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PBL year 2 (Sam) > Unit 14 week 4 > Flashcards

Unit 14 week 4 Flashcards

1
Q

Localisation of function

A

Specific neurological dysfunctions arise based on tumour/lesion location, indicating that there are neural areas/pathways dedicated to speech, language, motor control, and brain stem functions

Neurological deficits can indicate lesion location

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2
Q

• Review brain anatomy

− Especially cranial nerves

− Sensory cortical regions

− Motor cortex

− Vasculature

− Blood-brain barrier, role in drug choices

A
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3
Q

LIFESTYle and cqncer risk

A

no link between cortisol and cancer formation

however those that are more stressed tend to engage in cancer promoting behaviours e.g., smoking, drinking alcohol, overreating

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4
Q

Potemtial causes of lump in breast

A

non-cancerous lump e.g., fibroadenoma, breast cyst, lipoma, puberty, , mastitis, cancer

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5
Q

comparison of benign and malignant neoplasm

A

Neoplasm:

Benign

Malignant/cancerous

Definition

Slow-growing, non-invasive cells with lost proliferation control. If mass of cells, can call tumour (solid or fluid-filled). Lymphoma, leukaemia

are neoplasias but not tumours.

Invasive (local) or metastatic (distant) spread

Cells

May be heterogeneous

Clonal, essentially immortal

Capsule

(fibrous)

Typically present

Usually absent

Borders

Typically smooth, sharply demarcated

Irregular

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6
Q

Signs of breast cancer

A
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7
Q

Anatomy of breast

A

anterior thoracic wall

at the centre of the breast is the areola which contains sebaceous glands

contains mammory glands- involved in lactation and controlled by pituitary

fibrous troma condenses to form suspensory ligaments which secures the breast to the dermis of the underlying pectoral fascia

supplied by the internal thoracic artery medially and the lateral thoracic + thoracromial laterally

3 groups of lymoh nodes receive drainage from the breast:

axillary nodes (75%)

parasternal (20%)

posterior intercostal (5%)

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8
Q

definitions of:

dysplasia

carcinoma in situ

invasive carcinoma

A

dysplasia- Cellular proliferation (hyperplasia) showing some but not all the molecular and morphological characteristics

carcinoma in situ- Severe dysplasia without spread across the limiting basement membrane: thus without invasion of tissue and without metastatic potential. Usually treated, due to high risk of developing into cancer. Removal is considered cure

invasive carcinoma- Cancer

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9
Q

Difference between hyperplasia and neoplasia

A

Hyperplasia is a physiological (normal) response to a stimulus that leads to normal cell proliferation and enlargement of a tissue

Neoplasia is an abnormal cell proliferation in a non-physiological manner, which is unresponsive to a stimulus

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10
Q

Models of response to diagnosis

A

kubler ross 5 stages of grief

response can change over time e.g., reoccurence

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11
Q

general pattern of referral

A

within 14 days

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12
Q

examples of local therapy and systemic therapy for cancer

A

local: surgery, radiotherapy
systemic: chemo, hormonal, immuno

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13
Q

What is a mammogram?

how is a needle core biopsy linked?

A

A mammogram is an X-ray examination of the breast showing extent of the tumour and may indicate benign or malignant processes- Ultrasound may also be used

Needle core biopsy can be guided using the mammogram, producing tissue for histological examination

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14
Q

general progression of normal cells to metastisis

A

Normal → Dysplasia → Carcinoma in situ → Invasive carcinoma

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15
Q

is it the primary or secondary tumour that usually kills people?

A

secondary

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16
Q

what are the cues for wide local excision rather than local excision

A

well transcribed, no evidence of spread

▪ A wide local excision is performed for cancer (due to infiltrative margins), extending beyond the apparent clinical surgical or radiological margin (benign tumours often removed with a narrow margin)

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17
Q

what is the sentinel lymph node procedure?

qhat are the general methods of cancer spread?

A

staging method which attempts to define how far a cancer has spread

  1. lymphatics
  2. blood
  3. local
  4. in body cavities
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18
Q

Classification of tumours

A

tumours based on primary site, cell type and cellular morphological predictors of behaviour

primary site: breast, colon,

cell type: epithelial, CT, melanocytic

morphological predictors of behaviour: [architectural disorganisation, pleomorphism (size/shape variation), mitoses, nuclear hyperchromasia (more intense chromatin staining), necrosis, invasion of tissues/blood vessels/lymphatic channels, differentiation (similarity to corresponding normal tissue)].

Benign

Malignant

Epithelium any type

Add -oma

Carcinoma

Epithelium from glandular organs e.g. breast, stomach, colon, prostate

Adenoma

Adeno-carcinoma

Epithelial from a squamous tissue e.g. skin, mouth, larynx, lung [after metaplasia i.e. change of one mature cell type to another]

Squamous cell papilloma

Squamous cell carcinoma

Epithelium of transitional type e.g. bladder

Transitional cell papilloma

Transitional cell

carcinoma

Connective tissue Fat

Chondrocyte Blood vessels

Add - oma

LipomaChondroma

Angioma

-sarcoma

Lipo sarcoma

Chondro sarcoma

Angiosarcoma etc

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19
Q

How are malignant tumours graded?

A

by biological aggresiveness:

1/2/3

or

well, moderately or poorly differentiated

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20
Q

metastasis can be split into 5 basic steps:

A

1) invasion of the basement membrane and cell migration

  • cells mechanically remodel the ECM through a cycle of cell protrusion and contraction
  • they chemically degrade the ECM using MMPs
  • become motile by undergoing epithelial to mesenchymal transition

2) intravastion into surrounding vasculature or lymphatic system
* tumour angiogenesis brings nutrients to the gorwing mass of cells while also offering them a route into the circulatory system for haematogenous spread
3) survival in circulation

within the blood stream, the cancer must survive:

a) haemodynamic forces
b) immune stresses
c) red blood cell collisions
* the tumour cells undergo mutations which allow them to survive e.g., PAR2 proteins recruit adaptor proteins to mediate cancer cell migration.

4) Extravasation from vasculature into secondary tissue

  • involves a cascade of events inc. the tumour cell arrest on the endothelium and making contact with platelets. cell displaces an endothelial cell in the lining
  • invsation of surrounding tissue

5) colonisation at secondary tumour site

21
Q

relevence of headaches in the morning and cancer

A

intracranial pressure is greatest when horizontal

not specifically alarming but you should still refer to neurology???

cancers can cause headaches as they are space occupying lesions

22
Q

hypertonia

hyperreflexia

aphasia

A

Hypertonia is likely a central nervous system deficit: upper motor neuron, basal ganglia or frontal lobes

▪ Hyperreflexia: increased speed or amplitude; presence helps localise lesion

aphasia

language impairment, either speech or comprehension: (students should)

understand basics of producing speech, in that it involves shaping the tongue, lips, vocal folds (within larynx).

23
Q

common differential diagnosis for brain dysfunction

A

ischaemic stroke

haemorrhagic stroke

lesion to cranial nerves

lesion to motor tracts

24
Q

brain anatomy- cortex landamarks

A

25
Q

damage to brocca’s and Wernicke’s area

A

Broca’s area produces coherent speech (damage causes Expressive aphasia)

Wernicke’s area (superior temporal area) is required for comprehension (damage causes

Receptive aphasia)

26
Q

mass effect

midline shifts

odema

A

▪ Mass effect implies mass(es) with possible oedema…… May impose pressure on CNS structures, impairing function

▪ Often causes midline shifts with increased complications, contralateral signs, hydrocephalus, increased intracranial pressure

oedema is the cause–> leaky blood vessels due to inflammation

skull is a rigid structure with little space unoccupied in it. increased intracranial pressure can lead to spinal cord hernation or injury which can be fatal

27
Q

frontal and parietal lobes of the brain + pons and effect of tumour in each

A
28
Q

Differentiating between upper and lower motor neurone lesion

A

UMN

lesions occur in the brain or spine- i.e. they lead to a lack of higher control:

  • Pyramidal weakness, ie flexors stronger than extensors in arms, extensors stronger than flexors in legs
  • Spasticity
  • Brisk reflexes
  • Upgoing (extensor) plantar reflex
  • Clonus- nvoluntary muscle contractions. This results in uncontrollable, rhythmic, shaking movements

LMN

lesions occur in the nerve root, plexi or peripheral nerve

Flaccid weakness

Normal or reduced tone

Reduced or absent reflexes

Wasting

Fasciculation (ie no nerve supply)

29
Q

association

commissural

projection fibres in the brain

A

association- white matter tract that connects 2 areas within the same hemisphere

commissural/ transverse- connect 2 hemispheres through the corpus callosum

projection- type of white matter tract that connects the cortex with other areas of the CNS e.g., to brainstem or spine

30
Q

Her-2 positive cancer therefore which drug should you use as chemotherapy?

A

trastuzumab

CLASS: recombinant IgG1 kappa humanised monoclonal antibody

INDICATION: HER2+ metastatic breast cancer. HER-2 triggers downstream signalling when bound to EGF and cell proliferation. monotherapy or as adjunct to cis-platin

PHYS: Target: extracellular domain of HER-2 action: nhibition

  • downstream signalling involves Ras/ Raf/ mitogen-activated protein kinase (MAPK) that acticates cell prolif and growth.
  • inhinbits angiogenesis and activates antibody-dependant cell-mediated cytotoxicity

Side effects: anxiety, alopecia, appetite, depression

31
Q

alternative target for anti breast cancer drugs?

A

oestrogen receptor

32
Q

grading lymoh node involvement

A
33
Q

large molecular weight limits delivery across the blood brain barrier but:

A
  • radiotherapy damages BBB endothelium, increasing permeability
  • neurovascularistion in tumours are already leaky
34
Q

dexamethasone

A
  • Unbound corticosteroids diffuse through the plasma membrane and bind to the cytoplasmic corticosteroid receptor, allowing the steroid–receptor complex to move into the nucleus.
  • In the nucleus, glucocorticoids bind directly to specific DNA sequences called glucocorticoid response elements (GREs) that regulate the transcription of nuclear DNA.
  • Downstream, this affects the production of mRNA and subsequent protein synthesis (e.g., decreased anti-inflams)

upregulate tight junction protein occludin and cadherin

35
Q

name some psychological and behavioural interventions available to cancer patients

A

Behavioural therapy for pain and nausea

  • Educational therapy to improve coping skills,
  • Psychotherapy to reduce anxiety and depression
  • Support groups
36
Q

which 3 cn’s contribute to eye movement?

what movements do they control?

A

oculomotor III- elevates, depresses, adducts

trochlear IV- medial + depression???

abducens VI- abduction

37
Q

cn responsible for sensation on the face

A

trigeminal nerve

facial nerve for ear way

38
Q

cranial nerves involved in taste

A

Olfactory is Ist cranial nerve;

  • Sense of taste via facial VIIth
  • Glossopharyngeal IXth
39
Q

What kind of particles bind to olfactory receptors?

messenger system of olfactory receptors?

where do olfactory projections go?

A

airbone molecules

G protein coupled receptor and cAMP-gated channels

projections to temporal lobe (pyriform cortec and limbic system) and then to hypothalamus

40
Q

taste receptors are clustered into what on the tongue?

what are the modalities of taste? how are they transduced?

anterior 2/3 of tongue taste is conveyed by:

posterior third by:

taste projections are to the?

A

papillae

sweet, salt, bitter, sour, umami

mediated by effects on ion channels via G proteins or via cAMP-gated channels

anterior 2/3 via chorda tympani of the facial nerve (VII)

posterior 1/3 via the glossopharyngeal nerve (IX)

taste projections: nucleus tractus solitarius in the medulla –> thalamus –> somatosensory and insular cortex

41
Q

olfactory pathway

A
  1. Olfactory nerve pathway
  2. Originates in olfactory receptors within nasal epithelium.
  3. Axons (known as fila olfactoria) assemble into bundles of true olfactory nerves which penetrate small foramina in cribriform plate of ethmoid bone.
  4. Fibres enter olfactory bulb which lies in olfactory groove within anterior cranial fossa.
  5. Olfactory nerve fibres synapse with specialised neurones called mitral cells in olfactory bulb – this forms collections known as synaptic glomeruli.
  6. From here second order neurons pass posteriorly into olfactory tract.
  7. Olfactory tract travels posteriorly on inferior surface of frontal lobe then divides into medial and lateral stria:
  8. Lateral stria – carries axons to primary olfactory cortex within temporal lobe.
  9. Medial stria – carries axons across medial plane of anterior commissure where they meet the olfactory bulb of the opposite side.
42
Q

Bell’s palsy pathphysiology

symptoms

A

The facial nerve courses through a portion of the temporal bone commonly referred to as the facial canal. A popular theory proposes that edema and ischemia result in compression of the facial nerve within this bony canal.

symptoms:

  • weakness in facial muscles
  • makes half of the face droop
  • mouth droops ad eye resists closing
  • drooling
  • loss of taste
  • weakness is temporary
43
Q

distinguish between bells palsy and ischaemic stroke

A

stroke spares forehead and patient can raise eyebrows symmetrically

bell’s palsy should not have anhy limb effects

bells temporary

treat with prednisolone and facial exercises

44
Q

accronym for breaking bad news

A

Setting- arrange for privacy and practice what you’ll say

Perceptions- elicit the patient’s perception

Invitation- ask the patient what they would like to know

Knowledge- provide info in small pieces

Emotions- recognises and empathises with emotions

Strategy and summary- set out a pan of action and to meet again

45
Q

dorsal column medial lemniscus pathway

A

vibration, proprioception and fine touch

46
Q

Anterolateral system- spinothalamic tract

A

anterior segment- crude touch and pressure

lateral segment- pain and temperature

decussates at the level of the spinal cord in which it enters

ascending tract

47
Q

give 2 examples of breat cell cancer

A

ductal carcinoma

lobule carcinoma

48
Q

BBB and choice of drug

A

only ways through the BBB are:

  1. Passive movement of water-soluble agents across the BBB cannot be facilitated due to the close nature of the tight junctions between the endothelial cells.
  2. Small, lipid-soluble agents, such as antidepressants, cross the BBB through diffusion through the endothelial cells.
  3. Specialized transport proteins transport glucose, amino acids and drugs such as cyclosporin across the BBB
  4. Receptors mediate transcytosis of proteins like insulin
  5. Proteins, such as albumin are absorbed and transported via transcytosis (through the cell) Efflux transporters counter passive diffusion by pumping foreign agents out of the brain.

PBL year 2 (Sam) (12 decks)

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