Paper 1 Flashcards

(41 cards)

1
Q

List four (4) clinical features of diabetes mellitus.

A

Fasting hyperglycaemia
Glycosuria
Angiopathy (macro and micro)
Neuropathy

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2
Q

If Mrs White fell pregnant, list two (2) fetal complications if her diabetes is not controlled.

A

congenital malformation, large foetus, obstructed labour, polyhydramnios, neonatal distress
syndrome

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3
Q

Outline the macrovascular complication that she is at risk for if her diabetes is not well controlled.
Briefly explain the mechanism by which this complication occurs.

A

Myocardial infarction/stroke/diabetic foot (0.5)
2. Increased glucose levels result in endothelial wall damage (glycation) (0.5) and increased
permeability (0.5) which leads to accelerated atherosclerosis (0.5).

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4
Q

Outline three (3) WHO recommendations that you would advise this patient with respect to
exercise.

A

The WHO recommendations for this individual would be 1) any exercise is better than no exercise for
his health, 2) that he should ideally aim to accumulate between 150-300 min of moderate exercise
during the week (or 75 min of vigorous, or some combination of both), 3) that muscle strengthening is
also important for health, and particularly in his line of work, and that he should undertake this 2 x per
week minimum, and whenever possible, limit time in sitting and sedentary activities.

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5
Q

Outline to what extent regular exercise would reduce his risk for all-causes of death and multi-
morbidity.

A

Studies show that he can reduce his risk of all cause mortality by at least 20-25% by meeting these
guidelines.

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6
Q

Outline four (4) reasons why exercise will benefit his health, to help motivate him to exercise.

A

Regular exercise may prevent him from having to take hypertensive medication or oral hypoglycaemic
agents. Regular exercise increases vessel diameter and causes vasodilation, it improves his insulin
sensitivity, which can help to lower blood glucose, even in the absence of weight loss, and it can
increase his lean muscle mass and reduce his central adiposity. It may also make it easier for him to be
insured.

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7
Q

Obesity is typically characterised by hyperinsulinaemia or elevated insulin concentrations, with
either normal glucose concentrations, or impaired glucose control. Explain why this occurs.

A

In the obese, insulin-resistant state, adipose tissue, muscle and other target cells are less sensitive to
prevailing circulating insulin concentrations, either as a function of fewer receptors, or altered insulin
signalling pathways. With a reduction in insulin sensitivity, the beta cells of the pancreas will secrete
more insulin, in response to prevailing glucose concentrations, which then results in hyperinsulinaemia.
If the beta-cell can no longer produce enough insulin to maintain euglycaemia, then the person will
progress to Type 2 diabetes.

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8
Q

List the three (3) most common types of support cells in the CNS (1½ marks) and briefly describe
how they affect axon regeneration after traumatic injury

A

(Astrocytes, reactive gliosis/glial scar; oligodendrocytes, neurite growth inhibitory proteins block axon
regrowth; microglia, clear cell debris but may further damage neurons by releasing cytotoxic factors)

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9
Q

Name the cell types that will be primarily affected by de-myelinating diseases. CNS and PNS

A

a. of the CNS
Oligodendrocytes
b. of the PNS
Schwann cells)

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10
Q

State the principal structural difference between these cell types.

A

(Schwann cells myelinate only one axon segment, oligodendrocytes many)

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11
Q

State the clinical diagnosis of this patient.

A

Meningococcal meningitis/ bacterial meningitis

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12
Q

List all the laboratory investigations that you would request to assist you in managing this patient.

A

Cerebrospinal fluid (CSF) microscopy, culture and susceptibility testing; CSF cell count and chemistry,
blood culture, full blood count, SARS-CoV-2 PCR

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13
Q

State the definitive treatment of this condition and outline the infection prevention precautions that
you would implement.

A

Intravenous penicillin for 7 days, institute droplet precautions to prevent spread on the infection

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14
Q

Is this a notifiable condition.

A

Yes

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15
Q

In this case all the patients close contacts must be given post exposure prophylaxis, briefly explain
the term close contact.

A

Close contacts are people living in the same house or sharing eating utensils (1) with the index case in
the seven days (1) prior to the onset of illness

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16
Q

Complete the table below describing cerebrospinal fluid (CSF) characteristics in different infections.
Use the following terms: elevated, increased, moderately increased, decreased or normal.

A

Bacterial meningitis Elevated, polymorphonuclear
leaucocytes
Increased Decreased
Tuberculous meningitis Elevated, lymphocytes Increased Decreased
Viral meningitis Elevated, lymphocytes Moderately
increased
Normal
Fungal meningitis Elevated, lymphocytes Increased Decreased

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17
Q

List the routes by which a brain abscess can develop.

A

Haematogenous, direct trauma, contiguous spread

18
Q

State three (3) organisms that can cause brain abscesses (use full name where possible).

A

Streptococcus anginosus
Anaerobes
Gram negative bacilli e.g. E. coli
Staphylococcus aureus
Nocardia
Actinomyces

19
Q

State the anatomical location of the inflammation in each of the following syndromes. Meningitis, encephalitis, myelitis

A

a. Meningitis
Meningitis – meninges
b. Encephalitis
Encephalitis – brain parenchyma
c. Myelitis
Myelitis – spinal cord

20
Q

List two (2) symptoms or signs of each syndrome.Meningitis, encephalitis, myelitis

A

a. Meningitis
Meningitis – headache, neck stiffness, photophobia, nausea and vomiting - with normal brain
function
b. Encephalitis
Encephalitis – altered brain function – various: decreased level of consciousness, altered mental
status, motor or sensory deficits, altered behavior and personality changes, and speech or
movement disorders
c. Myelitis
Myelitis – paralysis of parts of body, incontinence

21
Q

Outline the concept of acute disseminated encephalomyelitis (ADEM).

A

Associated with many different viral/bacterial infections. Usually post-infectious. Usually in the
convalescent phase. Not directly caused by the organism. Auto-immune response to myelin by T-cells.

22
Q

The typical cell predominance, glucose level, and protein level in aseptic viral meningitis is: Use
the following terms: increased, decreased or normal.

A

Cells: Lymphocytes
Glucose: Normal
Protein: Normal

23
Q

List the three (3) different types of CNS disease caused by measles, state the status of the affected
person’s immune system, and state the most likely outcome.

A

With or after the
rash, Days
Acute measles post-
infectious
encephalitis / ADEM
/ PIEM
Immunocompetent Recovery
Months Measles inclusion
body encephalitis
Immunocompromised Death
Years Subacute sclerosing
pan-encephalitis
Immunocompetent Death

24
Q

Explain why normal chloride levels are higher in cerebrospinal fluid than in plasma.

A

CSF has very low protein levels compared to plasma. Most plasma protein is albumin that carries a negative
charge at physiological pH. To maintain electroneutrality in the CSF in the absence of protein Chloride anions
increase.

25
State the normal Cerebrospinal Fluid/Plasma glucose ratio.
Approximately 60%
26
Identify the three (3) major “true” barrier systems contributing to the physiological blood-brain barrier.
(Cerebral capillaries, choroid plexus and meninges/arachnoid mater)
27
The inner ear contains three (3) distinct sensory structures. a. Identify these and their primary functions
(Organ of Corti – detection of sound waves; Macula – static equilibrium; Crista Ampullaris – dynamic equilibrium/acceleration and deceleration)
28
Identify the type of receptor cell that is common to the above sensory structures.
(Hair cells)
29
Identify the cranial nerve that conveys the sensory stimuli from the above sensory structures to the brain.
(Cranial nerve XIII)
30
Briefly explain which structural features distinguish the Blind Spot from other parts of the neural retina.
(No photoreceptor cells and other neuronal cell bodies; exit point of optic nerve/retinal ganglion cell axons)
31
The Blind Spot is not normally perceived in the field of vision. Give a brief explanation for this.
(The visual centres in the brain extrapolate visual information through binocular vision and from the areas of the visual field adjacent to the Blind Spot to fill the space of the receptor-free area)
32
Discuss the pathological sequalae of a subdural haematoma.
* Initially the subdural haematoma is a flat blood clot not attached to the dura. (1) * Fibroblast ingrowth causes organization after 5-6 days resulting in loose attachment. (1) * After 10-20 days – outer membrane is formed. (1) * Then inner membrane forms, resulting in complete encapsulation. (1) * Further organization leads to formation a sac with a fibrous wall (chronic subdural haematoma) and blood is resorbed resulting in a cavity containing clear yellow fluid. (1)
33
Give a physiological explanation for the development of memory loss in the patient.
TBI may result in primary or secondary damage to the structures/areas of the brain that are associated with learning and memory (1) e.g. the hippocampus and the cortex (1). TBI may also cause a disruption of the neurotransmitter system that mediates memory function. (1)
34
Give a physiological explanation for the increased muscle tone in the patient.
TBI causes upper motor neuron (UMN) damage (1) and results in the removal of the normal inhibitory effects that UMN have on lower motor neurons (LMN) (1). Lack of inhibition results in increased firing of LMN and increased contractility/tone/activity in muscle and dystonia (1). OR A disruption of the neurotransmitter systems (1) (e.g. the dopaminergic system) (1) that mediates motor control may also cause increased muscle tone (1).
35
33. Briefly explain whether the symptoms exhibited by the patient show signs of upper or lower motor neuron damage.
The patient shows signs of UMN damage (1) as evidenced by the spasticity/increased muscle tone (1)
36
In addition to physical injury of brain tissue, TBI is also often associated with alterations of neurotransmitter release. Using your knowledge of the function of neurotransmitters, explain the changes in brain function you would expect should the patient have: (3x4 =12 marks) a. reduced dopamine release
disrupted motor control, * disrupted cognitive/executive functions, * disrupted emotional/behavioural functions, * other dopamine-deficiency related symptoms (half a mark for each correct answer)
37
excessive glutamate release
increased glutamate release leads to excitotoxicity and damage to neurons and thus may affect functions mediated by the frontal lobe – motor function, executive functions, behaviour and personality, learning and memory etc. OR any acceptable dysfunctions associated with frontal lobe damage (half a mark for each correct answer)
38
reduced serotonin release
depression and mood disorders, anxiety, sleep problems, behavioural compulsions OR any acceptable dysfunctions associated with serotonin deficiency. (half a mark for each correct answer)
39
reduced GABA release
Seizures, impaired executive functions, behaviour and personality, learning and memory etc. OR any acceptable dysfunctions associated with GABA deficiency (half a mark for each correct answer)
40
Identify the anatomical structure containing the cell bodies (somata) of the neurons that convey mechanosensory stimuli to the CNS. State how these neurons are classified in terms of their morphology
(Spinal/dorsal root ganglion; pseudo-unipolar)
41
Briefly describe the structure and function of the cell type after which the “Substantia Nigra” is named, give a unique diagnostic feature of these cells and state in what neurological disorder these cells play a key role.
(Multipolar, dopamine-releasing neurons; modulate the activity of the direct and indirect pathways involved in motor control in the basal nuclei; contain neuromelanin pigment inclusions; Parkinson’s disease)