure deficiencies

A
  • reflects cutaneous and dietary sources of vitamin D
  • has a fairly long half-life (2–3weeks)
  • is not subject to tight homeostatic control
105
Q

How would you administer GH in hormone therapy?

A

SC injection daily, can’t be given orally due to it being a peptide  will get digested in the stomach

106
Q

Overdose on an anticoagulant

A

Give factors II VII IX X

Give vit K

107
Q

Endocrine causes of short stature

A

Laron dwarfism, Prader Willi Syndrome, Pituitary dwarfism (GH deficiency), Cushing’s syndrome, poorly controlled T1DM

108
Q

Can atropine be used for asthma

A

Atropine solution should not be nebulized because atropine crosses the blood-brain barrier, leading to sedation and worsening of asthma

109
Q

Why is GTN given sublingually

A

High first pass metabolism

110
Q

3 causes of hyperparathyroidism and if radioiodine would work

A

Graves - Yes
Plummers - Yes
Viral toxicosis – No it is self resolving

111
Q

Omeprazole’s MoA-compare and contrast with the Antihistamine named above. (4)

A

Omeprazole is a proton pump inhibitor. PPIs are irreversible inhibitors of H+/K+ ATPase. It inhibits basal and stimulated gastric acid secretion from the parietal cells by over 90%. Protonated in acid environment and active form binds covalently to gastric proton pump. Localised due to inactivity at netural pH

H2 receptor antagonists suppress acid secretion by blocking the binding of Histamine onto H2 receptors ( à reduced acid secretion) and reducing the affect of other substances when bound

112
Q

Types of cell in cervix and vagina

A
  1. Cervical Squamous

2. Vaginal Columnar, glandular

113
Q

Further tests after water deprivation and DDVAP

A

Stimulation with IV hypertonic saline - Nephrogenic Diabetes insipidus - Vasopressin increase, Cranial DI - No change
MRI (cranial), Urea and creatinine (Nephrogenic)

114
Q

What is the oestrogen status of PCOS patients? Describe 3 ways you could demonstrate this. (4 marks)

A

Low oestrogen. Hirsuitism, menstrual cycle disturbance, infertility

115
Q

3 advantages of mini-mental state exam

A

Short, inexpensive
Multiple cognitive domains
Different translations available
Tested & validated in different populations

116
Q

3 cons of mini-mental state exam

A

Age, education(verbal numerical skills), cultural and socioeconomic background have an effect
Not good at picking up mild cognitive impairment (with all these tests there is a large degree of false positive output ->typical case that someone with poor educational background/depression/acute illness diagnosed with dementia when they dont have it. Becoming increasingly common to see this mis-diagnosis

117
Q

Issues of giving mini-mental state exam to elderly

A

Age, education(verbal numerical skills), cultural and socioeconomic background have an effect
Not good at picking up mild cognitive impairment (with all these tests there is a large degree of false positive output ->typical case that someone with poor educational background/depression/acute illness diagnosed with dementia when they dont have it. Becoming increasingly common to see this mis-diagnosis

118
Q

Why is person weighed in water deprivation test

A

There is a limit of safe water depravation  if the patient loses more than 3% of their body weight the test should be stopped due to risk of severe dehydration

119
Q

Receptor for kisspetin

A

GPR54

120
Q

Describe neural tube formation and when it happens

A

Week 3: mesenchymal cells ingress through primitive streak to form notochord. Primitive pit extends into process forming a notochord canal. Floor fuses with underlying endoderm. Notochordal cells proliferate and infold to form the notochord. Neuralation: the developing notochord induces the overlying ectoderm to thicken and form the neural plate
Plates elevates to form neural folds which fuse to form neural tube. Neural tube closes by day 22 (4th week)

121
Q

Failings of neural tube development

A

Anencephaly: failure of rostral fusion
Spina bifida: failure of caudal fusion.
Spina bifida occulta- small internal defect marked by a patch of hair or dimples overlying defect.
Meningocele - membrane bulged out - contains CSF but not neural tissue
Myelomeningocele - neural tissue has bulged out - severe defect - derangement of function

122
Q

When are folate supplements given for prevention of neural tube deficits

A

Folate supplements BEFORE pregnancy (through conception) and in first trimester

123
Q

Risk factors for preeclampsia

A

RFs: mother is a smoker, has DM, previous preeclampsia/FGR pregnancy, already has high blood pressure, kidney disease, increased age, FHx, pregnant with multiple babies, high BMI.

124
Q

What to recommend someone coming in with a diabetic foot and is hypertensive and smokes

A

Check feet everyday. Stop smoking. Wear supportive shoes that prevent pressure on particular parts of the foot. Treat the diabetic foot. Look for other things that may be happening due to his diabetes e.g. eyes, kidneys, other neurological problems

125
Q

What causes diabetic foot

A

Motor neuropathy causes a claw-like foot. Increased pressure on protruding joints. Sensory neuropathy means cuts on foot are not felt due to lack of sensation, and cuts become infected.

126
Q

Describe absorption rates of each administration route

A

Orally - very slow speed of onset - need to travel through GIT to stomach or intestines then get absorbed, travel through liver to heart before they can be exposed to the rest of body
Injection e.g. IV - rapid onset as straight into blood stream. Though injected into vein so needs to pass through venous system first
Inhalation - v fast - faster than injection as blood from lungs go straight to the body
Snort - slow - needs to diffuse across mucus membrane

127
Q

How will warfarin aspirin and amiodarone affect phenytoin concentration

A

i) Amiodarone
Inhibit phenytoin metabolism -> increase levels
ii) Aspirin
Displaces from binding protein -> only issue if near saturation -> increase levels
iii) Warfarin
None (Actually increases clearance of warfarin with chronic use -> decreased warfarin -> decreased INR)

128
Q

Necessities of a good first trimester

A
formation of trilaminar disc
formation of placental villi
closure of neural tube
Good anchorage 
Remodeling of spiral arteries
129
Q

Why are amoxicillin and clavulanic acid given together

A

Clavulanic acid is a beta lactamase inhibitor

130
Q

Define vit b deficiency

A

Lack of mineralisation in bone resulting in softening of the bone, bone deformities, bone pain, proximal myopathy

131
Q

Causes of vit d deficiency

A

Lack of sunlight - need UV to synthesise it in skin
Dietary
Malabsorption
Renal failure

132
Q

Issues of delivering MOCA to the elderly

A

Less ability to use strategies
• Lower levels of attention or concentration
• Slower processing speeds
• Slower reaction times

133
Q

What are the structural differences of heroin and morphine which makes heroin a stronger analgesic?

A

Heroin has acetyl groups in place of the OH groups seen in morphine, making it more lipid soluble hence it has better access to the brain and could have a better effect there than morphine

134
Q

How does the increase in free thyroxine cause lid lag?

A

There is increased sympathetic nervous system activation due to increased sensitivity of adrenoceptors to adrenaline which prevents the eyelids from fully closing