Questions for SBAs

Question 1

How does a fasciculation occur (3)

Answer 1

• Motor neuron dies, and so muscles fibres of the motor unit lose their nerve supply (denervation)
• Axons of the remaining motor unit grow and reach out to the denervated muscles fibres (reinnervation).
• The resulting new motor unit is larger and less stable and prone to ectopic generation of electrical stimuli in the distal axon that cause contraction of the muscle fibres ( a fasciculation).

Question 2

Name 2 signs of an UMN lesion (seen in the patient) (2)

Answer 2

Tone increased spastic, clonus present, power weakness (pyramidal distribution flexors stronger than extensors UL and extensors stronger than flexors
in LL), reflexes brisk, extensor plantar responses, no wasting and no fasciculations.

Question 3

Name 2 signs of a LMN lesion (seen in the patient) (2)

Answer 3

LMN: Tone flaccid, power weakness (distal weaker than proximal), no clonus, reflexes reduced or absent, flexor plantar responses, wasting may be present, fasciculations may be present.

Question 4

What pathways are affected in NMS (1)

Answer 4

Pyramidal tracts (these are the corticospinal and corticobulbar tracts)

Question 5

Describe how the counter-current mechanism is established and why its useful (4)

Answer 5

• The counter-current mechanism is established by Na+ reabsorption (ascending limb of LoH)
• urea recycling
• and the countering direction of flow of vasa recta.
• The counter-current mechanism is useful in enabling water reabsorption/removing more urea using less water/concentrates urine

Question 6

How does vasopressin aid in the counter-current multiplication for water reabsorption (2)

Answer 6

Boots UT-A1 and UT-A3 numbers (apical and basolateral membrane of collecting duct)

Question 7

What factors stimulate ADH release (2)

Answer 7

Increased osmolarity
Hypovolaemia
Decrease in BP

Nausea
Angiotensin II
Nictotine

Question 8

What factors inhibit ADH release (2)

Answer 8

Decreased osmolarity
Hypervolaemia
Increase in BP

Ethanol
ANP (atrial natriuretic peptide)

Question 9

How does ADH affect aquaporins (2)

Answer 9

ADH up/downregulates AQP2 (apical) & AQP3 (basolateral) numbers as required

Question 10

How does ADH support Na+ reabsorption at the kidney (3)

Answer 10

• Thick ascending limb: Increase Na+/K+/2Cl- symporter
• DCT: Increase Na+/Cl- symporter
• CD (principle cell): Increase Na+ channel

Question 11

What is the role of the kidney to maintain acid-base balance (3)

Answer 11

Secretion + excretion of H+
Reabsorption of HCO-3
Production of new HCO-3

Question 12

Describe how increased tubular sodium affects GFR (3)

Answer 12

High tubular sodium -> Increased sodium/chloride uptake via triple transporter
Adenosine release from Macula Densa cells -> Detected by extraglomerular mesangial cells -> Reduces renin production
Promotes afferent SMC contraction -> Reduces perfusion pressure and so GFR

Question 13

Where are the low pressure baroreceptors located (3)

Answer 13

Atria
Right ventricle
Pulmonary vasculature

Question 14

Where are the high pressure baroreceptors located (3)

Answer 14

Carotid sinus
Aortic arch
Juxtaglomerular appartus

Question 15

What is potassium secretion stimualted by (4)

Answer 15

Increased:
Plasma K conc
Tubular flow rate
Aldosterone
Plasma pH

Question 16

Causes of hypokalaemia (5)

Answer 16

Inadequate dietary intake (too much processed food)
Diuretics (due to increase tubular flow rates)
Surreptitious vomiting
Diarrhoea
Genetics (Gitelman’s syndrome; mutation in the Na/Cl transporter in the distal nephron)

Question 17

Causes of hyperkalaemia (5)

Answer 17

Severe diabetes
Elderly
ACE inhibitors
Seen in response to K+ sparing diuretics
Kidney disease

Question 18

How does a prolactinoma cause infertility (4)

Answer 18

• Prolactin binds to prolactin receptors on kisspeptin neurons in hypothalamus
• Inhibits kisspeptin release.
• Decreases in downstream GnRH/LH/FSH/T/Oest
• Oligo-amenorrhoea/Low libido/Infertility/Osteoporosis

Question 19

Describe process of plaque formation (4)

Answer 19

1. Damage occurs to endothelial lining (due to high BP, smoking, diabetic glycosylation end products etc.) especially at vascular branching points (as a result of turbulent flow → endothelial stress)
2. Lipids leak through damaged endothelium and accummulate in intima → oxidised by free radicals
3. Macrophages scavenge the oxidised lipids → turn into foam cells and deposit in blood vessel walls
4. Foam cells secrete growth factors (like platelet derived growth factor) that result in smooth muscle proliferation + extra-cellular matrix deposition → plaque formation

Question 20

How are DVTs are often precipitated by Virchow’s triad (3)

Answer 20

• Blood stasis (eg. like a long haul flight or bed rest)
• Endothelial damage (eg. traumatic vessel injuries)
• Hypercoagulability (eg. oral contraceptive use, pregnancy)

Question 21

Cellular pathology of MS (4)

Answer 21

Inflammation
Demyelination
Axonal loss
Neuro degeneration

Question 22

Types of MS (4)

Answer 22

Relapsing-remitting
Primary progressive
Secondary progressive
Progressive-relapsing

Question 23

Name and describe the paradox seen involving angiogenesis and cardiovascular disease (3)

Answer 23

The Janux paradox.
Angiogenesis (within vaso vasorum of the adventita) promotes plaque growth
Therapeutic angiogenesis (revascularisation) prevents damage post-ischemia

Question 24

Describe how early onset pre-eclampsia affects the fetus (4)

Answer 24

Shallow trophoblast invasion
Maladation of materal spiral artery
Poor placental perfusion
Fetal growth reduction

Question 25

What is recurrent pregnancy loss/recurrent miscarriage (1)

Answer 25

(In the UK, defined by) 3 or more pregnancy losses (consecutive or non-consecutive

Question 26

What signalling pathways might underpin RPL/RM (2)

Answer 26

Reduced levels of LIF in the uterine secretions of sub fertile women Non-selective uterus hypothesis in those patients - uterus permits implantation of poor quality embryos and changes in uterine mucin expression in women with RM/RPL

Question 27

What is the major cause of early clinical pregnancy loss (<12 weeks gestation) (1)

Answer 27

Aneuploidity

Question 28

How does this increase with age (2)

Answer 28

Cohesion proteins are lost, leading to loss of cohesion between chromatids with increasing age of the oocytes Chromatids can seperate and drift during meiotic division, rather than being segregated accurately by the spindle

Question 29

Risk factors for ectopic pregnancy (5)

Answer 29

``` Prior ectopic pregnancy Prior fallopian tube surgery Certain STIs Pelvic inflammatory disease Endometriosis ```

Question 30

How does smoking increase the risk of ectopic pregnancy (3)

Answer 30

Continine, a component of cigarette smoke, regulates the expression of PROKR1, a regulator of fallopian tube smooth muscle contractabiltiy Conitinine also induces pro-apoptosis protein expression in fallopian tube explants It is hypothesised that tobacco smoke inhibits ciliary function therefore reducing tubal transit of the embryo

Question 31

What is an ectopic pregnancy (1)

Answer 31

Implantation of the embryo at a site other than the uterine endometrium

Question 32

What are two ways in which cannabis may affect the fallopian tube (2)

Answer 32

Cannabionoid receptor CB1 levels are reduced in ectopic pregnancy patients Alter the endocannabionoid tone (balance) in the tube leading to a disrupted embryo environment

Question 33

What is stigma (1)

Answer 33

Stigma refers to challenges faced by people with mental illness related to knowledge, attitudes, and behaviour of people they meet

Question 34

What are the types of stigma (3)

Answer 34

•Intrapersonal stigma Direct effect on the individual Internalised discrimination Compounded by direct effects of illness •Interpersonal stigma Family Friends Colleagues •Structural stigma Poor resources and funding Access to physical health care

Question 35

What are the consequences of stigma (3)

Answer 35

Barrier to care Abuse Rejection + Isolation

Question 36

Causes of mental health stigma (3)

Answer 36

* Poor understanding of mental health * Negative attitude * Social exclusion

Question 37

Pathophysiology of Achondroplasia (3)

Answer 37

Inhibition of chondrocyte proliferation in proliferation zone of physis (secondary) Defect in endochondral bone formation Long bones affected

Question 38

Describe the formation of a plaque (4)

Answer 38

1. Damage occurs to endothelial lining (due to high BP, smoking, diabetic glycosylation end products etc.) especially at vascular branching points (as a result of turbulent flow → endothelial stress) 2. Lipids leak through damaged endothelium and accummulate in intima → oxidised by free radicals 3. Macrophages scavenge the oxidised lipids → turn into foam cells and deposit in blood vessel walls 4. Foam cells secrete growth factors (like platelet derived growth factor) that result in smooth muscle proliferation + extra-cellular matrix deposition → plaque formation

Question 39

*SSSS described* how in most and why

Answer 39

Neonates Exfoliative toxin Kidneys cannot excrete it quickly

Question 40

Pathophysiology of Osteogenesis Imperfecta? (2)

Answer 40

Decreased type 1 collagen due to decreased secretion and production of abnormal collagen Insufficient osteoid production

Question 41

What two things contribute to developing proteinuria (2)

Answer 41

Hyperglycaemia | Glomerular HTN

Question 42

FIX Describe the mechanism of damage in retinopathy (4)

Answer 42

Mitochondrial superoxide free radicals in endothelium Glycated plasma proteins -> AGEs advanced glycated end products Inflammatory pathways Damaged endothelium

Question 43

What happens in compation? (5)

Answer 43

Cells start pressing up against the zona pellucida Go from spherical to wedge-shaped Outer cells connect to each other through tight gap junctions and desmosomes Forms barrier to diffusion between inner and outer embryo Outer cells become polarised

Question 44

Describe the structure of the primary chorionic villi and outline the stages in its development (5)

Answer 44

Developed from cytotrophoblast which form finger-like projections through the syncitiotrophoblast layer into the maternal endometrium Terminal villus - convoluted knot of vessels and vessel dilation Primary development - outgrowth of the cytotrophoblast and branching of these extensions Secondary - growth of the fetal mesoderm into the primary villi Tertiary - growth of the umbilical artery and umbilical vein into the villus mesodderm, providing vasculature