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ELC > Physiology > Flashcards

Physiology Flashcards

1
Q

Definition of a hormone?

A

A substance secreted by living cells in trace amounts, transported to a distance site where it is used to regulate or initiate reactions.

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2
Q

How do steroid and thyroid hormones travel in the blood?

A

Bound to plasma proteins

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3
Q

What does the response to a hormone mostly rely on?

A

Depending on receptor number

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4
Q

What are the two lobes of the pituitary called, their separate functions?

A

Anterior pituitary - adenohypohysis - part of the gut

Posterior pituitary - neurohypohysis - part of the CNS

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5
Q

Two hormones the posterior pituitary secretes? Where are they synthesised?

A

ADH and oxytocin - synthesised in the hypothalamus (SON and PVN)

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6
Q

What does oxytocin do and what causes it’s release and what inhibits it’s release?

A

Causes uterine contraction and milk let down

stimulated by stretch of the cervix and suckling

Inhibited by stress and alcohol

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7
Q

What does ADH do and what causes it’s release and what inhibits it’s release?

A

Causes water reabsorption in the kidney by insertion of aquaporins

Stimulated by high plasma osmotic pressure, low blood volume and stress

Inhibited by alcohol

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8
Q

What does lack of ADH cause?

A

Diabetes insipidus (high flow of dilute urine)

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9
Q

What can cause lack of ADH?

A

Whiplash injury to the tract
Pituitary tumour
Local damage to hypothalamus

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10
Q

What does over-secretion of ADH (SIADH) cause?

A

Low flow of concentrated urine

Water is retained

Cells become over-hydrated

Plasma [Na+] falls

Fatigue

Confusion

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11
Q

Common causes of SIADH?

A

Carcinoma

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12
Q

Diagnosis of SIADH

A

Presence of high urine [Na+] and low plasma osmolarity

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13
Q

Treatment of SIADH?

A

Fluid restriction and very slow NaCl infusion.6

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14
Q

What hormones does the anterior pituitary secrete?

A

Thyroid stimulating hormone

Adrenocorticotrophic hormone

Growth hormone

FSH

LH (leuteinising hormone)

Prolactin

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15
Q

What is the anterior pituitary stimulation test?

A

ACTH and GH stimulated by injecting insulin

TSH and prolactin stimulated by TRH injection

LH and FSH stimulated by GnRH

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16
Q

What inhibits growth hormone?

A

Somatostatin

High blood glucose

Chronic stress

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17
Q

Actions of GH?

A

Fasting state:

  • Gluconeogenic AA taken up and converted to glucose
  • Mobilises fat to FFA
  • Powerfully anti-insulin in action

Insulin Concentrations High:

  • Stimulates AA uptake
  • Stimulates protein synthesis largely via IGFs
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18
Q

GH stimulated by?

A

Low blood glucose concentration

High plasma AA concentration

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19
Q

Results of lack of GH?

A

In adults, disordered metabolism but other systems compensate

In children causes failure to grow

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20
Q

Causes of lack of growth hormone in children?

A

Chronic stress e.g. bullying/parental divorce

Treatment of asthma or IBD causing high plasma cortisol

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21
Q

Tests for GH?

A

Stimulation: give insulin then glucose

Suppression: Glucose tolerance test

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22
Q

Three areas of the adrenal cortex and the hormones they produce?

A

Zona Glomerulosa: Mineralocorticoid

Zona fasciculata: Glucocorticoid

Zona reticularis: Sex steroid production

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23
Q

Results of excess GH?

A

Children: Gigantism

Adults: acromegaly

Diabetes mellitus and heart disease risk

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24
Q

What can cause primary under-production in the adrenal cortex?

A

TB/HIV

Addison’s disease (inherent disorder of the adrenal cortex)

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25
Q

Excess mineralocorticoid production can cause what?

A

Conn syndrome

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26
Q

How do you differentiate between ACTH dependent causes of cushings?

A

Low dose dexamethasone suppression test - diagnoses cushings

High dose test:

> 50% suppression of following 9am cortisol - corticotroph/pituitary tumour (‘cushings disease’)

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27
Q

Two types of under-production of the adrenal cortex?

A

Primary: Entire cortex affected
Secondary: Hypopituitarism, loss of ACTH

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28
Q

Cushing syndrome symptoms and signs? (get some)

A 
Moon face
Weight gain with central obesity
Hypertension
Diabetes
Depression
Hypogonadism
Osteoporosis
Poor wound healing
Acne
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29
Q

Diagnosing glucocorticoid excess?

A

Midnight/bedtime cortisol levels

24hr urinary free cortisol

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30
Q

Medical treatment for cushings?

A

Block cortisol production: metyrapone, ketoconazole

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31
Q

Pituitary tumour treatment?

A

Trans-sphenoidal hypophysectomy +/- radiotherapy

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32
Q

Causes of hypoadrenalism?

A

TB/AIDS
Addison’s disease
Metastatic tumour
Lymphoma

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33
Q

Clinical features of hypoadrenalism?

A 
Tiredness 
Weakness
Weight loss
postural hypotension 
hypoglycaemia
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34
Q

Diagnosis of hypoadrenalism?

A

Short synacthen test - Give ACTH and measure cortisol later

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35
Q

Treatment for hypoadrenalism?

A

Hydrocortisone lifelong

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36
Q

What is endocrine hypertension?

A

Hypertension caused by demonstrable hormone excess

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37
Q

What is Conn syndrome? symptoms?

A

Primary hyperaldosteronism

Few symptoms, hypokalaemia, weakness, lethargy, headaches

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38
Q

Classic presentation of Conns syndrome?

A

Young, severe hypertension, high sodium, low potassium

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39
Q

Where do spironolactone and eplerenone act?

A

Mineralocorticoid receptor in distal convoluted tubule, they antagonise the MR receptor.

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40
Q

Two examples of catecholamines?

A

Adrenaline

Noradrenaline

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41
Q

What is a phaeochromocytoma?

A

Tumour of the adrenal medulla, secreting catecholamines (adrenaline and noradrenaline)

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42
Q

Actions of catecholamines?

A

acts on α and β adrenoreceptors

alertness, anxiety, agitation

Pupil dilatation

Bronchodilation

Increased glucagon and decreased insulin

Increased renin release in the kidney

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43
Q

Treatment of phaeochromocytoma?

A

Surgery or α and β blocker (phenoxybenzamine or propranolol)

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44
Q

How do the adrenals regulate the stress response?

A

Catecholamines prepare for flight or fight

Glucocorticoids and mineralocorticoids ‘raise the alarm’

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45
Q

What does the cortex and medulla of the adrenals secrete ?

A

Cortex - steroid hormones, glucocorticoids, mineralocorticoids, sex hormones

medulla (part of the SNS) secretes catecholamines

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46
Q

What type of hormone is cortisol? Where does it act?

A

Glucocorticoid receptor very strongly

Mineralocorticoid receptor weakly

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47
Q

11β-HSD 1 and 2 actions?

A

2 prevents flooding of mineralocorticoid receptors by cortisol (converts it to cortisone)

1 amplifies glucocorticoid action

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48
Q

Steps of cortisol synthesis?

A

Hypothalamus affects the pituitary through CRF and ADH

Pituitary releases more ACTH in response to the above two

ACTH stimulates cortisol production

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49
Q

What is the HPA axis?

A

The classic negative feedback system functioning in between the hypothalamus, pituitary and the adrenals

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50
Q

Actions of cortisol?

A

Catabolic:
- Stimulates protein breakdown in muscle bone e.t.c.

Anabolic:

  • Increases gluconeogenesis
  • Decreases glucose and AA utilisation
  • Increases glycogen synthesis

Maintains fluid volume in the CV system

Immunosuppression and anti-inflammatory effects

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51
Q

What type of hormone is aldosterone? What are it’s main actions?

A

Mineralocorticoid

Promotes sodium reabsorption in the distal convoluted tubule

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52
Q

Main hormonal system that regulates aldosterone production?

A

RAAS pathway

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53
Q

What is DHEA, when is it secreted in the adrenals?

A

A sex steroid large amount secreted at birth and then stops till 7-8 where more is secreted.

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54
Q

What cells are in the adrenal medulla?

A

chromaffin cells - like specialised postganglionic cells without axons

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55
Q

How are catecholamines released, in response to what?

A

In response to stimulation of splanchnics causes exocytosis of secretory granules of

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56
Q

What exactly is cushings syndrome?

Causes

A

Cortisol excess (not that is not cushings disease)

Primary cause - ACTH independent e.g. adrenal tunour (this is cushings disease)

Secondary cause - ACTH-independent e.g. excess ACTH e.g. secretion from pituitary tumour

Prolonged corticosteroid treatment

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57
Q

What exactly is addison’s disease and it’s causes?

A

Glucocorticoid/mineralocorticoid deficiency

Primary cause - adrenal damage or auto-immunity

Secondary - pituitary dysfunction leading to low ACTH

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58
Q

Features of addison’s disease?

A

Progressive weakness and weight loss

Low plasma glucose and sodium, high Potassium

Dehydration

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59
Q

What is different in the fetal adrenal gland? What does this area do?

A

Has a large inner fetal area that makes DHEA, which is used as a precursor to produce oestrogens by plancenta

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60
Q

What is congenital adrenal hyperplasia? Most common type?

A

Congenital enzyme deficiencies, most common by far is 21-hydroxylase

causes excess sex steroids but decreased gluco/mineralocorticoids

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61
Q

Examples of hormones that regulate blood pressure?

A

Ang II

Aldosterone

Cortisol

Adrenaline/Noradrenaline

Calcium

GH

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62
Q

Common causes of Conn syndrome?

A

Aldosterone producing tumour (adrenal adenoma)

Micro/macro-nodular disease

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63
Q

Examples of thyroid hormones?

A

Thyroxine

Triodothyronine

(Thyro)calcitonin

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64
Q

What element do thyroid hormones contain (and is therefore required for synthesis)

A

Iodine

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65
Q

How are thyroid hormones synthesised?

A

Iodine uptake from blood into follicle cell

Transported to colloid surface

inserted into tyrosines

Couple together to form thyronines

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66
Q

What does TSH (thyrotrophin) stimulate?

A

Iodine uptake/oxygenation

T3/T4 release

Causes secretion and gland growth

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67
Q

What is TBG?

A

Thyroxine binding globulin, binds thyroid hormones with very high affinity

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68
Q

Actions of thyroid hormone, where do they act?

A

Acts in intracellular receptors and DNA

Raised BMR

Raises number of adrenergic beta receptors in tissues and therefore increase sympathetic function

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69
Q

Thyroid hormone excess (hyperthyroidism) symptoms?

A

Weight loss

Heat intolerance

Sweating

tremor

Lid retraction and staring eyes

high heart rate

Diarrhoea

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70
Q

Causes of hyperthyroidism?

A

Graves disease (Gland diffusely enlarged)

Toxic nodules

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71
Q

Hyperthyroidism treatment?

A

Surgery + replacement T4

Radioiodine + replacement T4

Antithyroid + replacement T4

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72
Q

Hypothyroidism symptoms?

A

Cold intolerance

Low heart rate

Constipation

Weight gain

Loss of interest in life

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73
Q

What is Myxoedema?

A

Hypothyroidism

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74
Q

Where is TSH secreted from, what controls it’s secretion?

A

Secreted from anterior pituitary

Controlled by hypothalamic TRH

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75
Q

What is T4 and T3?

A

T4 is prohormone, T3 is active

They are thyroid hormones

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76
Q

What is hashimoto’s thyroid disease?

A

T cell infiltrate within the thyroid

Presence of autoantibodies to thyroglobulin and thyroid peroxidase

Leads to hypothyroidism

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77
Q

Which gender is more likely to acquire an autoimmune disease?

A

female in most cases apart from UC and diabetes

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78
Q

What is graves disease, clinical manifestation?

A

Autoimmune thyroid disorder, causing hyperthyroidism autoantibodies against TSH receptor and thyroglobulin:

  • Tremor
  • Heat intolerance
  • Sweating
  • Anxiety
  • Weight loss
  • Palpitations
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79
Q

Common issues in diabetes?

A

Retinopathy

Neuropathy

Macrovascular and cerebrovascular disease

Foot ulcers (possible amputations)

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80
Q

Diagnosis of diabetes with glucose tests?

A

2-hour plasma glucose: >7.8 - 11.1

Fasting plasma glucose: >6.1 - 7

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81
Q

HbA1c level for diabetes diagnosis?

A

> 6.5

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82
Q

4 main classifications of diabetes?

A

Type 1

Type 2

Secondary

Gestational

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83
Q

Type 1 diabetes pathogenesis?

A

T-cell mediated autoimmune destruction of β-cells in the pancreas

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84
Q

Type 1 diabetes aetiology/triggers?

A

Mostly genetic, however other environmental factors also considered such as bacterial/viral and perinatal factors

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85
Q

Presentation of type 1 diabetes?

A

Increased thirst (polydipsia)

Polyuria

Nocturia

Drowsiness/dehydration

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86
Q

Causes of secondary diabetes?

A

Pancreatic disease (e.g. pancreatitis)

Endocrine disease (e.g. acromegaly)

Drugs and chemicals (e.g. Diuretics glucocorticoids)

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87
Q

What cells secrete insulin and glucagon? Where?

A

Alpha cells - glucagon

Beat cells - Insulin

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88
Q

Process of events that lead to the release of insulin?

A

Glucose taken up by beta cells, metabolised to form ATP

Increased ATP causes cascade leading to exocytosis of the insulin containing vesicles

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89
Q

Insulin receptor’s effects when insulin is bound?

A

Increased glucose transport by moving transporters to cell surface

Increased protein and fat synthesis

Increased Glucose synthesis

Growth and gene expression

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90
Q

What breaks down insulin?

A

Mostly the liver, by insulinase

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91
Q

Insulins effect on the livers release of glucose?

A

Decreases it

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92
Q

Effects of insulin on the liver?

A

Inhibits glycogenolysis

Stimulates glycogen synthesis

Stimulates glucose uptake

Stimulates glycolysis

Indirectly inhibits gluconeogenesis, inhibits fatty acid mobilisation from adipose tissue

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93
Q

What are the 4 glucose transport proteins?

A

GLUT 1: basal glucose uptake

GLUT2: pancreatic beta cells

GLUT3: basal glucose uptake

GLUT4: insulin sensitive (the only one)

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94
Q

What does insulin do to GLUT 4 receptors?

A

Makes them fuse with the membrane

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95
Q

Insulins effect on the lipid metabolism in the liver?

A

Increased lipoprotein synthesis

Reduced β-oxidation

Reduced ketogenesis

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96
Q

Effects of insulin on protein metabolism?

A

Stimulates protein biosynthesis in muscle

Reduces AA release from muscle

97
Q

Effects of insulin?

A 
Glucose and aa uptake
Increased protein synthesis 
Triglyceride synthesis 
Increased glycogenesis
Inhibits lipolysis
Inhibits gluconeogenesis 
Inhibits ketone bodies 
Inhibits glycogenolysis
98
Q

Anabolic and Catabolic meanings?

A

Anabolic is building up, catabolic breaking down.

99
Q

Examples of anabolic hormones?

A

Insulin

GH

Thyroid (low Conc)

100
Q

Examples of catabolic hormones?

A

Glucagon

Catecholamines

Cortisol

Thyroid (high Conc)

101
Q

Effects of glucagon?

A

Increased glycogenolysis
Increased gluconeogenesis
Increased ketone body formation
Increased lipolysis (weak)

102
Q

Main control of glucagon release?

A

Reduced glucose
Fatty acids inhibit
Insulin inhibits
Catecholamines

103
Q

Mechanism of glucagon’s action?

A

Plasma membrane receptor

Activated Adenylyl cyclase

Activates cAMP-dependent protein kinase

Substrate phosphorylation

104
Q

What increases and decreases glucagon secretion?

A

Increases:

  • Low plasma glucose
  • Raised plasma amino acids
  • CCK
  • PNS and SNS

Decreases:

  • High plasma glucose
  • Insulin
  • Energy substrates
105
Q

Catabolic and anabolic effects of GH?

A

Anabolic effects:

  • Protein synthesis, AA uptake

Catabolic effects:

  • Lipolysis
  • Glycogenolysis
  • Reduced glucose utilisation
106
Q

Effects of somatomedins (IGFs)

A

Anabolic effects:

  • Growth
  • Cell division
  • Protein synthesis
  • Glucose utilisation
107
Q

Changes in early starvation?

And Late starvation

A

KB produced and used by brain and body

Late:

  • Brain adapts to using KB
  • Muscles switch to using FA
108
Q

What is graves opthalmology?

A

Accumulation of hyaluronan, CAGs and collagen in perioccular space, infiltrate with CD4 T cells and B cells

109
Q

Symptoms of graves opthalmology?

A

Proptosis (bulging of eye)

Oedema of the conjunctiva (chemosis)

Eye-lid retraction

110
Q

Thyroid hormone changes in hyperthyroidism?

A

T4 increase and TSH decrease

111
Q

Clinical signs of hypothyroidism?

A

Slow pulse

Carpal tunnel

Myopathy

Ataxia

112
Q

Biochemical changes in thyroid hormones in hypothyroidism?

A

Decreased T4 increased TSH

113
Q

Main functions of the testes? and of the ovaries?

A

Testes :

  • Produce sperm
  • Produce testosterone

Overies:

  • Mature oocytes
  • Produce oestrogen
114
Q

What is the hypothalamic-pituitary-testis axis, explain it?

A

GnRH produced in the hypothalamus cause the secretion of LH and FSH in the pituitary which go on to stimulate the production of testosterone in the testes

115
Q

Pubertal and mature response of the hypothalamic-pituitary-gonadal axis?

A

Pulsatile secretion of GnRH about every 90mins

116
Q

Function of leydig cells?

A

Produce testosterone

117
Q

Effects of GnRH on males and females?

A

Males:

  • LH stimulated, producing testosterone
  • FSH stimulated, stimulating spermatogenesis

Females:

  • LH stimulates ovulation
  • FSH stimulates follicular development
118
Q

Wide ranging effects of oestrogen?

A

Fallopian tubes contractility

Cervix mucus consistency

Behavioural, reduced appetite

Fluid retention in kidney

119
Q

Wide ranging effects of progesterone?

A

Development of breasts

Mucus consistency in cervix

Increased appetite

increased body temperature

120
Q

Phases of the ovulatory cycle?

A

Pre-antral: Primordial to pre-antral follicle
- gets ready to respond to LH and FSH

Antral: forms antral follicle, responding to LH and FSH

Pre-ovulatory phase: occurs when there is lots of Lh and LH receptors on granulosa cells, causes oocyte to complete first meiotic division

Ovulatory: LH surge causes follicle rupture onto ovary surface

Follicular phase: low oestrogen exerts negative feedback on LH/FSH, high oestrogen exerts positive feedback, inhibit exerts negative feedback on FSH

Luteal phase: collapsed follicle becomes corpus luteum (dependent on LH) Granulosa cells secrete progesterone, thecal cells secrete oestrogen

If fertilisation does not occur: corpus luteum regresses to corpus albicans

If fertilisation does occur hCH is released and corpus luteum is maintained

121
Q

Stages of spermatogenesis?

A

Stage 1: mitotic proliferation

  • spermatogonium
  • Diploid spermatogonia
  • Primary spermatocytes

2: meiotic division
- Secondary spermatocytes
- Haploid spermatids

3: differentiation
- differentiating spermatids
- Mature sperm cells emerge from residual bodies

122
Q

What is the function of the blood-testes barrier?

A

Protects sperm from noxious circulating agents and immune response

123
Q

How do sperm move through the male genital tract?

A

Passively from rete testes to the epididymus by current of fluid

Actively through musculature of the epididymus to the Vas deferens

124
Q

What is capacitation?

A

Process that occurs naturally in the female genital tract that involves the removal of glycoproteins covering the sperm

125
Q

Where is cut in a vasectomy? Why does this stop the testes filling with fluid?

A

Vas deferens - Sperm build up behind the cut are removed by phagocytosis

126
Q

What do LH and FSH do in the testes?

A

LH - stimulates leydig cells to produce testosterone

FSH - acts on sertoli cells to stimulate testicular fluid formation and androgen binding proteins

127
Q

What hormones exert negative feedback on the HPT axis?

A

Oestradiol and inhibin on FSH

Testosterone on LH and FSH

128
Q

Definition of infertility?

A

When pregnancy fails to occur after a year, (normally fails in 4/5 cycles)

129
Q

Causes of male infertility?

A

Pre-testicular:
- Genetic e.g. XXY or hypogonadism

Sperm production/function (oligospermia):

  • Mumps
  • Chemotherapy/irradiation
  • autoimmunological

Sperm delivery:
- Epididymal obstruction

130
Q

Causes of male infertility?

A

Blocked or damaged tubes - Chlamydia

Ovulatory disorders:

  • Absent or irregular cycles
  • hyperprolactinaemia (prolactin inhibits GnRH)
  • Polycystic ovaries
  • Genetic ovarian failure
131
Q

Two reactions that the sperm undergoes before fertilization takes place?

A

Acrosome reaction

Capacitation

132
Q

The three blocks to polyspermy at fertilisation?

A

Fast block - Membrane potential changes, ion channels open

Slow block - cortical granules released, increased intracellular Ca2+ ZP3 receptors break down

Juno receptor block

133
Q

What is ICSI

A

ICSI - intracytoplasmic sperm injection

134
Q

What id PGD and PGS?

A

Pre-implantation genetic diagnosis/screening

135
Q

Reasons to perform pre-natal testing?

A

Advanced maternal age

Multiple pregnancy losses (>3)

Known or suspected family history of genetic disorder

Abnormal ultrasound

136
Q

Types of prenatal screening?

A

Non-invasive: ultrasound

Invasive:

  • CVS
  • Amniocentesis
137
Q

When would you perform CVS?

Miscarriage risk?

A

10-13 weeks of pregnancy

2-3%

138
Q

When would you perform Amniocentesis?

Miscarriage risk?

A

> 15 weeks

0.5-1%

139
Q

When can you do an ultrasound to detect abnormalities?

A

20 weeks

140
Q

Common clinical problems in early and in late pregnancy?

A

Early pregnancy: Miscarriage/ectopic pregnancy/Mola

Late pregnancy: Intrauterine growth restriction/pre-ecclampsia

141
Q

Where does ectopic pregnancy occur in 95% of cases?

A

Fallopian tube

142
Q

Classic symptoms of ectopic pregnancy?

A

Abdominal pain

Amenorrhoea

Vaginal bleeding

143
Q

Intra-abdominal bleeding signs?

A

Shoulder pain

Urge to defecate

Lightheadedness

144
Q

Ectopic pregnancy risk factors?

A

Previous ectopic

> 40

Smoking

IVF

Previous pelvic inflammatory condition

145
Q

Treatment for ectopic pregnancy?

A

Surgical salpingotomy

MTX (injection or other administration)

Tubal abortion/regression

146
Q

What is a molar pregnancy?

A

Unsuccessful pregnancy where there is no/abnormal placental tissue formation, large amounts of HCG

147
Q

What is NIPT?

A

Non-invasive prenatal testing

Next-gen sequencing technology with high specificity and sensitivity

148
Q

Difference in a screening test and a diagnostic test?

A

Diagnostic test:
- To account for symptoms or signs

Screening test:
- No prior evidence in the individual

149
Q

Pro’s and Con’s of screening tests?

A

Pros:

  • early detection - better treatment/early intervention
  • Identify people at risk for preventative treatment
  • Cost-effectiveness

Cons:

  • False positive and negatives
  • Invasive tests
  • Both cause psychological distress
150
Q

Definition for natural menopause?

A

12 consecutive months of amenorrhoea

151
Q

Average age of the menopause and duration?

A

Avg. Age 52

Avg. duration 3 years

152
Q

Menopausal symptoms?

A

Vasomotor symptoms e.g. hot flushes and night sweats

Irregular periods eventually amenorrhoea

Sexual dysfunction

Urinary symptoms

psychological symptoms

153
Q

Urogenital atrophy effects in menopause?

A

Vaginal atrophy (rise in pH)

Cervical atrophy

Loss of elasticity

Weakening of pelvic floor

Less sensitive to stimulation

154
Q

What causes osteoporosis in menopause?

A

Lack of E2 causes change in balance of HPG axis leadign to lack of oestrogen and decreased bone density

155
Q

Osteoporosis prevention mechanisms in menopausal women?

A

Recommended amounts of Calcium and Vit. D

Regular weight bearing exercises

Avoid smoking and excessive alcohol

156
Q

Osteoporosis treatment in menopausal women?

A

Bisphosphonates for post-menopausal women younger than 65

157
Q

Mechanism for bisphosphonates’ actions

A

Inhibit bone resorption by altering osteoclast function and activity

158
Q

What is given in HRT?

A

Oestrogen and progesterone for all women with a uterus and only oestrogen for hysterectomised women

Oestrogen alone increases risk of endometrial cancer in women with a uterus

159
Q

Two types of HRT?

A

Cyclical HRT: Oestrogen throughout with progestin 3 out of 4 weeks to produce bleed

Continuous combined HRT: ‘no-bleed’ Oestrogen and progesterone throughout

160
Q

Risks and benefits to HRT?

A

Relieves vasomotor symptoms

Sexual and urogenital symptoms respond well to HRT

Venous thromboembolism, stroke, CHD, breast cancer, ovarian cancer, - increased risk

161
Q

Will a larger maternal size affect the birth size of baby?

A

Yes

162
Q

What hormone does the growing fetus use to ‘signal’ it’s presence, used for pregnancy tests?

A

HcG

163
Q

Maternal metabolic changes in pregnancy?

A

Increase in protein reserves

Increase in fat reserves

Relative insulin resistance leads to increased circulating glucose levels

164
Q

Maternal cardiovascular adaptations in pregnancy?

A

Oestrogen causes generalised vasodilatation - decreased peripheral resistance

therefore maternal CO increased

165
Q

Maternal renal adaptations in pregnancy?

A

Blood volume expansion:

  • Increased activity in RAAS pathway
  • changes in blood osmolality

Increased GFR

166
Q

Why does the hypothalamus not decrease ADH secretion in pregnancy even though blood osmolality decreases significantly?

A

Hypothalamic osmoreceptors have decreased threshold

167
Q

Maternal respiratory changes in pregnancy?

A

Tidal volume increased by 40%

Pulmonary blood flow increased by 40%

Increased maternal red cell mass and DPG in red cells - increased O2 carrying capacity

168
Q

How does the fetus utilise IGF’s?

A

Fetal tissue release IGFs in response to raised glucose levels - they stimulate DNA production and cell division

169
Q

What age do you ultrasound the fetus during pregnancy (twice) why?

A

12 weeks - Date the pregnancy

18-20 weeks - growth and abnormalities

170
Q

Things to avoid eating during pregnancy due to risk of it being toxic to the baby?

A

Liver or liver-containing products

High dose multivitamin products

Shark, swordfish and limit tuna

171
Q

Micronutrients that should be provided in pregnancy, what they’re used for?

A

Folate/folic acid - DNA synthesis

Vitamin D - regulate calcium and phosphate

Iodine - synthesis of thyroid hormones

172
Q

What can happen if invasion of the cytotrophoblast is poor, formine less capillaries in the placenta?

A

Pre-ecclampsia

173
Q

What specifically does not cross the placental barrier?

A

Red cells

Large molecules

Lipophobic molecules (unless transported)

174
Q

What is the synctiotrophoblast?

A

Barrier that forms over villi in the placenta that prevents certain molecules passing through

175
Q

What can cause impaired placental function?

A

Reduced maternal blood flow

Too few villi

Too few transport proteins

Maternal illness

176
Q

What drugs do cross the placenta?

A

Most polypeptides do not - e.g. insulin/cortisol

177
Q

What is hyperemesis gravidarum?

A

Severe morning sickness, onset around 5-6 weeks

Diagnosis on clinical signs of dehyrdation and ketonuria

178
Q

What are twin-to-twin transfusions?

A

Artery to vein anastomoses from one umbilical cord to the other, if untreated likely to be lethal

179
Q

Complications associated with pre-ecclampsia?

A

Seizures ‘eclampsia’

Cerebral haemorrhage

Liver damage

Renal failure

180
Q

Main hormone relaxants and stimulants in pregnancy

A

Relaxants:

  • Progesterone
  • Relaxin
  • NO

Stimulants:

  • Oestrogen
  • Oxytocin
  • Prostaglandins
181
Q

During pregnancy what hormone is in abundance? At term how does the balance change?

A

Progesterone, at term balance changes to oestrogen

182
Q

During labour what hormones dominate, their roles?

A

Stimulants dominate:

Oestrogen:
- Stimulate proteolytic enzymes to dilate cervix

Oxytocin:

  • Initiates contractions,
  • Stimulates prostaglandin synthesis

Prostaglandins:
- Potentiate contractions induced by oxytocin

183
Q

Stages of labour (parturition)?

A

Pre-labour:

  • 4/5 weeks before
  • Braxton hicks contractions
  • Increase in uterine activity and change in cervical consistency

Dilation phase:

  • Cervical dilation
  • Preceded by water breaking

Expulsion stage:
- Uterine contractions and reduction in uterine volume push baby through pelvis

Placental stage:
- Delivery of the placenta ‘afterbirth’

184
Q

Uterine changes during pregnancy?

A

Hypertrophy and hyperplasia of myometrial cells

Increased contractile proteins

Increased numbers of mitochondria and cellular ATP

185
Q

What prostaglandin can be given to initiate labour, what else can be given?

A

Dinoprostone

Synthetic oxytocin can also be given

186
Q

How are oxytocin receptors affected in labour?

A

Increased receptor numbers by action of oxytocin

187
Q

Role of fetal cortisol?

A

Lung surfactant synthesis

Store of glycogen in liver

Synthesis of adrenaline in adrenal medulla

Maturation of islets in pancreas

188
Q

What is fetal distress during labour?

A

Reduced placental perfusion induced by strong uterine contractions, fetus can switch to anaerobic metabolism leading to acidosis

189
Q

Analgesia during labour?

A

Inhaled gas&air - entanox

Opioids - pethidine

Local nerve block

Epidural - lignocaine

190
Q

Treatment of post-partum haemorrhage?

A

Oxytocin - contraction to decrease blood flow

Ergometrine - increases contraction and vasoconstriction

Prostaglandins - e.g. misoprostol - increases uterine tone

191
Q

Drugs used for induction of abortion?

A

Prostaglandins - Gemeprost (PGE1)

Progesterone receptor antagonists - Mifeprestone

192
Q

Factors that adversely affect fertility?

A 
Age
Smoking
Coital frequency
Alcohol
Body weight
NSAIDS
Chemo
193
Q

Infertility investigations?

A

FSH/LH levels
Day 21 progesterone
Rubella/chlamydia status
Semen analysis

194
Q

Fertility treatment options?

A

Ovulation induction
Intra-uterine insemination
IVF
Intra-cytoplasmic sperm induction

195
Q

Common causes of pre-term labour?

A

Spontaneous (45%)

Delivery due to maternal or fetal infection (30%

Premature rupture of the membranes (25%)

196
Q

Risk factors of pre-term births?

A 
Tobacco use
Previous pre-term
Low BMI
Uterine abnormalities
Congenital uterine abnormalities

During pregnancy:

  • Multiple pregnancy
  • Vaginal bleeding
  • Systemic inflammation
  • Psychological stress/depression
197
Q

What can be detected to predict for pre-term delivery?

A

Fetal fibronectin

198
Q

What is tocolysis?

A

Drugs used to delay labour (stops contractions)

199
Q

What drugs are used for tocolysis?

A

Nifedipine - calcium channel receptor antagonist

Atosiban - oxytocin receptor antagonist

Magnesium

NSAIDS - Indomethecin

Calcium channel blockers

B2 adrenoceptor agonists

200
Q

In preterm labour what are the two general treatments

A

Delay birth

Mature fetal lung

201
Q

What can you give to mature the fetal lung?

A

Betamethasone - glucocorticoid steroid, increase the amount of surfactant produced

202
Q

How do NSAIDS work to prolong labour?

A

Inhibit the production of prostaglandins and:

Reduce uterine contractility
Reduce cervical softening

203
Q

How does Nifedipine work to prolong labour?

A

Blocks the calcium channel blocker that causes smooth muscle contraction in the uterus

204
Q

How does Ritodrine work to prolong labour?

A

B2 adrenoceptor agonist - activates intracellular cAMP and causes smooth muscle relaxation

205
Q

Best tocolysis drugs?

A

Atosiban and nifedipine: less side effects and effective

206
Q

What is surfactant?

A

Complex mix of phospholipids and surfactant proteins

207
Q

Two main surfactant therapies for the newborn child?

A

Synthetic surfactants:

Natural surfactants:

208
Q

Particular issues in neonatal physiology (what doesn’t work properly?

A

Immature liver function

Immature kidney function

Immature gut - lacking flora and ‘leaky’ endothelium

Immature immune system

Immature blood clotting

209
Q

What nutrients can be deficient in breast milk compared to formula?

A

Vitamin D

Iron

Vitamin K

210
Q

Some conditions that breast milk has been shown to reduce over formula milk?

A

Short term:

  • Otitis media
  • Respiratory infections

Long term:

  • Incidence if IBD
  • Risk of type 2 diabetes/Cardiovascular disease/obesity
211
Q

How does the histology of the breast work from milk producing glands to the nipple?

A

Made up of 15-20 lobes, divided by adipose

The lobes contain alveoli that synthesise and secrete milk

They then drain into lactiferous ducts

Then into the lactiferous sinus

The lactiferous converges on the nipple

212
Q

What hormone inhibits prolactin?

A

Dopamine

213
Q

What hormone triggers ‘let-down’ (milk ejection)?

A

Oxytocin - released during suckling

214
Q

What drugs could be used to first stimulate lactation and also to inhibit lactation?

A

Stimulate - domperidone, D2 receptor antagonist

Inhibit - D2 receptor agonists - bromocriptin

215
Q

What is colostrum?

A

They first milk for the first couple of days - low in fats and sugar, but high in protein minerals and vitamins, also contains lots of immunoglobulins

216
Q

What does prolactin inhibit? What is the function of this?

A

Inhibits GnRH so that LH and FSH are also inhibited, this is supposed to ensure that there cannot be another pregnancy so soon

217
Q

Piaget’s stages of development?

A

The sensori-motor stage (0-2)

The pre-opperational stage (2-7)

The concrete operational stage (7-12)

The formal operational stage (12-19)

218
Q

Interventions to reduce pain and anxiety in children in the medical setting?

A 
Distraction
Prep information
Play therapy
Hypnosis
Parental involvement
219
Q

The two different surfactant proteins?

A

SP-A/B/C and D

220
Q

Causes of short stature in infants?

A 
Familial short stature
Constitutional delay of growth and puberty
Intra-uterine growth retardation
Chronic disease
Psychosocial deprivation
Dysmorphic syndromes
Endocrine disorders
Skeletal dysplasia
221
Q

What is constitutional delay of growth and puberty? Treatment?

A

A condition with poorly understood aetiology that occurs more often in boys with a family history

Therapeutic intervention:

Boys: testosterone
Girls: oestradiol

222
Q

Where is GnRH released from, what are it’s actions?

A

Released from the hypothalamus acts on the pituitary to release LH/FSH

223
Q

Precocious puberty is what? In boys and girls what age?

A

Early puberty

224
Q

Causes of precocious puberty?

A

GnRH dependent:

  • Idiopathic
  • Tumour secreting GnRH
  • Chronic inflammation
  • Trauma
  • Sexual abuse

GnRH Independent:

  • Hypothyroidism
  • Ovarian cyst
  • Cushings
225
Q

Causes of delayed or incomplete puberty?

A

Hypogonadotrophic states:

  • Gonadotrophin deficiency e.g. CNS defects, Kallmann’s syndrome
  • Congenital adrenal hyperplasia

Hypergonadotrophic states:

  • Chromosome abnormalities e.g. turners and Klinefelters
  • Gonadal dysgenesis
  • Radio/chemotherapy
226
Q

Risk associated with gestational diabetes?

A

Miscarriage
Congenital malformations
Respiratory distress

Long term risks of: Obesity and Diabetes

227
Q

What diabetes drugs are contra-indicated in pregnancy?

A

Sulphonylureas apart from glibenclamide

228
Q

Suggested diabetes drugs in pregnancy?

A

Metformin

glibenclamide - only sulphylurea thats okay

229
Q

Treatment for diabetic ketoacidosis?

A

Resuscitation fluids: restore circulating volume, clear ketones, correct acidosis/electrolyte balance

Insulin infusion

230
Q

Triad of symptoms in PCOS?

A

Presence of polycystic ovaries
Signs of hyperandrogenism (hirsutism, acne, clitomegaly)
Oligo/amenorrhoea

231
Q

Why do ovaries become polycystic in PCOS?

A

Hypothalamic-pituitary-ovary feedback disorder causing ‘freezing’ of the ovary so that no dominant follicle is selected

232
Q

PMS physical symptoms?

A 
Swelling
Breast tenderness
Food cravings
Insomnia
Nausea
Sweating
233
Q

Definition of familial cancer, and hereditary cancer?

A

Familial: Family history of the same cancer but not clearly dominant or young in onset - includes environmental factors

Hereditary: Young onset, predisposition is uncommon in general population but very common in family

234
Q

Definitions of penetrance and expressivity relating to cancer genetics?

A

Penetrance - Chance of developing the disease if mutation is present

Expressivity - Disease manifestations may be different

235
Q

Functions of LH?

A

Formation and maintenance of the corpus luteum

Thinning of the graafian follicles membrane

236
Q

Functions of FSH?

A

Stimulation of development of follicles

237
Q

When is the proliferative phase of the menstrual cycle?

A

Begins immediately after the menstrual phase

days 5-14

238
Q

Results of increased oestrogen in the follicular phase (also signs a woman is about to ovulate)?

A

Thinning of cervical mucus

Thickening of endometrium

239
Q

Functions of progesterone?

A

Stimulation of oestrogen production

Initiation of secretory phase of endometrium

Inhibit LH and FSH

Increased basal body temperature

ELC (9 decks)

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