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Y2 - BRS 2 > Questions for SBAs > Flashcards

Questions for SBAs Flashcards

1
Q

How does a fasciculation occur (3)

A
  • 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).
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2
Q

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

A

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.

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3
Q

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

A

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.

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4
Q

What pathways are affected in NMS (1)

A

Pyramidal tracts (these are the corticospinal and corticobulbar tracts)

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5
Q

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

A
  • 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
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6
Q

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

A

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

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7
Q

What factors stimulate ADH release (2)

A

Increased osmolarity
Hypovolaemia
Decrease in BP

Nausea
Angiotensin II
Nictotine

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8
Q

What factors inhibit ADH release (2)

A

Decreased osmolarity
Hypervolaemia
Increase in BP

Ethanol
ANP (atrial natriuretic peptide)

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9
Q

How does ADH affect aquaporins (2)

A

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

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10
Q

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

A
  • Thick ascending limb: Increase Na+/K+/2Cl- symporter
  • DCT: Increase Na+/Cl- symporter
  • CD (principle cell): Increase Na+ channel
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11
Q

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

A

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

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12
Q

Describe how increased tubular sodium affects GFR (3)

A

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

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13
Q

Where are the low pressure baroreceptors located (3)

A

Atria
Right ventricle
Pulmonary vasculature

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14
Q

Where are the high pressure baroreceptors located (3)

A

Carotid sinus
Aortic arch
Juxtaglomerular appartus

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15
Q

What is potassium secretion stimualted by (4)

A 
Increased:
Plasma K conc
Tubular flow rate
Aldosterone
Plasma pH
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16
Q

Causes of hypokalaemia (5)

A

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)

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17
Q

Causes of hyperkalaemia (5)

A 
Severe diabetes
Elderly
ACE inhibitors
Seen in response to K+ sparing diuretics
Kidney disease
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18
Q

How does a prolactinoma cause infertility (4)

A
  • 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
19
Q

Describe process of plaque formation (4)

A
  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
20
Q

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

A
  • Blood stasis (eg. like a long haul flight or bed rest)
  • Endothelial damage (eg. traumatic vessel injuries)
  • Hypercoagulability (eg. oral contraceptive use, pregnancy)
21
Q

Cellular pathology of MS (4)

A

Inflammation
Demyelination
Axonal loss
Neuro degeneration

22
Q

Types of MS (4)

A

Relapsing-remitting
Primary progressive
Secondary progressive
Progressive-relapsing

23
Q

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

A 
The Janux paradox.
Angiogenesis (within vaso vasorum of the adventita) promotes plaque growth
Therapeutic angiogenesis (revascularisation) prevents damage post-ischemia
24
Q

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

A

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

25
Q

What is recurrent pregnancy loss/recurrent miscarriage (1)

A

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

26
Q

What signalling pathways might underpin RPL/RM (2)

A

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

27
Q

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

A

Aneuploidity

28
Q

How does this increase with age (2)

A

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

29
Q

Risk factors for ectopic pregnancy (5)

A 
Prior ectopic pregnancy
Prior fallopian tube surgery
Certain STIs
Pelvic inflammatory disease
Endometriosis
30
Q

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

A

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

31
Q

What is an ectopic pregnancy (1)

A

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

32
Q

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

A

Cannabionoid receptor CB1 levels are reduced in ectopic pregnancy patients

Alter the endocannabionoid tone (balance) in the tube leading to a disrupted embryo environment

33
Q

What is stigma (1)

A

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

34
Q

What are the types of stigma (3)

A

•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

35
Q

What are the consequences of stigma (3)

A

Barrier to care
Abuse
Rejection + Isolation

36
Q

Causes of mental health stigma (3)

A
  • Poor understanding of mental health
  • Negative attitude
  • Social exclusion
37
Q

Pathophysiology of Achondroplasia (3)

A

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

38
Q

Describe the formation of a plaque (4)

A
  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
39
Q

SSSS described how in most and why

A

Neonates
Exfoliative toxin
Kidneys cannot excrete it quickly

40
Q

Pathophysiology of Osteogenesis Imperfecta? (2)

A

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

41
Q

What two things contribute to developing proteinuria (2)

A

Hyperglycaemia

Glomerular HTN

42
Q

FIX Describe the mechanism of damage in retinopathy (4)

A

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

43
Q

What happens in compation? (5)

A

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

44
Q

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

A

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

Y2 - BRS 2 (5 decks)

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