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MD4001 > Week 9 > Flashcards

Week 9 Flashcards

1
Q

Describe the development of the Thyroid?

A
  • Thyroid tissue arises in midline at a point on tongue known as foramen caecum
  • Epithelial cells sink downwards anterior to hyoid & larynx (week7)
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2
Q

What does the Thyroglossal duct do?

A

Connects developing thyroid to the tongue

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3
Q

List what you would expect to see in a histology of the Thyroid Gland?

A
  • Follicle
  • Follicular cells
  • Colloid
  • Para-follicular C-cells
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4
Q

Where synthesises & secretes thyrotropin-releasing hormone (TRH)?

A

Small-bodied neurons in arcuate nucleus & median eminence

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5
Q

What carries TRH to the anterior pituitary?

A

Long portal vessels

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6
Q

How is T4 released?

A

Inside lysosomes of the follicular cells, enzymes will cleave 2 peptides on the backbone of thyroglobulin molecule

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7
Q

Describe the 1. “Trapping” process during the synthesis & secreting of T3 & T4?

A
  • TSH increases activity of Na/I co-transporter (NIS) on basolateral membrane of thyroid follicular cell
  • Increased iodine trapping
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8
Q

What happens to the ratio of follicular-cell iodine to plasma iodine during “Trapping”?

A

Increases under conditions of high TSH

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9
Q

Describe what happens to the trapped iodine during synthesis & secretion of T3 & T4?

A
  • Leaves cell, via pendrin, & enters lumen

- Thyroid peroxidase on luminal surface of secretory vesicle oxidises I- to Io

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10
Q

What does the follicular cell also secrete?

A

Thyroglobulin

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11
Q

Describe the 3. “Iodination” process during the synthesis & secretion of T3 & T4?

A

TSH stimulates iodination of thyroglobulin in the follicular lumen

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12
Q

Describe the 4. “Conjugation” process during the synthesis & secretion of T3 & T4?

A

TSH stimulates conjugation of iodinated tyrosine to form T4 & T3 linked to thyroglobulin

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13
Q

Describe the 5. “Endocytosis” process during the synthesis & secretion of T3 & T4?

A

TSH stimulates endocytosis of iodinated thyroglobulin into follicular cells from thyroid colloid

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14
Q

Describe the 6. “Proteolysis” process during the synthesis & secretion of T3 & T4?

A

TSH stimulates proteolysis of iodinated thyroglobulin, forming T3 & T4 in the lumen of lysoendosome

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15
Q

Describe the 7. “Secretion” process during the synthesis & secretion of T3 & T4?

A

TSH stimulates secretion of T4 & T3 into the circulation

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16
Q

Describe the “Hyperplasia” process during the synthesis & secretion of T3 & T4?

A

TSH exerts growth-factor effect, stimulating hyperplasia within the thyroid gland

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17
Q

What is 99.5% of T3 bound to in the blood plasma?

A

TBG (thyroxin-binding globulin)

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18
Q

What is 99.98% of T4 bound to in the blood plasma?

A

TBG (thyroxin-binding globulin)

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19
Q

How/What converts T4 to T3?

A

5’/3’ monodeiodinase activity removes the 5’ iodine

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20
Q

How do T4 & T3 enter the cytosol of a cell?

A

Either diffusion or carrier-mediated transport

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21
Q

What does TBG (thyroxin-binding globulin) do?

A

Along with other thyroid hormone binding proteins found in plasma (transthyretin & albumin) buffer free T3 & T4 levels in blood

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22
Q

What is the chain reaction when basal metabolic rate (BMR) increases?

A

Increased O2 consumption –> Increased heat production

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23
Q

What does hyperthyroidism do to the basal metabolic rate (BMR)?

A

Increased basal metabolic rate (BMR) upto 100%

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24
Q

What does hypothyroidism do to the basal metabolic rate (BMR)?

A

Decreased basal metabolic rate (BMR) to 50-60%

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25
Q

Describe the physiological actions of the thyroid hormones on carbohydrate, fat & protein stores?

A
  • Increased Glucose uptake from GI Tract & Glucose utilisation
  • Increased Liver glycogenolysis & gluconeogenesis
  • Increased Lipolysis in adipose tissue (plasma FFA)
  • Increased Tissue oxidation of FFA
  • Increase protein turnover with net increase in anabolism
  • Increase in specific enzymes/membrane proteins/hormone receptors
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26
Q

What other hormones does thyroid hormones have a permissive action on?

A
  • GH, prolactin, gonadal & adrenal steroids

- Essential for normal development & function of central & peripheral nervous systems

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27
Q

Describe the effect of hypothyroidism on the brain?

A
  • Poor mental ability

- Lack of memory & initiative

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28
Q

What 3 things does fetal hypothyroidism lead to?

A
  1. Neuronal hypoplasia
  2. Delayed myelination in specific neurones
  3. Mental retardation
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29
Q

Describe the Thyroid disorder- Goitrogens?

A
  • Excess iodide

- Thiocyanate or perchlorate cause excess TSH secretion & hypertrophy of thyroid & hypothyroidism

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30
Q

Describe the Thyroid disorder- Pituitary tumours?

A
  • Excess TSH= hypertrophy of thyroid & hyperthyroidism

- Lack of TSH= atrophy of thyroid & hypothyroidism

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31
Q

Describe the Thyroid disorder- Graves Disease?

A
  • Long-acting thyroid stimulator (LATS- autoimmune stimulation of thyroid)
  • Hypertrophy of thyroid & hyperthyroidism
  • Exophthalmos
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32
Q

Describe the Thyroid disorder- Hashimoto’s disease?

A
  • Autoimmune destruction of thyroid

- Atrophy of thyroid & hypothyroidism

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33
Q

When can Goitre’s be present?

A

In Hyper- or Hypothyroidism

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34
Q

What % of GP consultations are for neurological symptoms?

A

17%

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35
Q

What is Spina bifida?

A

Group of congenital conditions where there’s an incomplete development/covering of brain &/or spinal cord, caused by failure of foetal spine to close normally in 1st month of pregnancy

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36
Q

List the proposed aetiologies for Spina Bifida?

A
  • Multi-factorial inheritance
  • Potato blight
  • Vitamin deficiencies/folate
  • Maternal fever
  • Zinc deficiency
  • High sound intensity
  • Viral infection
  • Alcohol
  • Mineral deficiency
  • Medication: Phenytoin, Epilim
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37
Q

What is Cerebral Palsy (CP)?

A
  • Spectrum of motor disorders affecting posture, movement & co-ordination
  • Caused by brain lesion –> abnormal development of CNS
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38
Q

Describe the stages of Spinal cord during embryology?

A
  • Neural plate 14 days
  • Neural folds at 20 days
  • Ant. neuropore closes 26 days
  • Post. neuropore closes 29 days
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39
Q

What are the 2 minor spinal cord embryological defects?

A
  1. Spina Bifida occulta

2. Sacral dimple

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40
Q

What are the 2 cranial & vertebral neural tube abnormalities?

A
  1. Anencephalus

2. Spina bifida

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41
Q

Describe MILD spina bifida?

A
  • Sac contains meninges & CSF but not spinal cord
  • Mild disability
  • Least common
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42
Q

When is Spina Bifida described as a serious disability?

A

If cord is displaced from neural canal or has not developed

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43
Q

Describe the neurological consequences of severe Spina Bifida?

A
  • Lower motor neurone lesion

- Paralysis, loss of sensation & reflexes distal to abnormality

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44
Q

What are the pros & cons of surgical closure of the severe Spina Bifida defect?

A
  • PROS: stop the high risk of infection due to the open wound
  • CONS: not improve damage which is already done
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45
Q

Describe the neonatal consequences of severe Spina Bifida?

A
  • High risk meningitis in open lesions in the neonate

- Hydrocephalus in 70-90% because of interruption of the circulation of CSF

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46
Q

What can be a consequence of shunting in hydrocephalus?

A

Shunts can become infected or blocked

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47
Q

What are neurological disorders 4 associated conditions?

A
  1. Renal anomalies
  2. Sphincter function
  3. Intellectual impairments
  4. Musculoskeletal
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48
Q

How can you diagnose neurological disability in antenatal care?

A
  • Ultrasound spinal anomalies identifiable at 16-18 weeks

- α fetoprotein raised in neural tube defects maternal serum at 16-20 weeks, amniocentesis

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49
Q

Describe the neurological consequences of an L4 lesion?

A
  • No motor function below knee, apart from tibialis anterior
  • Weak glutei
  • No sensation distal to L4
  • Sphincters non-functioning (S2,3,4)
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50
Q

Describe the possible musculoskeletal problems associated with neurological disorders?

A
  • LMN, muscle weakness/paralysis
  • Difficulties walking
  • Spinal deformity
  • Disuse osteoporosis, risk of fracture
  • Skin ulceration
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51
Q

What are the 2 problems with paralytic deformities of the feet?

A
  1. Difficulties with shoe wear

2. Plantar ulceration

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52
Q

Describe Scoliosis?

A
  • Due to combo of
    congenital abnormalities of the spine & muscle weakness
  • If surgical correction is required, usually done after age of 10 years to allow sufficient spinal
    growth beforehand
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53
Q

What are 4 factors influencing walking?

A
  1. Neurological level
  2. Intellectual impairment
  3. Psychological
  4. Age
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54
Q

What is the prognosis for independent walking as a adult?

A
  • Thoracic & upper lumbar lesions: none

- Lower lumbar & sacral: can walk but will need splints to compensate for paralysed muscles

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55
Q

Is mobility the same as walking?

A

NO

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56
Q

Describe the flexed knee gait in a L4 lesion?

A
  • Patient relied on intact quadriceps
  • Paralysed calf muscles result in excess ankle dorsiflexion
  • Muscle fatigue
  • Energy inefficient gait
  • Knee pain
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57
Q

Describe why there are mobility challenges when a child grows into an adult with a L4 lesion?

A

Increasing height & weight as child grows but muscle strength does not change

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58
Q

Describe the challenges to mobility as an adult with a L4 lesion/

A
  • Muscle fatigue & knee pain may worsen & becomes more reliant on a wheelchair
  • Able to drive in adapted vehicle
  • Self propelling or electric wheelchair for shorter distances
  • Will require adapted housing if living independently
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59
Q

Describe Charcot joints?

A

Loss of protective sensation & proprioception in a joint can result in joint destruction

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60
Q

What are the 4 expectations of lower urinary tracts?

A
  1. Bladder should fill to good capacity
  2. Empty to completion
  3. Emptying should be under voluntary control
  4. Filling & emptying should not be
    detrimental to renal function
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61
Q

Describe the consequences of urinary incontinence (S2-4) in neurogenic bladder?

A

Incomplete emptying
leads to back pressure on ureters & eventual renal
parenchymal damage & failure if untreated

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62
Q

What are the possible treatments for urinary incontinence?

A
  • Nappies in kids
  • Permanent bladder catheterisation (UTIs)
  • Clean intermittent catheterisation often best option (carer or patient self)
  • Urinary diversion for physical or social reasons (stoma bag)
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63
Q

Describe the reasons/problems with Faecal incontinence?

A
  • Often a barrier to social acceptance
  • Paralysis of external anal sphincter & mechanism to indicate a full rectum
  • Some have weak abdominal & perineal muscles
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64
Q

What are the possible treatments for faecal incontinence?

A
  • Daily rectal enema
  • Constipation may require laxatives or manual evacuation
  • Surgical diversion for physical or social reasons
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65
Q

What are the sexual problems associated with neurological disorders?

A
  • Libido may be normal - Sensation absent (S2-4)
  • Erections possible due to spinal reflex
  • Fertility females normal, males usually sterile
  • Menstruation may cause further social difficulty
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66
Q

Describe different forms of education for people with neurological disorders?

A
  • Mainstream school
  • Special needs school: learning & physical disability
  • College to acquire life skills for those with learning difficulties
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67
Q

What do patients whose disabilities preclude employment do?

A

Attend a day centre

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68
Q

What is the disability paradox?

A

Poor function but excellent quality of life

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69
Q

What are the challenges to independent living as an adult?

A
  • Learning/ Behavioural difficulties
  • Social continence not achieved
  • Cannot transfer independently
  • Ageing parents
  • Live in a sheltered facility & looked after by a team of carers
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70
Q

What are the 2 types of Euthyroid?

A
  1. Diffuse- younger people

2. Multinodular- older

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71
Q

What are the 2 types of Hypothyroid & what cases them?

A
  1. Iodine deficiency- endemic, versus seaweed increase

2. Goitrogens- drugs (lithium, amiodarone) diet (cabbage, turnips)

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72
Q

What is the pathogenesis of goitre’s?

A
  • Reactive
  • Iodine block
  • Genetic
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73
Q

Describe the characteristics of a benign mass?

A

Usually movable, soft & non tender

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74
Q

Describe the characteristics of a malignancy?

A

Hard nodule, fixation to surrounding tissue & regional lymphadenopathy

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75
Q

Describe the signs & symptoms of hyperthyroidism?

A
  • Nervousness
  • Heat intolerance
  • Diarrohea
  • Muscle weakness
  • Loss of weight & appetite
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76
Q

Describe the signs & symptoms of hypothyroidism?

A
  • Cold intolerance
  • Constipation
  • Fatigue
  • Weight gain, in children, primarily accumulation of myxedematous fluid
  • Slow speech
  • Deep hoarse voice
  • Thickening of skin
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77
Q

Why do signs & symptoms of local nerve involvement trigger rapid investigation?

A
  • Involvement may be indicative of local invasiveness from malignancy
  • Most important signs are dysphagia & hoarseness
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78
Q

Describe the different diagnosis’s in Thyroid function tests?

A
  • Elevated thyroid-stimulating hormone (TSH) may indicate thyroiditis
  • Very low TSH level indicates autonomous or hyperfunctioning nodule
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79
Q

What is the Antithyroid antibodies helpful in diagnosing?

A

Chronic lymphocytic thyroiditis (Hashimoto thyroiditis)

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80
Q

What is complete blood count (CBC) helpful in diagnosing?

A

Abscess

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81
Q

What are the 4 different techniques for diagnosing thyroid pathology?

A
  1. Thyroid function test
  2. Antithyroid antibodies
  3. Complete blood count (CBC)
  4. Fine needle aspirate
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82
Q

What are the 5 different imaging studies used for thyroid pathology?

A
  1. Ultrasonography
  2. Radioiodine scintigraphy
  3. Chest radiography
  4. Computed tomography (CT)
  5. MRI
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83
Q

What is Ultrasonography useful for in thyroid pathology?

A

Determine whether nodule is cystic, solid, or mixed

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84
Q

What is Radioiodine scintigraphy useful for in thyroid pathology?

A

Determine whether nodule is cold, warm, or hot

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85
Q

Why is a Chest radiography used in thyroid pathology?

A

If malignancy is suspected, given the high incidence of early metastases to the lungs

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86
Q

What is CT & MRI useful for in thyroid pathology?

A

Analyse the extent of disease by scanning the neck & chest

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87
Q

List the different disease categories diseases of the thyroid?

A
  1. Trauma & toxicity
  2. Goitre, solitary nucleus, neoplasms
  3. Chronic inflammation (immune or not)
  4. Acute thyroiditis, abscess
  5. Metabolic, genetic
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88
Q

What is the commonest type of hyperthyroidism?

A

Graves (may present as diffuse toxic goitre)

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89
Q

What are the 3 different types of hyperthyroidism?

A
  1. Graves
  2. Functional goitre
  3. Toxic adenoma
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90
Q

What are the 2 types of hypothyroidism?

A
  1. Congenital

2. Autoimmune

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91
Q

What are the 3 causes of autoimmune hypothyroidism?

A
  1. Defective TH production
  2. Loss of parenchyma
  3. Deficient TSH
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92
Q

Describe Graves (hyperthyroidism)?

A
  • Autoimmune
  • Under 40 years
  • Female 10 : male 1
  • Immune: IgG against TSH receptor on thyrocytes
  • Strong family history HLA DR3 & CTLA-4
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93
Q

Who is Hashimoto thyroiditis (chronic autoimmune) most common in?

A

Females 30-50yrs

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94
Q

Describe Hashimoto thyroiditis (chronic autoimmune)?

A
  • Present as hyper- / hypo- thyroidism
  • Autoreactive CD8 T lymphocytes
  • Autoreactive antibodies: thyroid microsomal in almost all 95% thyroglobulin in 2/3’s, minority have blocking TSH receptor antibodies
  • Family history strong & other autoimmune diseases
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95
Q

What are 2 other causal risks for Hashimoto thyroiditis (chronic autoimmune)?

A
  1. Increased iodine intake

2. Viral infection

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96
Q

Name a benign thyroid neoplasm?

A

Follicular adenoma

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97
Q

Describe the 2 types of malignant thyroid neoplasms?

A
  1. Primary- 1% of cancers: PAPILLARY, FOLLICULAR, anapaestic, medullary, lymphoma
  2. Metastatic- lymphoma
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98
Q

Describe a Follicular adenoma (benign)?

A
  • 30-50y
  • Female>males
  • 1-3 cm at presentation
  • Different histological subtypes
  • Sometimes functional
  • Ras mutation?
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99
Q

Describe the prevalence of Papillary carcinoma (malignant)?

A
  • Around 80% of thyroid cancers
  • 20-50y
  • Females 3 : males 1
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100
Q

What are the 3 different causes of Papillary carcinoma (malignant)?

A
  1. RADIATION (Chernobyl)
  2. Family history
  3. Unknown
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101
Q

Describe the molecular pathology of Papillary carcinoma (malignant)?

A
  • Rearrangement of RET oncogene in most

- B-RAF mutation in half, increased risk of LN mets

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102
Q

Describe the prevalence of Follicular carcinoma (malignant)?

A
  • Around 20% of thyroid cancers
  • Older than 40
  • Female 3 : male 1
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103
Q

Describe the molecular pathology in Follicular carcinoma (malignant)?

A
  • RAS oncogene
  • PAX8/PPARG rearrangements
  • Minimally invasive versus invasive
  • Blood spread
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104
Q

Describe the prevalence of Anaplastic carcinoma (malignant)?

A

Female 4 : Male 1

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105
Q

Describe the molecular pathology of Anaplastic carcinoma (malignant)?

A
  • 1/2 have had chronic goitre
  • May have had previous thyroid neoplasia
  • p53 mutation common
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106
Q

Describe the prevalence of Medullary carcinoma?

A

20% familial (in younger patients)

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107
Q

Describe the molecular pathology of Medullary Carcinoma?

A

RET proto-oncogene activation

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108
Q

What are 3 diseases of the parathyroid glands?

A
  1. Primary hyperparathyoridism
  2. Secondary hyperparathyoridism
  3. Tertiary hyperparathyoridism
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109
Q

What are the 3 different types of Primary hyperparathyoridism?

A
  1. Adenoma: 4/5’s
  2. Hyperplasia (some familial)
  3. Parathyroid carcinoma (less than 1%)
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110
Q

What is the cause of Secondary hyperparathyoridism?

A

Low calcium (chronic renal failure & vitamin D deficiency)

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111
Q

What is the cause of Tertiary hyperparathyoridism?

A

Raised calcium in secondary hyperparathyoridism

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112
Q

What do you need to remember about endocrine neoplasia?

A

There are multiple (MEN1 & MEN2 examples)

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113
Q

What is a stressor?

A

Stimulus that disrupts homeostasis & causes stress response

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114
Q

What is the stress response?

A

Suite of physiological & behavioral responses to a stressor that help to restore homeostasis

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115
Q

Describe the 2-step physiological stress response?

A
  1. Sympathetic nervous system- Quick, within sec’s, release of epinephrine (adrenaline)
  2. HPA Axis (hypothalamic-pituitary-adrenal axis)- Slower, mins-hrs, release of cortisol
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116
Q

What 3 things does the adrenal cortex release?

A
  1. Glucocorticoids
  2. Mineralocorticoids
  3. Sex hormones
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117
Q

What 2 things does the adrenal medulla release?

A
  1. Epinephrine

2. Norepinephrine

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118
Q

Describe the HPA Axis (hypothalamic-pituitary-adrenal axis)?

A

Hypothalamus –> CRH –> Pituitary gland –> ACTH –> Adrenal cortex –> Cortisol –> Hypothalamus

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119
Q

What are the immediate effects of the stress response?

A
  • Increased heart rate & O2 intake
  • Increased blood glucose levels
  • Increased blood flow to muscles
  • Increased alertness
  • Inhibition of digestion, immune system
  • Release of endorphins
  • Dilation of pupils
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120
Q

Describe the consequences of Short-term versus long-term consequences of stress?

A

Beneficial in short-term or mild levels, but can cause major long-term problems if stress is chronic

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121
Q

What 5 health problems is chronic stress related to?

A
  1. Heart disease
  2. Diabetes
  3. Ulcers
  4. Growth problems
  5. Compromised immune system
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122
Q

What is the relationship between cortisol & depression?

A

Cortisol elevated in 50% of depressed patients

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123
Q

Describe the rhythm in cortisol production?

A
  • High in morning (7-9am)

- Low at night (11pm-4am)

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124
Q

Describe the Dexamethasone suppression test?

A

Causes HPA negative feedback to turn off, so no cortical surge (not true in depressed patients)

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125
Q

What 2 disease’s is depression a symptom of?

A
  • Cushing’s disease (high cortisol)

- Addison’s disease (low cortisol)

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126
Q

Describe the effect of the stress response on the immune system over time?

A
  • 1st few mins: enhanced immune system
  • After ~1hr: returns to normal
  • Chronic stress: suppresses immune system
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127
Q

Why is cortisol described as being a key anti-stress hormone?

A
  • It helps reduce inflammation during stress, also acts as immunosuppressent
  • Various components of immune system influenced by cortisol
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128
Q

What was the Experiment at the Catholic University in Korea?

A
  • Male & female undergraduate students all free of disease/illness
  • Blood samples taken on day of exam & 4 weeks later, monitored for no. of specific immune cells
129
Q

What were the results of the Experiment at Catholic University in Korea?

A
  • Lowered Interferon gamma (IFN-γ), which is normally released by T lymphocytes & natural killer (NK) cells
  • Examination Day IFN-γ: 190 pg/dl
  • Four Weeks IFN-γ: 500 pg/dl
  • Lowered T-helper 1 (Th1) cellular immunity
130
Q

What are the conclusions of the Experiment at Catholic University in Korea?

A
  • Although neuroendocrine status wasn’t monitored, cytokine profiles were taken which are an indirect link to immune system
  • Decrease in no. of macrophages, interferons, lymphocytes & natural killer (NK) cells
131
Q

What was the NASA study?

A
  • Relation between elevated stress hormones & reactivation of Epstein-Barr Virus (EBV) in astronauts
  • Study effects of stress due to space flight on levels of neuroendocrine hormones & immune cells
132
Q

Describe the method of the NASA study?

A
  • Blood samples taken, 10 days before launch, landing day, 3 days after landing
  • Urine samples for detecting hormones
133
Q

What were the conclusions of the NASA study?

A
  • Decrease in virus specific antibodies in all astronauts
  • Reactivation of EBV
  • Urinary cortisol & catecholamines elevated after flight
  • Stresses lead to decreased virus specific T-cell immunity
134
Q

Describe the classical mode of glucocorticoid action (transactivation)?

A

Cell producing a protein which has anti-inflammatory
effect, glucocorticoid receptor binding & driving more production of the anti-inflammatory which dampens down the ability to make an immune response

135
Q

Describe a model for glucocorticoid action (transrepression)?

A

Cell produces a protein
which drives inflammation, the cortisol is coming in & binding to stop the production of that inflammatory protein (indirect) which reduces ability to make an immune response

136
Q

What is the potency of Dexamethasone?

A

25-80

137
Q

What is the half life in hrs (t1/2) of Dexamethasone?

A

36-54hrs

138
Q

Give some examples of synthetic glucocorticoids?

A
  • Hydrocortisone
  • Cortisone acetate
  • Prednisone
  • Prednisolone
  • Dexamethasone
139
Q

Describe the immunosuppressive action of glucocorticoids?

A
  • Suppress cell-mediated immunity
  • Inhibit IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8, TNF-alpha
  • Suppress humoral immunity: B cells express less IL-2R & secrete less IL-2
  • Down regulation of Fc receptors on macrophages
    (reduced phagocytosis)
140
Q

List the possible side effects of glucocorticoids?

A
  • Immunosuppression
  • Hyperglycemia, insulin resistance, impaired glucose tolerance
  • Skin fragility, bruising
  • Osteoporosis
  • Weight gain
  • Adrenal insufficiency
  • Muscle breakdown
  • Irregular menstruation
  • Cushing’s syndrome
141
Q

What does excess use of high dose steroids do?

A

Suppress CRH & ACTH

142
Q

What does prolonged used of high dose steroids do?

A

Leads to adrenal atrophy, recovery can take months

143
Q

Describe the steroid withdrawal after less than 1 week treatment?

A
  • Usually ok to withdraw abruptly

- 1 week recovery

144
Q

Describe the steroid withdrawal after 6-10days treatment?

A
  • Reduce to replacement
  • Tape over 4 more days
  • Recover in 4 weeks
145
Q

Describe the steroid withdrawal after 11-30 days treatment?

A
  • Reduce to twice replacement, then by 25% every 4 days

- 3 months to recover

146
Q

Describe the steroid withdrawal after >30days treatment?

A
  • Reduce to twice replacement, then by 25% per week, then 0800h check with cortisone
  • Recovery may take 1yr
147
Q

What is type 1 diabetes (main type in juveniles)?

A

Destruction of insulin producing beta-cells in pancreas

148
Q

Describe the 2 stages of type 1 diabetes?

A
  • 1st stage: insulitis (lymphocyte invasion of pancreatic islets)
  • 2nd stage: overt diabetes, massive death of islet B cells & loss of glucose homeostasis
149
Q

Describe the autoimmune process involved in type 1 diabetes?

A
  • Immune assault on beta-cells mostly T lymphocytes
  • Naïve beta-reactive T cells meet antigen in pancreatic lymph nodes (PLN)
  • Antigens delivered to PLN by dendritic cells
  • Thus PLN is site where tolerance to pancreas is 1st broken down
150
Q

What problems also links to type 1 diabetes?

A
  • Alimentary problems

- Enteroviruses (coxackie virus), gluten, coeliac disease

151
Q

When does lymphocyte access to PLN occur?

A

During infancy

152
Q

What does altering the status of the gut also alter?

A

Insulitis

153
Q

What are the different types of pathological classifications?

A
  • Inherited/Acquired
  • Infections (viruses, bacteria etc)
  • Inflammation (vasculitis, paraneoplastic, idiopathic, MS)
  • Toxic (drugs, chemicals etc)
  • Metabolic (DM, vitamin deficiency, thyroid problems etc)
  • Degenerative
  • Trauma
154
Q

What are the 3 problems of relying on pathology?

A
  1. Sampling error
  2. Accessibility of tissue
  3. Often tissue only available late in disease process (post-mortem)
155
Q

What are “Dawson’s fingers”?

A
  • Pattern of plaques in the brains of people with multiple sclerosis
  • Located around ventricles
156
Q

Describe the pathology of Multiple Sclerosis?

A
  • An inflammatory, demyelinating disease of the CNS
  • Demyelinating lesions of MS, called plaques, appear as indurated areas
  • Absence of inflammation at edge of chronic lesions
157
Q

What are the 4 different classifications of Multiple Sclerosis?

A
  1. Relapsing-remitting MS: ~85% of cases
  2. Secondary progressive MS
  3. Primary progressive MS
  4. Progressive-relapsing MS
158
Q

What can relapsing-remitting MS go on to develop into after many yrs?

A

Secondary progressive

159
Q

Is Multiple Sclerosis related to genes or environment?

A

BOTH (polygenic disease)

160
Q

Describe the relationship of vitamin D & MS?

A
  • Prospective studies shows vitamin D deficiency prior to MS onset predisposes to increased risk of MS (geography & sunlight)
  • In RRMS every 10ng/mL increase in vitamin D level there’s a 34% decrease in rate of subsequent relapse
  • Vitamin D supplementation & disease activity in RRMS
161
Q

What can Vitamin D be used as?

A

Immunomodulator

162
Q

What are virtually all subjects with Multiple Sclerosis (>99%) infected with?

A

EBV compared to only ~90% of control subjects

163
Q

Describe the pathology of Alzheimer’s disease?

A
  • Neurofibrillary tangles

- Amyloid plaques

164
Q

Describe the pathology of Parkinson’s disease?

A

Lewy body present in dopaminergic neurons leading to loss in substantial nigra

165
Q

What causes peripheral neuropathy?

A

Axonal degeneration (diabetes, toxic, demyelination)

166
Q

List the potential causes of peripheral neuropathy (common, acquired)?

A
  • Diabetes
  • Idiopathic
  • Toxic (alcohol, drugs)
  • Vitamin Deficiency (B12)
  • Post-infectious (Guillain-Barre syndrome)
  • Paraneoplastic
  • Leprosy
  • Amyloid, inflammation (e.g. vasculitis)
167
Q

What is Charcot-Marie Tooth?

A
  • Inherited conditions that damage peripheral nerves
  • Also known as hereditary motor & sensory neuropathy (HMSN)
  • Progressive
168
Q

What are the consequences of Sural nerve biopsy?

A
  • Loss sensation

- 30% have neurpathic pain

169
Q

What is slow twitch (I) fibres innervated by?

A
  • Alpha 2 motor neurons

- Smaller of the 2 α motor neurons

170
Q

What is fast twitch (II) fibres innervated by?

A
  • Alpha 1 motor neurons
  • Larger of the 2 α motor neurons
    (higher excitation threshold & faster conduction velocity)
171
Q

What is the size principle?

A

Motor neurons recruited in order of size

172
Q

Describe the motor unit recruitment (size principle)?

A
  • 1st: Smallest alpha motor neurons (α2) slow twitch

- Last: Largest alpha motor neurons (α1) belong to fast twitch

173
Q

Describe the staining properties of slow twitch (type I)?

A

Myosin isoforms with low ATPase activity

174
Q

Describe the staining properties of fast twitch (type II)?

A

Myosin isoforms with high ATPase activity that promotes rapid breakdown of ATP for energy of high-speed muscle shortening

175
Q

Describe the distribution of muscle fibre types?

A
  • All muscle composed of slow & fast twitch fibres
  • Most individuals possess between 45-55% slow twitch
  • Mosaic pattern
176
Q

Where would you do a muscle biopsy?

A
  • Under LA
  • Usually deltoid, quadriceps or tibias anterior (muscle & nerve)
  • Done CPK & EMG 1st
177
Q

List 5 different types of inherited muscle diseases?

A
  1. Dystrophies (degen & regen)
  2. Congential myopathies (no regen)
  3. Mitochondrial
  4. Metabolic
  5. Myotonic
178
Q

List 5 different types of acquired muscle diseases?

A
  1. Inflammatory (polymyositis/dermato)
  2. Toxic (alcohol, simvastatin)
  3. Metabolic (Cushing’s)
  4. Disuse atrophy
  5. Rhabdomyolysis
179
Q

What is Duchennes muscular dystrophy caused by?

A

Absence of dystrophin, a protein that helps keep muscle cells intact

180
Q

What is the inheritance of Duchennes muscular dystrophy?

A

X-linked recessive

181
Q

What is Psychosis?

A

Any disorder so severe that the victim loses contact with reality

182
Q

List 5 different disorders which are associated with psychosis?

A
  1. Schizophrenia
  2. Bipolar disorder
  3. Dissociative identity disorder (split personality)
  4. Schizoaffective disorder
  5. Persistent delusional disorders
183
Q

How common is Schizophrenia?

A

1% of World population

184
Q

When are the usual ages for diagnosis of Schizophrenia?

A
  • Men early 20s

- Women late 20s

185
Q

Give 4 statistics for Schizophrenia disorder occurrence & its affects on people?

A
  • 20% who have 1st episode recover
  • 80% suffer either another acute episodes or more chronic condition
  • 10% successfully commit suicide
  • 19% diagnosed are employed
186
Q

List the (positive & negative) symptoms of Schizophrenia?

A
  • Pervasive thought disturbance
  • Difficulty ignoring irrelevant stimuli (external/internal)
  • Cognitive deficits
  • Withdrawal from personal contact
  • Delusions
  • Hallucinations
  • Emotional disorder
  • Behavioural disruption
187
Q

Describe the pattern of Schizophrenic symptoms?

A
  • Episodic

- Lack of insight

188
Q

Describe what is needed to diagnose Schizophrenia?

A
  • 2 Characteristic symptoms for significant time during 1 month
  • OR, 2 Less specific symptoms & social/occupational dysfunction & duration of symptoms (1 month)
189
Q

According to DSM-5 what are the 5 characteristics symptoms for diagnosing Schizophrenia?

A
  1. Delusions
  2. Hallucinations
  3. Disorganised speech
  4. Grossly disorganised or catatonic behaviour
  5. Negative symptoms (reduced emotional expression)
190
Q

According to ICD-10 what are the main characteristic symptoms for diagnosing Schizophrenia?

A
  • Thought echo/ insertion/ withdrawal/ broadcasting
  • Passivity, delusional perception
  • Voices commenting or discussing
  • Persistent bizarre delusions
191
Q

According to DSM-5 & ICD-10 what exclusions are there for diagnosing Schizophrenia?

A
  • Dominant mood symptoms
  • Schizoaffective disorder
  • Physiological effects of substance misuse (drug intoxication/ withdrawal)
  • Organic causes
  • Overt brain disease
192
Q

What cognitive deficits are there in Schizophrenia? (executive functions)

A
  • Sustained attention
  • Planning
  • Verbal & visuospatial working memory
  • Language skills
  • Explicit learning & memory
  • Perceptual/ motor processing
193
Q

Describe the delusional symptoms of Schizophrenia?

A
  • Ideas of reference/ changes in salience

- Delusional system

194
Q

What type of hallucination occurs in Schizophrenia?

A

Auditory

195
Q

Describe the behavioural disruption symptoms of Schizophrenia?

A
  • Catatonic

- Disorganised

196
Q

What are the 6 subtypes for Schizophrenia?

changed in DSM-5 to domains, gradients & dimensions

A
  1. Cataonic
  2. Disorganised (Hebephrenic)
  3. Paranoid
  4. Simple
  5. Undifferentiated
  6. Residual
197
Q

What are the causes of Schizophrenia?

A

Deficits in ability to keep thoughts & actions on track:

  • Genetics
  • Physiological
  • Anatomical
  • Psychosocial
198
Q

Describe the potential physiological causes of Schizophrenia?

A
  • Dopamine hypothesis (classical antipsychotic, overstimulation)
  • Dopamine-serotonin interaction hypothesis (atypical antipsychotics)
  • Acetylcholine?
  • Glutamate?
  • GABA?
199
Q

Describe the anatomical reasons of Schizophrenia development?

A
  • Reduction in global brain volume (hypoxia at birth)
  • Neuronal displacement
  • Abnormally sized neurones (in areas associated with corticostriatal-thalamic loop)
200
Q

Describe the potential psychosocial causes of Schizophrenia?

A
  • Social class
  • Minority position
  • Urban environment
  • Family environment
  • Cannabis use?
201
Q

What is the Diathesis model for Schizophrenia?

A

Vulnerability - Stress

202
Q

What are the 2 types of drug therapies for Schizophrenia?

A
  1. Classical antipsychotics

2. Atypical antipsychotics

203
Q

List the 3 possible psychological interventions for Schizophrenia?

A
  1. Family intervention
  2. Cognitive behaviour therapy
  3. Social-skill training
204
Q

List the ways of early intervention & assessment of Schizophrenia according to NICE?

A
  • Psychiatric
  • Medical
  • Physical
  • Psychological
  • Developmental
  • Social
  • Occupational & educational
  • QOL
  • Economic
205
Q

What is the NICE recommended treatment for 1st episode of Schizophrenia?

A

Oral antipsychotic medication with psychological intervention (family intervention & individual CBT)

206
Q

What does NICE say to “offer” for continuing treatment & care for Schizophrenic patients?

A
  • CBT to promote recovery (esp. persistent symptoms/ remission)
  • Family intervention
  • Consider depot/long-acting antipsychotic medication if patient prefers it after acute episode/to avoid covert non-adherence as a clinical priority
  • Monitor physical health regularly, esp. potential side effects
207
Q

Give 3 % statistics for the dependency outcome of Schizophrenic patients?

A
  1. Independent- 30%
  2. Relatively dependent- 50%
  3. Highly dependent- 20%
208
Q

What does activation of nuclear receptors induce?

A

New protein synthesis which produce physiological effects

209
Q

Where is especially is some of the T4 converted to T3 (thyroid hormones)?

A

In kidney & liver

210
Q

Describe actions of T3 (thyroid hormone) on the body’s growth system?

A
  • Increase soft tissue growth

- Increase bone maturation

211
Q

Describe the action of T3 (thyroid hormone) on the body’s Central nervous system?

A

Increase maturation of CNS

212
Q

Describe actions of T3 (thyroid hormone) on the body’s Basal metabolic rate (BMR)?

A
  • Increase Na+/K+-ATPase
  • Increase O2 consumption
  • Increase heat production
  • Increase BMR
213
Q

Describe actions of T3 (thyroid hormone) on the body’s Metabolism?

A
  • Increase glucose absorption
  • Increase glycogenolysis
  • Increase gluconeogenesis
  • Increase lipolysis
  • Increase protein synthesis & degradation
214
Q

Describe actions of T3 (thyroid hormone) on the body’s cardiovascular system?

A
  • Increase inotropic
  • Increase chronotropic
  • Increase cardiac output
215
Q

What are the 2 common manifestations of hyperthyroidism?

A
  1. Diffuse toxic goitre

2. Toxic nodular goitre

216
Q

Describe a diffuse toxic goitre?

A
  • Autoimmune disorder

- Antibodies to TSH receptor stimulate thyroxine secretion

217
Q

What is a toxic nodular goitre caused by?

A

Benign neoplasm/adenoma

218
Q

What are the 6 causes of hyperthyroidism?

A
  1. Graves disease (LATS/TSI)
  2. Overtreatment with thyroxine
  3. Thyroid/pituitary adenoma (rare)
  4. Transient neonatal thyrotoxicosis (mother with Graves disease)
  5. Inflammation of thyroid/thyroiditis
  6. Excess iodine in diet (very high- hypothyroidism)
219
Q

What are the investigations to assess hyperthyroidism?

A
  • Measure blood TSH, free T3 & T4 levels
  • Test for anti-thyroid antibodies (esp. TSH
    receptors antibodies)
  • Radionucleotide thyroid scan (123I- or 99mTcO4 -uptake) viewed by a gamma camera
220
Q

What are the 3 treatment modalities for thyroid disorders?

A
  1. Radioactive iodine
  2. Anti-thyroid drugs
  3. Surgery
221
Q

What are the negatives for the current 3 treatment modalities for thyroid disorders?

A
  • None is optimal
  • None interrupts the autoimmune process
  • Each has a drawbacks
222
Q

How is radioactive iodine given to treat diseases of the thyroid (hyperthyroidism)?

A
  • Radioiodine (131I) given orally & selectively taken up by thyroid
  • Given as single dose & lasts about 2 months (Not during pregnancy/ lactation)
223
Q

What does oral treatment of Radioiodine (131I) for hyperthyroidism do?

A
  • Damages cells
  • Emits short-range β radiation & affects only follicle cells
  • Hypothyroidism will eventually occur (replacement therapy)
224
Q

What 4 potential drugs can you use to treat hyperthyroidism?

A
  1. Thioureylenes (thioamides), Carbimazole (methimazole) & propylthiouracil
  2. Iodine
  3. Beta-blockers (propranolol)
  4. Calcium supplements
225
Q

What is the function of Thioureylenes (thioamides), Carbimazole (methimazole) & propylthiouracil drugs for hyperthyroidism?

A
  • Decrease synthesis of thyroid hormones
  • Inhibit thyroperoxidase so reducing the iodination of thyroglobulin
  • Acts over 3-4 weeks
226
Q

What is the function of iodine drug for hyperthyroidism?

A
  • Given orally in high doses & converted to iodide
  • Transiently
    reduces thyroid hormone secretion & vascularity of gland
227
Q

What is the function of calcium supplement drugs for hyperthyroidism?

A

Maintenance of normal bone density because parathyroid hormone demineralises the bone

228
Q

What is the thiocarbamide group in thioamides essential for?

A

Antithyroid activity

229
Q

What does hypothyroidism lead to in children?

A

Cretinism

230
Q

What is hypothyroidism also known as?

A

Myxedema

231
Q

Describe the process of Myxedema in hypothyroidism/ hyperthyroidism?

A

Accumulation of increased amounts of hyaluronic acid & chondroitin sulphate in the dermis of both lesioned & normal skin, causing swelling/puffiness of subcutaneous tissue

232
Q

What 4 things can potentially cause decreased thyroid hormone levels?

A
  1. Low T4
  2. Possibly low T3 too
  3. Raised TSH (test with protirelin)
  4. Possibly various anti-thyroid antibodies
233
Q

What are the 6 potential etiologies for congenital hypothyroidism?

A
  1. Hypoplasia (agenesis/dysgenesis)
  2. Familial enzyme defects (dyshormonogenesis)
  3. Iodine deficiency (endemic cretinism)
  4. Intake of goitrogens during pregnancy
  5. Pituitary defects
  6. Idiopathic
234
Q

Describe the effects of newborns with congenital hypothyroidism?

A
  • May have few/no clinical manifestations of thyroid deficiency
  • Longer the condition goes undetected the lower the IQ
235
Q

What are the 6 potential aetiologies for acquired hypothyroidism?

A
  1. Iodine deficiency
  2. Auto-immune thyroiditis
  3. Thyroidectomy or RAI therapy
  4. TSH or TRH deficiency
  5. Medications (iodide & cobalt)
  6. Idiopathic
236
Q

What is the most common cause of hypothyroidism?

A

Hashimoto’s disease

237
Q

Describe Hashimoto’s disease?

A
  • Autoimmune lymphocytic thyroiditis
  • Females > Males
  • Runs in families
238
Q

What are the 3 different anti-thyroid antibodies involved in Hashimoto’s disease?

A
  1. Thyroglobulin Ab
  2. Microsomal Ab/Thyroid peroxidase (TPO) Ab
  3. TSH-R Ab (blocking antibodies)
239
Q

What are the 2 possible treatments for hypothyroidism?

A
  1. Levothyroxine

2. Liothyronine

240
Q

Describe Levothyroxine & what it’s used for?

A
  • Synthetic analogue of
    thyroxine
  • Has all the actions of endogenous thyroxine
  • Standard T4 replacement therapy for hypothyroidism
241
Q

Describe Liothyronine & what it’s used for?

A
  • Synthetic analogue of triiodothyronine
  • Has all the actions of endogenous triiodothyronine
  • Treatment of choice for myxedema coma
242
Q

What is a Myxedema coma?

A

Extreme form of hypothyroidism compounded by some stressful state such as infection, myocardial infarction or stroke

243
Q

In Graves disease what are the symptoms limited to?

A

Pretibial myxedema (only 1-5% of patients)

244
Q

Why do we need statistics to interpret evidence?

A

Because of variability between people (side effects, effectiveness of treatment) & within people (BP, strength of left & right hands)

245
Q

What are the 3 different ways of calculating risk?

A
  1. Absolute risk reduction (ARR)
  2. Relative risk (RR)
  3. Number needed to treat (NNT)
246
Q

What are the 2 types of Numerical data?

A
  1. Continuous ie. height, BP

2. Discrete ie. no. of children in family, no. of hand nodes

247
Q

What are the 2 types of Categorical data?

A
  1. Ordinal ie. social class, pain severity

2. Nominal ie. marital status, blood group

248
Q

What 3 different types of data are used for calculating an average (central tendency)?

A
  1. Mean
  2. Median
  3. Mode
249
Q

What are the 2 different types of data used to show variability?

A
  1. Standard deviation

2. Inter-quartile range

250
Q

Describe what the mean uses?

A

All data but can be influenced by outliers

251
Q

Describe what the median uses?

A

Not influenced by outliers, but doesn’t use all data (less informative)

252
Q

What are the 3 types of graph distribution for data (mean, median, mode)?

A
  1. Negatively skewed
  2. Normal (no skew)
  3. Positively skewed
253
Q

What is the equation to calculate risk?

A

Number with disease/ Total number at risk

254
Q

What is the equation to calculate Absolute Risk reduction (ARR)

A

Risk group 1 - Risk group 2

255
Q

What is the equation to calculate Relative risk (risk ratio)?

A

Risk group 1/ Risk group 2

256
Q

What is the equation to calculate number needed to treat (NNT)?

A

1/ARD proportion

257
Q

What is relative risk independent of?

A

The original prevalence

258
Q

Since relative risk can be misleading, what should you always state?

A

Baseline absolute risks as well as relative risks

259
Q

When is the odds ratio used?

A
  • Case-control studies
  • Observational studies
  • Regression models
260
Q

What is the equation for odds ratio?

A

Cases or controls with exposure/ Cases or controls without exposure

261
Q

What is the odds ratio if odds are equal in case & control group?

A

OR= 1

262
Q

If events are rare, then what is odds ratio a good approximation to?

A

Relative risk (RR)

263
Q

What is population in evidence?

A

Theoretical concept to describe the group of individuals of interest to the research question

264
Q

What is the sample in evidence?

A
  • Preferably random sample, that is representative of the population in which we are interested
  • Usually smaller than population in which we are interested
265
Q

What do we use the mean, relative risk & prevalence of the sample to estimate?

A

“True” mean/relative risk/proportion of the population

266
Q

When do we have more confidence in results of a sample?

A

If the sample is LARGE

267
Q

What is the standard error of the mean (SE)?

A

Measure the variability of the sample means

268
Q

What does a large standard error of the mean (SE) indicate?

A
  • Much variability in sample means

- Many lie a long way from the population mean

269
Q

What does a small standard error of the mean (SE) indicate?

A

Not much variability between the sample means

270
Q

Why is standard error of the mean (SE) always SMALLER than standard deviation (SD)?

A

Because there is less variability between sample means than between individual values

271
Q

What does larger samples lead to?

A

Smaller standard error of the mean (SE)

272
Q

What does a confidence interval give?

A

A range of values, estimated from sample data, which is likely to include the, unknown, population parameter (mean)

273
Q

What is a 95% confidence interval?

A
  • Range of values within which we are 95% confident the true population mean lies
  • Sample mean +/- 1.96*SE
274
Q

What is the confidence interval good for?

A

Making decisions about whether observed differences are likely to be due to chance alone, or likely to be a true effect

275
Q

What is a null hypothesis?

A

No significant difference between specified populations, any observed difference being due to sampling or experimental error.

276
Q

What is an alternative hypothesis?

A

Statistical significance/ difference between two variables

277
Q

Where/How does the pancreas develop?

A

As an out growth of the gut tube, closely associated with gall bladder development

278
Q

What are the endocrine functions of the pancreas?

A

Islets of Langerhans produce hormones (glucagon, insulin, somatostatin, pancreatic polypeptide)

279
Q

What is the weight of the endocrine pancreas?

A

Less than 2% of the total mass of the pancreas

280
Q

What do the A (α, α2) cells of the endocrine pancreas synthesis?

A

Glucagon

281
Q

What do the B (β) cells of the endocrine pancreas synthesis?

A

Insulin

282
Q

What do the D (α1, γ, δ) cells of the endocrine pancreas synthesis?

A

Somatostatin

283
Q

What are the exocrine functions of the pancreas?

A

Pancreatic acini produce pancreatic amylase etc.

284
Q

Describe the anatomy of the Islet of Langerhans in the pancreas?

A
  • α cells around the periphery
  • δ & β cells at the centre
  • Blood flows from the centre to the periphery
285
Q

Describe the 4 steps of synthesis & processing of insulin?

A
  1. Insulin mRNA translated as single chain precursor (preproinsulin) & removal of signal peptide during insertion into endoplasmic reticulum generates proinsulin
  2. Proinsulin has amino-terminal B chain, carboxy-terminal A chain & connecting C peptide
  3. Within endoplasmic reticulum, proinsulin exposed to endopeptidases which excise C peptide, generating mature insulin
  4. Insulin & free C peptide packaged in Golgi into secretory granules which accumulate in cytoplasm
286
Q

What chain reaction does absorption of food in the GI tract cause?

A

Increase blood glucose –> β cells stimulated –> Insulin release –> Physiological actions

287
Q

What 6 factors potentiate β cell’s producing insulin release once there is an increased blood glucose?

A
  1. α cell producing Glucagon
  2. Free fatty acids
  3. GI tract hormones/ incretins/ GIP/ GLP-1/ CCK
  4. Certain amino acids
  5. Parasympathetic stimulation (Ach)
  6. β adrenergic stimulation (Adrenaline)
288
Q

What 3 factors inhibit β cell’s producing insulin once there is an increased blood glucose?

A
  1. α adrenergic stimulation (Noradrenaline)
  2. δ cells producing somatostatin
  3. Autocrine effects of insulin
289
Q

Describe the 7 steps to the mechanism of insulin release from the pancreatic β cell?

A
  1. Glucose enters cell via GLUT2 transporter (facilitated diffusion)
  2. Glucose metabolism leads to increase [ATP]i or [ATP]i/[ADP]i
  3. Increased [ATP]i &/or [ATP]i/[ADP]i inhibits an ATP-sensitive K+ channel
  4. Causes Vm to become more positive (depolarisation)
  5. Actives voltage-gated Ca2+ channel in plasma membrane
  6. Ca2+ influx & increased [Ca2+]i which evokes Ca2+-induced Ca2+ release
  7. Elevated [Ca2+]i leads to insulin exocytosis & release into blood
290
Q

What insulin’s action of increased protein synthesis effect?

A

Growth & maintenance

291
Q

What chain reaction does absorption of a high protein meal in the GI tract OR starvation cause?

A

Decreased blood glucose –> α cell stimulation (because there is no insulin inhibition) –> Glucagon –> Physiological actions

292
Q

What are the 3 physiological actions of insulin?

A
  1. Increased protein synthesis (most tissues)
  2. Increased glycogenesis (liver, muscle)
  3. Increased lipogenesis (liver & adipose tissue)
293
Q

What is the chain reaction for insulin increasing glycogenesis?

A

Increased glycogenesis –> Increased glucose transport into cells (muscle/adipose tissue) –> Decreased blood glucose

294
Q

What 5 factors potentiate α cells producing glucagon?

A
  1. GI tract hormones
  2. Certain amino acids
  3. Parasympathetic stimulation (Ach)
  4. β adrenergic stimulation (Adrenaline)
  5. α adrenergic stimulation (Noradrenaline)
295
Q

What 2 factors inhibit α cells producing glucagon?

A
  1. β cell producing insulin

2. δ cell producing somatostatin

296
Q

Where do the physiological actions of Glucagon predominate?

A

In the liver

297
Q

What is the physiological actions of glucagon with no insulin?

A
  • Decrease lipogenesis
  • Increased lipolysis
    (increased fatty acids & glycerol)
298
Q

What is the main physiological action of glucagon?

A

Increased glycogenolysis (via raising cAMP) –> Increased blood glucose

299
Q

What is the physiological action of glucagon with cortisol?

A

Increased gluconeogenesis

300
Q

How common is Diabetes Mellitus?

A

2-3% of the population although higher in 50-60 year olds (15-20%) & within some races (African & Native Americans)

301
Q

What 2 things does Diabetes Mellitus result from?

A
  1. Insulin deficiency (5-10%)

2. Insulin insensitivity (>90%)

302
Q

How much blood glucose is defined as hyperglycaemia?

A

> 10mM or 180mg%

303
Q

Describe the 3 main signs of hyperglycaemia?

A
  1. Glucosuria- tubular fluid exceeds renal threshold for re-absorption
  2. Polyuria- osmotic diuresis due to glucose in tubular fluid
  3. Polydipsia- dehydration increasing angiotensin II levels which act as dipsogen on thirst centres in brain
304
Q

What is type 1 Diabetes Mellitus?

A

Insulin dependent diabetes mellitus (IDDM/ Juvenile-onset DM)

305
Q

What is increased blood FFA & glycerol in Diabetes Mellitus due to?

A

Increased lipolysis in adipose tissue

306
Q

What is ketoacidosis in Diabetes Mellitus due to?

A

Incomplete oxidation of fatty acids & ketogenic amino acids

307
Q

Describe the cause of type 1 Diabetes Mellitus?

A

Destruction of pancreatic beta cell (autoimmune disease after viral attack esp. Coxsackie B virus)

308
Q

Describe the treatment of type 1 Diabetes Mellitus?

A
  • Insulin administration (IM injections of short/long acting formulations of recombinant human insulin)
  • Restricted carbohydrate diet (<45% of total calorific intake)
309
Q

What is type 2 Diabetes Mellitus?

A

Non insulin-dependent diabetes mellitus (NIDDM/ Maturity onset DM)

310
Q

Describe the treatment for type 2 diabetes mellitus?

A
  • Restricted diet (1000 callories per day)
  • Sulphonyl ureas (increase beta cell response to glucose)
  • Biguanides (stimulate glucose uptake in muscle)
  • When uncontrolled: Insulin injection!
311
Q

What is type 2 Diabetes Mellitus related to?

A

Obesity (relative inactivity & over eating)

312
Q

What are the 6 acute effects of Diabetes Mellitus (insulin deficiency)?

A
  1. Increased hepatic glucose output
  2. Decreased glucose uptake by cells
  3. Decreased triglyceride synthesis
  4. Increased lipolysis
  5. Decreased αα uptake by cells
  6. Increased protein degradation
313
Q

What does the acute effects of Diabetes Mellitus (insulin deficiency) eventually lead to if untreated?

A

Renal failure –> Death!!!

314
Q

What 2 processes are increased during long term Diabetes Mellitus?

A
  1. Fat metabolism

2. Blood glucose

315
Q

What 2 things does loss of arterial compliance in long-term diabetes mellitus cause?

A
  1. Diabetic atherosclerosis

2. Hypertension

316
Q

What are the 3 common cardiovascular pathologies due to long-term diabetes Mellitus?

A
  1. Angina
  2. Cardiac arrhythmias
  3. Renal disease
317
Q

Describe the embryonic development of the thymus gland?

A
  • Develops from 3rd pharyngeal pouch

- Migrates inf to superior mediastinum & loses connection with larynx

318
Q

What incase & colonise in the thymus gland?

A

Lymphoid thymocytes derived from bone marrow

319
Q

What does the thymus control the development & “education” of?

A

T lymphocytes

MD4001 (11 decks)

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