Brainscape's Knowledge GenomeTM

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


See full index

PHYL2065 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the functions of the endocrine system?

A
  • regulate metabolism, water and electrolyte balance
    -allow body to cope with stress
  • regulate growth
  • control reproduction
  • regulate circulation and red blood cell production
  • control digestion and absorption of food
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the components of the endocrine system?

A

All hormone-secreting tissues:
- in the brain
- hypothalamus
- pituitary and pineal gland
- periphery in the thyroid, parathyroid and adrenal glands
- gonads
- pancreas
- kidneys
- liver
- thymus
- parts of the intestines, heart and skin

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

What are peptides?

A
  • a class of hormone
  • chains of amino acids, e.g. antidiuretic hormone (vasopressin), growth hormone
  • hydrophilic (water soluble)
  • stored prior to release
  • fast acting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are amines?

A
  • class of hormones
  • derived from amino acid ‘tyrosine’
  • all are stored
  • some hydrophilic (catecholamines - adrenaline, noradrenaline and dopamine)
  • some lipophilic - i.e. fat soluble (thyroid hormones)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are steroids?

A
  • class of hormone
  • derived from cholesterol where appropriate enzymes for conversion are present (e.g. cortisol, testosterone, oestrogens)
  • lipophilic
  • not stored, made when needed, and released by diffusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

List features of hydrophilic hormones (peptides and catecholamines)

A
  • most transported in blood dissolved in plasma (some also carried on binding proteins)
  • can’t pass through cell membrane, therefore binds to specific receptors on surface of target cell
  • elicit response either by changing cell permeability (few) or activating ‘second-messenger’ system to alter activity of intracellular proteins (most)
  • vulnerable to metabolic inactivation so short-term effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List features of lipophilic hormones (thyroid hormones and steroids).

A
  • transported in blood mostly bound to plasma proteins
  • small unbound amount dissolved - only dissolved portion physiologically active
  • free hormone (unbound) easily passes through cell membrane, binds to specific receptor within target cell (mostly in cell nucleus)
  • elicit response by activating specific genes within target cell to cause formation of new intracellular proteins
  • less vulnerable to metabolic inactivation so effects last longer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Summarise differences between hydrophilic and lipophilic hormones

A
  • hydrophilic likes water, lipophilic hates water
  • hydrophilic can’t get through plasma membrane, lipophilic can diffuse across plasma membrane
  • hydrophilic have fast onset and are fast acting, whereas lipophilic have slower onset, and are longer acting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the five steps involved in the regulation of hormone activity, and what are some considerations at each stage?

A
  1. secretion (stimulation, feedback, reflexes, rhythms)
  2. transport (binding proteins, free/unbound balance)
  3. metabolism (activation/inactivation, differs for hydrophilic vs lipophilic due to accessibility
  4. excretion (unregulated - but can be affected by renal/urinary disease)
  5. target cell responsiveness (receptor expression, amplification, combination with other hormones - ‘permissiveness, synergism and antagonism’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the control pathways for secretion in the regulation of hormone activity?

A
  1. central regulation
  2. direct regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Discuss features of the central regulation control pathway for secretion.

A
  • controlled by brain
  • affected by positive and negative-feedback loops, neuroendocrine reflexes, rhythms (e.g. diurnal)
  • can be fast, slow or long term responses
  • coordinated by hypothalamus and pituitary gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is an example of a rhythm that affects the central regulation of secretion?

A

Diurnal:
- melatonin (produced by pineal gland - responds to light)
- cortisol
- growth hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Discuss features of the direct regulation control pathway for secretion

A
  • endocrine cells respond directly to changes in extra-cellular fluid (especially plasma) levels of substances (e.g. glucose, calcium)
  • very rapid response to critical needs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are two groups of anterior pituitary hormones, when considering actions?

A
  • ‘trophic’ hormones control activity of another endocrine gland (thyroid stimulating hormone, adrenocorticotrophic hormone, luteinising hormone, follicle stimulating hormone)
  • hormones which have a direct effect in their own right (prolactin and growth hormone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does growth occur and what does it involve?

A
  • primarily through the actions of growth hormone
  • involves structural growth of tissues: synthesis or proteins, lengthening of long bones, soft tissue cell size and number increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some other factors that influence the extent of growth?

A
  • genetic determination of height and shape
  • dietary impact - especially amino acids
  • chronic disease or stressful environment (as cortisol inhibits growth)
  • other hormones influencing growth (thyroid hormone, insulin, sex steroids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Discuss the impacts of the a) anabolic and b) metabolic actions of GH

A

a) - growth
- increases length and thickness of long bones
- increases size and number of cells in soft tissues
b)
- increases fat breakdown/increases circulating fatty acids
- decreases glucose uptake by muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the action of growth hormone in muscles?

A
  • (direct via Gh-receptor)
  • stimulates amino acid uptake
  • decreases glucose uptake
  • inhibits protein breakdown
    = increase muscle mass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the action of growth hormone in adipose tissue?

A
  • (direct via GH-receptor)
  • decreases glucose uptake
  • increases fat breakdown (lipolysis)
    = decrease in fat deposits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the action of growth hormone in the liver?

A
  • (direct via GH-receptor)
  • increases protein synthesis
  • increases gluconeogenesis
    = increase metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Provide a one word summary of the action of growth hormone when received directly via GH-receptors.

A
  • primarily metabolic effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the action of growth hormone when indirectly mediated by somatomedins (IGFs)?

A

IGF-I:
- proliferation of chondrocytes at epiphyseal plates increasing bone length
- stimulates osteoblast activity to produce organic matrix increasing bone thickness
- promotes soft tissue growth through hyperplasia and hypertrophy (increased no. and size of cells respectively)
IGF-II:
- promotes soft tissue and organ growth by increasing protein, RNA and DNA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What other hormones influence growth hormone’s synthesis and release, and in what ways?

A
  • thyroid hormones: permissive, low TH = low growth
  • glucocorticoids: excess inhibits growth
  • sex steroids: synergistic, androgens important for pubertal growth spurt, but ultimately promote closure of epiphyses
  • insulin: (deficiency = low growth, excess = high growth)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is a growth abnormality resulting from excess growth hormone in children, and what is a feature of it?

A

Gigantism
- normal body proportions

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

What is a growth abnormality in adult resulting from excess growth hormone, and what are some features of it?

A

Acromegaly
- enlarged extremities
- course/malformed facial features, enlarged tongue, thickened lips, deep voice, sleep apnoea, cadiomegaly, degenerative arthropathy, muscle hypertrophy but weakness
- generally due to pituitary tumour

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

What is the result of growth hormone deficiency in a) adults and b) children?

A

a) no major symptoms
b) ‘pituitary dwarfism’
- short stature, normal body proportions, poor muscle development, excess subcutaneous fat

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

What is the physiological importance of calcium?

A
  • structural component of bones and teeth
  • contributes to resting membrane potential
  • maintains normal excitability of nerve and muscle cells
  • involved in neurotransmitter and hormone release
  • muscle contraction (skeletal and cardiac)
  • activation of many enzymes
  • coagulation of blood
  • milk production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How is calcium regulated in the body?

A
  • hormone control - balance maintained between ECF, and GIT, kidney and bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Compare acute and chronic control of calcium

A

Acute:
- must maintain constant free Ca2+ concentration in plasma
- mostly by rapid exchange between bone and ECF
Chronic:
- maintain total Ca2+ level in body long-term
- adjust gastrointestinal absorption and urinary excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the three main hormones that regulate Ca2+ metabolism?

A
  • parathyroid hormone (PTH)
  • vitamin D3
  • calcitonin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What three types of cells are important for bone formation and resorption?

A
  1. osteoblasts - synthesise and secrete collagen and promote deposition of CaPO4 crystals
  2. osteoclasts - promote resorption of bone
  3. osteocytes - essential role in exchange of calcium between ECF and bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

List some features of the parathyroid hormone, including its actions and half-life

A
  • parathyroid glands are 4 glands located on posterior surface of thyroid gland
  • PTH secreted from chief cells in direct response to changing plasma Ca2+ concentrations
  • overall increase calcium, decrease phosphate in plasma
  • is a peptide
  • half-life in plasma of <20 minutes
  • actions on bone, kidneys and GIT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the functions on bone of parathyroid hormone?

A

Short-term:
- stimulates Ca2+ membrane pump in osteocytes, so Ca2+ moves from bone fluid to plasma in central canal
Long-term:
- stimulates osteoclasts
- inhibits osteoblasts
- so Ca2+ and PO4 increase in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What function does parathyroid hormone have on the kidney?

A
  • decreases Ca2+ loss - increased tubular reabsorption of Ca2+ and decreased tubular reabsorption of PO4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What function does parathyroid hormone have on the GIT?

A
  • indirectly increases Ca2+ and PO4 - increases absorption by small intestine by stimulating activation of vitamin D3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the function of vitamin D?

A
  • produced either in skin or ingested, and is activated by liver and kidney to vitamin D3
  • promotes absorption of Ca2+ from that intestine by increasing its transport across intestinal membrane
  • (most ingested Ca2+ is not absorbed by GIT, but lost in faeces)
  • promotes absorption of PO4 in intestine
  • increases bone reabsorption
  • stimulates Ca2+ and PO4 reabsorption in kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Where is calcitonin produced, and what is its function?

A
  • produced in the C cells of the thyroid gland in response to high plasma Ca2+ levels
  • decreases bone resorption (effects osteoclasts)
  • decreases Ca2+ reabsorption in kidneys, promotes increased excretion
  • overall action = decreased Ca2+ and PO4 in plasma
  • protects against hypercalcemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is hyperparathyroidism, and how is it caused?

A
  • most frequently caused by PTH-secreting adenomas, leads to hypercalcemia
  • increased Ca2+ mobilisation from bones causes softening and fractures
  • increased Ca2+ excretion through kidneys causes polyuria, polydipsia and nephrocalcinosis
  • decreased excitability of nerves and muscles leads to weakness, depression and coma
  • hypercalcemia leads to nausea, constipation and increased incidence of peptic ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is hyperparathyroidism, and what is its cause?

A
  • most frequently caused by PTH-secreting adenomas, leads to hypercalcemia
  • increased Ca2+ mobilisation from bones causes softening and fractures
  • increased Ca2+ excretion through kidneys causes polyuria, polydipsia and nephrocalcinosis
  • decreased excitability of nerves and muscles leads to weakness, depression and coma
  • hypercalcemia leads to nausea, constipation and increased incidence of peptic ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is hypoparathyroidism, and what is its cause?

A
  • most frequently caused by gland destruction, leads to severe hypocalcemia
  • hypocalcemia causes increased nerve and muscle excitability
  • severe hypocalcemia leads to death by asphyxiation caused by laryngospasm
  • mild hypocalcemia causes cramps, twitches and tingles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are some other causes of hypocalcemia?

A
  • high demand for Ca2+ in pregnancy/lactation (causes tetany or paralysis)
  • lack of vitamin D/sunlight
    (causes rickets in children, osteomalacia in adults)
  • change in blood pH
    (alkalosis - less free Ca2+)
  • pancreatitis
41
Q

What is osteoporosis?

A
  • reduction in the mass (density) of bone and impairment of integrity of spongy bone
  • weaker bone = prone to fracture
  • progression from osteopenia to osteoporosis
42
Q

What are risk factors of osteoporosis?

A
  • poor nutrition (particularly low calcium)
  • low oestrogen levels, early menopause or loss of normal menstruation
  • inadequate sunlight exposure (Vitamin D deficiency)
  • smoking, excessive alcohol and caffeine intake
  • sedentary lifestyle
  • low testosterone
  • corticosteroid use
  • aortic calcifications
43
Q

What can be the result of decreased bone mass and structural disruption?

A
  • fractures after minimal trauma
44
Q

How does oestrogen tie into bone formation/resorption?

A
  • Increased oestrogen -> decreased osteoclast activity and decreased bone resorption
  • Less oestrogen (after menopause) -> more bone resorption
45
Q

What happens when testosterone is converted to oestrogen in bone in males?

A

Less testosterone -> more bone resorption

46
Q

How can osteoporosis be prevented?

A
  • good nutrition (Ca2+ and Vitamin D)
  • post-menopause (hormone replacement therapy, however side effects include increased risk of cardiovascular disease and cancer)
  • maintaining exercise (particularly weight bearing) in older age: reduces bone loss, prevents fractures, and prevents falls
47
Q

Differentiate the terms ‘genetic sex’, ‘gonadal sex’ and ‘phenotypic sex’.

A

Genetic sex: sex detemrined by chromosomes
Gonadal sex: if male, gonads differentiate into tests from seventh week of gestation, ovaries form after ninth week
Phenotypic sex: after 8 weeks gestation, testosterone production by testes causes development of Wolffian ducts into male internal reproductive organs, dihydrotestosterone causes masculinisation of external genitalia

48
Q

What influences the onset of puberty?

A
  • body weight/obesity
  • genetics
  • health
  • melatonin
49
Q

What does the pre-pubertal increase in pulses of of gonadotrophin-releasing hormone trigger?

A
  • triggers production of gonadotrophins (luteinizing hormone and follicle stimulating hormone) from anterior pituitary, which trigger gonadal activity
50
Q

What is the result of the production of sex steroids?

A
  • development of secondary sexual characteristics and fertility
51
Q

How does the hypothalamus control reproduction?

A
  • produces pulses of gonadotrophin-releasing hormone
  • stimulates pulsatile release of luteinizing hormone and follicle stimulating hormone
52
Q

What are two testicular cells and what are their functions?

A
  1. Leydig cells:
    - produce testosterone and small amounts of other steroids in response to luteinizing hormone
    - testosterone: either acts on adjacent Sertoli cells or is released in the blood, actions outside testes
  2. Sertoli cells: (with support from testosterone and follicle stimulating hormone)
    - maintain tight junctions (to create seminiferous tubules)
    - nourish germ cells and support spermatogenesis
    - secrete androgen binding protein (ABP)
    - convert testosterone to dihydrotestosterone or oestradiol
53
Q

What are the actions of the testosterone androgen?

A
  • sex determination in foetus
  • at puberty: growth spurt, closure of epiphyses
  • development and maintenance of male secondary sexual characteristics - external genitalia, deep voice, hair growth pattern, skin, body shape (lean muscle mass, low body fat)
  • development and maintenance of accessory sex organs and libido
  • anabolic actions, effects on brain and bone
54
Q

What is the process of female sexual development, commencing from the ‘awakening’ of the ovary?

A
  • ovary awakened because of LH and FSH release from anterior pituitary: considered the start of follicular development
  • developing follicles release oestrogens: development of female secondary characteristics, e.g. fat deposition, growth and maturation of reproductive tract
  • growth of auxiliary hair, libido and pubertal growth spurt due to pubertal rise in adrenal androgens
  • when sufficient gonadotrophin releasing hormone, LH and FSH to support follicular development to ovulation first ‘period’ - ‘menarche’
  • oestrogens cause closure of epiphyses
55
Q

What are the four stages of the menstrual cycle, and what is the main occurrence at each stage?

A
  1. Follicular phase
    - follicular and luteal changes in ovary
    - oocyte development and follicular growth
    - follicle secretes oestrogen (at end)
  2. Ovulation
    - LH surge coincides with ovulation
    - development of corpus luteum (at end)
  3. Luteal phase
    - corpus luteum secretes progesterone and oestrogen
    - degeneration of corpus luteum
  4. New follicular phase
56
Q

What happens to the plasma concentration of oestrogen throughout the different phases of the menstrual cycle?

A

Follicular phase: very low oestrogen
Ovulation phase: oestrogen level rises, causes thickening of endometrium - oestrogen levels peak (LH surge follows this rise)
Luteal phase: progesterone increases number of blood vessel and secretory glands in endometrium, oestrogen rises again slightly
New follicular phase: returns to low levels

57
Q

What happens to the plasma concentration of progesterone throughout the different phases of the menstrual cycle?

A

Follicular phase: very low progesterone
Ovulation phase: progesterone levels rise follow LH surge
Luteal phase: progesterone level peak, and increase in progesterone increases number of blood vessels and secretory glands in endometrium
New follicular phase: returns to low levels

58
Q

What are the effects of female sex steroids?

A
  • in normal cycle, brief ‘steroid fee period’ followed by sequential exposure to oestrogen then progesterone + oestrogen
  • oestrogen stimulates both E-receptor and P-receptor expression
  • alone progesterone has very few effects, as its actions require oestrogen priming
  • menopause: very low oestrogen and progesterone as menstrual cycles cease, regression of reproductive tract, reversed by treatment with oestrogen
59
Q

What bodily systems does oestrogen affect, and what are its principle functions?

A
  • oviduct
  • uterus
  • cervix
  • vagina
  • breasts (duct growth)
  • fat/protein deposition
  • brain
  • skeleton
  • electrolyte balance
  • skin
    Principle functions:
  • cellular proliferation
  • growth of tissues of sexual organs
  • growth/modification of other tissues related to reproduction
60
Q

True or false: the hormones oestrogen and progesterone cause the mucus of the cervix to be receptive to sperm?

A

True, and false:
- oestrogen, yes - very receptive to sperm
- progesterone, no - hostile and impermeable to sperm

61
Q

What bodily systems does progesterone effect, and what are its principle functions?

A
  • oviduct
  • uterus (inhibits proliferation and promotes accumulation of secretory products)
  • cervix (secretion of hostile mucous)
  • vagina
  • increase basal body temperature
  • breasts (alveolar development)
  • brain
    Principle functions:
  • prepares the reproductive tract (and other organs) for pregnancy, modifies or blocks (antagonises) the action of oestrogen
62
Q

What is the chief difference between progesterone levels in a conception cycle vs. a regular menstrual cycle, and why does this occur?

A
  • progesterone levels do not decline at the end of a conception cycle
  • occurs because the corpus luteum does not undergo luteolysis and continues to produce progesterone
63
Q

What hormone does the foetus produce that triggers birth? Once labour starts, what hormone, produced by the mother, helps the womb contract?

A
  • corticotrophin releasing hormone
  • mother’s own oxytocin
64
Q

Discuss the development of lactation throughout the course of a pregnancy.

A
  • During pregnancy, oestrogen stimulates duct growth, progesterone stimulates alveolar-lobule formation in breasts
  • Prolactin and human chorionic somatomammotropin promotes gland development and induces enzymes for milk production
  • high levels of oestrogen and progesterone (from placenta) prevent initiation of lactation until after birth
65
Q

Discuss the hormones involved in birth and the onset of lactation.

A

Oxytocin: high placental oestrogens in late pregnancy increase number of oxytocin receptors in uterus, oxytocin stimulates rhythmic uterine contractions in labour, through neuroendocrine reflex/positive feedback loop)
Progesterone and oestrogen: decrease after birth, permits lactation to commence
Oxytocin: stimulated by suckling, causes contraction of myoepithelial cells in breast (promotes milk ejection)
Prolactin: suckling stimulus promotes release of prolactin, which acts on alveolar epithelial cells to increase milk secretion (maintains milk production)

66
Q

Discuss the reproductive disorder of prolactinoma

A
  • prolactinomas are the commonest pituitary adenomas, produce high levels of prolactin, also cause compression of pituitary and optic chiasm
    Symptoms: caused either by increased prolactin levels (hyperprolactinemia) or by ‘mass’ effect (due to size of tumour)
    Hyperprolactinemia cause:
  • amenorrhea (no cycles)
  • galactorrhoea
  • loss of axillary and pubic hair
  • hypogonadism, gynecomastia, erectile dysfunction
    Mass effects include:
  • bi-temporal hemianopsia (as optic chiasm compressed)
  • vertigo, nausea, vomiting
67
Q

What is the basal metabolic rate, and what is it primarily determined by?

A
  • energy used at rest
  • thyroid hormones
68
Q

Define follicle.

A

a fluid-filled sack

69
Q

What are the follicular cells of the thyroid full of?

A
  • colloid - no connection to rest of body, reason being to make and store thyroid hormone
70
Q

What are the functions of the thyroid?

A
  • contains follicles, comprised of follicular cells and colloid, that produce the thyroid hormones T3 and T4 from tyrosine and iodine
  • thyroid hormones are amines, lipophilic, are transported in plasm bound to carrier proteins, with a balance between bound and free hormone
  • most thyroid hormones are secreted as T4 which is converted to T3 in tissues
  • virtually every tissue in the body is affected by thyroid hormones
71
Q

Where is the thyroid gland located?

A

Lies over the trachea in the neck

72
Q

What is the effect of thyroid hormone on cells?

A
  • increases metabolism (‘goes faster’) by influencing fuel metabolism (i.e. synthesis and breakdown of protein, fat, and carohydrates)
73
Q

True or false: T3 is four times more potent than T4

A

True

74
Q

Discuss thyroid hormone’s ‘sympathomimetic’ effect

A
  • increases target cell responsiveness to catecholamines (effects cardiac output by increasing heart rate and contractility)
75
Q

List the four main types of thyroid tumours, as well as their symptoms

A
  • papillary thyroid cancer
  • follicular thyroid cancer
  • medullary thyroid cancer
  • anaplastic thyroid cancer
    Symptoms:
  • nodule in thyroid region; enlarged lymph node; pain in anterior neck, vocal changes
  • thyroid hormones can be normal, low or high
76
Q

List the risk factors and diagnosis & treatment of thyroid tumours

A

Risk factors:
- radiation exposure, enlarged thyroid
- family history, thyroid disorders
Diagnosis and treatment:
- ultrasound/fine needle aspiration
- surgery, radiation therapy, chemotherapy

77
Q

List the causes and symptoms of hyperthyroidism

A

Causes:
- Grave’s disease
- excess thyrotropin-releasing hormone, thyroid stimulating hormone or thyroid hormone production (from tumour in hypothalamus, pituitary, or thyroid gland)
Symptoms:
- increased metabolism, excessive sweating, increased appetite but weight loss, muscle weakness, anxiety, palpitations
- GOITRE (enlargement of thyroid gland)
-exophthalmos (protrusion of eyes)

78
Q

Discuss Grave’s Disease, mentioning its risk factors, symptoms and treatment

A

-an autoimmune disease (produces autoantibodies)
- thyroid stimulating immunoglobin
Risk factors:
- family history, other autoimmune diseases, smoking
Symptoms:
- increased metabolism, excessive sweating, increased appetite but weight loss, muscles weakness, anxiety, palpitations, exophthalmos, goitre
Treatment:
- radioiodine therapy, antithyroid medications, thyroid surgery

79
Q

Discuss the differences between primary and secondary hypothyroidism, as well as in pregnancy.

A

Primary:
- thyroid gland failure; resection/radiotherapy
- Hashimoto’s thyroiditis
Secondary:
- deficiency of thyrotropin releasing hormone or thyroid stimulating hormone (hypothalamus or pituitary failure)
Pregnancy:
- can cause congenital iodine deficiency syndrome (cretinism) in neonates

80
Q

Discuss the symptoms, diagnosis, prevention & treatment of hypothyroidism

A

Symptoms:
- decreased metabolism, poor cold tolerance, excessive weight gain, fatigue; bradycardia, weak pulse, slow reflexes and mental function, myxoedema (puffiness), goitre
Diagnosis:
- blood tests for thyroid stimulating hormone, thyroxine (T4)
Prevention & treatment:
- salt iodisation (where iodine deficient)
- levothyroxine (synthetic TH)

81
Q

Discuss Hashitomo’s thyroiditis, mentioning its symptoms, diagnosis and treatment.

A
  • Autoimmune disease - autoantibodies attack the thyroid gland
  • caused by combination of genetic and environmental factors
  • more common in women, family history of autoimmune diseases
    Symptoms and treatment:
  • goitre, decreased metabolism, poor cold tolerance, excessive weight gain, fatigue, etc.
  • diagnosis: blood tests for thyroid stimulating hormone, T4 and anti-thyroid antibodies
  • levothyroxine
82
Q

Discuss congenital iodine deficiency syndrome, making specific mention to the signs and symptoms (severe and mild), and prevention & treatment.

A

Signs and symptoms:
- goitre, poor growth, thick skin, hair loss, enlarged tongue, protruding abdomen, delayed bone maturation and puberty, small adult stature, infertility
- cognitive and neurological impairment (severe, can’t talk, stand or walk; mild, learning disabilities, reduced muscle tone and coordination)
Prevention and treatment:
- iodine supplementation of food, screening pregnant women and neonates
- lifelong administration of thyroid hormone

83
Q

What are some psychological stressors?

A

Stimuli which lead to fear, anxiety or frustration
- includes traumatic events such as death, divorce, conflict, abuse, war, and natural disasters

84
Q

What are some physical stressors?

A

Stimuli which disrupt normal body function, can be due to internal factors or external environment
- hypoxia, hypoglycaemia, infection, physical strain, injury, starvation, dehydration
- exposure to heat or cold

85
Q

What is an acute stress response?

A
  • a normal and beneficial adaptive response
  • increases alertness and focus, provides energy to respond and cope with stressful situation
  • extent of response is dependent on severity of stressor, and on the individual
  • mild stress improves mood, creates new memories , encourages creative thinking, promotes neural growth in brain, facilitates problem solving
86
Q

What can severe stress cause?

A
  • detachment
  • reduction in awareness
  • derealisation
  • depersonalisation
  • dissociate amnesia
87
Q

What is a chronic stress response?

A
  • when stress is prolonged, homeostasis is unable to be maintained
  • the body enters an exhausted state, when damage to health can occur, immune suppression, hypertension, gastrointestinal disturbances
  • can have detrimental psychological effects - anxiety and mental dysfunction, social withdrawal
88
Q

What is the ‘General Adaptation Syndrome’ response to stress?

A
  • describes the stages of the bodies response to stress, three phases:
    1. alarm - preparing ‘fight-or-flight’
    2. resistance - staying alert, but keep on with normal functioning (adaptation), homeostasis maintained
    3. exhaustion - resources are depleted, ‘burnout’ sets in, homeostasis cannot be maintained so function impaired
89
Q

In what ways does the acute stress response ready the body for action?

A
  • increased cardiovascular function - heartrate, contractility, mostly vasoconstriction, with vasodilation to muscles
  • increased respiratory function: resting rate and tidal volume, bronchodilation
  • liberation of nutrients - increased blood glucose and fatty acids
  • skin - paling or flushing, sweating, piloerection
  • muscle tension and shaking
  • inhibition of gastrointestinal motility, contraction of sphincters
  • inhibition of the lacrimal gland and salivation
  • relaxation of bladder, inhibition of erection
90
Q

What is the physiological response to stressors coordinated by?

A
  • the hypothalamus
91
Q

What is the sympathetic nervous system’s involvement in the physiological response to stress?

A
  • adrenaline (epinephrine) from adrenal medulla
  • noradrenaline (norepinephrine) from neurons
  • inhibition of parasympathetic nervous system
92
Q

What is the endocrine’s system’s involvement in the the physiological response to stress?

A
  • cortisol and corticosterone from adrenal cortex
  • vasopressin (anti-diuretic hormone) from posterior pituitary
  • activation of renin-angiotensin-aldosterone (‘RAAS’, involves liver, kidneys, lungs and adrenal cortex)
  • insulin and glucagon from pancreas
93
Q

Why is aldosterone produced in response to, and what is its function?

A
  • produced in response to changes in ECF volume/blood pressure and stress
  • promotes water retention in kidneys by increasing Na+ reabsorption
94
Q

What are the actions of glucocorticoids (cortisol/corticosterone)?

A
  • allows body to cope with stress by increasing availability of energy and amino acids
  • increases vascular reactivity (by largely unknown mechanisms)
  • affects mood and behaviour - improving mood, increasing alertness
  • stimulates brain function - promotes neural growth in brain which improves memory, creative thinking, problem solving ability
  • in chronic stress, may be responsible for immune suppression and other health defects
95
Q

What is the adrenal medulla and what does it produce?

A

Part of the sympathetic nervous system

  • produce the catecholamines adrenaline and noradrenaline in response to direct stimulation by sympathetic pre-ganglionic neurones from the splanchnic nerve
  • hormones are released directly into the bloodstream, and act on distant target tissues including heart, blood vessels, bronchioles, GIT
96
Q

What do adrenaline and noradrenaline do?

A
  • elicits acute physical reactions of body to prepare for ‘fight or flight’
  • increases cardiac and respiratory function, slows digestion/kidney function, tenses muscles, increases sweating
  • vasoconstriction to skin and organs (including kidneys), vasodilation to skeletal muscles
  • inhibits parasympathetic nervous system
  • act on pancreas to reduce insulin secretion, increase glucagon secretion to increase blood glucose
97
Q

What can chronic stress cause?

A
  • immune suppression through excess glucocorticoid production, increasing risk of infection
  • hypertension and cardiovascular disease
  • disruption of body weight
  • poor growth in children through suppression of growth hormone production
  • inhibition of parasympathetic nervous system can result in reproductive failure, poor digestion
  • mental disorders
  • associated with higher mortality
98
Q

What is Cushing’s syndrome, and what are the symptoms?

A

Excess glucocorticoids, due to excess ACTH or adrenal tumour -> excess glucocorticoid secretions (Cushing’s Disease) or excess glucocorticoid administration
Symptoms:
- protein depletion -> muscle weakness
- poor healing, immunodeficiency
- thin skin, prone to damage and hirsutism (hairy)
- obesity and body fat redistribution
- Type II diabetes

99
Q

What are the symptoms of Addison’s disease?

A

Chronic failure of adrenal cortex
Symptoms:
- electrolyte imbalance - loss of aldosterone
- dehydration and hypotension
- reduction in stress response (loss of glucocorticoids)
- Addisonian crisis (hypoglycaemia - coma, death)
- loss of vascular reactivity (vasodilation/shock)
- melanin pigmentation (loss of negative feedback causes increased production of ACTH and melanocyte-stimulating hormone

100
Q

What is adrenogenital syndrome, and what are the symptoms?

A

Excess levels of androgens due to 21-hydroxylase deficiency or adrenal tumour
Symptoms:
- pre-pubertal females - pseudohermaphroditism
- pre-pubertal males - precocious pseudopuberty
- adult females - virile characteristics, hirusutism, deep voice, increased muscularity, amenorrhea
- adult males - no apparent effect

101
Q

What is the treatment and management of a) Cushing’s syndrome, and b) Addison’s disease?

A

Cushing’s: aim to reduce cortisol levels
- surgery, radiotherapy or chemotherapy (if tumour) or medication; diabetes management

PHYL2065 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions