Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

203: Theme 1 - 304 - Endocrinology > The Endocrine System > Flashcards

The Endocrine System Flashcards

+ diagnostic biochemistry

1
Q

What is the main role of the autonomic nervous system?

A
  • 1.contraction and relaxation often vascular and visceral smooth muscles
    1. all exocrine and certain endocrine secretions
    1. control of the heartbeat
    1. energy metabolism, particularly in the liver and skeletal muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Give examples of fast neurotransmitters and how they function

A
  • Glutamate & GABA
    • operate through ligand-gated ion channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give examples of slow neurotransmitters and neuromodulators and how they function

A
  • DA, neuropeptides
    • operate mainly through G-protein coupled receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the response when the Blood-brain barrier has dysfunction/ damage

A
  • Injury causes oxidative stress, and the increased production of proinflammatory mediators
  • there is an upregulation of expression of cell adhesion molecules on the surface of brain endothelium which promotes the influx of inflammatory cells into the traumatized brain parenchyma.
  • this causes swelling and the following symptoms seen in a brain haemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the Endocrine System?

A
  • collection of ductless glands produce hormones that regulate internal process
    • metabolism
    • growth
    • development
    • tissue function
    • sexual & reproductive function
    • sleep
    • mood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What organs make up the Endocrine System?

A
  • Pineal gland
  • Hypothalamus
  • Pituitary gland
  • Parathyroid gland
  • Thyroid gland
  • Thymus
  • Adrenal glands
  • Kidneys
  • Pancreas
  • Ovary (females)
  • Testes (males)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the six Anterior Pituitary hormones?

A
  • FSH- Follicle-stimulating hormone
  • LH- Luteinizing hormone
  • GH- Growth Hormone
  • TSH- Thyroid-stimulating hormone
  • PRL- Prolactin
  • ACTH- Adrencorticotropic hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the two Posterior Pituitary hormones

A
  • Oxytocin
  • ADH -Antidirutiec Hormone (vasopressin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give an overview of the biochemical pathway of the Anterior Pituitary Hormones

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the location of the Pituitary gland

A
  • inferior to the hypothalamus and the Infundibulum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the overall role of the Thyroid and the Parathyroid gland?

A
  • control of metabolic rate and calcium homeostasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the overall role of the Adrenal glands?

A
  • the inner medulla produces hormones related to the stress response
    • NE and Epinephrine
  • the outer cortex works to control, sodium and glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the overall role of the Pancreas

A
  • secretes Glucagon and Insulin to control the blood glucose levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the overall role of the Gonads?

A
  • they secrete the female and male reproductive hormones responsible for the development of secondary sexual characteristics and reproduction
    • Female: Oestrogen, Progesterone
    • Male: Testosterone, Androsterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the major receptor groups that interact with hormones?

A
  • Steroid Hormone Receptors
  • G-Protein Coupled receptors
  • Tyrosine Kinase Receptors

these may be intracellular or membrane-bound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do Steroid Hormones and their receptors work?

A
  • Steroid Hormones (SHs) are lipophilic molecules derived from cholesterol and made in
    • the adrenal cortex
    • the testes
    • the ovary and placenta
  • they reach their target cells via the blood where they bind to carrier proteins and pass the cell membrane by simple diffusion (lipophilic nature)
  • it then binds to the receptor which may be cytoplasmic or nuclear
  • the hormone-receptor complex binds to the hormone response element of the DNA to influence gene transcription
    • the receptor may be constitutively active ( resulting in the production of a second messenger in the absence of an agonist)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Explain hormone-receptor complexes removal after they have been internalised

A
  • the hormone-receptor is internalised within a vesicle formed of clathrin-coated pits, which allows the hormone to be removed from its receptor
  • in the vesicle arrestin, may replace the hormone on the receptor and prevent the receptor-interacting with its G-protein
  • overall internalised receptors are inactive, broken down or recycled
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the biological characteristics of hormones

  • the classes of hormones
A
  • Peptide hormones
    • chains of aa, highly water-soluble, susceptible to protease attach
    • unable to cross cell membrane without a carrier protein
    • act on membrane-bound receptors
  • Steroid hormones (+ thyroid hormones)
    • highly lipid-soluble, poorly water-soluble
    • must be transported in the blood and bound to plasma protein
    • only biologically active in its unbound state
    • able to cross cell membrane and acts as intracellular receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the biochemical characteristics of hormones

  • the classes of hormones
A
  • Peptide Hormones
    • not orally active
    • rapid onset and duration of action
    • short plasma half-life
    • synthesised and stored as an inactive precursor
      • maybe ‘stored’ in platelets; plasma-protein bound steroids may be a storage reservoir
  • Steroid & Thyroid Hormone
    • ​orally active
    • synthesised on demand
    • slow onset of action
    • long plasma half-life and duration of action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is the endocrine system controlled?

A
  • secretion from the anterior pituitary gland is controlled by the hypothalamus
    • the hypothalamus secretes the releasing hormone
  • the secretion of a hormone from a gland is controlled by the anterior
    • the APG releases Stimulating (trophic) Hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Match the hormones released by the hypothalamus to those that it stimulates in the Anterior Pituitary gland

  • Thyrotrophin Releasing Hormone (TRH)
  • Corticotrophin Releasing Hormone (CRH)
  • Gonadotrophin Releasing Hormone (GnRH)
  • Growth Hormone Releasing Hormone (GHRH)
A
  • Thyrotrophin Releasing Hormone (TRH)
    • Thyroid Stimulating hormone
  • Corticotrophin Releasing Hormone (CRH)
    • Adrenocorticotrophic hormone (ACTH)
  • Gonadotrophin Releasing Hormone (GnRH)
    • Follicle-stimulating hormone (FSH)
  • Growth Hormone Releasing Hormone (GHRH)
    • Growth Hormone (GH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where do the hormones of the Anterior Pituitary gland act on?

A
  • Thyroid Stimulating Hormone (TSH)
    • Thyroid Gland
      • produces Thyroxine
  • Adrenocorticotrophic hormone (ACTH)
    • Adrenal Cortex
      • produces Cortisol
  • Follicle Stimulating Hormone (FSH)
    • Ovary
      • ​produces Oestrogen
  • Luteinising Hormone (LH)
    • Ovary
      • ​produces Progesterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Explain the effect of nocturnal ACTH (adrenocorticotropin) and Cortisol secretion and long or short sleep duration

A
  • at the time of sleep the SSG (short sleep gp) had higher plasma cortisol levels compared to the LSG (long sleep gp)
  • however, the ACTH levels were not reduced or tended to be higher in the LSG, whereas they were lower in the SSG
  • this may be explained by the negative feedback effect high cortisol levels has on plasma ACTH,

Conclusions

  • the transition from sleep to wakefulness in the morning, irrespective whether spontaneous or induced, stimulates ACTH and cortisol release
  • the switch from darkness to lights on after awakening may have contributed to the awakening-dependent ACTH and cortisol peak.
  • the decline of plasma ACTH and cortisol during wakefulness supports the view that quietly lying awake inhibits adrenocortical activity in the morning, as already suggested by results from previous studies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Define Endocrine

A

• Action of the hormone on a target organ away from the secreting cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Define Autocrine

A

• Action of the hormone on the secreting cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Define Paracrine

A

• Action of the hormone on the adjacent cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Define Neuroendocrine

A

• Neural stimulation of endocrine cells to secrete hormones e.g. the medulla of adrenal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Give a general overview of endocrine gland structure

A
  • cuboidal secretory cells with a lumen at the centre
    • not all endocrine functional units have a lumen
      • e.g pituitary and parathyroid gland cells
  • secretory cells are supported by myoepithelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What hormones are released by the Posterior and Anterior Pituitary gland

  • where do they affect?
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which cells are found in the anterior pituitary gland?

  • what hormones do they release?
  • what is the target organ?
A
  • Somatrotroph
    • Growth Hormone –> Bones
  • Lactotroph
    • ​Prolactin –> Breasts
  • Corticotroph
    • Adrenocorticotrophic hormone (ACTH) –> Adrenal glands
  • Gonadotroph
    • Follicle stimulating hormone (FSH) –> Ovary & testis
    • Luteinising hormone (LH) –> Ovary & testis
  • Thydrotroph
    • Thyroid-stimulating hormone (TSH) –> Thyroid gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What hormones are released from the posterior pituitary gland?

A
  • ADH
    • increase water reabsorption from the collecting ducts in the kidneys
  • Oxytocin
    • promotes contractions of the smooth muscle in the uterus during childbirth and myoepithelial cells in the breast during breastfeeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Explain the clinical features of a Pituitary Adenoma

A
  • these are benign tumours that arise from the anterior lobe
  • can be functional or non-functional
    • productive adenomas cause hyperpituitarism
    • pressure effect can cause hypopituitarism
  • constitute 10% of intra-cranial neuplasms
  • space-occupying effect of functional non-functioning adenomas can cause
    • headaches, vomiting & nausea
    • diplopia, impaired vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What pathology is this?

  • what are the presenting symptoms of this pathology?
A
  • Pituitary adenoma
  • patients present with bitemporal hemianopsia due to compression of the optic chiasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which two hormones does the thyroid gland synthesis

  • what are their functions?
A
  • Thyroxine (T3)​
  • Triiodothyronine (T3)
    • ​stimulate the metabolic rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What pathologies are associated with the Thyroid gland?

A
  • Goitre (euthyroid)
    • enlargement of the thyroid gland due to lack of iodine
    • sea salt is rich in Iodine
  • Grave’s Disease (hyperthyroid)
  • Hashmoto’s disease (hypothyroid)
  • Adenoma (euthyroid)
  • Cancer (euthyroid)
  • Myxedema & Cretinism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe the structure and composition of a normal thyroid gland

A
  • between 35-45g
  • 2 lobes and an isthmus
  • Very vascular
    • endothelial cells lining the capillaries are fenestrated allowing passage of hormones into the circulation
  • thyroid tissues composed of follicles with variable sized lumina
    • follicles contain colloid with an eosinophilic or pink appearance
    • the follicles are lined by cuboidal cells
  • Para-follicular cells or C-cells are found between the follicles
    • these secrete calcitonin which promotes the reduction of calcium conc. in the blood
    • C cells are the origin of medullary carcinoma of the thyroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is this an image of? Explain the pathology and treatment

A
  • Multi nodular Goitre
  • enlargement of the thyroid gland due to hyperplasia and hypertrophy of the thyroid cells due to decreased iodine levels
    • enlargement increases absorbance of iodine counteracting any hormone deficiency
    • therefore the patient is euthyroid
  • may compress trachea needs to be carefully assessed radiologically before thyroidectomy
  • may cause softening of the trachea which collapses and obstructs the airways
38
Q

What is this an image of?

  • explain the pathology and histology
  • clinical features relating to the pathology
A
  • Thyroidectomy due to Grave’s Disease
  • caused by auto-antibodies stimulating TSH receptors- hyperactivity
    • in histology, a the colloid has a ‘soap bubble’ appearance due to hyperactivity
  • leading to diffuse enlargement of the thyroid gland
  • causes
    • Infiltrative ophthalmopathy: accumulation of soft tissue and inflammatory cells behind the yer leading to proptosis
    • Infiltrative dermopathy: thickening and induration of the skin on the anterior shin –> pre-tibial myxoedema
39
Q

What is this an image of?

  • explain the pathology
A
  • Hashimoto’s Thyroiditis
    • an autoimmune disease that destroys its own thyroid tissue
  • causes progressive depletion of thyroid cells by inflammation & replaced by fibrosis
    • in histology, there is prominent lymphocytic infiltrate/ inflammation
  • decreased T3/T4 but increased TSH levels
  • its the most common cause of hypothyroidism in areas where iodine is really available
40
Q

What type of thyroid tumours are there?

A
  • Follicular adenoma - benign tumour of the thyroid follicular cells
  • Carcinoma – Four main types
    • Papillary ( 75-85%); ↑ risk of lymph node metastasis
    • Follicular (10-20%); ↑ Mets to bone, lung and liver
    • Medullary (5%); arises from C cells ; 20% ass with MEN 2 syndrome (multiple endocrine neoplasm)
    • Anaplastic (<5%); older patients; poor prognosis
41
Q

What is the role of the Parathyroid gland?

A
  • secrete parathyroid hormone PTH
  • control the levels of calcium in the blood
    • a decrease in blood Ca2+ stimulates PTH
  • contains chief cells with no lumen
  • highly vascular
42
Q

What pathologies are associated with the parathyroid gland?

A
  • Adenoma- involved one gland
    • increased size, less vascular
  • Hyperplasia- involves all four glands
  • both of these cause hypercalcaemia
43
Q

Where des the Adrenal cortex and the adrenal medulla embryologically originate from?

A
  • the adrenal cortex is derived from the mesoderm
  • the adrenal medulla is derived from the neural crest
44
Q

Describe the structure and organisation of the adrenal cortex

A
  • Divided into three zones
    • Zona Glomerulosa
      • closely packed round cells
    • Zona Fascinculata
      • clear cells arranged in cords
    • Zona Reticularis
      • smaller darker staining cells
  • in general, the adrenal glands appear yellow as the cells are rich in lipids
    • yellow appearance lost during histological preparation, cells appear clear under observation
45
Q

What are the functional purposes of the different adrenal cortex zones?

A
  • Zona glomerulosa
    • Mineralocorticoid
    • Aldosterone
    • For absorption of sodium
  • Zona fasciculata
    • Glucocorticoids
    • Cortisol & corticosterone
    • Sex hormones
  • Zona reticularis
    • 17 Ketosteroids
    • Sex hormones
46
Q

What pathologies are associated with the adrenal gland?

A
  • Adrenocortical hyperactivity
    • Due to hyperplasia, adenoma or cancer (rare)
    • Cushing’s Syndrome ( excess cortisol)
    • Conn’s Syndrome ( excess aldosterone)
    • Adrenogenital syndrome ( excess androgens)
  • Adrenocortical insufficiency
    • Addison’s disease (chronic low adrenal hormone release)
  • Adrenal Cortex Adenoma
    • functional adenomas can cause Cushing’s syndrome or Cohn’s syndrome
47
Q

Describe the appearance of the adrenal medulla compared to the adrenal cortex

A
  • Adrenal medulla cells are neuroendocrine
  • have darker staining than adrenal cortex cells
48
Q

What is Phaeochromocytoma?

  • symptoms
  • epidemiology
A
  • tumour of the adrenal medulla
    • caused by high levels of catecholamines
  • Precipitous
    • ↑ BP + tachycardia, palpitations,
    • headache, sweating,
    • tremor & sense of apprehension
  • Complications
    • of ↑ BP
    • CCF, IHD, cardiac arrhythmias, CVA
  • 0.1-0.3% cause of treatable hypertension
  • 10% tumour
    • 10% are familial as part of the MEN2
    • 10% are extra-adrenal
    • 10% bilateral
    • 10% are malignant
    • 10% arise in childhood
49
Q

What hormone controls appetite?

  • where is it produced?
A
  • Leptin
  • produced in adipose tissue: acts on the hypothalamus to inhibit appetite
50
Q

What are eh various perspectives on ageing?

A
  • Evolutionary perspective
    • we are outliving our natural lifespan
    • hormonal function
  • Cultural Perspective
    • anti-ageing is a big societal topic
  • Pharma perspective
    • there’s an enormous market
      • testosterone ad GH
51
Q

Reflect on the medicalisation of ageing

  • usual ageing
  • role of hormones
  • benefits vs harm
A
  • increased life expectancy does not always equate to increased health expectancy
  • How is ‘usual ageing’ viewed?
    • is it a ‘normal’ physiological process
    • is it pathological
    • can your ageing be made optimal
  • Is hormonal influence dwarfed by
    • genetic, environmental psychosocial factors
    • and co-morbidities
  • Balance of benefits & harm of treatment
    • Risks - cancer risk in elderly
    • Hassle - GH/testo not orally active
    • Costs
52
Q

What is ageing associated with/ caused by?

A
  • Hypogonadism/ GH deficiency/ aging have similar phenotypes
    • increased fat mass increased visceral fat
    • sarcopenia
    • decreased bone mineral density
    • decreased QOL/ mood
    • increased risk of cardiovascular diseas
  • These phenotypes are non-specifc and have a high prevalence
    • universal?
53
Q

What changes occur to your nutritional status as you age?

A
  • Weight: increased from mid-30s, stays stable between your 50-70’s
  • Lean body mass: decreases 6-8% / decade from your mid-30’s
  • Diet: trend towards lower total energy & protein intake with increased age
54
Q

How does Insulin/glucose change with age?

A
  • increased insulin and glucose with increased age
    • increased insulin resistance
    • increased peripheral glucose uptake
  • increased prevalence of metabolic syndrome with increased age
55
Q

What is Metabolic Syndrome?

A
  • ‘Constellation of closely associated CV risk factors’
    • Visceral obesity
    • Dyslipidaemia
    • Hyperglycaemia
    • Hypertension
  • INSULIN RESISTANCE is the underlying pathophysiological mechanism
56
Q

Review the Gonadal Axis

A
57
Q

What is Menopause

  • clinically
  • symptoms
  • morbidity
A
  • essentially ovarian failure
  • Oestrogen levels
    • very low constant levels no more cycling
      • decreased E2, increased LH/ FSH
    • age of menopause 50+- 2 years
    • Symptoms:
      • Hot flushes, night sweats
      • median duration of menopausal symptoms 7 years
    • Morbidity
      • increased osteoporosis, increased CHD, increase in sexual dysfunction
58
Q

Post-menopausal Hormone-Replacement Therapy

  • benefits vs risks
  • goal
A
  • balance of risk : benefit ratio
    • other risk factors
    • Age of woman and duration of HRT use
      • greater risk of >60yrs, >10yrs Post MP
    • type of HRT - Oestrogen, progestogen, route
  • no longer replacement more focused on the treatment of menopausal symptoms

Benefits

  • Rx menopausal Sx
  • decreases osteoporosis/ fracture risk for the duration of Rx

Risks

  • increase venous thrombo-embolism
  • increase breast cancer esp. >5 years of treatment
  • increase endometrial cancer
    • if unopposed E2 is used
59
Q

How does age affect the male gonadal axis?

A
  • gradual decrease of testo with age
  • wide range of normality at all ages
  • at 75 yrs the mean testo level is ~ 2/3rds that at 25years
  • there is poor association libido/erectile dysfunction and testo
    • testo prescription increased 500% over the past decade
  • Clinical hypogonadism
    • decreased sexual function
    • decreased muscle strength
    • increased osteoporosis
60
Q

Review Testosterone treatment in men

  • effect
  • efficacy
  • risks
A
  • Bones
    • increase bone mineral density if hypogonadal
    • biphosphonates work, independent of androgen
  • Body composition
    • increase lean body mass, decrease fat mass
    • increase muscle strength with supra-physiological doses
    • no convincing functional benefits demonstrated
  • Little evidence/ insufficient evidence for the following
    • atherosclerosis, coronary artery diseases
    • sexual function
    • cognitive function
    • mood/quality of life
  • Risks
    • Prostate hyperplasia
    • Erythropoiesis (increased haematocrit)
    • ? CV risk)
61
Q

Review the GH-IGF-I axis

A
62
Q

How does age affect the GH - IGF-I axis

(Growth Hormone, Insulin-Like Growth Factor)

A
  • decreased integrated GH with age
  • decreased IGF-I with age
  • wide variation in a ‘normal range’
63
Q

Review the use of GH Treatment

  • effect
  • efficacy
  • risk
A
  • Body composition
    • increased lean body mass ~ 2kg
    • decreased fat mass ~2kg
    • no convincing functional benefits demonstrated
  • No significance change
    • bone mineral density
    • lipids
      • decreased Total Cholesterol
  • Potential risks
    • increased risk of cancer, increased
  • Side-effects
    • Soft tissue oedema
    • Arthralgias (joint pain)
    • Carpal tunnel syndrome
    • Carpal tunnel syndrome
64
Q

Review the HPA axis

A
65
Q

How does age affect Cortisol?

A
  • increased trough levels with age
    • increased average levels of cortisol
  • Phase advance of diurnal rhythm
    • time at trough and peak are both earlier
66
Q

Go over Sapolsky’s glucocorticoid cascade hypothesis

A
  • ↓ hippocampal glucocorticoid & mineralocorticoid receptors
    • leads to ↓ sensitivity to glucocorticoid negative feedback
    • therefore ↑ glucocorticoids levels
  • –> hippocampal neurons vulnerable to damage
  • ‘feed forward cascade’
    • ↓ volume hippocampus on MRI – no differences in volume of adjacent structures
    • Other roles of hippocampus are effected: learning, memory
      • ↑ cortisol associated with ↑ decline cognitive function
67
Q

How are other circulating Androgens affected by age?

A
  • Decline in DHEA (Dehydroepiandrosterone)
    • not very clear on the effect of this hormone due to other more potent androgens circulating
    • decreased DHEA is seen as a non-specific marker fo ill health
      • decreased DHEA/ cortisol found in cancer, inflammatory diseases, T2DM, CV disease
  • observational studies suggest increased DHEAS
    • increased QOL, increased bone mineral density
    • decreased cognitive decline, decreased CHD
68
Q

Effects of DHEA treatment

A
  • no real evidence for efficacy and no adverse effects demonstrated
69
Q

Review the Thyroid Axis

A
70
Q

How does age affect Thyroid function?

  • treatment?
A
  • slight increase of TSH with age
    • T4 remains stable
  • a decrease in peripheral T4 –> T3 conversion with age
  • decreased T3 with age

No evidence for the beneficial effects of T4 treatment may cause harm:

  • ? increases risk of osteoporosis, atrial fibrillation
  • ? risk in elderly with atherosclerotic coronaries
71
Q

What is the physiological effect of Starvation/ Anorexia Nervosa?

  • Insulin
  • Glucose
  • Leptin
A
  • ↓ insulin, ↓ glucose, ↑ insulin sensitivity
  • LEPTIN
    • Produced by white adipose tissue this correlates with BMI and body fat
    • Reports nutritional information to the hypothalamus
      • ‘Starvation signal’: signals energy availability
      • ↓leptin leads to ↑ food intake, ↓ energy expenditure,
      • ↓leptin leads to ↓ fertility
        • Permissive factor for initiation of puberty
72
Q

What is the physiological effect of Starvation/ Anorexia Nervosa?

  • Oestrogen
  • Testosterone
A
  • ↓ LH, ↓ FSH,
  • ↓ oestrogen / testosterone
  • ↓ fertility, amenorrhoea
    • ‘hypothalamic amenorrhoea’
    • makes ‘evolutionary sense’ in times of famine
  • Osteoporosis
    • Rx HRT / COCP
73
Q

Give an overview of the link between metabolism and reproduction

A
  • hyperphagic and obese mice –>
    • low gonadotrophins
    • incomplete development of reproductive organs
    • does not reach sexual maturity –> infertile
    • Leptin replacement resolves issues
  • the Kisppeptin system acts as a +ve and-ve mediator for sex steroids via GnRH production
    • highly responsive to oestrogen
  • metabolic influences on reproduction are mediated by leptin via the kisspeptin system exerting effects on
    • puberty and
    • reproduction
74
Q

What is Kisspeptin?

A
  • a hypothalamic neuropeptide that binds to the GPR54 receptor
  • this signalling is known to be crucial for the development of puberty and effects reproduction
75
Q

How does Starvation/ Anorexia Nervosa affect the GH - IGF-I axis?

A
  • Growth hormone resistance
    • increased GH, but decreased IGF-I
  • this is seen in acute starvation and in AN
    potential due to the downregulation of hepatic GH receptor an/ or post-receptor defect
  • reversible with re-feeding
76
Q

How does Starvation/ Anorexia Nervosa affect thyroid function?

A
  • TSH and T4 are at the lower limits of normal
  • ↓ T4 conversion to T3 leads to ↓ active T3
  • ↑ T4 conversion to rT3 leads to ↑inactive rT3
  • Consequences
    • Lower basal metabolic rate
    • Conserve energy
77
Q

Why is TSH a more significant biochemical marker of dysfunction?

A
  • small changes in freeT4 cause a large reciprocal change in TSH
    • therefore acts as a sensitive indicator of thyroid activity in the target tissue
    • with TSH on a logarithmic scale a 2.5 x change in fT4, TSH changes 100x
  • In steady-state TSH is a better index of dysfunction than freeT4, used in
    • Thyroxine replacement
    • Diagnosing 1y hypo & hyper- thyroidism
78
Q

How can freeT3 measurements be used clinically?

A
  • used to diagnose hyperthyroidism
  • monitoring therapy when using
    • carbimazole
    • Propylthiouracil (PTU)
    • I131
      (all treatments for hyperthyroidism)
79
Q

Give an overview of the pathway of thyroid hormone metabolism

  • start from when TRH is released from the hypothalamus
  • inhibiting factors?
A
80
Q

What biochemical results would you see that would indicate 1y Hyperthyroidism?

  • causes
  • treatment?
A
  • High freeT4 and freeT3
  • TSH <0.03
    • ​usually due to Grave’s disease
    • Toxic nodular goitre, thyroiditis
  • TSH receptor autoantibodies are +ve
    • ​seen in an ultrasound
  • Treatment: carbimazole
    • monitor TFT 1-2 months until stable, then 3 months, then 6-12 if on long term treatment
81
Q

What is the diagnosis of a 80y M presenting with

  • TSH 86mU/L (0.3-4.2)
  • FT4 7 pmol/L (12-22)
  • tiredness and lethargy
  • dry coarse and sparse hair/ lateral eyebrows thining
  • periorbital oedema/ puffy dull face with dry skin
A
  • 1y Hypothyroidism
  • treat with Thyroxine (T4)
    • low dose and titrate up
    • monitor TFT 6-8 weeks after starting thyroxine
82
Q

Why is there a delay after adjusting the thyroxine dose (when treating hypothyroidism) before requesting a TSH?

A
  • the t1/2 of thyroxine is 1 week
  • to reach steady state is 6 x t1/2 (6 weeks)
  • FT4 achieves as a steady state in 6 weeks
    • this will feed-back tot he pituitary (where TSH is released)
  • so TSH achieves steady state in 2 months
83
Q

What thyroid function tests can be done?

  • which disease is it used for
A
  • TSH
  • Free T4 & T3
  • Thyroid peroxidase antibodies - TPOAb
    • marker of chronic autoimmune thyroiditis (destructive)
  • TSH receptor autoantibodies
    • seen in Graves disease
    • binds to or near TSH receptors ( stimulates)
84
Q

What are the diagnostic steps when presented with this case?

  • 50y G, tiredness, lethargy, weight gain
  • TSH 11 mU/L 0.3 - 4.2
  • FT4 12 pmol/L 12 - 22
  • potential diagnosis?
A
  • take a further history of their symptoms
  • due to equivocal or borderline results request a TPOAb (a marker of chronic autoimmune thyroiditis)
    • ​can confirm chronic autoimmune hypothyroidism
  • Subclinical hypothyroidism
85
Q

Should borderline raised TSH be treated?

  • a normal FT4 & TSH 4-10 mIU/L
A

Treated with Thyroxine, in the following

  • patients with goitre
  • patients seeking pregnancy
  • patients TPO Ab +ve and raising TSH
86
Q

How should different cases of Subclinical hypothyroidism be treated?

  • TSH > 10
  • TSH 4-10 with either +ve / -ve TPO Ab
A
  • FT4 low normal TSH >10
    • …treat with thyroxine
  • FT4 normal, TSH 4-10, TPO Ab +ve
    • …treat with thyroxine/annual tests
  • FT4 normal, TSH 4 -10, TPO Ab –ve
    • ….tests 2 yearly
87
Q

What is the diagnosis of this case?

  • what investigations should be done
  • what is the treatment plan
  • 23y F bends to tie a shoelace
  • Experiences intense low back pain
  • Presents to A&E
  • O/E:
  • Severe back pain in lumbar region.
  • Abdominal striae, Gravidity2,Parity2
  • Pigmentation in palmer creases & gums.
  • Central weakness.
A
  • Cushing’s disease
  • Lumbar X-ray
88
Q

What is pro-opio-melanocortin (POMC)

  • how is it relevant to Addison’s disease
A
  • a hypothalamic precursor protein that is processed to
    • ACTH –> alpha-melanocyte-stimulating hormone (alpha-MSH)
    • beta-endorphin
  • in primary adrenal insufficiency (Addison’s disease) lack of cortisol negative feedback causes an increase in POMC
    • you can see hyperpigmentation generally across the skin and in areas wich experience pressure and sunlight
      • elbows, cheecks, knees, spine, knuckle, bra straps
89
Q

What is the action of Cortisol?

A
  • breaks down protein and converts it to glucose
  • Major sources of protein
    • Muscle
    • Collagen: bones, connective tissue (skin)
  • high cortisol mimics the action of aldosterone in the DCT in the kidneys
    • causes reabsorption of Na+ + water –> hypertension & hypernatraemia
    • loss of K+ and H+ (increased HCO3-) –> hypokalaemic alkalosis
90
Q

What is a simple test to assess muscle weakness?

A

get the patient to stand up from a chair without using their arms to help

91
Q

What biochemical assessments would be used if Cushing’s disease is suspected?

A
  • Check cortisol - it would be raised
    • Loss of diurnal rhythm, monitor cortisol
  • a Dexamethasone suppression test (it’s a potent glucocorticoid)

203: Theme 1 - 304 - Endocrinology (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions