Exam Questions

Question 1

1. Describe the reasons behind the differing clinical presentation of a patient with an upper (UMN) versus a lower (LMN) motor neurone lesion.
   (4 marks)

Answer 1

UMN is inhibitory over LMN. LMN stimulates the effector (e.g. skeletal muscle).
UMN lesion causes loss of inhibition of LMN and therefore spastic paralysis.
LMN lesion results in a lack of stimulation of effector and therefor flaccid paralysis.

Question 2

x

Answer 2

x

Question 3

4. Give an overview of the closure of the neural tube in the human embryo. You may use a well labelled diagram in your answer.
   (6 marks)

Answer 3

Answer: The diagram on the left side = multi-site closure of neural tube in humans; primary (1-4) and secondary (5) neurulation.

Question 4

5. List two (2) possible names for the bulging cyst on the back of the infant.
   (1 mark)

Answer 4

[meningocoel, meningomyelocoele—NOT myelocoele]

Question 5

9. List five (5) other causes of clubfoot

2 ½ marks

Answer 5

[causes of anhydramnios eg bilateral renal agenesis/bilateral cystic renal dysplasia/urethral atresia; causes of fetal akinesia/absent movement eg cerebral pathology, other causes of spinal disease (neuronal loss); muscle weakness]

Question 6

11. State the mechanism for the increase of this alpha-feto protein
    (1 mark)

Answer 6

b. Neural tube defects: The open nature of the neural tube allows the transudation of AFP from foetal serum directly into amniotic fluid in amounts greater than might be expected physiologically. This then results in increased amounts of AFP in maternal serum.

Question 7

12. State one other pregnancy-related condition (besides NTD) where alpha-feto protein will be elevated in maternal serum.

Answer 7

c. Multiple pregnancy; foetal conditions (renal disease, abdominal wall defects)

Question 8

13. List two (2) non-pregnancy-related conditions in which this alpha-feto protein is elevated.

Answer 8

d. Non-pregnancy-related: liver cirrhosis, hepatitis, hepatoma, non-seminomatous germ cell tumours

Question 9

14. List four (4) other biochemical tests that may be performed antenatally for screening of foetal anomalies. (4 x ½ = 2 marks)

Answer 9

e. PAPP-A
f. Free or total beta human chorionic gonadotropin
g. Estriol
h. Inhibin

Question 10

16. Outline six (6) factors / reasons that may prevent access of women to termination of pregnancy (TOP) services in South Africa.
    (6 marks)

Answer 10

1. Inequitable distribution of services- not all designated services are providing TOP, greater gap in rural areas
2. Staff resistance : conscientious objection,
3. Abusive treatment by hospital staff- women are insulted, judgemental & rude staff
4. Fear of breaching confidentiality by nurses- women would not use legal abortion services as they were scared that staff members would leak the information
5. Lack of trained personnel- There is also a lack of providers trained to perform TOP services
6. Long waiting lists –in some instances, long waiting lists for abortions have deterred women from using public health abortion services
7. Lack of knowledge of the TOP legislation
8. Lack of knowledge of facilities providing abortions- many women are aware of the TOP legislation, but do not know which health facilities offer TOP services, so they don’t know where to go
9. Stigma associated with abortions- Many women would not have an abortion due to religious and social stigmas

Question 11

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

Answer 11

(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)

Question 12

19. 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.
    (2 marks)

Answer 12

(Spinal/dorsal root ganglion; pseudo-unipolar)

Question 13

Briefly describe the structure and function of the cell type after which the “Substantia Nigra” is named.

Answer 13

(Multipolar, dopamine-releasing neurons; modulate the activity of the direct and indirect pathways involved in motor control in the basal nuclei

Question 14

21. Name the cell types that will be primarily affected by de-myelinating diseases
    (2 marks)

a) of the CNS:
b) of the PNS:
c) state the principal structural difference between these cell types.
(1 mark)

Answer 14

a) of the CNS:

Oligodendrocytes:

b) of the PNS:
Schwann cells

c) state the principal structural difference between these cell types.
(1 mark)
Schwann cells myelinate only one axon segment, oligodendrocytes many

Question 15

a) Describe the synthesis, release and degradation of Acetylcholine.
b) State what subtype of acetylcholine receptor is located at the neuromuscular junction (NMJ) and explain how is it adapted to mediate muscle contraction.
(8 marks)

Answer 15

Answer:
-Acetylcholine (ACh) is the neurotransmitter in cholinergic neurons. ACh is synthesized in nerve terminals from choline and acetyl coenzyme A. (1 mark)
-Choline is transported into the nerve terminal by a high affinity choline transporter. (1 mark)
-Choline is combined with acetyl-CoA by the enzyme choline acetyltransferase. Acetyl-CoA comes from metabolic pathways in the mitochondria which are found in high concentration in
nerve terminals. (1 mark)
-ACh synthesis occurs in the cytoplasm. ACh is transported into synaptic vesicles by the vesicular ACh transporter. (1 mark)
-ACh is released into the synaptic cleft where it diffuses to the postsynaptic cell to activate ACh receptors. (1 mark)
-The action of acetylcholine is terminated by the enzyme acetylcholinesterase. (1 mark)

ACh binds to nicotinic ACh receptors on the skeletal muscle fibre endplate and are ligand-gated ion channels whose activation causes the influx of Na+ and efflux of K+. (1 mark)
This produces an end-plate potential (EPP) which activates voltage-gated sodium channels in the muscle, thus depolarizing the muscle, eliciting a contraction. (1 mark)

Question 16

23. Describe the mechanism by which the cerebellum is able to correct for motor signal errors and how synaptic plasticity within the cerebellum circuitry contributes to motor learning.
    (6 marks)

Answer 16

Answer:
The mossy fibre inputs to the cerebellum convey the sensory information used to evaluate the overall sensory context of the movement. (1 mark)
The error signal is believed to be conveyed by the climbing fibre inputs. (1 mark)
Climbing fibres are known to be especially active when an unexpected event occurs, e.g. when a greater load than expected is placed on a muscle. (1 mark)
The large divergence of input from the mossy fibres to the granule cells to the parallel fibres is believed to create complex representations of the entire sensory context and the desired motor output. (1 mark)
When the desired output is not achieved, the climbing fibres signal this error and trigger a calcium spike in the Purkinje cell. (1 mark)
The influx of calcium changes the synaptic connection strengths (plasticity) between parallel fibres and Purkinje cells, such that the next time the same behavioural context occurs, the motor output will be modified to more closely approximate the desired output. (1 mark)

Question 17

24. Outline the function of muscle spindles by describing the synaptic connections between Group Ia spindle afferents and alpha motor neurons, and the efferent control of spindle sensitivity.
    (6 marks)

Answer 17

Answer:
Synaptic connections between Ia spindle afferents and α motor neurons:
1. Ia afferent fibers synapse directly with motor neurons. They are the only sensory afferent to do so. (1 mark)
2. Each Ia afferent makes only a few (2-6) synapses with any one motor neuron - glutamate is released. (1 mark)
3. Release of glutamate acting on motor neuron dendrites activates monosynaptic EPSPs (1 mark).

Efferent control of spindle sensitivity

1. Spindles are also innervated by special motor neurons called gamma motor neurons. Gamma motor neurons cause the intrafusal fibres of the muscle spindle to contract, thus shortening the spindle (2 mark).
2. Gamma motor neurons are activated along with alpha motor neurons during voluntary muscle contraction (“alpha-gamma coactivation”) to prevent the spindle from becoming slack, thus maintaining sensitivity throughout the range of muscle contraction (1 mark).

Question 18

25. With the aid of a clear diagram, show how

a) a CONTRALATERAL lesion can cause the symptom of Right sided motor weakness (ie Left sided lesion causing Right sided weakness)
(2 marks)
b) an IPSILATERAL lesion can, in the face of raised intracranial pressure, cause the symptom of Right sided motor weakness (ie Right sided lesion causing Right sided weakness), indicating the tracts involved.
(5 marks)

Answer 18

A] * L sided lesion involving motor cortex of R side. Diagram must show decussation and crossing over to explain laterality.

B] R sided supratentorial lesion  R sided transtentorial herniation of parahippocampal gyrus [usually ipsilateral] [1]  pressure on brain stem with shift to L [1] . Outer edge of pons is compressed against the free edge of the tent on the L side [Kernohan’s notch] [1]. This carries long motor tracts from the R [1] . Decussation is at a lower level so the weakness is on the R side [ false localizing sign].[1]

Question 19

26. List five (5) biochemical analytes (in blood) that would support this diagnosis of hyperaldosteronism. For each analayte, state the direction of change.
    (5 x ½ = 2 ½ marks)

Answer 19

a. Increased aldosterone
b. Decreased renin
c. Hypokalaemia
d. Hypernatraemia
e. Metabolic alkalosis (high pH, low [H+], high [HCO3-])

Question 20

27. State the two (2) analytes that would differentiate between a renin producing tumour and primary hyperaldosterone according to their direction of change. For each, state the direction of change in the case of a renin producing tumour.
    (4 x ½ = 2 marks)

Answer 20

a. Renin increased/normal

b. Sodium normal

Question 21

28. List three (3) tests used to screen for cushings syndrome.
    i. (3 x ½ = 1½ marks)

Answer 21

a. Midnight cortisol (serum / saliva)
b. 24 hour urine cortisol
c. Low dose dexamethasone suppression test
d. Loss of diurnal rhythm

Question 22

29. Name four (4) potential complications of recurrent urinary tract infections that have been missed and not treated.
    (2 marks)

Answer 22

Septic shock, scarring, pyelonephritis, renal damage/renal scarring and renal dysfunction/hypertension/renal abscesses.

Question 23

33. Identify the three (3) major “true” barrier systems contributing to the physiological blood-brain barrier
    (3 marks)

Answer 23

(Cerebral capillaries, choroid plexus and meninges/arachnoid mater)

Question 24

34. The inner ear contains three (3) distinct sensory structures.

a) Identify these and their primary functions
(3 marks)

b) Identify the type of receptor cell that is common to the above sensory structures
(½ mark)

c) Name the cranial nerve that conveys the sensory stimuli from the above sensory structures to the brain.
(½ mark)

Answer 24

(Organ of Corti – detection of sound waves; Macula – static equilibrium; Crista Ampullaris – dynamic equilibrium/acceleration and deceleration)

b) (Hair cells)
c) (Cranial nerve XIII)

Question 25

35. Name the structural features that distinguishs the Blind Spot from other parts of the neural retina. (2 marks) 36. The Blind Spot is not normally perceived in the field of vision. Give a brief explanation for this.

Answer 25

(No photoreceptor cells and other neuronal cell bodies; exit point of optic nerve/retinal ganglion cell axons) (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)

Question 26

41. Give two (2) haematogenous routes whereby an organism causing otitis media could have entered the brain. (2 marks)

Answer 26

i] septicaemia | Ii] diploic veins

Question 27

42. Give two (2) conditions which would make this child at increased risk for S. pneumoniae. (1 mark)

Answer 27

``` i] asplenia ii] Sickle cell iii] HIV iv] splenectomy v] proteinuria ```

Question 28

47. If this was a case of neonatal meningitis, name three (3) organisms/organism groups that you would consider as most likely causes. (3 marks)

Answer 28

E.coli and other Enterobacteriaceae, Streptococcus agalactiae (Group B Strep) and Listeria monocytogenes.

Question 29

49. Describe the post-exposure prophylaxis you would give someone who has just been bitten by a potentially rabid dog. (5 marks)

Answer 29

Wash wound. Do not suture. Tet tox. Antibiotics. Vaccine – deltoid, baby = anterolateral thigh. Vaccine days 0/3/7/14/(28). Immunoglobulin into wound; excess into deltoid opposite vaccinated deltoid.

Question 30

50. A person who has just been bitten by a potentially rabid dog requests to be tested for rabies hopefully to avoid all the unpleasant injections. State whether requesting these tests is a good or bad practice, and explain your answer. (3 marks)

Answer 30

Bad idea – rabies virus will not be detected in this patient. Antibodies would not be detected in this patient unless this patient previously had been vaccinated.

Question 31

51. Outline the pathogenesis of progressive multifocal leukoencephalopathy. (2 marks)

Answer 31

JC virus, latent in most of the population. Immunocompromise  reactivation.

Question 32

53. Compare and contrast the oral polio vaccine and the injectable polio vaccine. (3 marks)

Answer 32

``` OPV = Sabin, live attenuated, 3 strains (now dropping to 2), risk of mutation, sterilising immunity, IgA in gut IPV = Salk, inactivated, 3 strains, no risk of mutation, immunity = disease prevention, IgG in blood ```

Question 33

58. Outline the public health response to a suspected case of meningococcal disease. (5 marks)

Answer 33

Every suspected case should prompt an urgent response to include: Immediate telephonic notification to the local health authority by a healthcare worker in the facility, followed by written notification. Rapid investigation of the case Classification of the case as confirmed or probable Provision of post exposure prophylaxis to close contacts Identification of other cases in the same institution or community that may suggest a cluster.

Question 34

60. Define what is meant by a teratogen. | 2 marks

Answer 34

Teratogen = a drug or other substance or event capable of interfering with the physical formation and/or development of an embryo and fetus, causing birth defects or termination of pregnancy.

Question 35

61. Briefly describe the mechanism behind the teratogenic effect of alcohol. (2 marks)

Answer 35

Students can write around any of the following: Numerous mechanisms likely contribute to the damaging effects of prenatal alcohol exposure on the developing fetus and particularly the developing central nervous system: necrosis and apoptosis; free radicals, oxidative stress, and mitochondrial dysfunction; interference with growth factors regulating cell proliferation and survival; negative effects on glial cell function; negative effects on neurotransmitter systems; affects glutamate and serotonin; excitotoxicity; affects glucose transport and uptake; effects on cell adhesion; altered developmental regulation of gene expression.

Question 36

63. List two (2) possible causes of low birth weight. (1 mark)

Answer 36

[alcohol ingestion; GPH; premature infant]

Question 37

68. List five (5) metabolic abnormalities associated with acute alcohol intoxication. For each abnormality, briefly outline the mechanism. (5 x 1½ = 7 ½ marks)

Answer 37

a. Hypoglycaemia – inhibition of gluconeogenesis (due NAD/NADH imbalance favouring NADH accumulation) b. Ketoacidosis / ketosis – low carbohydrate intake; inhibition of gluconeogenesis. c. Hypertriglyceridaemia – lack of NAD prevents acetylCoa entry into Kreb cycle, acetylCoA is diverted to fatty acid synthesis instead. d. Lactic acidosis – high NADH/NAD ratio favours lactate formation e. Hyperosmolarity – alcohol molecules contribute to osmolarity f. Diuresis and mild dehydration (decreased ADH release) g. Dilutional hyponatraemia: ingestion of vast quantities of water (hypotonic fluid) in the form of beer. h. Hyperuricaemia – increased AMP production and therefore breakdown into urate; inhibition of renal urate secretion by ketones and lactate (anions compete for transporter); increased flux through purine breakdown pathway due to increased diversion of acetyl CoA to fatty acid synthesis (NADPH)

Question 38

40. List the principle functional cortical areas. | (5½ marks)

Answer 38

Broca’s motor speech area (.5), Wernicke’s auditory association area (.5), primary motor area (.5), primary sensory area (.5), motor association area (.5), sensory association area (.5), prefrontal cortex (.5), frontal eye field (.5), primary auditory cortex (.5), primary visual cortex (.5), limbic association cortex (.5)

Question 39

41. List the nuclear components of the basal ganglia/nuclei (2½ marks)

Answer 39

Caudate nucleus (.5), nucleus accumbens (.5), putamen (.5), globus pallidus (.5), substantia nigra (.5)

Question 40

43. List the biochemical changes in blood typically present in hyperaldosteronism: (3 x ½ = 1 ½ marks)

Answer 40

Hypernatraemia Hypokalaemia Metabolic alkalosis