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Yr1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is endocrinology?

A

The study of hormones, their receptors, the intracellular signalling pathways and associated diseases

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2
Q

What are the three types of hormone action?

A
  • Endocrine - blood-borne, acting at distant sites
  • Paracrine - acting on adjacent cells
  • Autocrine - feedback on same cell that secreted hormone
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3
Q

What is an endocrine gland?

A

Secretes into the blood stream

- Examples are thyroid, adrenal, beta cells of pancreas

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4
Q

What is an exocrine gland?

A

Secretes through a duct

- Examples include pancreas amylase and lipase

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5
Q

What is synergism?

A

The combined effect of two hormones amplified

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6
Q

What is permissiveness?

A

A hormone needed for another full potential effect

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7
Q

Function of thyroid hormone? (5)

A
  • Accelerates food metabolism
  • Increases protein synthesis
  • Enhances fat metabolism
  • Increase in ventilation rate, cardiac output
  • Growth rate accelerated
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8
Q

Function of growth hormone?

A
  • Stimulates production of IGF-1. This induces metabolic changes
  • Decreases adipose
  • Increases liver function/muscle
  • Increases protein synthesis and lipolysis
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9
Q

What hormone stimulates GH?

A

GHRH

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10
Q

What hormone inhibits GH?

A

Somatostatin

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11
Q

What is acromegaly? (2)

A
  • Overgrowth of all organ systems, bones, joints, soft tissues
  • Due to excessive GH secretion after epiphyseal plate fusion
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12
Q

What is hyperprolactinaemia?

A
  • A condition with elevated serum prolactin
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13
Q

What is satiety?

A

The feeling of fullness - disappearance of appetite after a meal

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14
Q

Which part of the brain plays a central role in appetite regulation?

A

Hypothalamus

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15
Q

What are the main ‘players’ in appetite regulation?

A
  • Peripheral factors e.g. leptin and insulin
  • Gut peptides
  • Hypothalamus
  • Central areas
  • Brain stem
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16
Q

What is the role of leptin?

A
  • Binds to leptin receptor

- Switches off appetite and is immune-stimulatory

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17
Q

Why is diabetes a public health issue?

A
  • Mortality
  • Disability
  • Co-morbidity
  • Reduced quality of life
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18
Q

What is an ‘obesogenic’ environment?

A
  • Physical environment - TV remote controls, lifts, cars
  • Economic environment - cheap TV watching, expensive fruit and veg
  • Sociocultural environment - safety fears, family eating patterns
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19
Q

What is different about the anterior pituitary blood supply?

A
  • Has no arterial blood supply

- Receives blood through portal venous circulation from the hypothalamus

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20
Q

Would the removal of the thyroid cause an increase or decrease in TSH?

A

Increase

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21
Q

Would an overreactive thyroid cause an increase or decrease in TSH?

A

Decrease

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22
Q

What are two examples of diseases of the pituitary?

A
  • Benign pituitary adenoma
  • Craniopharygioma
  • Trauma
  • Apoplexy
  • Sarcoid/ TB
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23
Q

What can a tumour of the pituitary cause?

A
  • Pressure on local structures e.g. optic nerves
  • Pressure on normal pituitary
  • Functioning tumour
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24
Q

What can pressure on local structures of a pituitary tumour cause?

A
  • Headaches
  • Visual field defects
  • Cranial nerve palsles
  • Rhinorrhoea
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25
Q

What is bitemporal hemianopia?

A
  • affects peripheral view

- lose colour vision first

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26
Q

What are examples of functioning pituitary tumours?

A
  • Prolactinoma
  • Acromegaly/giantism
  • Cushing’s Disease
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27
Q

What are the symptoms of prolactinoma?

A
  • present with galactorrhoea (excessive production of milk) and/or infertility
  • Loss of libido
  • visual field defect
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28
Q

What is the treatment for prolactinoma?

A
  • Dopamine agonist = cabergoline
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29
Q

What are the symptoms of acromegaly?

A
  • thick skin, greasy, sweating, prognathism, frontal bossing

- ABCDEFGHIJ

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30
Q

What are the symptoms of Cushings?

A

Central obesity, red face, proximal myopathy, short stature, thin skin, brusing

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31
Q

What is mean age of diagnosis of acromegaly?

A

44

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32
Q

What are the co-morbidities related to acromegaly?

A
  • hypertension
  • Sleep apnoea
  • Arthritis
  • Type 2 diabetes
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33
Q

How can acromegaly be diagnosed?

A
  • Clinical features - includes facial enlargement, maxfax changes, excessive sweating and headaches
  • Increasaed GH and IGF-1
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34
Q

What therapy is used for treating acromegaly?

A
  • Restore basal GH and IGF-1 to normal levels (surgery
  • Relieve symptoms
  • Prevent further skeletal deformities
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35
Q

What surgery can be used in acromegaly

A
  • Pituitary surgery

- success dependent on size of tumour and surgeon

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36
Q

What medication is used for acromegaly? (3)

A
  • Cabergoline (dopamine agonist)
  • Somatostain analogue
  • GH receptor antagonist
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37
Q

What symptoms would occur with prolactinoma?

A
  • Effect of tumour = headache, visual field defect

- menstrual irregularity, infertility, low libido, galactorrhoea

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38
Q

What is the main type of treatment for acromegaly?

A
  • Pituitary surgery is the main therapy

- Medical management is improving

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39
Q

What is the main type of treatment for prolactinoma?

A
  • Medication rather than surgery

- Unlike other pituitary tumour management

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40
Q

What medication is used in prolactinoma?

A
  • Cabergoline - dopamine agonist
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41
Q

What part of the body can determine circadian rhythm?

A
  • The eyes (cells)
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42
Q

What are the symptoms of Addison’s Disease?

A
  • Fatigue
  • Lethargy
  • Muscle weakness
  • Mild depression
  • Loss of appetite/dehydration
  • Can go on to develop other common symptoms
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43
Q

What is the pathology of Addison’s Disease?

A
  • Primary adrenal insufficiency

- Disruption of production of the steroid hormones aldosterone and cortisol

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44
Q

What are the symptoms are hypopituitarism?

A
  • Fatigue
  • Weight Loss
  • Decreased sex drive
  • Decreased appetite
  • Anaemia
  • Infertility
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45
Q

What is the treatment for Addison’s and hypopituitarism?

A
  • Hydrocortisone 2-3x

- Also in primary adrenal insufficiency replace aldosterone with fludrocortisone

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46
Q

What is the common presentation of adrenal crisis?

A
  • Hypotension
  • Fatigue
  • Fever
  • Hypoglycaemia
  • Hyponatraemia/ hyperkalaemia
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47
Q

How can you manage adrenal crisis?

A
  • Immediate hydrocortisone
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48
Q

Name two types of thyroid autoimmunity.

A
  • Postpartum thyroiditis
  • Hashimoto’s thyroiditis
  • Atrophic thyroiditis
  • Graves’ disease
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49
Q

What is Graves’ Disease?

A
  • Autoimmune condition

- Body attacks thyroid so it is overreactive

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50
Q

What can predispose someone to thyroid autoimmunity?

A
  • Genetic factors
  • Female, especially post-partum
  • Environmental factors e.g. stress, iodine intake and smoking
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51
Q

What is a goitre?

A

A palpable and visible thyroid enlargement

52
Q

What can hyperthyroidism be due to?

A
  • Overproduction of thyroid hormone
  • Leakage of preformed hormone from thyroid
  • Ingestion of excess thyroid hormone
53
Q

What are the features of a patient with hyperthyroidism?

A
  • Weight loss
  • Tachycardia
  • Hyperphagia
  • Heat intolerance/sweating
  • Menstrual issues
54
Q

How would you investigate hyperthyroidism?

A
  • Thyroid function test
55
Q

What is the treatment for hyperthyroidism?

A
  • Anti-thyroid drugs = thionamides
  • carbimazole
  • Radioiodine
  • Surgery
56
Q

What is the common side effect of thionamides?

A
  • Rash
57
Q

What is the medication used for hyperthyroidism?

A
  • Carbimazole

- Thionamides

58
Q

What are two causes of hypothyroidism?

A
  • Hashimoto’s thyroiditis
  • Iodine therapy
  • Drugs
  • Pituitary disease
  • Hypothalamic disease
59
Q

What are the features of hypothyroidism?

A
  • Fatigue
  • Weight gain
  • Cold intolerance
  • Constipation
  • muscle cramps
  • dry, rough skin
  • oedema
60
Q

How would you investigate hypothyroidism?

A
  • levels of TSH (would be increased)
61
Q

What is the treatment for hypothyroidism?

A
  • synthetic L-thyroxine
62
Q

What is Hashimoto’s thyroiditis?

A

The immune system attacks the thyroid gland so that it swells and becomes damaged
- Symptoms include tiredness, weight gain and dry skin

63
Q

What are the consequences of hypocalcaemia?

A
  • parasthesia
  • muscle spasms
  • seizures
  • cataracts
64
Q

What is puberty?

A

The physiological, morphological and behavioural changes as the gonads switch from infantile to adult

65
Q

What are the secondary sex characteristics that occur at puberty for girls and boys?

A
  • Girls = ovarian oestrogens - growth of breast and female genitalia. Ovarian and androgens control pubic hair and axillary hair
  • Boys = testicular androgens - genitalia and pubic hair growth. Also enlargement of larynx
66
Q

What do you stage male/female genitalia/characteristics with?

A
  • Tanner stages
67
Q

What can delayed puberty lead to?

A

Reduced peak bone mass and osteoporosis

68
Q

What is delayed puberty?

A
  • delayed activation of the hypothalamic pulse generator (idiopathic)
  • hypogonadotrophic hypogonadism
  • hypergonadotrophic hypogonadism
69
Q

What can delayed puberty lead to?

A
  • Delay in secondary sex charactertistics
  • psychological problems
  • defects in reproduction
  • reduced peak bone mass
70
Q

What is primary hypogonadism?

A
  • ovary and testis failing
  • Female = oestrogen decreases, lack of feedback and LH and FSH increase
  • Males = testosterone goes down, lack of feedback so LH and FSH increase
71
Q

What is secondary hypogonadism?

A
  • hypothalamus/ pituitary failing
  • female = LH and FSH low, no response to feedback and oestrogen decreases
  • Male = LH and FSH low so testosterone decreases
72
Q

What are the symptoms of diabetes insipidus?

A
  • polyuria
  • polydypsia
  • no glycosuria (excess sugar in urine)
73
Q

How can you diagnose DI?

A
  • measure urine volume
  • check renal function/serum calcium
  • water deprivation test
  • serum osmo >300 AND urine osmo <200
74
Q

What are some causes of cranial diabetes insipidus?

A
  • lack of vasopressin
  • acquired - idiopathic, tumours, trauma, infections
  • genetic = DIDMOAD, autosomal dominant
75
Q

What are some causes of nephrogenic diabetes insipidus?

A
  • resistance to vasopressin action
  • Acquired = diabetes mellitus, drugs, renal failure
  • Familial = X-linked, or autosomal recessive
76
Q

How can you manage cranial diabetes insipidus?

A
  • Treat any underlying condition

- Desmopressin

77
Q

How can you manage nephrogenic diabetes insipidus?

A
  • Try and avoid precipating drugs
  • high dose of desmopressin
  • hydrochlorothiazide or indomethacin
78
Q

What is hyponatraemia?

A
  • Serum sodium <135mmol/l

- low sodium

79
Q

What are some symtpoms of hyponatraemia?

A
  • headache
  • lethargy
  • anorexia and abdominal pain
  • weakness
  • agitation
  • decreased conscious level
  • fitting/coma
80
Q

What is the difference between acute vs chronic hyponatraemia?

A
  • Acute - 48 hours. Rapid correction safer and may be necessary
  • Chronic - CNS adapts. Correction must be slow
81
Q

How can you investigate hypomataemia?

A
  • Plasma osmolality
  • Urine osmolality
  • Plasma glucose
  • Urine sodium
  • others
82
Q

What are the different types of causes of hyponatraemia?

A
  • Fluid overload
  • Normovolaemic
  • Dehydrated
83
Q

What is Rathke’s Cyst?

A
  • derived from remnants of Rathke’s pouch
  • single layer of epithelial cells
  • present with headache, amenorrhoea and hypopituitarism
84
Q

What is the most common and 2nd most common tumour region?

A
  1. pituitary adenoma

2. meningioma

85
Q

What is meningioma associated with?

A
  • visual disturbance and endocrine dysfunction

- presents with loss of visual acuity and visual field defects

86
Q

What are effects of a local mass on pituitary?

A
  • visual field defects
  • CSF rhinorrhoea
  • headaches
  • cranial nerve palsy
87
Q

How would you investigate a non-functioning tumour?

A
  • There would be absence of hormone secretion

- Test normal pituitary function

88
Q

What can prolactin levels be raised due to?

A
  • Stress
  • Drugs: anti-psychotics
  • Stalk pressure
  • Prolactinoma
89
Q

Why use an MRI compared to CT for studying the pituitary?

A
  • better visualisation of soft tissues and vascular structures
  • no exposure to ionizing radiation
  • can see fat e.g. fatty marrow and orbital fat
90
Q

When is a CT preferred over an MRI?

A
  • better at visualising bony structures and calcifications within soft tissue
  • diagnose tumours with calcification
91
Q

If a patient has low GH, how would they present?

A
  • short stature
  • abnormal body composition
  • reduced muscle mass
  • poor quality of life
92
Q

If a patient has low LH/FSH, how would they present?

A
  • reduced sperm count
  • infertility
  • menstration problems
93
Q

If a patient has low ACTH, how do they present?

A
  • Adrenal failure

- decreased pigment

94
Q

Who would you give thyroxine replacement to?

A

Patients with low TSH

95
Q

What are the presenting features of diabetes?

A
  • Thirst
  • Polyuria
  • Weight loss and fatigue
  • Hunger
  • Pruritis vulvae
  • blurred vision
96
Q

What are some suggestive features of type 1 diabetes?

A
  • onset in childhood
  • lean body habitus
  • prone to ketoacidosis
97
Q

What are some suggestive features of type 2 diabetes?

A
  • Usually presents in over 30s
  • Onset is gradual
  • FH is often positive
98
Q

What is ketoacidosis?

A
  • Absence of insulin and rising counter-reg hormones leading to increased hyperglycaemia
  • Ketones cause anorexia and vomiting
99
Q

What is the definition of diabetic ketoacidosis (DKA)?

A
  • Hyperglycaemia

- Raised plasma ketones

100
Q

What are the symptoms of DKA?

A
  • develop over days
  • polyuria/polydipsia
  • nausea and vomiting
  • weight loss
  • abdominal pain
101
Q

What are the signs of DKA?

A
  • hyperventilation
  • dehydration
  • hypotension
  • tachycardia
  • coma
102
Q

How can you manage DKA?

A
  • rehydration
  • insulin
  • replacement of electrolytes
103
Q

What are the aims of treatment for T1D?

A
  • relieve symptoms and prevent ketoacidosis

- prevent microvascular and macrovascular complications

104
Q

What are the consequences of diabetic neuropathy?

A
  • Pain
  • insensitivity - includes foot ulceration, infection
  • Autonomic - orthostatic hypotension, incontinence, erectile dysfunction
105
Q

How can you treat diabetic neuropathy?

A
  • glycaemic control
  • anti-depressants/ SSRIs
  • IV lignocaine
  • psychological interventions/hyponosis
106
Q

What is diabetic foot ulceration?

A
  • occurs in 15% of people with DM during their lifetime

- most people won’t show symptoms until the ulcer has become infected

107
Q

What can occur with DFU?

A
  • sensory nerve damage
  • motor nerve damage
  • localised callus
  • autonomic nerve damage
108
Q

How would you screen for diabetic peripheral neuropathy?

A
  • test sensation
  • vibration perception
  • ankle reflexes
109
Q

How does peripheral vascular disease present?

A
  • Intermittent claudication (cramping in leg induced by exercise)
  • rest pain
  • diminished pedal puses
  • coolness of feet and toes
  • poor skin and nails
  • absence of hair on feet and legs
110
Q

What is the treatment for peripheral vascular disease

A
  • quit smoking
  • walk through pain
  • surgical intervention
111
Q

What is the cause of diabetic amputation?

A
  • Neuropathy occurs
  • Trauma
  • Leads to ulcer
  • failure to heal
  • infection leads to amputation
112
Q

What is the best way to detect early diabetic retinopathy?

A
  • Eye screening
113
Q

What is the treatment for diabetic retinopathy?

A
  • Laser therapy

- treatment does not improve sight, just stabilise the changes

114
Q

What are the risks of laser treatment?

A
  • difficulty with night vision

- loss of peripheral vision

115
Q

What is the treatment for diabetic nephropathy?

A
  • blood pressure control
  • glycemic control
  • ARB
116
Q

What is the pathogenesis of T1D?

A
  • Insulin deficiency with a loss of beta cells due to autoimmune destruction
117
Q

What does the failure of insulin secretion lead to?

A
  • Continued breakdown of liver glycogen
  • increase in hepatic glucose output
  • suppression of peripheral glucose uptake
118
Q

What does the reduction insulin lead to?

A
  • fat breakdown

- formation of glycerol and FFA

119
Q

What is ketoacidosis?

A
  • absence of insulin and rising hormones

- leasds to hyperglycaemia and rising ketones

120
Q

What can ketones cause?

A
  • Anorexia and vomiting
121
Q

What is the pathogenesis of T2D?

A
  • impaired glucose tolerance

- due to a combination of genetic predisposition and environmental factors

122
Q

If there is impaired insulin secretion in T2D, what does this lead to?

A
  • Hepatic insulin resistance
  • Muscle/fat insulin resistance
  • leads to hyperglycaemia
123
Q

What is hypoglycaemia?

A
  • low plasma glucose

- causes impaired brain function

124
Q

What are the symptoms of hypoglycaemia?

A
  • trembling/palpitations
  • sweating
  • difficulty concentrating, confusion
  • weakness, dizziness
125
Q

What is the treatment for hypoglycaemia?

A
  • Recognise symptoms
  • treat with 15g fast-acting carbohydrate
  • retest in 15 mins
126
Q

Why does hypoglycaemia occur?

A
  • due to the inability of insulin therapy to mimic the physiology of the beta cell

Yr1 (13 decks)

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