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Endocrinology Ella K only > Endocrinology only > Flashcards

Endocrinology only Flashcards

1
Q

Give an example of a water-soluble hormone

A

Peptides
TRH, LH, FSH

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2
Q

Are water-soluble hormones stored in vesicles or synthesized on demand?

A

Stored in vesicles

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3
Q

How do water soluble hormones like peptides get into a cell?

A

Bind to cell surface receptors

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4
Q

Give an example of a fat soluble hormone

A

Steroids, like cortisol

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5
Q

Are fat-soluble hormones stored in vesicles or synthesized on demand?

A

Synthesised on demand

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6
Q

Give an example of an amine hormone

A

Noradrenaline and adrenaline

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7
Q

Describe the pathway for noradrenaline synthesis

A

Phenylalanine->L-tyrosine->L dopa->NAd and Ad

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8
Q

Name 2 enzymes that break down catecholamines

A

MAO and COMT

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9
Q

What are noradrenaline and adrenaline broken down into?

A

Normetadrenaline and metadrenaline

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10
Q

Where in a cell are the peptide cell receptors located?

A

Located on the cell membrane

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11
Q

Where in a cell are steroid cell receptors located?

A

Located in the cytoplasm

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12
Q

Where in a cell are the thyroid/vitamin A and D cell receptors located?

A

Act on nuclear receptors

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13
Q

Give 5 ways in which hormone action is controlled

A
  1. Hormone metabolism
  2. Hormone receptor induction
  3. Hormone receptor down-regulation
  4. Synergism, like glucagon and adrenaline
  5. Antagonism like glucagon and insulin
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14
Q

What layer of the trilaminar disc is the anterior pituitary derived from?

A

Ectoderm-Rathke’s pouch

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15
Q

Name 6 hormones produced by the anterior pituitary

A
  1. TSH
  2. FSH
  3. LH
  4. ACTH
  5. Prolactin
  6. GH
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16
Q

What is the posterior pituitary derived from?

A

The floor of the ventricles

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17
Q

Where are the posterior pituitary hormones synthesized?

A

Synthesized in the para-ventricular and supra-optic nuclei

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18
Q

Name 2 hormones released from the posterior pituitary

A
  1. Oxytocin
  2. ADH
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19
Q

What is the function of ADH?

A

Acts on the collecting ducts of the nephron and increases insertion of aquaporin 2 channels to increase H2O retention

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20
Q

Give 2 functions of oxytocin

A
  1. Milk secretion
  2. Uterine contraction
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21
Q

Which has a longer half-life: triiodothyronine or thyroxine?

A

Thyroxine: 5-7 days
Triiodothyronine: 1 day

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22
Q

Describe the thyroid axis

A

Hypothalamus->TRH->AP->TSH->thyroid->T3 and T4
T3 and T4 have a negative feedback effect on the hypothalamus and anterior pituitary

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23
Q

What would be the effect on TSH if you had an underactive thyroid?

A

TSH would be raised as you have less T3/T4 being produced so no negative feedback

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24
Q

What would a low TSH tell you about the action of the thyroid?

A

Low TSH: over-active thyroid
Lots of T3 and T4 being produced so more negative feedback on the pituitary and less TSH

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25
Q

Describe the mechanism of action of ACTH

A

Hypothalamus->CRH->AP->ACTH->adrenal cortex (zona fasciculata)->glucocorticoid synthesis like cortisol
Cortisol has a negative feedback effect on the hypothalamus and the anterior pituitary

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26
Q

Give 3 functions of thyroid hormones (T3/T4)

A
  1. Food metabolism
  2. Protein synthesis
    3, Increased sympathetic action like CO and HR
  3. Heat production
  4. Growth and development
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27
Q

Give 3 functions of cortisol in response to stress

A
  1. Mobilises energy sources->lipolysis, gluconeogenesis, and protein breakdown
  2. Vasoconstriction
  3. Suppresses inflammatory and immune responses
  4. inhibits non-essential functions like growth and reproduction
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28
Q

Briefly describe the mechanism of FSH and LH

A

Hypothalamus->GnRH->AP->FSH/LH->ovaries/testes
FSH acts on granulosa cells to produce oestrogen and Sertoli cells to stimulate spermatogenesis
LH acts on theca cells to produce androgens or Leydig cells to produce testosterone

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29
Q

What cells does FSH act on?

A

In the ovaries: granulosa cells
In the testes: sertoli cells

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30
Q

What cells does LH act on?

A

In the ovaries: theca cells
In the testes: leydig cells

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31
Q

What is the function of theca cells?

A

Stimulated by LH to produce androgens that diffuse into granulosa cells to be converted into oestrogen

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32
Q

What is the function of granulosa cells?

A

Stimulated by FSH to convert androgens into oestrogen using aromatose

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33
Q

What is the function of Sertoli cells?

A

Produce MIF(Mullerian inhibiting factor) and inhibin and activin which act on the pituitary gland to regulate FSH

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34
Q

What is the function of Leydig cells?

A

Stimulated by LH to produce testosterone

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35
Q

Describe the GH/IGF-1 axis

A

Hypothalamus->GHRH or SMS->AP->GH->liver->IGF-1

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36
Q

What is the function of IGF-1?

A

Induces cell division, cartilage and skeletal growth and protein synthesis

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37
Q

Briefly describe the mechanism of action of prolactin

A

Hypothalamus->dopamine->AP->prolactin
Prolactin acts on the mammary glands to produce milk

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38
Q

What would happen to serum prolactin levels if something was to impact on the pituitary stalk and block dopamine release?

A

Prolactin levels would increase

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39
Q

Give 3 potential consequences of a pituitary tumour

A
  1. Pressure on local structures like an optic chiasm
    Hypo-pituitary
    Functioning tumours like in Cushing’s, gigantism, prolactinoma
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40
Q

Give 2 causes of prolactinoma

A
  1. Pituitary adenoma
    2, Anti-dopaminergic drugs
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41
Q

Give 5 signs of prolactinoma

A
  1. Infertility
  2. Galactorrhea
  3. Amenorrhoea
  4. Loss of libido
  5. Visual field defects due to local effect of the tumour
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42
Q

What investigation would you do on someone presenting with difficulty getting pregnant, galactorrhoea, amenorrhea, loss of libido and headaches?

A

Measure serum prolactin: symptoms of prolactinoma

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43
Q

Describe the treatment for prolactinoma

A

Dopamine agonist like cabergoline

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44
Q

Describe growth hormone secretion from the anterior pituitary

A

Secreted in a pulsatile fashion and increases during deep sleep

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45
Q

What can cause acromegaly?

A

Benign pituitary adenoma producing excess GH

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46
Q

Give 5 symptoms of acromegaly

A
  1. Changes in appearance
    2, increase in the size of hands and feet
    3, Excessive sweating
  2. Headache
  3. Tiredness
  4. Weight gain
  5. Amenorrhoea
  6. Deep voice
  7. Goitre
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47
Q

Give 5 signs of acromegaly

A
  1. Prognathism
  2. Interdental separation
  3. Large tongue
  4. Spade-like hands and feet
  5. Tight rings
  6. Bi-temporal hemianopia
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48
Q

What co-morbidities are associated with acromegaly?

A
  1. Arthritis
  2. Cerebrovascular events
  3. Hypertension and heart disease
  4. Sleep apnea
  5. T2DM
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49
Q

What investigations might you do on someone who you suspect has acromegaly?

A
  1. Plasma GH-can exclude acromegaly
  2. Serum IGF-1 levels-raised
  3. Oral glucose tolerance test-diagnostic
  4. MRI of pituitary
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50
Q

What test is diagnostic for acromegaly?

A

Oral glucose tolerance test-failure of glucose to suppress serum GH

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51
Q

Describe the treatment for acromegaly

A
  1. Trans-sphenoidal surgical resection
  2. Radiotherapy
  3. Medical therapy: somatostatin analogues, dopamine agonists like cabergoline
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52
Q

Give 3 potential complications of trans-sphenoidal surgical resection for the treatment of acromegaly

A
  1. Hypopituitarism
  2. Diabetes insipidus
  3. Haemorrhage
  4. CNS injury
  5. Meningitis
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53
Q

Give 3 advantages of using dopamine agonists in the treatment of acromegaly

A
  1. No hypopituitarism
  2. Oral administration
  3. Rapid onset
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54
Q

Give 2 disadvantages of using dopamine agonists in the treatment of acromegaly

A
  1. Can be ineffective
  2. Risk of side effects
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55
Q

Name a dopamine agonist that can be used in the treatment of acromegaly

A

Cabergoline

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56
Q

Give 5 causes of hypothyroidism

A
  1. Autoimmune thyroiditis like Hashimoto’s thyroiditis and atrophic thyroiditis
  2. Post-partum thyroiditis
  3. Iatrogenic thyroidectomy
  4. Drug-induced: carbimazole, amiodarone, lithium
    Iodine deficiency
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57
Q

Name 3 antibodies that may be present in the serum of someone with autoimmune thyroiditis

A
  1. TPO(thyroid peroxidase)
  2. Thyroglobulin
  3. TSH receptor
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58
Q

Give an example of a transient cause of hypothyroidism

A

Post-partum thyroiditis

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59
Q

Give 2 examples of iatrogenic causes of hypothyroidism

A
  1. Thyroidectomy
  2. Radioiodine therapy
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60
Q

Name 3 drugs that can cause hypothyroidism

A
  1. Carbimazole
  2. Amiodarone
  3. Lithium
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61
Q

How can amiodarone cause hypo-hyperthyroidism

A

Because it is iodine rich

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62
Q

Give 5 symptoms of hypothyroidism

A
  1. Menorrhagia: heavy bleeding
  2. Obesity/weight gain
  3. Malar flush
  4. Fatigue
  5. Cold intolerance
  6. Eyebrow loss
  7. Goitre
  8. Depression
  9. Dry skin/hair
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63
Q

Give 5 signs of hypothyroidism

A
  1. Mental slowness
  2. Dry, thin hair
  3. Bradycardia
  4. Anaemia
  5. Hypertension
  6. Loss of eyebrows
  7. Cold peripheries
  8. Carpal tunnel syndrome
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64
Q

What investigations might you do in someone you suspect has hypothyroidism?

A

-TFT’s-serum TSH will be raised and T3/T4 will be low
-Thyroid antibodies

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65
Q

Describe the management for hypothyroidism

A

Levothyroxine

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66
Q

What is thyrotoxicosis?

A

Excess thyroid hormone due to any cause

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67
Q

Give 5 causes of thyrotoxicosis

A
  1. Increased production like Grave’s, toxic adenoma
  2. Leakage of T3/T4 due to follicular damage
  3. Ingestion
  4. Thyroiditis
  5. Drug induced
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68
Q

Give 2 causes of hyperthyroidism

A
  1. Grave’s disease
  2. Toxic adenoma
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69
Q

Briefly describe the pathophysiology of Grave’s disease

A

Autoimmune
TSH receptor antibodies stimulate thyroid hormone production->hyperthyroidism

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70
Q

Give 5 symptoms of Grave’s disease that don’t include ophthalmopathy signs

A
  1. Weight loss
  2. Increased appetite
  3. Irritability
  4. Tremors
  5. Palpitations
  6. Goitre
  7. Diarrhoea
  8. Heat intolerance
  9. Malaise
  10. Vomiting
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71
Q

Give 5 signs of Grave’s disease that don’t include ophthalmopathy signs

A
  1. Tachycardia
  2. Arrhythmias like AF
  3. Warm peripheries
  4. Muscle spasms
  5. Pre-tibial myxoedema(raised purple lesions over the shins)
  6. Thyroid acropachy (clubbing and swollen fingers)
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72
Q

With what disease would you associate pre-tibial myxoedema ad thyroid acropachy?

A

Grave’s disease

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73
Q

Give 5 Grave’s ophthalmopathy signs

A
  1. Exophthalmos (bulging eyes)
  2. Lid lag stare
  3. Redness
  4. Conjunctivitis
  5. Pre-orbital edema
  6. Bilateral
  7. Extra-ocular muscle swelling
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74
Q

What investigations might you do in someone who you suspect has hypothyroidism?

A

TFT’s: TSH suppressed and T3/T4 elevated

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75
Q

What would you see histologically in someone with Grave’s disease?

A

Lymphocyte infiltration and thyroid follicle destruction

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76
Q

Describe the treatment for Grave’s disease

A
  1. Anti-thyroid drugs like carbimazole
  2. Radioiodine drugs
  3. Surgery-partial thyroidectomy
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77
Q

How does carbimazole work in treating Grave’s disease?

A

Targets thyroid peroxidase so prevents the formation of T3/T4

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78
Q

Give a potentially serious side effect of taking carbimazole to treat Grave’s disease

A

Agranulocytosis

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79
Q

What advice should you give a patient when prescribing carbimazole to treat Grave’s disease

A

Seek medical attention if they develop an unexplained sore throat or fever-signs of agranulocytosis

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80
Q

How do radioiodine drugs work in treating Grave’s disease?

A

Radioiodine drugs emit beta particles that destroy thyroid follicles so thyroid hormone production is decreased

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81
Q

Give 3 potential complications of a partial thyroidectomy

A
  1. Bleeding
  2. Hypocalcaemia
  3. Hyporthyroidism
  4. Recurrent laryngeal nerve palsy
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82
Q

What disease would you treat with carbimazole?

A

Grave’s disease

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83
Q

What disease would you treat with levothyroxine?

A

Hypothyroidism

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84
Q

Give 5 metabolic changes that occur in pregnancy

A
  1. Increased EPO, cortisol and NAd
  2. High CO
  3. High cholesterol and triglycerides
  4. Pro thrombotic and inflammatory state
  5. Insulin resistance
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85
Q

Give 5 gestational syndromes

A
  1. Pre-eclampsia
  2. Gestational diabetes
  3. Obstetric cholestasis
  4. Gestational thyrotoxicosis
  5. Postnatal depression
  6. Post partum thyroiditis
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86
Q

At what week are foetal thyroid follicles and T4 synthesised?

A

Week 10

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87
Q

Why can HCG activate TSH receptors and cause hyperthyroidism?

A

HCG and TSH are glycoprotein hormoens with very similar structures so HCG can activate TSH receptors

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88
Q

Is hypothyroidism or thyrotoxicosis more common in pregnancy?

A

Hypothyroidism more common

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89
Q

How can you differentiate between Grave’s disease and gestational thyrotoxicosis?

A

Grave’s: symptoms predate pregnancy and get more severe during pregnancy: goitre and TSH-R antibodies present
Gestational thyrotoxicosis: symptoms don’t predate pregnancy, lots of N/V-hyperemesis gravidarum associated. No goitre or TSH-R

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90
Q

Give 3 potential consequences of untreated hypothyroidism in pregnancy

A
  1. Gestational hypertension
  2. Placenta abruption
  3. Post partum haemorrhage
  4. Low birth weight
  5. Neonatal goitre
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91
Q

Give 3 potential consequences of untreated hyperthyroidism in pregnancy

A
  1. Intra-uterine growth restriction
  2. Low birth weight
  3. Pre-eclampia
  4. Risk of still birth/miscarriage
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92
Q

What is diabetes mellitus?

A

Disorder of carbohydrate metabolism characterised by hyperglycaemia

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93
Q

Which 4 cells make up the islets of Langerhans?

A
  1. Beta cells (70%)
  2. Alpha cells (20%)
  3. Delta cells (8%)
  4. Polypeptide secreting cells
94
Q

What do beta cells produce?

95
Q

What do alpha cells produce?

96
Q

What do delta cells produce?

A

Somatostatin

97
Q

What is the importance of the alpha and beta cells being located next to each other in the islets of langerhans?

A

Enables them to ‘cross talk’-insulin and glucagon show reciprocal action

98
Q

Describe the mechanism of insulin secretion form beta cells

A

Glucose binds to beta cells->glucose 6 phosphate->ADP->ATP->K+ channels close->membrane depolarisation->Ca2+ channels open, influx->insulin release

99
Q

Describe the physiological processes that occur in the fasting state in response to low blood glucose

A

Low blood glucose=high glucagon and low insulin
-Glycogenolysis and gluconeogenesis
-Reduced peripheral glucose uptake
-Stimulates the release of gluconeogenic precursors
Lipolysis and muscle breakdown

100
Q

Describe the effect on insulin and glucagon secretion in the fasting state

A

Fasting state=low blood glucose
Raised glucagon and low insulin

101
Q

How many carbon precursors are needed for gluconeogenesis?

102
Q

Describe the physiological processes that occur after feeding in response to high blood glucose

A

High blood glucose = high insulin and low glucagon
-Glycogenolysis and gluconeogenesis are suppressed
-Glucose taken up by peripheral muscle and fat cells
-Lipolysis and muscle breakdown suppressed

103
Q

Describe the effect on insulin and glucagon secretion after feeding

A

Insulin is high and glucagon is low

104
Q

What would a persons fasting plasma glucose be if they were diabetic?

A

Fasting plasma glucose >7mmol/L

105
Q

What would a persons random plasma glucose be if they were diabetic?

A

Random plasma glucose >11mmol/L

106
Q

What would the results of the oral glucose tolerance test be if someone was diabetic?

A

Fasting plasma glucose >7mmol/L
2 hour value >11mmol/L

107
Q

What would someones HbA1c be if they have diabetes?

A

> 48mmol/mol

108
Q

What is the effect of cortisol on insulin and glucagon?

A

Cortisol inhibits insulin and activates glucagon

109
Q

Describe the aetiology of T1DM

A

Beta cells express HLA antigens
Autoimmune destruction->beta cells loss->impaired insulin secretion

110
Q

Is T1DM characterized by a problem with insulin secretion, insulin resistance, or both?

A

Impaired insulin secretion-severe insulin deficiency

111
Q

At what age do people with T1DM present?

A

Most often in childhood

112
Q

Give 2 potential consequences of T1DM

A
  1. Hyperglycaemia
  2. Ketoacidosis
113
Q

Describe the natural history of T1DM

A

Genetic predisposition + trigger->insulitis, beta cell injury->pre-diabetes->diabetes

114
Q

Describe the pathophysiological consequence of impaired insulin secretion in T1DM

A

Severe insuline deficiency->glycogenolysis/gluconeogenesis/lipolysis all not suppressed and reduced peripheral glucose uptake->hyperglycaemia and glycosuria.
Perceived stress-?cortisol and Ad secretion-?catabolic state-?increased plasma ketones

115
Q

Give 3 symptoms of T1DM

A
  1. Weight loss
  2. thirst (fluid and electrolyte losses)
  3. polyuria (due to osmotic diuresis)
116
Q

Is ketoacidosis associated with T1 or T2 dm?

A

Type 1-occurs due to absence of insulin

117
Q

Describe the pathophysiology of DKA

A

No insulin->lipolysis->free fatty acids->oxidised in liver->ketone bodies and ketoacidosis

118
Q

Name 3 ketone bodies

A

-Acetoacetate
-Acetone
-beta hydroxybutarate

119
Q

Where does ketogenesis occur?

A

In the liver

120
Q

Give 4 signs of DKA

A
  1. Hypotension
  2. Tachycardia
  3. Kussmaul’s respiration
  4. Breath smells of ketones
  5. Dehydration
121
Q

Describe the treatment for T1DM

A
  1. Education: make sure patient understands benefits of good glycaemic control
  2. Healthy diet: low in sugar, high in carbohydrates
  3. Regular activity, healthy BMI
  4. BP and hyperlipidemia control
  5. Insulin
122
Q

How is insulin administered in someone with T1DM?

A

Injected into SC fat

123
Q

Other than SC injections, how else can insulin be administered?

A

Insulin pump

124
Q

Give 4 potential complications of insulin therapy

A
  1. Hypoglycaemia
  2. Lipohypertrophy at ejection site
  3. Insulin resistance
  4. Weight gain
  5. Interference with life style
125
Q

Is T2DM a problem with insulin secretion, resistance or both?

A

Impaired insulin secretion and insulin resistance

126
Q

Describe the aetiology of T2DM

A

Genetic predisposition and environmental factors like obesity and lack of exercise

127
Q

Why is insulin secretion impaired in T2DM?

A

Thought to be due to lipid deposition in the pancreatic islets

128
Q

Describe the pathophysiology of T2DM

A

Impaired insulin secretion and resistance->IGT->T2DM->hyperglycaemia and high FFA’s

129
Q

Is insulin secretion or insulin resistance the driving force of hyperglycaemia in T2DM?

A

Hepatic insulin resistance is driving force of hyperglycaemia

130
Q

Give 3 risk factors for insulin resistance in T2DM

A
  1. Obesity
  2. Physical inactivity
  3. Family history
131
Q

What happens to insulin resistance, insulin secretion and glucose levels in T2DM?

A

-Insulin resistance increases
-Insulin secretion decreases
-Fasting and post prandial glucose increase

132
Q

Why do you rarely see DKA in T2DM

A

Insulin secretion is impaired but there are still low levels of plasma insulin. Even low levels of insulin can prevent muscle catabolism and ketogenesis

133
Q

Describe the treatment pathway for T2DM

A
  1. Lifestyle changes: lose weight, exercise, healthy diet
  2. Metformin
  3. Metformin + sulfonylurea
  4. Metformin + sulfonylurea + insulin
  5. Increase insulin dose as required
134
Q

How does metformin work in treating T2DM?

A

Increases insulin sensitivity and inhibits glucose production

135
Q

How does sulfonylurea work in treating T2DM?

A

Stimulates insulin release

136
Q

Give a potential consequence of taking sulfonylurea for the treatment of T2DM

A

Hypoglycaemia
Sulfonylurea stimulates insulin release

137
Q

Give 3 microvascular complications of diabetes mellitus

A
  1. Diabetic retinopathy
  2. Diabetic nephropathy
  3. Diabetic peripheral neuropathy
138
Q

Give a macrovascular complication of diabetes mellitus

A

CV disease and stroke

139
Q

What is the main risk factor for diabetic complications?

A

Poor glycaemia control

140
Q

Give a potential consequence of acute hyperglycemia

A

DKA and hyperosmolar coma

141
Q

Give a potential consequence of chronic hyperglycemia.

A

Micro/macrovascular complications like diabetic retinopathy, nephropathy, neuropathy, CV disease etc

142
Q

What is the commonest form of diabetic neuropathy?

A

Distal symmetrical polyneuropathy

143
Q

Give 3 major consequences of diabetic neuropathy

A
  1. Pain
  2. Autonomic neuropathy
  3. Insensitivity
144
Q

Describe the pain associated with diabetic neuropathy

A

-Burning
-Paraesthesia
-Nocturnal exacerbation

145
Q

What is autonomic neuropathy?

A

Damage to the nerves that supply body structures that regulate functions like BP, HR , bowel, bladder emptying

146
Q

Give 5 signs of autonomic neuropathy

A
  1. Hypotension
  2. HR affected
  3. Diarrhoea/constipation
  4. Incontinence
  5. Erectile dysfunction
  6. Dry skin
147
Q

What are the consequences of insensitivity as a result of diabetic neuropathy?

A

Insensitivity->foot ulceration->infection->amputation

148
Q

Describe the distribution of insensitivity as a result of diabetic neuropathy

A

Insensitivity starts in the toes and moves proximally
Glove and stocking distribution

149
Q

Give 5 risk factors for diabetic neuropathy

A
  1. Poor glycaemic control
  2. Hypertension
  3. Smoking
  4. HbA1c
  5. Overweight
  6. Long duration of DM
150
Q

Describe the treatments for diabetic neuropathy

A
  1. Improve glycaemic control
  2. Antidepressants
  3. Pain relief
151
Q

PVD is a potential complication of diabetes. Give 6 signs of acute ischaemia

A
  1. Pulseless
  2. pale
  3. perishing cold
  4. Pain
  5. paralysis
  6. paraesthesia
152
Q

Give 5 ways in which amputation can be avoided in someone with diabetic neuropathy

A
  1. Screening for insensitivity
  2. Education
  3. MDT foot clinic
  4. Pressure relieving footwear
  5. Podiatry
  6. Revascularisation and antibiotics
153
Q

Would there be increased or decreased pulses in a diabetic neuropathic foot?

A

Increased foot pulses

154
Q

Give 5 risk factors for diabetic retinopathy

A
  1. Long duration DM
  2. Poor glycaemic control
  3. Hypertension
  4. Insulin treatment
  5. Pregnancy
  6. High HbA1c
155
Q

Describe the pathophysiology of diabetic retinopathy

A

Micro-aneurysms->pericyte loss and protein leakage->occlusion->ischaemia

156
Q

How can diabetic retinopathy be sub-divided?

A

Can be divided into:
-Proliferative: evidence of neovascularization in the retina
-Non-proliferative

157
Q

What would you see in someone with an R1 retinopathy grade?

A

R1-non-proliferative/background
-Micro-aneurysms
-Intraretinal haemorrhage
-Exudates

158
Q

What would you see in someone with an R2 retinopathy grade?

A

R2-pre proliferative
-Venous bleeding
-Growth of new vessels

159
Q

What would you see in someone with an R3 retinopathy grade?

A

R3-proliferative
-New blood vessel on disc

160
Q

What is the treatment for diabetic retinopathy?

A

-Regular screening to assess visual acuity
-Laser therapy treats neovascularisation

161
Q

What is the hallmark of diabetic nephropathy?

A

Development of proteinuria and progressive decline in renal function

162
Q

What happens to the glomerular basement membrane in someone with diabetic nephropathy?

A

On microscopy there is thickening of the glomerular basement membrane

163
Q

Give one way in which the presentation of diabetic nephropathy differs between T2 and T2DM

A

T1DM: microalbuminuria develops 5-10 year after diagnosis
T2DM: microalbuminuria often present at diagnosis

164
Q

Describe the treatment for diabetic nephropathy

A
  1. Glycaemia and BP control
  2. ARB/ACEi
  3. Proteinuria and cholesterol control
165
Q

Name the suprasellar neoplasm that can result from benign cysts and calcification of Rathke’s pouch?

A

Craniopharyngioma

166
Q

Give 4 signs of craniopharyngioma

A
  1. Raised ICP
  2. Vision affected
  3. Growth failure
  4. Puberty affected
167
Q

Give 4 local effects of pituitary adenoma

A
  1. Headaches
  2. Visual field defects-bitemporal hemianopia
  3. CN palsy and temporal lobe epilepsy
  4. CSF rhinorrhoea
168
Q

What is the effect of hypothyroidism on TSH and T4 levels?

A

High TSH
Low T4

169
Q

What is the affect of hyperthyroidism on TSH and T4 levels?

A

Low TSH
High T4

170
Q

What is the affect of hypopituitarism on TSH and T4 levels?

A

Low TSH
Low T4

171
Q

What is the treatment for thyroid hypopituitarism?

A

Levothyroxine

172
Q

Give a cause of primary hypogonadism.

A

Klinefelter’s syndrome-extra X chromosome

173
Q

What is the effect of primary hypogonadism on testosterone and FSH/LH levels?

A

Testosterone will be low
FSH/LH will be low

174
Q

What is the effect of hypopituitarism on testosterone and FSH/LH levels?

A

Low testosterone
Low FSH/LH

175
Q

When should serum testosterone be measured?

A

At 9am due to circadian rhythm

176
Q

Give 5 consequences of androgen deficiency in a male

A
  1. Loss of libido
  2. High pitched voice
  3. Loss of facial, axillary, limb and pubic hair
  4. loss of erection
  5. Poorly developed scrotum and penis
177
Q

What is the treatment for hypogonadism?

A

Testosterone gel/injection
Can improve BMD, QOL and libido etc

178
Q

What syndrome is characterised by a congenital deficiency of GnRH

A

Kallmann’s syndrome

179
Q

Are the levels of oestradiol and FSH/LH low or high before puberty?

A

Before puberty: very low levels of these hormones in the serum

180
Q

What is the effect of primary ovarian failure on oestradiol and FSH/LH levels?

A

FSH/LH high
Oestradiol is low

181
Q

What is the effect of hypopituitarism on oestradiol and FSH/LH levels?

A

FSH/LH low
Oestradiol low

182
Q

What is the effect of primary adrenal insufficiency on cortisol and ACTH levels?

A

Low cortisol
High ACTH

183
Q

What is the effect of hypopituitarism on cortisol and ACTH levels?

A

Low cortisol
Low ACTH

184
Q

What can lead to elevated levels of prolactin?

A
  1. Stress
  2. Drugs
  3. Pressure on the pituitary stalk
185
Q

What stimulates the posterior pituitary to release ADH?

A

Osmoreceptors in the hypothalamus detect raised plasma osmolarity->posterior pituitary is signalled to release ADH

186
Q

Give 5 signs of diabetes insipidus

A
  1. Excessive urine production (>3L/24hrs)
  2. Very dilute urine <300mOsmol/kg
  3. Severe thirst
  4. Hypernatraemia
  5. Dehydration
187
Q

What investigations might you do to determine if someone has diabetes insipidus?

A
  1. Measure 24 hr urine volume >3L/24 hr
  2. Plasma biochemistry -hypernatraemia
    Water deprivation test-urine won’t concentrate when asked not to drink
188
Q

What is the treatment for neurological diabetes insipidus?

A

Desmopression

189
Q

Give 4 causes of polyuria

A
  1. Hypokalaemia
  2. Hypercalcaemia
  3. Hyperglycaemia
  4. Diabetes insipidus
190
Q

Would TSH and T4 be high or low in someone with sub-clinical hypothyroidism?

A

High TSH but normal T4-often asymptomatic patients

191
Q

What is Cushing’s syndrome?

A

A set of signs/symptoms resulting from chronic glucocorticoid excess with a loss of normal feedback mechanisms

192
Q

What can cause Cushing’s syndrome?

A
  1. Adrenal tumour (adenoma or carcinoma)
  2. Pituitary tumour (Cushing’s disease)
  3. Exogenous steroids
  4. Ectopic ACTH syndrome
193
Q

What is Cushing’s disease?

A

A set of signs/symptoms resulting from inappropriate ACTH secretion form the pituitary
ACTH dependent

194
Q

Give 7 signs/symptoms of Cushing’s disease

A
  1. Central obesity
  2. Moon face
  3. Hypertension
  4. Skin thinning
  5. Abdominal striae
  6. Mood changes
  7. Osteoporosis
  8. Muscle thinning
  9. Weight gain
195
Q

What investigations might you do in someone with Cushing’s syndrome?

A
  1. Overnight dexamethasone suppression test-failure to suppress cortisol
  2. Late-night salivary cortisol -loss of circadian rhythm
  3. Urinary free cortisol raised
  4. Loss of circadian rhythm
196
Q

What is the treatment for Cushing’s syndrome

A
  1. Surgical removal of pituitary tumours
  2. Drugs to inhibit cortisol synthesis like metyrapone, ketoconazole
197
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion
Too much ADH-very concentrated urine and hyponatraemia

198
Q

Give 3 symptoms of SIADH

A
  1. Anorexia
  2. Nausea
  3. Malaise
  4. Headache
  5. Confusion
199
Q

Give 3 causes of SIADH

A
  1. Malignancy
    2, CNS disorders: meningitis, brain tumors, cerebral hemorrhages
  2. TB
  3. Pneumonia
  4. Drugs
200
Q

Describe the treatment for SIADH

A
  1. Restrict fluid
  2. Give salt
  3. loop diuretics like furosemide
  4. ADH-R antagonists like vaptans-useful when fluid restriction is challenging
201
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism-high aldosterone levels independent of RAAS activation->H2o sodium retention and potassium excretion

202
Q

What are the 2 main signs of Conn’s syndrome?

A
  1. Hypertension
  2. Hypokalaemia
    Sodium will be normal or slightly raised
203
Q

Give 3 symptoms of Conn’s syndrome? Which electrolyte deficiency causes these symptoms?

A
  1. Muscle weakness
  2. Tiredness
  3. Polyuria
    Due to potassium deficiency-hypokalaemia
204
Q

What can cause Conn’s syndrome?

A

Adrenal adenoma

205
Q

What hormone is raised in Conn’s syndrome and what hormone is reduced? Where are these hormones synthesised?

A
  1. Aldosterone is raised-synthesized in zona glomerulosa
  2. Renin is reduced-synthesised by juxtaglomerular cells
206
Q

What investigations might you do in someone to confirm a diagnosis of Conn’s syndrome?

A
  1. Bloods: U&E, renin (low) and aldosterone (high)
  2. Plasma aldosterone renin ratio can be used as an initial screening test-raised result indicates the need for more tests
207
Q

Give 4 ECG changes you might see in someone with Conn’s syndrome

A
  1. INcreased amplitude and width of P waves
  2. Flat T waves
  3. ST depression
  4. Prolonged QT interval
  5. U waves
208
Q

What is the treatment for Conn’s syndrome?

A
  1. Laparoscopic adrenalectomy
  2. Sprionolactone (aldosterone antagonist)
209
Q

What does the parathyroid control?

A

Serum calcium levels
A low serum calcium triggers release of PTH and a high serum calcium triggers c-cells to release calcitonin

210
Q

What hormone does the parathyroid secrete and what is its function?

A

PTH-secreted in response to low serum calcium
PTH increases bone resorption, increases calcium reabsorption at the kidney and activates vitamin D which then acts on the intestines to increase calcium absorption

211
Q

What is released by c-cells in the parathyroid in response to high serum calcium?

A

Calcitonin

212
Q

What is the effect of hyperparathyroidism on serum calcium levels?

A

Hyperparathyroidism->hypercalcaemia

213
Q

Give 5 symptoms of hyperparathyroidism

A

Hyperparathyroidism->hypercalcaemia
1. Renal/biliary stones
2. Bone pain
3. Abdominal pain
4. Polyuria
5. Depression, anxiety, malaise

Stones, bones, groans, thrones, moans

214
Q

Give 3 causes of hyperparathyroidism

A
  1. Primary: parathyroid adenoma: high PTH, high calcium, low phosphate
  2. Secondary: physiological hypertrophy in an attempt to correct low calcium
  3. Prolonged uncorrected hypertrophy
215
Q

Describe the treatment for hyperparathyroidism

A
  1. High fluid intake, low calcium diet
  2. Excision of adenoma
  3. Correct the underlying cause
  4. Parathyroidectomy
216
Q

What is the effect of hypoparathyroidism on serum calcium levels?

A

Hypoparathyroidism->hypocalcaemia

217
Q

Give 5 symptoms of hypoparathyroidism

A

Hypoparathyroidism->hypocalcaemia
1. Spasm
2. Paraesthesia around mouths and lips
3. Anxious and irritable
4. Seizures
5. Increased muscle tone
6. Confusion
7. Dermatitis
8. Impetigo herpetiformiis
9. QT prolongation

218
Q

What is the treatment for hypoparathyroidism

A

Calcium supplements

219
Q

Give 5 causes of hypocalcaemia

A
  1. Dietary insufficiency
  2. Anticonvulsant therapy
  3. CKD
  4. Vitamin D defieiceny
  5. Osteomalacia
  6. Hypoparathyroidism
220
Q

Give 2 ECG changes that you might see in someone with hyperparathyroidism

A

Hyperparathyroidism->hypercalcaemia so:
-Tall T waves
-Shorted QT interval

221
Q

Give 2 ECG changes that you might see in someone with hypoparathyroidism

A

Hypoparathyroidism->hypocalcaemia
-Small T waves
-Long QT interval

222
Q

What is phaeochromocytoma?

A

A rare catecholamine secreting tumour in the adrenal medulla

223
Q

Give 5 symptoms of phaeochromocytoma

A

Classic triad of:
-Headache
-Sweating
-Tachycardia
Also:
-Hypertension
-Palpitations
-Tremor
-Arrhythmia
-Confusion

224
Q

What investigation might you do in order to diagnose someone with having a phaeochromocytoma

A

Bloods-raised WCC, increased plasma metadrenaline and normetadrenaline

225
Q

What is the treatment for phaeochromocytoma?

A
  1. Alpha blocker like phenoxybenzamine
  2. Beta-blockers
  3. Surgical resection of a tumour
226
Q

What is the major concern in someone with pheochromocytoma?

A

Dangerous but treatable cause of hypertension

227
Q

Describe the different types of SC insulins that can be given to people with T1DM

A
  1. Ultra-fast acting like Humalog taken before eating in conjunction with long-acting insulin at night
  2. Long-acting insulin like insulin glargine before going to bed
  3. Pre-mixed insulin like NovoMix taken twice daily
228
Q

What is adrenal insufficiency?

A

Adrenocortical insufficiency resulting in a reduction of a mineralocorticoids and glucocorticoids and androgens

229
Q

Give 6 symptoms of adrenal insufficiency

A
  1. Tanned pigmentation
  2. Tired
  3. Tearful
  4. Thin-weight loss
  5. Headaches
  6. Abdominal cramps
  7. Myalgia
  8. Throwing up
  9. Weakness
230
Q

Give 5 primary causes of adrenal insufficiency

A
  1. Addison’s disease
  2. Congenital adrenal hyperplasia
  3. TB
  4. Adrenal metastases
  5. Drugs
  6. Haemorrhage
  7. Infection

Endocrinology Ella K only (1 decks)

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