PPE Questions Flashcards

1
Q

Give 2 changes in lipid levels produced by statins

A

reduced LDL/VLDL/triglycerides

increased HDL

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2
Q

State 2 ADRs of simvastatin

A

rased transaminases
myalgia/myopathy
diarrhoea

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3
Q

Give 4 secondary benefits of statins.

A

anti-inflammatory, plaque reduction, improved endothelial function, antithrombotic

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4
Q

Give the preferred 2nd line lipid lowering drug used if statins alone are ineffective

A

ezetimibe: Ch absorption inhibitor

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5
Q

Give 2 effects of giving pre-medication during anaesthesia

A

sedation, anxiolysis

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6
Q

Name the one physiochemical property of inhalational agents that best predicts its potency

A

? lipophhilicity

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7
Q

MAC of 0.5 for 60% N2O.
1MAC = 1.2% for isoflurance.
If give both N20 and isoflurane in combination what % isoflurane would you have to give.

A

0.6

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8
Q

Name 2 inhibitory ligand gated ion channels involved in MOA of inhalational agents

A

GABA, glycine

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9
Q

Explain GABA and glycine MOA in terms of their pharmacodynamic effect, resulting ion transfer and action
potential generation.

A

Positive allosteric modulation: increased potency and efficacy of GABA
and glycine  cl- entry into cell  hyperpolarizes cell  depresses CNS)

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10
Q

Give a respiratory ADR for N2O and one agent given to alleviate this.

A

Respiratory depression

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11
Q

Describe phase 2 metabolism of paracetamol in liver.

A

conjugation to sulphate and glucuronide

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12
Q

What crucial changes happen in metabolism of paracetamol in overdose.

A

saturation of phase

2 metabolism, glutathione depletion, build up of NAPQI

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13
Q

What class of drugs do fluoxetine and paroxetine belong to?

A

SSRIs

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14
Q

Ki for paroxetine is lower than fluoxetine.
Using this determine which drug is more potent
Explain why

A

Paroxetine

lower Ki in paroxetine = a lower concentration of the drug required to
achieve 50% occupancy
so has a greater affinity and therefore potency (potency = affinity
+ efficacy))

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15
Q

Patient presents with right sided hemiparesis, slurred speech, visual disturbances.
What is the most likely diagnosis?
Which side of the brain is affected
Which tract is most likely to be affected to cause muscle weakness in the body
Where do most fibres of this tract decussate

A

Stroke

Left

left lateral corticospinal tract

Medulla

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16
Q

Between which layers of the meninges is a subdural haematoma contained?
What is nature of the vessel affected?
which local circulation does it contribute
to?

A

meningeal layer of dura matter, arachnoid matter

venous

Dural venous sinus

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17
Q

Patient initially collapse at home. He was later brought to the hospital and regain consciousness. The level GSC score was 15/15. A few hours later, he started to deterioriate and GSC started to drop. What is the clinical term used to describe the short period of full
consciousness?

A

Lucid interval

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18
Q

Explain why elderly more prone to subdural haematomas

A

cortical atrophy increases
stretching of the bridging veins so more vunerable to tear when the brain moves inside the
cranium, weaker vessel walls

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19
Q

Suggest how would you treat a patient with subdural haematoma to save his life?

A

craniotomy + drain the

haematoma)

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20
Q

results of Weber’s and Rhinne’s test:
Right ear Left Ear
Weber’s test Quiet Loud
Rhinne’s test AC>BC BC>AC

State the type of hearing loss found in this patient and in which ear. Explain your reasons.

A

conductive hearing loss in the left ear.

(No lateralisation on Weber’s test + AC>BC in both
ears on Rhinne’s test are normal findings)

Lateralisation to the left ear suggests conductive in
left or SN in the right. BC>AC in the left confirms conductive loss in the left ear.

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21
Q

20 year old presents with fever, neck stiffness, rash photophobia
A blood test is performed. Name the principle marker of inflammation in the blood
What other test would you need to perform?
Give 4 changes in CSF seen in a patient with bacterial meningitis
What is the most likely pathogen involved

A

C reactive protein

Lumbar puncture

raised WCC/PMNs,
increased protein, decreased glucose, increased tubidity, increased pressure

N.meningitides in 5-30 year olds
Another bacterial cause of meningitis (S. pneumoniae, H. influenza type B)

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22
Q

Where do the dorsal columns decussate

A

Medulla

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23
Q

Patient has muscle wasting. What can you infer about the type of neuron involved

A

LMN

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24
Q

Patient has breast cancer. Xray shows microcalcification.

Give two conditions in which microcalcification is a feature.

A

Often benign:
Fibroadenoma
Breast cyst

Can be sign of first stages of breast cancer

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25
Q

tests to find out predisposition to breast cancer

A

BRCA1/2

mutation leading to breast/ovarian cancer syndromes)

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26
Q

Patient attend antenatal assessment and undergo ultrasound assessment.
In this assessment, what measurements used to determine the gestational age of fetus in
a) first trimester
b) second trimester

A

a) crown-rump length

b) biparietal diameter, abdominal circumference, femur length

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27
Q

Which palpable structures used to measure symphysis-fundal height?

A

Pubic symphysis

Fundus of uterus

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28
Q

Explain how amniotic fluid is a)produced b)reabsorbed in third trimester.

A

produced by fetal

metanephric kidney producing urine, reabsorbed by fetal swallowing

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29
Q

clinical term for excessive amniotic fluid.

A

Pilyhydraminos

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30
Q

Baby born and projectile vomits when fed. duodenal atresia is diagnosed.
2 other fetal causes for excessive amniotic fluid other than duodenal atresia.

A

Bartter syndrome causing increased urine production, anencephaly impairing the swallowing reflex
and causing reduced reabsorption)

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31
Q

Where along the GI tract atresia can occur and what may have caused the defect
embryologically?

A

bile duct, oesophagus- caused by recanalisation failure

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32
Q

A lady reported chest pain relieved by rest. A diagnosis of angina was made.
What test to investigation the cause of her chest pain?
What would be the findings from the investigation?

A

ECG stress test

ST depression

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33
Q

Patient is given nitroglycerin spray. What is the active substance?
How does it relieve symptoms

A

NO

venodilation  reduced preload on the heart, 2.
vasodilation of collateral coronary vessels  improved blood/O2 delivery to heart

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34
Q

Patient has aortic stenosis due to myocardial infarction. Which phase in the cardiac cycle is
the murmur heard?

A

Systolic

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35
Q

Explain the normal mechanism of aortic valve closure.

Which heart sound is heard when the aortic valve closes?

A

aortic pressure > ventricular pressure
towards the end of systole  brief backflow of flood  pushes valve leaflets closed)

s2

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36
Q

Explain the reasons for dizziness, angina and SOB in aortic stenosis

A

dizziness: reduced brain perfusion
angina: ventricular hypertrophy causing increased O2 demand, SOB: backflow of flood into pulmonary circulation affecting gas exchange

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37
Q

Patient presents with moon face and central obesity. Diagnosis of Cushing’s made.
Give 3 other signs seen in this patient and give a metabolic reason for each

A

buffalo hump in
the neck/area around collar bone as abnormally high cortisol switches action from lipolysis to
lipogenesis, muscle wasting/skin striae due to increased proteolysis in skin/muscle,
hyperglycaemia due to increased glycogenolysis and gluconeogenesis in liver

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38
Q

What detects changes in osmolarity and where are they located?
What detects changes in blood plasma [Na+] and where exactly are they located?

A

Hypothalmic osmoreceptors

Macula densa: DCT of kidney

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39
Q

State 2 main mechanisms used to control plasma osmolarity

Explain how these 2 mechanisms utilise a negative feedback mechanism to control plasma osmolarity

A

ADH, thirst

  1. raised osmolarity  ADH secretion by p.pituary  production of small amounts
    of hyperosmotic urine  decreases osmolarity back to normal.
  2. raised osmolarity 
    initiates thirst mechanism  consumption of hypoosmotic fluid  decreases osmolarity back
    to normal).
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40
Q

What is the plasma volume in 70kg man

What is the total body volume in 70kg man

A

Approx
2.8L
42L

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41
Q

how cells prevent dehydration and how ICF is affected during
changes to plasma osmolarity

A

? Movement of osmotically active ions such Na , H

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42
Q

Patient with persistent vomiting.
Name the 3 most important ions lost in vomit.
Name the acid base disturbance vomiting can lead to.
Explain the mechanism leading to this AB disturbance.

A

H+, Na+, K+, (NOT cl-)

metabolic alkalosis

loss of protons in vomitus  body
produces more to replace those lost, in the process also produces HCO3- which goes into
ECF  raised HCO3-:pCO2 ratio  raised plasma pH)

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43
Q

If plasma sodium increased, what changes in plasma osmolarity?

A

no change as water follows

by osmosis

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44
Q

Why is the thirst mechanism not stimulated as seen in simple dehydration?

A

Loss of isoosmotic fluid so no change in osmolarity.

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45
Q

How does the body compensate for metabolic alkalosis (as seen in persistent vomiting)

A

partially compensates by reducing ventilation rate  raising
pCO2  decreasing HCO3-:pCO2 ratio  decreasing pH back to normal

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46
Q

Patient with acute cholecystitis.

Explain why pain is felt 1 hour after a meal

A

cholecystokinin release and contraction of the

inflamed gall bladder to release bile occurs after food leaves stomach and enters duodenum

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47
Q

Patient with liver disease gets ascites.
Define acites
Explain how liver disease leads to ascites.
Explain one other cause of abdominal distention and how it would present

A

abnormal presence of fluid in peritoneal cavity

cirrhosis  fibrosis compresses portal vein  PH
 increased hydrostatic pressure in capillaries  increased tissue fluid leaving capillary)

bowel obstruction
with vomiting and constipation

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48
Q

Patient is diagnosed with bronchial adenocarcinoma
What is the Epithelium of the main bronchus
Is this benign or malignant?
2 histological types of bronchial carcinoma

A

pseuodostratified ciliated columnar with goblet cells

Malignant

adenocarcinoma, squamous carcinoma, large
cell, small cell

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49
Q

Give two neurones that are damaged if there is bronchial carcinoma around
left hilar region of the lung and give the symptoms that would result.

A

left recurrent laryngeal

nerve  hoarse voice, phrenic nerve  dyspnoea

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50
Q

2 narrowest parts of the oesophagus

A

as it crosses left main bronchus, LOS

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51
Q

FVC : 3.2 litre (predicted is 3 litre), FEV1: 2.5 litre. Comment on these results.

A

normal as

FEV1:FVC>0.7, FVC as predicted

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52
Q

give two investigation/tests to differentiate between obstructive or restrictive deficit in this
patient

A

Spirometry

Peak flow

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53
Q

Give two reasons for reduced pO2 in PE

A

impaired gas exchange in some alveoli

leading to VQ mismatch

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54
Q

Name 2 regional lymph nodes

Name the terminal group that drains these

Give important fibrous structure that encircle the terminal lymph node

A

submental, submandibular, buccal, pre/post auricular, occipital, ant/post cervical

Jugulo-digastric

Investing layer of deep
cervical fascia

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55
Q

2 neurovascular structures that can be found on posterior triangle of neck

One cranial nerve in posterior triangle that can be affected and its innervations

Give two MAJOR groups of nerves that may also be disrupted in the posterior triangle.

A

Subclavian artery, spinal accessory nerve

spinal accessory- SCM, trapezius

Cervical and brachial plexus

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56
Q

A 9 year old boy is diagnosed with DMD. His older brother and sister are asymptomatic. Older brother is expecting a baby.
why boys more likely to get the disease than girls

prevelance of the mutant dystrophin gene (~1/1100). use this to calculate the probability of the asymptomatic older brother having a child who has the disease if they are

a) male
b) female

A

x-linked recessive condition/ dystrophin gene located on x chromosome  so males only carry one
copy of the gene so having the mutant gene means they have the disease, women carry two copies the gene so require 2 copies of the mutant gene to have the disease

a) 1/1100
b) 0

(The probability of him having a partner who is a
carrier, XDXd, is 1/1100 and his genetype must be XDY-  so a baby boy would have 1/1100
chance of being XdY- and having the disease and a baby girl would have a zero chance of
being XdXd as would have at least 1 normal gene from her father)

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57
Q

Back pain radiates to the back of the leg. Patient is diagnosed with sciatica
Name ligament that runs anteriorly to the vertebra
Give another ligament or any processes of the vertebra

A

Anterior longitudinal ligament

Posterior longitudinal ligament

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58
Q

Which structure of the intervertebral disc a) that is ruptured b) herniated
What imaging technique is best to investigate this injury?

A

a) annulus fibrosis
b) nucleus propulsus

MRI

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59
Q

Compression of the L5 nerve. Explain dermatomal distribution of L5.

A

lateral leg + middle 3

digits of the foot + lateral half of the great toe + medial half of small toe

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60
Q

Give two muscles involved in dorsiflexion of the ankle

A

tibialis anterior, extensor hallucis

longus, extensor digitorum longus, fibularis tertius)

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61
Q

Give nerve root involved if:

a) Hip flexion, adduction and cremasteric reflex is compromised.
b) Sensation in the lateral edge of lower leg is compromised

A

a) L2 as femoral nerve is L2-
L4, obturator never is L2-L4, cremasteric reflex is L1-L2)

b) S1

62
Q

State 2 abnormalities that might be seen on Xray of a colles fracture

A

dorsal displacement of radial fragment-
dinner fork deformity, reversal of radio/ulnary styloid process axis (radial shortening),
avulsion of ulnar styloid process)

63
Q

What is grading?

What is its significance?

A

measure of degree of anaplasia

informs prognosis along with staging

64
Q

What type of necrosis seen in MI

Give 2 microscopic changes seen in this type of necrosis

A

Coagulative

protein denaturation, maintenance
of tissue architecture)

65
Q

Name the ion channel involved in the phases 1-3 of ventricular action potential
Comment on the movement of the ions for each.

A

Na+, Ca+, K+ respectively)

(in, in, out respectively)

66
Q

Explain how myelin increases nerve impulse transmission

A

reduced capacitance, increased

resistance  increased conduction velocity

67
Q

B-adrenoreceptor mechanism:
Name the effector activated following agonist binding to GPCR.
Name the intracellular mediator produced.
What enzyme does this mediator then activate.

A

Adenyl cyclase
cAMP
PKA

68
Q

Name the enzyme inhibited by statins

A

HMG CoA reductase

69
Q

New drug for duodenal ulcer… IRR is 0.9 (new drug in
compare to placebo). (CI between 0.85-0.95 but H null is not included la)
Explain the value
Give one reason that will cause u to be cautious with it

A

Answer

70
Q

Define specificity

A

proportion of those who do not have the disease who test negative, detects health

71
Q

Define NPV

A

proportion of those who test negative who actually do not have the disease

72
Q

Explain discreditable and discredited stigma

A

discretible= nothing can be seen but can be
found out e.g. mental health problems
discredited= physically visible characteristic e.g.
paraplegia

73
Q

Patient noticed changes but didn’t choose to see her doctor because it wasn’t affecting her
activities of daily living. Explain how lay beliefs impact when a patient presents.

Two other things that could have prevented her from presenting.

A

lay beliefs =
people’s general understanding of health and illness. Patient has a functional definition of
health so deems herself healthy despite the symptoms and therefore doesn’t consider it
appropriate to see her doctor.

discouragement from social networks (e.g. husband) to seek professional help, time management issues, transport problems etc

74
Q

Explain the transactional model of stress

A

The transactional model of stress shows how the experience of stress is
subjective – it depends on the way each individual person appraises
potentially stressful events [1] and the resources available to cope with
these events [1]. Appraisal of events has been categorised in to primary
appraisal (what is the nature of the threat?), and secondary appraisal (can I
cope?). [1]

Therefore, the way people appraise events is unique and depends on the
nature of the event (e.g. its salience to the individual), individual
characteristics and experiences (e.g. the extent to which they are
optimistic by nature), and their social context (e.g. their family support),
so one person may consider the situation to be stressful when the other
does not [1]

75
Q

Briefly describe
what is meant by predisposing factors, precipitants, and maintaining
factors in sexual dysfunction, and give an example of each.

A

PREDISPOSING - Early experiences which make an individual
vulnerable to developing sexual difficulties at a later stage,
eg Restrictive upbringing, inadequate sexual information,
traumatic early sexual experiences
 PRECIPITANTS - Events or experiences associated with the
initial appearance of a dysfunction, eg Childbirth, infidelity,
dysfunction in partner, depression, random failure, physical
illness.
 MAINTAINING - Intervening factors which allow the dysfunction
to persist. e.g. Performance anxiety, guilt, poor communication,
relationship discord, restricted foreplay, environmental factors.

76
Q

Explain briefly why all human beings are pre-disposed to

stereotypical thinking and how this can lead to prejudice.

A

Knowledge is thought to be organised into cognitive structures called
schemas or schemata. Schema about social groups are called stereotypes.
[1] We sometimes access these stereotypes unconsciously and ‘pre-judge’
people on the basis of the social group that they belong to rather than
assessing them as an individual. [1]

77
Q

Briefly describe one emotion-focused approach and one problem-
focused approach to coping

A

Emotion focussed coping (change the emotion)
 Access social support (talking to friends & family, contact with
support groups)
 Cognitive approaches: change how she thinks about situation, e.g.
focus on positive aspects of good self-management
Problem focussed coping (change the problem or your resources)
 Reduce demands of stressful situation, e.g. get aids in the home
 Expand resources to deal with it, e.g. mindfulness
[1 mark for point relating to emotion-focused, and 1 mark for point
relating to problem-focused]

78
Q

Describe the health belief model and how it relates to someone presenting to STI clinic

A

Health belief model indicates that this health related behaviour is influenced
by:
1. Beliefs about health threat:
Perceived susceptibility – he may be concerned he has been exposed to STIs,
or is at risk due to un-safe sex behaviour. [1]
Perceived severity of the outcome – he may believe the consequences of
having an STI without knowledge or treatment are significant enough to try
to avoid [1]

  1. Beliefs about the pros and cons of the health behaviour
    He has recognised the benefits of getting tested for STIs— possibly by
    allowing him to get early treatment or preventing him from infecting others.
    [1]
    He has been able to identify any personal barriers to getting tested (i.e.,
    getting to the clinic, fears about confidentiality or being recognised) and
    explore ways to get over these barriers (i.e., find out about transport, choose
    a quiet time of day, use an alias).
    [1]
    Or 1 mark for cues to action (e.g. he saw a poster about the risks of STIs)
79
Q

Name 2 improvements in ADR profile in using paracetamol over other NSAIDS

A

COX2 inhibition but not COX1 so better side effect profile

No increased risk peptic ulcers, no anti platelet actions

80
Q

Which fascial layer makes the parotid sheath?

A

Investing layer of deep cervical fascia

81
Q

Mumps affecting parotid gland: Why do you have intense pain while chewing?

A

Swelling of parotid gland impacting on facial nerve running through it

82
Q

Where does the parotid papilla open at?

Why is the papilla red in mumps?

A

Parotid papilla = small elevation of tissue that works opening of parotid duct on inner surface of cheek

Viral infection in mumps

83
Q

Why is the papilla red?

A

A

84
Q

Give two neurovascular structures that go through the gland.

A
(Lateral to medial)
Facial nerve
Retromandibular vein
External carotid artery
Superficial temporal artery
Great auricular nerve
Maxillary artery
85
Q

Vaccination for mumps is given as active immunization. Which kind of vaccine is given in
this type of immunisation and at what age?

A

Live attenuated virus

Part of combined MMR vaccine: Single injection usually within a month of a baby’s first birthday

86
Q

What cell of the innate immune system involve in viral killing (and some cancerous cells)
and why innate immune system is required before adaptive immune system

A

Killer T cells:
Activated when their T cell receptor binds to the antigen in a complex with the MHC class I receptor of another cell
Recognition of this MHC:antigen complex aided by co-receptor on T cell: CD8

Antigen must first be processed and recognised before an antigen-specific immune response can be carried out by adaptive immune sys

87
Q

What is the effect of sodium to plasma osmolarity in a cell

A

Sodium a major determinant of plasma osmolarity
Na the major osmotically active ion in the ECF
total body Na content determines ECF vol

88
Q

How does a cell prevent dehydration?

Name one membrane protein that is involved

A

Movement of osmotically active ions e.g. Na+, K+, Cl-
Water follows

E.g. Na/Cl, Na/K/Cl co-transporters, Na/H exchanger

89
Q

what regulates osmolarity and where is it located?

A

Osmolarity if blood detected in osmoreceptors in OVLT in hypothalamus

Releases ADH

Causes acquporin channels to be inserted into cells of DCT and CT

90
Q

explain polydipsia in T2DM

A

Hyperglycaemia
Tm of glucose exceeded in kidney
Glucose remains in urine, increasing osmolarity
Water remains and more fluid lost in urine

91
Q

Give four personality/behavioural changes due to frontal lobe atrophy.

A
Inhibition
Behaviour regulation
Impulsiveness
Apathy and indifference
Socially inappropriate behaviour
92
Q

Patient with Alzheimers later presents with tremors, rigidity and myoclonic jerks. Explain why

A

Loss of neurons and synapses in cerebral cortex and some subcoritcal regions

93
Q

What is the pathology in Alzheimers that could affect the blood vessel that supply the frontal lobe?

Which layer of the blood vessel is affected?

A

A

94
Q

Which major blood vessel is most likely affected in patient with frontal lobe atrophy?

Name another commonly affected blood vessel in Alzheimer’s Disease

A

A

95
Q

Explain ‘normal pressure hydrocephalus’.

Can it be managed by draining to peritoneal and explain why?

A

Decreased absorption of CSF
Can be idiopathic or secondary (e.g. Due to SAH)

Increased ICP, ventricles then enlarge, lowering ICP
(So do not suffer normal symptoms of RICP)

Can be managed with shunt, but outcomes are variable

96
Q

A 23 year old patient comes with epilepsy. diagnosed with epilepsy since childhood. She’s on Carbamazepine but has been having seizures as of late. patient is a heavy drinker.
● Give two precipitants to seizures in this patient.
● What is the mechanism of action of this drug and site of action?
● Under what main class of drugs does this belongs to?
● what need to be considered in this patient when taking this drug and how does it affect
its half life?
● what major drug (other than Anti-epileptic drug) interfere with serum level of this drug.
Patient wants to have baby and she’s on oral contraceptives. What is the proportion of
failure rate of contraception when using ocp with carbamezapine?
● What is the proportion of birth defect percentage when use valporate?
● What replacement drug would you give and why?

A

Carbamazepine: stabilised inactivated VG Na channels: cells less excitable
Half life diminishes as given repeatedly; a strong CYP inducer

Decreasing metab of the drug: erythromycin, cimetidine, CaCB

97
Q

2 endoscopic features of uc and crohns

A
UC:
Ulceration
Pseudo polyps (surviving mucosa)
Loss of haustra
Crypts
Continuous involvement
Crohns:
Cobble-stoning
Fissures
Thickened bowel wall
Skip lesions
98
Q

patient is diagnosed with UC and given medication. later, why does the patient have recurrent UTIs

A

Remicade (infliximab): anti TNF-alpha
Prevent induction of pro-inflammatory cytokines
Immunosuppression: more prone to opportunistic infections

99
Q

Explain mechanism of fever in relation to thermoregulation.

A

Temp regulated by hypothalamus
Trigger of fever = release prostaglandin E2
Acts on hypothalamus: systemic response back to rest of body
Heat-crating effects to match new temp lvl

100
Q

what type of drug to control fever, give a common name of the drug and its mechanism of action

A

Antipyretics:
E.g. NSAIDS e.g. Ibuprofen
Inhibit COX enzyme: inhibit prostaglandin synthesis
Fever caused by elevated PGE2, which alters firing rate of neurones on hypothalamus

101
Q

What protein is involved in opsonisation

A

Antibodies (IgG, IgM indirectly)
Complement proteins: C3b, C4b,
Circulating proteins: CRP

Molecule that enhances phagocytosis by markimg antigem for immune response

102
Q

What cytokines are released to induce acute phase response. And give clinical significance of measuring CRP

A

Interleukins (IL1, IL6, IL8), TNF alpha
Secreted by local inflammatory cells (neutrophil geanulocytes, macrophages)
Liver responds by producing acute phase reactants

CRP:
Found in plasma
Rises in response to inflammation
Is an acute phase protein, originating in liver

103
Q

●What stimulates thirst in a patient with T2DM?
● What hormone would be produced from the posterior pituitary gland in this patient?
● Where does the hormone act?
● What is the name of the membrane protein where it acts on?

A

Increased osmolarity of plasma (more water lost in urine)

ADH

Kidney: increases aquaporin channels on apical membrane of DCT and CD

104
Q

What is the Plasma volume in 70kg man

What is the Total body fluid in 70kg man

A

~4.6 L

~46 L

105
Q

Distinguish between gastric ulcer and duodenal ulcer.

A

Gastric:
Less common
Pain soon after eating
Pain increased by eating

Duodenal:
More common
Pain later after eating
Relieved by eating
May wake at night with pain
106
Q

Ulceration of Posterior wall of duodenal cap might affect what structure. Give 2. And choose 1 & give the immediate complication.

A

Gastroduodenal artery

Haemorrhage

107
Q

If MCV and Hb are low in a blood result, What does the result show?
Give an example of the etiology
What else would u want to see from the blood result to confirm the diagnosis?

A

Microcytic anaemia

E.g. Iron defociency

108
Q

What protective mechanism induced to protect from acid secretion in

a) stomach
b) duodenum

Why is stress considered as a process?

A

Stomach: mucus production
Duodenum: bicarb production

109
Q

Briefly explain what is meant by ‘severe

dependence’ in alcohol

A

Low risk drinking: within DoH sensible drinking guidelines

Hazardous drinking: over sensible drinking limits (regular excessive consumption or
less frequent but heavy drinking) but so far avoided sig alcohol related probs

Harmful drinking: above recommended sensible drinking but typically higher than
most ͚hazardous drinkers͛ & show clear evidence of some alcohol related harm

Moderate dependence: have a degree of dependence but not reached stage of ͚relief
drinking͛ (to avoid physical discomfort from withdrawal symptoms)
May require community detox

Severe dependence: serious & long standing problems & experienced sig alcohol
withdrawal, may be drinking to stop withdrawal symptoms
o may require inpatient detox
o may have complex needs e.g. psychiatric problems, poly-drug dependence

110
Q

A lady reported chest pain relieved by rest. A diagnosis of angina was made.
● What test to investigation the cause of her chest pain?
● What is the findings from the investigation?

A

ECG stress test

ST depression

111
Q

What are the chest surface marking of the heart valves (mitral, aortic and pulmonary) for auscultation

A

pulmonary valve: junction of superior and middle thirds of body of sternum and slightly to the left side; near to left third costal cartilage
aortic valve: just below and to the right of the pulmonary valve on left side of middle third of sternum; level with the third intercostal space
tricuspid valve: median plane in the inferior third of the sternal body; opposite the fourth costal cartilage
mitral valve: overlapping tricuspid area but more superior and to the left of sternal body

112
Q

Patient is being given nitrates. What is the active substance does nitrates produce?
What is the effect of it?

A

Venodilation

Reduce pressure in ventricles

113
Q

aortic stenosis: Which phase

in the cardiac cycle is the murmur heard?

A

Mid-systolic, ejection

114
Q

Role of NICE before treatment being made available in the NHS hospitals.

A

Treatment guidance based on current evidence

115
Q

Explain the normal mechanism of aortic valve closure.

Which heart sound is heard when the aortic valve is closed?

A

Increased aortic pressure,higher then left ventricle
Normally has 3 cusps

S2

116
Q

A kid who fell down from climbing a frame and fractured his right humerus at the midshaft level
● What runs in the radial groove together with the radial nerve?
● Muscle for extension is supplied by the radial nerve. Will extension be ABSENT, NORMAL or COMPROMISED? (give reasons)
● Why does the extension at the elbow is only weakened?

A

deep brachial artery

Supplies motor to triceps and anconeus, brachioradialis, extensors of hand
Sensory to dorsum of hand

Mid shaft fracture =
Weakened supination 
Loss of extension of hand and fingers
Wrist drop
Sensory deficit: posterior forearm, radial half of dorsum of hand and radial 3.5 digits excluding nail beds

Long head of triceps can be innervated by axillary nerve

117
Q

Draw the distribution of the radial nerve on the dorsum of the hand. Indicate with
x where will you specifically test for radial nerve.

A

A

118
Q

Name 1 muscle which causes the extension of the wrist and another muscle which causes the extension of the digits.

A

Extend wrist:extensor carpi radialis longus, extensor carpi ulnaris.
Extend digits: extensor digitorum

119
Q

In mid shaft humeral fracture affecting the radial nerve, Name 1 muscle which causes adduction of the wrist And name 1 muscle which also causes adduction but is not affected.

A

Affected:
Extensor carpi ulnaris.

Not affected:
Flexor carpi ulnaris

120
Q

Loss of fine touch and proprioception:
What ascending tract involve?
where does it decussate
where does 1st order neurone synapse with 2nd order

A

Dorsal column
decussate in medulla.
Synapse in the nuclei gracillis and cuneatus.

121
Q

A lady came with hypothyroidism and she is tired and obese.
● Explain thyroid test results (low T4 and high TSH and explain why) HPA axis.
● Why thyroid gland enlarged ?
Why give thyroxine replacement using T4 and not T3.

A

May be Enlarged due to inflammation and infiltration of lymphocytes

T4: longer half life, less active, can be converted to active T3 as needed

122
Q

Kid with DM type 1 collapse while playing football. Ketoacidosis is diagnosed.
result :
High glucose, HbA1c, creatinine, urea and beta hydroxybutyrate, sodium and cortisol. Low Bicarbonate.
● Give two clinical signs that can be seen in this patient
● What is beta hydroxybutyrate and Why is it high in this patient
Why is bicarbonate low in this patient
● Why cortisol is high and what does it do in this case?

A

Beta hydroxybutyrate:
Synthesised in liver from acetoacetate (ketone)
Can be used as energy source by brain when blood glucose low
(TCA cycle stalled and shift glucose towards ketone body production)

Cortisol released in response to low blood glucose
Stimulates gluconeogenesis, glycogenolysis, (later) proteolysos, lipolysis

123
Q

Give volume of urine produced if patient has
a) oliguria b) anuria c) polyuria.
Which of the three can be seen in a patient with diabetic ketoacidosis

A

a) 2.5-3L/day

polyuria in ketoacidosis

124
Q

what is HbA1c and what does it indicate?

A

Glycated haemaglobin

Avg plasma glucose conc over prolonged period

Normally approx 5%

125
Q

Give 2 clinical features of a Subdural haematoma seen on imaging

Between which two layers subdural haematoma formed.

Which type of vessel may involved in this type of haemorrhage, and which local circulation it contributes to.

A

Crescent shaped
Crosses sutire lines

Memingeal layer of dura - Arachnoid mater

126
Q

What is the role of sacral parasympathetic fibres in micturition

A

Micturition: contraction of detrusor

127
Q

Which tract is involved in:

a) two point discrimination in the hand
b) vibration in the ankle
c) itsneurone originates from precentralgyrus
d) affectipsilateral movement of lower leg and it gives pyramidal signs

A

a) DCML: cuneatus
b) DCML: gracillus
c) corticospinal?
d) corticospinal?

128
Q

Hyperextension of the neck. Sudden loss of consciousness, with spontaneous breathing unaffected. All four limbs are paralysed, but shoulder movement is not affected. Loss of
sensation below neck. Lower motoneuron signs elicited in patient. Doctor found out there is complete transection of the spinal cord
● Which neural level is affected
● Explain why (give three reasons)
● Give three lower motoneuron signs in this patient
2 lower motoneuron signs seen later in this patient

A

A

129
Q

Epithelium of the main bronchus

A

PseudoStratified columnar with goblet cells

130
Q

Patient is diagnosed with bronchial adenocarcinoma
Is this benign or malignant?
2 histological types of bronchial carcinoma.

A

Malignant

Non small cell
Non-invasive/minimally invasive ot invasive

131
Q

Explain surface markings of the lobes of the lung

A

Lung:
T6: mid clavicular line
T8: mid axillary line
T10: lower lobe posteriorly

Pleura extends 2 ribs lower

132
Q

What changes in ovary that induces menopause

Briefly explain what happens to the level of hormones in HPG axis

A

Lack of oocyte (normally produce oestrogen)

Low oestrogen = no -ve feedback on HPG axis = increased LH and sig increased FSH (no inhibin)

133
Q

Which layer of endometrium involved in menstruation

What two effects of oestrogen on this tissue

A

superficial part of endometrium (statum functionalis) subject to cyclical growth, degeneration & shedding of dead tissues

(Deeper part of endometrium (sturatus basalis) in vicinity of myometrium; doesnt show cyclical changes. Responsible for regeneration of upper endometrium)

Oestrogen promotes proliferation of functional layer: thickening, glandular invagination
Also promotes growth and motility of myometrium

134
Q

How does increased BMI contribute to increased risk of endometrial carcinoma

A

increased oestrogen from endogenous sources (e.g. adipose tissue) can promote endometrial hyperplasia which increases risk of endometrial carcinoma

135
Q

How does history of irregular menstruation lead to development of endometrial carcinoma

A

Endometrial hyperplasia assoc with prolonged oestrogenic stimulation, which increases risk of developing into endometrial carcomoma

136
Q

What is grading and what does it signify

A

Based on degree of differentiation and growth rate: a measure of appearance

Together with staging (measure of metastasis), informs on prognosis

137
Q

Distinguish chronic from acute pain.

A

Chronic pain can be defined as ‘pain or discomfort persisting continuously or intermittently forgreater than 3 months’
Can be further sub-divided into nocioceptive pain, neuropathic pain, or mixed.

Acute pain has survival value

138
Q

Give two reasons for delayed referral.

A

A

139
Q

Give 2 avoidant strategies in coping

A

Emotion focused coping (rather than problem focused):
Behavioural approaches; do something e.g. alcohol, finding a distraction

Cognitive approaches: change how you think about the situation, e.g. denial

140
Q

Explain clinical audit.

A

A quality improvement process that seeks to improve patient care and outcomes through systematic review of care against criteria and the implementation of change

Main stages:
Choose a topic
Research evidence
Set criteria and standards
1st evaluation/audit
Implement change
2nd evaluation/audit
(Back to setting criteria and standards)
141
Q

Inheritance pattern of huntingtons disease

A

Autosomal dominant

A trinucleotide repeat disorder (length of releated section lf gene exceeding normal range)

142
Q

Explain one study design of prospective and retrospective cohort study

A

Cohort: start with disease-free individuals and follow them up, often over a long period
Good for rare exposures, mot good for rare diseases

Prospective:
recruit outcome-free individuals and classify them according to
their exposure status

Retrospective:
cohorts ‘recruited’ historically, using existing records
recruit outcome-free individuals and classify their initial exposure status and subsequent outcome status using historical records
Follow up data collection starts in the past

143
Q

What is confounding factor

A

factor linked to both exposure & outcome but not on causal pathway

144
Q

11 year old boy presented with adenoids. Patient has cough, fever and dysphagia
● Where is adenoid located
● What surrounding structure may be obstructed
● Which palpable lymph node enlarged and where can it be palpated
● Give three specific consequence of this condition
● Doctor recognised it as viral infection. Give one common viral agent to this.
● Is ampicillin a suitable treatment to this patient
● What is a bacterial agent that may cause adenoid. And comment on its gram staining

A

(Naso)pharyngeal tonsil, posterior to nasal cavity in roof of nasopharynx

Can obstruct airflow through nasal cavity, affecting speech and nose breathing

Cervical lymph nodes

Difficulty breathing/swallowing/speaking, potential spread of infection (pharyngitis)

Adenovirus, rhinovirus, influenza

Unlikely as most likely cause is viral, and is treatment for group B strep

Group A streptococci (pyogenes): gram positive cocci

145
Q

Define portosystemic anastomosis and give examples
● Explain development of oesophagealvarices
● Patient also has splenomegaly. Explain why

A

Anastamosis that occurs between veins of portal circulation and systemic corculation

E.g.
Oesophagus (portal = L gastric, systemic = azygous)
Rectum (portal = sup rectal, systemic = middle and inf rectal)
Paraumbilical (portal= paraumbilical, systemic = superficial epigastric)
Intrahepatic (portal = L branch portal, systemic = IVC)

Oesophageal varices:
Dilated submucosal vein
Portal hypertension (e.g. From cirrhosis): blood flow thru hepatic portal sys redirected from liver to areas of lower venous pressure (Collateral circulation dev e.g. In oesophagus)
= small blood vessels distended, thin-walled and cause varcosities
Prone to rupture

Splenomegaly from blood being forced down alternate channels (via splenic vein) by increased resistance to flow thru systemic venous system

146
Q

Patient vomits blood from ruptured oesophageal varices. Is there any change in immediate haematocrit level. Explain
why?

Patient is given normal isotonic saline solution. Will the intracellular volume change? Explain why?

A

Haematocrit: Vol % of rbc’s in blood (as compared to total vol)
Level will now low straight after vomiting as plasma and blood lost in equal proportion

Intracellular volume will not change in isotonic saline, because no significant fluid shift across membranes
(Hypotonic solution e.g. NaCl will move into cells, Hypertonic solution e.g. Dextrose will move from intravascular to intracellular and interstitial)

147
Q

What Are the sites of action of cytotoxic agents used in chemotherapy

A

DNA synthesis: antimetabolites (e.g. Methotrexate)
DNA replication: intercalating agents
DNA Transcription/duplication: alkylating agents (platinum compounds e.g. Cisplastin)
Mitosis: Spindle poisins (inhibit tubulin- vinca alkyloids, stabilise tubulin - taxoids)

148
Q

Give two patient factors to be considered before starting chemotherapy

A

A

149
Q

Vincristine is given to the patient. Give the mechanism of action of this drug

A

Inhibit tubulin production in metaphase

150
Q

Patient is given cyclophosphamide. It is an alkylating agent. What is the mechanism of action of alkylating agent and where does it act.

A

DNA replication
allowing covalent bonds to form between DNA strands (either interstrand or intrastrand adducts), meaning that replication cannot occur thus preventing the tumour to grow
anyfurther.

151
Q

Patient with COPD:
Action of macrophage in lung damage.

How does phosphodiesterase inhibitor helps to alleviate the symptoms

A

Alveolar macrophages = leukocyte
Immune response in infection and injury
In COPD, they do not resolve inflammation

Produce proteases e.g. Neutrophil elastase (also produce neutrophils which also secrete these)
= alveolar wall destruction (emphysema) and mucus hypersecretion

Phosphodiesterase inhibitor prevents inactivation of cAMP and cGMP
includes methylxanthines e.g. Theophylline - a bronchodilator