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Med Student Finals > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Classification of Endocrine Hormones (3)

A

Peptide hormones- composed of chains of amino acids
Steroid hormones- derived from cholesterol
Amine hormones- derived from one of two amino acids (tryptophan/tyrosine)

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2
Q

Hypothalamus (3)

A

Main hormones: Trophic hormones and non-trophic
Primary targets: Anterior and posterior pituitary
Main effects: Release/inhibit pituitary hormones (trophic –> ant. pituitary, non-trophic –> post. pituitary)

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3
Q

Hypothalamic-Pituitary Hormones (4)

A

The hypothalamus and anterior pituitary release trophic and non-trophic hormones
Hypothalamus releases neurohormones
Posterior pituitary releases neurohormones
Anterior pituitary releases endocrine hormones

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4
Q

What are the 5 Hypothalamic Releasing Hormones? (5)

A

Thyrotrophin releasing hormone (TRH)
Corticotrophin releasing hormone (CRH)
Growth hormone inhibiting hormone (GHIH)
Gonadotrophin releasing hormone (GnRH)
Prolactin releasing hormone (PRH), aka. dopamine

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5
Q

What are the 2 Hypothalamic Inhibiting Hormones? (2)

A

Growth hormone inhibiting hormone- somatostatin

Dopamine- prolactin inhibiting hormone

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6
Q

Define Trophic Hormone (2)

A

Govern the release of another hormone

Secreted into anterior pituitary

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7
Q

Define Non-Trophic Hormones (1)

A

Travel to posterior pituitary via neuronal axons

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8
Q

Hypothalamo-Pituitary Axis (2)

A

The hypothalamus and pituitary are the principal organisers of the endocrine system
Hypothalamic communication with the pituitary gland is neural and endocrine

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9
Q

Compare the Anterior (5) and Posterior (5) Pituitaries

A 
Anterior: 
-true endocrine tissue 
-epithelial origin 
-connected to hypothalamus via capillary portal system 
-aka adenohypophysis 
-makes up 2/3 of gland
Posterior: 
-neuroendocrine tissue 
-neural tissue origin
-neural connection to hypothalamus 
-secretes neurohormones made in hypothalamus 
-aka. neurohypophysis 
-makes up 1/3 of gland
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10
Q

Anterior Pituitary

  • main hormones (5)
  • primary targets (5)
  • main effects (6)
A

Prolactin–>breast–>milk production
Growth hormone (somatotrophin)–>liver–>growth factor secretion
Corticotropin (ACTH)–>adrenal cortex–>growth + metabolism
Thyrotrophin (TSH)–>thyroid gland–>cortisonal release and thyroid hormone synthesis
Follicle stimulating hormone (gonadotrophin)–>gonads–>egg/sperm production and sex hormone production

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11
Q

What is Growth Hormone and Where is it Released? (5)

A

aka. somatotrophin
Promotes growth
Requires permissive action of thyroid hormones and insulin before it stimulates growth
Peptide hormone (but 1/2 of it circulates bound to carrier proteins)
Released from anterior pituitary

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12
Q

Stimuli that Increase GHRH Secretion (5)

A 
Actual/potential decrease in supply to cells 
Increased amino acids in the plasma 
stressful stimuli 
Delta sleep 
Oestrogen and androgens
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13
Q

Growth Hormone/IGF-1 Effects on Bone (4)

A

GH stimulates pre chondrocytes in the epiphyseal plates to differentiate into chondrocytes
During differentiation the cells begin to secrete IGF-1 and to become responsive to IGF-1
IGF-1 then acts as an autocrine or paracrine agent to stimulate the differentiating chondrocytes to undergo cell division and produce cartilage
Epiphyseal plates close during adolescence under the influence of sex steroid hormones

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14
Q

Direct Effects of Growth Hormone (5)

A

Increased gluconeogenesis by the liver
Reduces ability of insulin to stimulate glucose uptake by muscle and adipose tissue
Makes adipocytes more sensitive to lipolytic stimuli
Increased blood glucose when present in excess
Increased muscle, liver and adipose tissue amino acid uptake and protein synthesis (anabolic effect)

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15
Q

Growth Hormone Negative Feedback (1)

A

IGF-1 inhibits GHRH and stimulates somatostatin

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16
Q

Stimuli that Increase GHIH (Somatostatin) Secretion (4)

A

Glucose
Free fatty acid
REM sleep
Cortisol

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17
Q

Hypersecretion of Growth Hormone (4)

A

Usually caused by endocrine tumours
Surgery to remove tumour or somatostatin analogues to treat
Gigantism: excess GH due to pituitary tumour before epiphyseal plates of long bones close
Acromegaly: excess GH due to pituitary tumour after epiphyseal plates close, no increase in height but can still grow in other directions eg. large hands and feet

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18
Q

Reduced Growth (Dwarfism) (3)

A

Deficiency of GHRH (so less GH production)
Laron Dwarfism- end organ unresponsive to GH
Pygmies have genetic mutation that impairs ability of cells to produce IGF-1 in response to GH

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19
Q

What 2 Peptide Hormones are Released by the Posterior Pituitary?

A

Vasopressin (ADH)

Oxytocin

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20
Q

Hypopituitarism

Aetiology (3)

A

Hypothalamus: Kallman’s syndrome (anosmia and GnRH deficiency), tumour, inflammation, infection
Pituitary stalk: trauma, surgery, tumour
Pituitary: tumour, radiation

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21
Q

Hypopituitarism

Signs + symptoms (5)

A

Growth hormone deficiency: central obesity, reduced strength and balance, atherosclerosis, dry skin
LH/FSH deficiency in males: reduced libido, erectile dysfunction, hypogonadism (less hair, small testes, small ejaculate volume)
LH/FSH deficiency in females: reduced libido, amenorrhoea, osteoporosis, subfertility
TSH deficiency: hypothyroidism
ACTH deficiency: secondary hypoadrenalism (no skin pigment change as ACTH is low)

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22
Q

Hypopituitarism

Investigations (3)

A

Basal hormone tests: LH + FSH (low or normal), TFT:TSH ratio (low or normal), T4 (low), cortisol (low)
Short Synacthen test
MRI pituitary fossa: look for hypothalamic/pituitary lesion

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23
Q

Hypopituitarism

Treatment (5)

A

Hydrocortisone for secondary adrenal failure before any other hormones given
Thyroxine for hypothyroid
Testosterone enanthate for males or oestradiol patches/COCP for females
Gonadotrophin therapy to induce fertility
May give somatotrophin to treat GH deficiency

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24
Q

Pituitary Tumours

Definition (2)

A

Almost always benign adenomas

Account for 10% of intracranial tumours

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25
Q

Pituitary Tumours

Types (3)

A

Chromophobe (70%): many are non-secretory, half produce prolactin, a few produce GH (acromegaly) or ACTH (Cushing’s Disease)
Acidophil (15%): secrete GH/prolactin
Basophil (15%): secrete ACTH

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26
Q

Pituitary Tumours

Investigations (4)

A

MRI: defines intra- and supra-sellar extension
Hormones: prolactin, GH, ACTH, cortisol, TFT (because secondary hypothyroidism occurs as pituitary tumour invades gland), LH, FSH, short Synacthen test
Glucose tolerance test: assess for acromegaly
Water deprivation test: assess for diabetes insipidus

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27
Q

Pituitary Tumours

Treatment (3)

A

Hormone replacement (must ensure give steroids before thyroxine as it could precipitate an adrenal crisis)
Transphenoidal pituitary excision
Radiotherapy for residual/recurrent adenomas

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28
Q

Acromegaly

Aetiology (1)

A

99% due to pituitary tumour (acidophil)

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29
Q

Acromegaly

Pathology (1)

A

Increased GH secretion leads to bone and soft tissue growth through increased secretion of IGF-1

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30
Q

Acromegaly

Symptoms (7)

A 
Acroparaesthesia (numb extremities) 
Amenorrhoea 
Reduced libido 
Headache 
Sweating 
Snoring 
Galactorrhoea
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31
Q

Acromegaly

Signs (6)

A

Increased growth of hands (spade-like), jaw and feet
Coarse facial features and wide nose
Macroglossia
Skin darkening
Carpal tunnel syndrome
Signs from pituitary mass: hypopituitarism +/- local effect (reduced vision, hemianopia, fits)

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32
Q

Acromegaly

Investigations (5)

A 
High glucose 
High calcium 
High phosphate 
OGTT: GH is normally suppressed by glucose but this doesn't occur in acromegaly 
MRI pituitary fossa
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33
Q

Acromegaly

Treatment (2)

A

Transphenoidal excision

If surgery fails use somatostatin analogues

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34
Q

Hyperprolactinaemia

Aetiology (3)

A

Excess pituitary production: pregnancy, breastfeeding, prolactinoma
Disinhibition by pituitary stalk compression: pituitary adenoma
Dopamine antagonists: eg. anti-emetics, anti-psychotics

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35
Q

Hyperprolactinaemia

Signs + symptoms (5)

A 
Amenorrhoea 
Infertility 
Galactorrhoea 
Reduced libido 
Erectile dysfunction
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36
Q

Hyperprolactinaemia

Investigations (4)

A

Basal prolactin
Pregnancy test
TFT
MRI pituitary if other causes ruled out

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37
Q

Hyperprolactinaemia

Treatment (2)

A

Dopamine agonists 1st line

Transphenoidal surgery 2nd line (if visual/pressure symptoms are unresponsive to medical management)

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38
Q

Diabetes Insipidus

Definition (2)

A

Passage of large volumes (>3L/day) of dilute urine due to impaired water resorption by the kidney
Because of reduced ADH secretion from the posterior pituitary (cranial) or because of impaired response of the kidney to ADH (nephrogenic)

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39
Q

Diabetes Insipidus

Aetiology (2)

A

Cranial: idiopathic (50%), tumour, trauma, sarcoidosis
Nephrogenic: congenital, low K, high Ca, CKD

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40
Q

Diabetes Insipidus

Signs + symptoms (4)

A

Polydipsia (uncontrollable and all-consuming)
Polyuria
Dehydration
Hypernatraemia

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41
Q

Diabetes Insipidus

Investigations (6)

A 
U&E 
Calcium 
Glucose (exclude DM) 
Urine and plasma osmolality 
Water deprivation test (stage 1- fluid deprivation and collect urine, stage 2- differentiate between cranial and nephrogenic, give desmopressin): primary polydipsia- urine concentrates but less than normal, cranial- urine osmolality increased after desmopressin, nephrogenic- no increase in urine osmolality after desmopressin 
MRI pituitary fossa
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42
Q

Diabetes Insipidus

Treatment (2)

A

Cranial: desmopressin
Nephrogenic: treat underlying cause

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43
Q

What Makes up the Adrenal Gland? (2)

A

Adrenal medulla

Adrenal cortex

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44
Q

What does the Adrenal Medulla Secrete? (1)

A

Catecholamines, mainly epinephrine but also norepinephrine and dopamine

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45
Q

What do the Different Parts of the Adrenal Cortex Secrete (4)

A

Zona reticularis: sex hormones
Zona fasciculata: glucocorticoids (eg. cortisol)
Zona glomerulosa: mineralocorticoids (eg. aldosterone)
Steroid hormones in response to ACTH

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46
Q

What are all Steroid Hormones Derived from? (1)

A

Cholesterol

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47
Q

Cortisol

Release (4)

A

Circadian rhythm
Preceded by ACTH release
Cortisol bursts persists longer than ACTH bursts because 1/2 life much longer
Peak levels upon waking and due to stressful stimuli

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48
Q

Cortisol

Importance (3)

A

Protects brain from hypoglycaemia
Maintaining blood glucose levels
Maintaining ECF

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49
Q

Cortisol

Actions on glucose metabolism (4)

A

Gluconeogenesis: enhances
Proteolysis: breakdown of muscle protein
Lipolysis: stimulates
Decreases insulin sensitivity of muscles and adipose tissue

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50
Q

What are the Side Effects of Glucocorticoid Therapy and Why? (4)

A 
Increased severity and frequency of infection (because cortisol normal function suppresses immune system) 
Muscle wasting (normal cortisol catabolises muscle) 
Appearance of thin skin and fragile skin due to loss of percutaneous fat stores (normal cortisol causes lipolysis)
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51
Q

Aldosterone (6)

A

Mineralocorticoid
Acts on distal tubule of kidney to determine levels of minerals reabsorbed/excreted
Increased reabsorption of Na
Promotes excretion of K
Secretion of aldosterone by adrenal cortex is controlled by renin-angiotensin-aldosterone system
End effect is Na and H2O retention and K depletion, resulting in increased blood volume and increased BP

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52
Q

Cortisol

Non-glucocorticoid actions (4)

A

Negative effect on Ca balance (net loss increasing bone resorption- osteoporosis)
Impairment of mood and cognition
Permissive effect on norepinephrine (vasoconstrictive, hypertension from too much)
Suppression of immune system (cortisol reduces lymphocyte count, inhibits inflammation and reduces antibody formation)

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53
Q

CRH + ACTH

3

A

Release is promoted by stress
Alcohol/caffeine/lack of sleep disinhibit the hypothalamo-pituitary-adrenal axis
Elevation of cortisol turns down the immune system

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54
Q

Withdrawing Chronic Glucocorticoid Treatment (3)

A

Therapeutic cortisol enhances the negative feedback on hypothalamus and pituitary, reducing release of CRH + ACTH
Loss of trophic action of ACTH on adrenal gland causes atrophy of gland
Risk of adrenal insufficiency if withdrawal too fast

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55
Q

Cushing’s Syndrome (Hyperadrenalism)

Aetiology (2)

A

ACTH dependent: Cushing’s disease (bilateral adrenal hyperplasia from an ACTH-secreting pituitary adenoma), ectopic ACTH production (SCLC or carcinoid tumour) - TOO MUCH ACTH
ACTH independent: steroids, adrenal adenoma/carcinoma- REDUCED ACTH DUE TO -VE FEEDBACK

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56
Q

Cushing’s Syndrome (Hyperadrenalism)

Symptoms (5)

A

Weight gain
Mood change (depression, lethargy, irritability, psychosis)
Proximal weakness
Gonadal dysfunction (irregular menses, hirsutism, erectile dysfunction)
Virilisation in females (more masculine)

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57
Q

Cushing’s Syndrome (Hyperadrenalism)

Signs (9)

A 
Central obesity 
Facial plethora 
Moon face 
Buffalo neck hump 
Bruises 
Purple abdominal striae 
Osteoporosis 
High BP 
High glucose
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58
Q

Cushing’s Syndrome (Hyperadrenalism)

Investigations (3)

A

1st line: overnight dexamethasone suppression test
2nd line: 48h dexamethasone suppression test
Plasma ACTH

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59
Q

Cushing’s Syndrome (Hyperadrenalism)

Treatment (3)

A

Iatrogenic: stop medications
Cushing’s disease: trans-sphenoidal excision of pituitary adenoma
Adrenalectomy if adrenal adenoma/carcinoma

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60
Q

Addison’s Disease (Adrenal Insufficiency)

Aetiology (2)

A

Primary adrenocortical insufficiency (Addison’s disease): autoimmune
Secondary adrenal insufficiency: long term steroids

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61
Q

Addison’s Disease (Adrenal Insufficiency)

Pathology (2)

A

Primary: adrenal cortex destruction leads to glucocorticoid and mineralocorticoid deficiency, high ACTH binds to melanoreceptors causing hyperpigmentation
Secondary: long-term steroid therapy suppresses the pituitary adrenal axis and when steroids are withdrawn the body is unable to make its own glucocorticoids, but mineralocorticoids unaffected so no hyperpigmentation

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62
Q

Addison’s Disease (Adrenal Insufficiency)

Signs + symptoms (8)

A 
Weight loss 
Fatigue 
Skin hyperpigmentation 
Dizziness 
Faints 
Mood disturbance 
Unexplained abdo pain and vomiting pigmented palmar creases and mucosa
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63
Q

Addison’s Disease (Adrenal Insufficiency)

Investigations (5)

A 
U&E (low Na, high K) as reduced aldosterone 
Blood glucose (low) as reduced cortisol 
Serum calcium (high) 
9am ACTH (high in Addison's, low in secondary causes) 
Synacthen test (short ACTH stimulation test): plasma cortisol before and 30 mins after Synacthen, Addison's if cortisol doesn't rise
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64
Q

Addison’s Disease (Adrenal Insufficiency)

Treatment (2)

A 
Steroid replacement (hydrocortisone daily) 
Mineralocorticoid replacement (fludrocortisone)
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65
Q 
Addison's Disease (Adrenal Insufficiency)
Addisonian Crisis (4)
A

Aetiology: infection, trauma, stopping long term steroids
Signs + symptoms: shock (tachycardia, vasoconstriction, postural drop), oliguria, confusion, low GCS
Investigations: cortisol, ACTH, U&E (AKI), blood + urine + sputum cultures, blood glucose, ECG (hyperkalaemia)
Treatment: IV fluids, correct hypoglycaemia, IV hydrocortisone for glucocorticoid replacement

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66
Q

Primary Hyperaldosteronism

Aetiology (2)

A

Conn’s syndrome: solitary aldosterone releasing adenoma

Bilateral adrenal-cortical hyperplasia

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67
Q

Primary Hyperaldosteronism

Pathology (1)

A

Excess production of aldosterone independent of the renin-angiotensin system, causing increased sodium and water retention and suppression of renin release

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68
Q

Primary Hyperaldosteronism

Signs + symptoms (6)

A 
Often asymptomatic or signs of hypokalaemia 
Weakness 
Cramps 
Paraesthesia 
Polyuria 
Polydipsia
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69
Q

Primary Hyperaldosteronism

Investigations (4)

A

U&E
Renin and aldosterone (suppressed renin, increased aldosterone)
K low
Na high

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70
Q

Primary Hyperaldosteronism

Treatment (2)

A

Conn’s: laparoscopic adrenalectomy and spironolactone to control BP and hypokalaemia
Hyperplasia: spironolactone

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71
Q

Phaeochromocytoma

Epidemiology (1)

A

Rule of 10s: 10% malignant, 10% extra-adrenal, 10% bilateral, 10% as part of hereditary syndromes

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72
Q

Phaeochromocytoma

Aetiology (2)

A

Catecholamine producing tumours arising from adrenals

Associated with MEN 2a + 2b

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73
Q

Phaeochromocytoma

Symptoms (1)

A

Classic triad: episodic headache, sweating, tachycardia

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74
Q

Phaeochromocytoma

Investigations (3)

A

High WCC
Plasma and 3x24h urine for free metadrenaline and normetadrenaline
Abdominal CT/MRI for localisation

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75
Q

Phaeochromocytoma

Treatment (1)

A

Surgery: alpha blocker pre-op to avoid crisis from unopposed alpha-adrenergic stimulation

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76
Q

What are the 4 types of Islet Cells and what do they Produce?

A

Alpha cells: glucagon
Beta cells: insuline
Delta cells: somatostatin
F cells: pancreatic polypeptide

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77
Q

How is Insulin Synthesised and Stored? (4)

A

Synthesised as preproinsulin which is then converted into proinsulin in the endoplasmic reticulum
Proinsulin is then packaged as granules in secretory vesicles
Within the granules the proinsulin is cleaved to give insulin and C-peptide
Insulin is stored in this form until the B cells are activated

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78
Q

What Stimuli Increase Insulin Release? (5)

A 
Increased BG
Increased amino acid in the plasma 
Glucagon 
Incretin hormones controlling GI secretion and motility (eg. gastrin, secretin, CCK) 
Vagal nerve activity
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79
Q

What Stimuli Inhibit Insulin Release? (4)

A

Low BG
Somatostatin
Sympathetic alpha2 effects
Stress (eg. hypoxia)

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80
Q

How Does the Autonomic Nervous System Innervate Islet Cells? (2)

A

Increased parasympathetic activity (vagus)–> high insulin and high glucagon (to a lesser extent), in association with the anticipatory phase of digestion
Increased sympathetic activation promotes glucose mobilisation –> high glucagon, high epinephrine and insulin inhibition

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81
Q

Explain the Primary Action of Insulin (2)

A

Binds to tyrosine kinase receptors on the cell membrane of insulin-sensitive tissues to increase glucose uptake by these tissues
Insulin stimulates the mobilisation of specific glucose transporters (GLUT-4)

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82
Q

What are some additional actions of insulin? (6)

A

Inhibits catabolism by:

  • high glycogen production by muscle and liver
  • high amino acid uptake by muscle
  • high protein synthesis and inhibits proteolysis
  • stimulates lipogenesis and inhibits lipolysis
  • inhibits gluconeogenesis enzymes in liver
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83
Q

How Does the Liver take up Glucose? (3)

A

The liver isn’t an insulin-sensitive tissue
Liver takes up glucose by GLUT-2, which are insulin independent
Glucose enters down a concentration gradient

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84
Q

Explain the Mechanism of Control of Insulin Secretion by BG? (5)

A

B-cells have a specific type of K channel sensitive to ATP within the cell: KATP channel
When glucose is abundant it enters cells through GLUT and metabolism increases
Increases ATP within cell causing KATP to close
Intracellular K rises, depolarising the cell
Voltage-dependent Ca channels open and trigger insulin vesicle exocytosis into the circulation

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85
Q

How is BG Maintained? (2)

A

Glycogenolysis- synthesising glucose from glycogen

Gluconeogenesis- synthesising glucose from amino acids

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86
Q

What is the Half Life of Insulin? Where is Insulin Degraded?

A

5 minutes

In liver and kidneys

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87
Q

How is Excess Glucose Stored? (2)

A

Glycogen in liver and muscle

Triacylglycerols in liver and adipose tissue

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88
Q

Actions of Glucagon (6)

A

Opposes action of insulin
Part of glucose counter-regulatory control system
Most active in the post-absorptive state
Receptors are G-protein coupled receptors linked to cAMP system
When activated, phosphorylate specific liver enzymes
Results in: increased glycogenolysis, increased gluconeogenesis, formation of ketones from fatty acids (lipolysis), elevated blood glucose

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89
Q

Which Stimuli Promote Glucagon Release? (5)

A 
Low BG 
High amino acids- prevents hypoglycaemia following insulin release in response to amino acids 
Sympathetic innervation and epinephrine 
Cortisol 
Stress, eg. exercise
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90
Q

Which Stimuli Inhibit Glucagon Release? (4)

A

Glucose
Free fatty acids and ketones
Insulin
Somatostatin

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91
Q

What Happens to Insulin and Glucagon if BG Changes? (2)

A

High glucose –> high insulin and low glucagon

Low glucose –> high glucagon and low insulin

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92
Q

What Effect does Amino Acid Concentration Have on Insulin and Glucagon? (2)

A

Amino acids –> high insulin –> low BG

Amino acids –> high glucagon –> high BG

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93
Q

Type 1 Diabetes

Aetiology (1)

A

HLA DR3+/-DR4 (>90%)

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94
Q

Type 1 Diabetes

Secondary causes of diabetes (3)

A

Pathological process damaging pancreatic cells: chronic pancreatitis, pancreatic cancer, CF, haemochromatosis
Drugs: corticosteroids, anti-HIV drugs
Endocrine: Cushing’s, acromegaly, hyperthyroidism

95
Q

Type 1 Diabetes

Latent autoimmune diabetes of adults (LADA) (3)

A

Form of type 1
Present later in life and misdiagnosed as type 2
Slower progression to insulin dependence

96
Q

Type 1 Diabetes

Pathology (2)

A

Autoimmune disruption of B-cells = unable to produce insulin
Means unable to utilise glucose in peripheral muscles and adipose, which stimulates counter-regulatory hormones to promote gluconeogenesis, glycogenolysis and ketogenesis

97
Q

Type 1 Diabetes

Signs + symptoms (7)

A 
Polyuria 
Polydipsia 
Unexplained weight loss 
Blurred vision 
Lethargy 
DKA/ketones on breath 
Low-grade infections eg. thrush
98
Q

Type 1 Diabetes

Signs + symptoms in children <5 (6)

A 
Return to bedwetting in a previously dry child 
Heavier nappies 
Candidiasis (oral/vulval) 
Constipation 
Recurring skin infections
Irritability
99
Q

Type 1 Diabetes

Investigations (3)

A

Symptoms + one diagnostic lab glucose (randome >11.1 mmol/l or fasting >7 mmol/l)
Two diagnostic lab glucose results on 2 separate occasions (could use oral glucose tolerance test- >11.1 2h after 75g oral glucose load)- don’t need symptoms
HbA1c >48mmol/l indicates hyperglycaemia over preceding 3 months (don’t need symptoms)

100
Q

Type 1 Diabetes

When HbA1c can’t be used (7)

A 
Haemoglobinopathies 
Haemolytic anaemia 
Untreated iron deficiency anaemia 
Suspected gestational diabetes 
Children 
CKD 
Medications that cause hyperglycaemia eg. steroids
101
Q

Type 1 Diabetes

Education (6)

A

Carb counting: dose adjustment for normal eating
Measure glucose before and after exercise
Travel: diabetes ID, take double quantities and split them up in case one lost
Driving: inform DVLA for restricted licence if on insulin, check levels before driving and every 2h on long journeys, if >1 severe hypo inform DVLA and stop driving
Alcohol: check levels before drinking, not empty tummy
Training on hypo management, monitoring, injection technique, sick day rules (never miss insulin)

102
Q 
Type 1 Diabetes 
Insulin treatment (4)
A

Rapid-acting insulin analogues- at start of meal or just after
Short acting insulin
Intermediate acting insulin
Long acting insulin analogues- no awkward peak so good if overnight hypos are a problem

103
Q 
Type 1 Diabetes 
Additional Treatment (3)
A

Metformin (add in if BMI >25)
Statins if >40, established nephropathy, other cardiovascular risk factors
Monitoring: annual retinal and foot screening

104
Q

Type 2 Diabetes

Pathology (3)

A

Relative deficiency of insulin due to excess of adipose tissue
Peripheral tissues become insensitive to insulin (abnormal response by receptors or reduced numbers)
B-cells remain intact, may even be hyperinsulinaemia

105
Q 
Type 2 Diabetes
Risk factors (9)
A 
Strong family history 
Obesity 
Black/Asian ethnicity 
History if gestational diabetes 
Poor diet 
Steroids 
Statins 
PCOS 
Inactivity
106
Q

Type 2 Diabetes

Signs + symptoms (4)

A

Asymptomatic (often incidental finding)
Polydipsia
Polyuria
Acanthosis nigricans (hyperpigmentation in body folds)

107
Q

Type 2 Diabetes

Investigations (4)

A

Random plasma glucose >11.1 mmol/l
HbA1c >48 mmol/mol
Fasting plasma glucose >7mmol/l
Confirmed by 1 test if symptomatic or 2 on separate occasions if asymptomatic

108
Q

Type 2 Diabetes

Treatment (6)

A

Lifestyle modification: weight loss (aim 5-10%, low carb and sugar), BP (target <140/80 or <130/80 if end kidney/eye/cerebrovascular damage) with lifestyle advice but if not improved in 2 months then ACE-i (if black CCB/diuretic), atorvastatin if cVS risk
Driving: same as type 1 if sulfonylurea/insulin
HbA1c target: monitor 3-6 months until stable then 6
Metformin 1st line if Hba1c >48mmol/l
If HbA1c >53 16 weeks later: sulfonylurea –> SGLT-2 inhibitor/DPP-4 inhibitor or thiazolidinediones
3rd line: triple therapy then try insulin

109
Q

Type 2 Diabetes

Maturity Onset Diabetes of the Young (MODY) (1)

A

Rare autosomal dominant form of type 2 diabetes

110
Q

Diabetes Medication

Biguanides (metformin) (5)

A

Mechanism: increased insulin sensitivity and reduced hepatic gluconeogenesis
Contraindications: acute metabolic acidosis, general anaesthesia (withold on day)
Caution: renal impairment (risk of lactic acidosis)
Side effects: GI upset, lactic acidosis
Interactions: excessive alcohol increases risk of lactic acidosis

111
Q

Diabetes Medication

Sulfonylureas (eg. glicazide, glimepiride) (3)

A

Mechanism: stimulate pancreatic B-cells to secrete insulin
Cautions: renal impairment (can cause hypo), hepatic impairment, pregnancy and breastfeeding (risk of neonatal hypo)
Side effects: hypos, increased weight, GI upset, hypersensitivity (rash)

112
Q

Diabetes Medication

Thiazolidinediones (Glitazones) (4)

A

Mechanism: activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake
Contraindications; hepatic impairment, pregnancy and breastfeeding
Side effects: hypos, weight gain, fluid retention, liver dysfunction, GI upset, fractures, impotence
Caution: CV risk, risk of fractures

113
Q

Diabetes Medication

SGLT-2 inhibitors (glifozins) (5)

A

Mechanism: inhibit resorption of glucose in kidney by SGLT-2 in the proximal tubule
Contraindications: renal impairment, pregnancy and breastfeeding
Caution: CV dsiease, elderly, hypotension
Side effects: weight loss, GU infection, thirst, polyuria, DKA at only mildly raised glucose levels
Interactions: anti-hypertensives

114
Q

Diabetes Medication

DPP-IV Inhibitors (gliptins eg. sitagliptin) (4)

A

Increases incretin (GLP-1 and GIP) levels
Contraindications: pregnancy and breastfeeding
Caution: renal/hepatic impairment, history of pancreatitis
Side effects: hypos, GI upset, oedema, increased risk of pancreatitis

115
Q

Diabetes Medication

GLP-1 Analogues (eg. liraglutide) (4)

A

Mechanism: GLP-1/incretin is released by small intestine in response to oral glucose and increased insulin secretion and inhibit glucagon synthesis, also causes weight loss
Contraindications: pregnancy and breastfeeding, GI disease
Caution: elderly, hepatic impairment
Side effects: hypos, N&V, pancreatitis, weight loss

116
Q

Hypoglycaemia

Definition (1)

A

Plasma glucose <3mmol/l

117
Q

Hypoglycaemia

Aetiology (5)

A 
Too much insulin 
Sulfonylurea 
Inadequate food intake/fasting 
Exercise 
Alcohol
118
Q 
Hypoglycaemia
Risk factors (7)
A 
Tight glycaemic control 
Long duration of diabetes 
Cognitive impairment 
Extremes of age 
Renal/hepatic impairment 
Inadequate monitoring 
Reduced carbohydrate intake: coeliac disease, gastroenteritis, alcohol
119
Q

Hypoglycaemia

Pathology (2)

A

Hyperinsulinaemia leads to a lack of glucose in blood travelling to the brain, causing neurological symptoms
Sympathetic response due to adrenaline release

120
Q

Hypoglycaemia

Edinburgh Hypoglycaemia Scale (3)

A

Autonomic: sweating, palpitations, shaking, hunger
Neuroglycopenic: confusion, drowsiness, odd behaviour, speech difficult, incoordination
General malaise, headache, nausea

121
Q

Hypoglycaemia

Types of hypoglycaemia (2)

A

Type 1s usually get fasting hypos (insulin/sulfonylurea induced or exercise, missed meal)
Type 2s usually get post-prandial hypos (prolonged OGTT)

122
Q

Hypoglycaemia

Non-diabetic causes (6)

A 
Drugs: B-blockers 
Pituitary insufficiency
Liver failure 
Addison's disease 
Islet cell tumours: insulinoma 
Dumping syndrome post gastric/bariatric surgery (post-prandial)
123
Q

Hypoglycaemia

Treatment (3)

A

Treat with oral sugar and a long-acting starch (eg. toast)
If can’t swallow, 25-50ml 50% glucose IV with 0.9% saline flush (prevents phlebitis)
Glucagon IM if no IV access (short duration of effect so repeat 20 mins later)

124
Q

Diabetic Ketoacidosis

Pathology (4)

A

Unable to utilise glucose in adipose and muscle tissues causing release of glucagon, adrenaline, cortisol and growth hormone
Glucagon promotes glycogenolysis, gluconeogenesis and ketogenesis in the liver leading to hyperglycaemia
Accumulation of ketone bodies –> metabolic acidosis
Osmotic diuresis causes electrolyte shifts + fluid depletion (usually hyperkalaemia when admitted but becomes hypo when insulin given

125
Q 
Diabetic Ketoacidosis
Risk factors (3)
A

Type 1 DM
Inadequate insulin
Infection

126
Q

Diabetic Ketoacidosis

Symptoms (8)

A 
Onset over hours 
Polyuria 
Polydipsia 
Weight loss 
Weakness 
N&amp;V
Abdo pain 
SOB
127
Q

Diabetic Ketoacidosis

Signs (7)

A 
Dry mucous membranes 
Sunken eyes 
Tachycardia 
Hypotension 
Sweet smelling ketotic breath 
Altered mental state 
Sighing deep breathing (Kussmaul hyperventilation)
128
Q

Diabetic Ketoacidosis

Investigations (8)

A 
ECG
CXR
Urine dipstick (ketonuria) 
Capillary + lab glucose (>11.1mmol/l) 
Ketones (blood): >3mmol/l 
VBG: blood pH <7.3
Bicarbonate <15 mmol/l 
High anion gap
129
Q 
Diabetic Ketoacidosis
Severe DKA (9)
A 
Blood ketones >6mmol/l 
Bicarbonate <5mmol/l 
pH <7
Hypokalaemia on admission 
GCS <12
SpO2 <92% 
BP <90 
Pulse >100 or <60 
Anion gap >16
130
Q

Diabetic Ketoacidosis

Treatment (5)

A

If SBP <90: give 500ml NaCl 0.9% IV over 10-15 mins, if SBP >90: give NaCl 0.9% IV at rate that replaces deficit (maintenance) (both with KCl unless anuria)
IV insulin fixed rate of 0.1 units/kg/hour
Monitor blood ketone and glucose concentrations hourly and adjust rate accordingly
Once blood glucose concentration falls below 14 mmol/l, give glucose 10% IV + NaCl 0.9%
Continue infusion until blood ketone conc. <0.5mmol/l, pH >7.3 and patient can eat and drink, then give subcut fast acting insulin and meal

131
Q

Diabetic Ketoacidosis

Complications (3)

A

Cerebral oedema (may be due to cerebral hypoperfusion and subsequent reperfusion)
Hypokalaemia
Hypoglycaemia

132
Q

Hyperglycaemic Hyperosmolar State (HHS)

Epidemiology (2)

A

Elderly

Type 2

133
Q

Hyperglycaemic Hyperosmolar State (HHS)

Aetiology (5)

A

Illness: MI, infection, stroke, AKI, acute abdo, pancreatitis, hyperthyroidism
Medication: metformin during intercurrent illness, diuretics, B-blocker
Substance misuse: alcohol, cocaine
Poor diabetic control/compliance
May be 1st presentation of diabetes

134
Q

Hyperglycaemic Hyperosmolar State (HHS)

Pathology (3)

A

Hyperglycaemia leads to osmotic diuresis and renal losses of water in excess of sodium and potassium
Severe volume depletion leads to increased serum osmolality leading to blood hyperviscosity
Hypertonicity leads to preservation of intravascular volume so patient may not look dehydrated

135
Q 
Hyperglycaemic Hyperosmolar State (HHS) 
Risk factors (6)
A 
Older 
Type 2 DM 
Nursing home residents/live alone 
Dementia 
Sedative drugs 
Immunosuppression/steroids
136
Q

Hyperglycaemic Hyperosmolar State (HHS)

Symptoms (8)

A 
Generalised weakness 
Leg cramps 
Visual impairment 
Bedbound 
Lethargy 
Confusion 
Seizures 
Coma
137
Q

Hyperglycaemic Hyperosmolar State (HHS)

Signs (3)

A

Increased respiratory rate to lower metabolic acidosis
Raised blood urate: sunken eyes, limb weakness
Severe hypovolaemia: tachycardia and/or hypotension, reduced turgor

138
Q

Hyperglycaemic Hyperosmolar State (HHS)

Investigations (3)

A

Hyperglycaemia >30 mmol/l WITHOUT hyperketonaemia (<3 mmol/l) or acidosis (pH >7.3, bicarb >15 mmol/l)
Osmolality (measure serum osmolality: 2Na + glucose + urea
Hypovolaemia

139
Q

Hyperglycaemic Hyperosmolar State (HHS)

Treatment (4)

A

Fluid replacement should be low to prevent acute heart failure
May require potassium replacement
Insulin: low dose when glucose no longer falling with IV fluids alone or significant ketonaemia
May need to replace magnesium + phosphate as hypos are common

140
Q

Hyperglycaemic Hyperosmolar State (HHS)

Complications (6)

A 
Cerebral oedema 
Arterial/venous thrombosis 
Foot ulceration 
ARDS
Multi-organ failure 
Rhabdomyolysis
141
Q

Diabetic Foot Disease

Aetiology (3)

A

Neuropathy (injury/infection over pressure points)
Ischaemia (critical toes +/- absent dorsalis pedis pulses and worse outcome)
Mixed neuropathy + ischaemia

142
Q 
Diabetic Foot Disease 
Risk factors (3)
A

Peripheral arterial disease (smoking, hypertension, hyperlipidaemia)
Previous ulceration
Joint deformity

143
Q

Diabetic Foot Disease

Signs + symptoms (5)

A

Neuro-ischaemia: critical toes, absent dorsalis pedis, cold
Neuro-ischaemic ulcers: painful, punched out lesions at foot margins and pressure points
Neuropathy: loss of protective sensation in stocking distribution, absent ankle jerks, warm dry skin
Neuropathic ulcers: painless, punched out, injury + infection over pressure areas
Neuropathic deformity (Charcot joint): swelling, instability, loss of arch, claw toes

144
Q

Diabetic Foot Disease

Investigations (4)

A

Neuropathy: clinical assessment with monofilament
Ischaemia: clinical, ABPI, doppler, angiography
Bony deformity: X-ray
Infection: swabs, blood cultures, X-ray for osteomyelitis

145
Q

Diabetic Foot Disease

Treatment (4)

A

Conservative: daily foot inspection, footwear, regular podiatry, wound debridement and dressings
Medical: IV antibiotics for cellulitis, TCAs for painful neuropathy
Absolute indications for surgery: abscess/deep infection, spreading infection, gangrene
Vascular (angioplasty, stents, amputation) or orthopaedic (excision and drainage of abscess) surgery

146
Q

Diabetic Neuropathy

Aetiology (1)

A

Metabolic and microvascular damage to vasa nervorum

147
Q

Diabetic Neuropathy

Signs + symptoms (4)

A

Symmetric sensory polyneuropathy and glove and stocking tingling, numbness and pain
Mononeuritis multiplex: usually CNIII/IV
Amyotrophy: painful wasting of quads and other pelvifemoral muscles
Autonomic neuropathy: postural hypo, reduced cerebrovascular autoregulation, urinary retention, erectile dysfunction, diarrhoea

148
Q

Diabetic Neuropathy

Treatment (4)

A

Symmetrical sensory polyneuropathy: 1st paracetamol, 2nd amitryptiline
Mononeuritis multiplex: immunosuppression (corticosteroids)
Amyotrophy: usually just gradual (often incomplete) improvement
Autonomic neuropathy: codeine for diarrhoea, sidafenil for ED, fludrocortisone for BP

149
Q

Diabetic Retinopathy

Aetiology (1)

A

Microvascular injury to retinal arteries leads to injury to retinal neuromas

150
Q

Diabetic Retinopathy

Pathology (4)

A

Increased blood flow to retinal arteries due to hyperglycaemia causes retinal capillary leakage which leads to intraretinal haemorrhage, cholesterol exudate deposition and retinal oedema
Macula may become involved causing reduced central vision
Occlusion of retinal capillaries causes micro-aneurysms, cotton wool spots, intra-retinal microvascular damage and ultimately proliferative diabetic retinopathy
Neovascularisation is due to VEG-F release in response to hypoxia and these new vessels form on the disc and at ischaemic areas may be proliferative

151
Q

Diabetic Retinopathy

Findings on annual retinal screening (3)

A

Background retinopathy: microaneurysms (dots) , haemorrhages (blots), hard exudates (fat deposits)
Pre-proliferative retinopathy: cotton wool spots eg. infarcts, haemorrhages, venous bleeding
Proliferative retinopathy: new vessel formation (urgent referral)

152
Q

Diabetic Retinopathy

Treatment (3)

A

Pan-retinal laser photocoagulation: stops production of angiogenic factors from the ischaemic retinopathy
Anti-VEGF (intra-vitreal)
Vitrectomy

153
Q

Diabetic Retinopathy

Complications (5)

A 
Vitreous haemorrhage 
Cataract 
Rubeosis iridis (new vessels on iris, occurs late and may lead to glaucoma) 
Macular oedema 
Visual field loss
154
Q

Diabetic Nephropathy

Pathology (5)

A

High glucose and high glomerular pressure result in mesangial expansion and a transient increase in GFR
Mesangial expansion gradually leads to microalbuminuria which causes nephropathy (low GFR and high proteinuria)
Fibrosis which eventually leads to Kimmelesteil-Wilson nodules which are the hallmark of diabetic glomerulosclerosis
Increased glomerular basement membrane width, diffuse mesangial sclerosis, microaneurysm and arteriosclerosis
Hypertension aggravates the process via mesangial stress

155
Q

Diabetic Nephropathy

Signs + symptoms (1)

A

Normally asymptomatic until late stages

156
Q

Diabetic Nephropathy

Investigations (3)

A

Annual screening for microalbuminuria with specialised dipstick
24h urinary collection
Urinary albumin creatinine ratio

157
Q

Diabetic Nephropathy

Treatment (1)

A

Start ACE-i or ARB even if BP normal to reduce intraglomerular pressure and proteinuria

158
Q

Thyroid Hormone Synthesis (4)

A

Tyrosine and iodide obtained from diet
Follicular cells manufacture enzymes required for thyroid production, manufacture thyroglobulin and actively concentrate iodide from the plasma
Enzymes and thyroglobulin are packaged into vesicles and exported to the colloid along with iodide
Thyrosine and iodide are combined to form thyroid hormones by thyroid peroxidase enzymes

159
Q

Thyroid Hormone Release (3)

A

In response to TSH, follicular cells take back up portions of colloid which form vesicles inside the cell and proteolytic enzymes cut thyroglobulin to release thyroid hormones
T3 + T4 are lipid soluble so pass through cell membrane to the plasma to bind to thyroxine binding globulin (TBG)
Hypothalamus (TRH) –> ant. pituitary (TSH) –> thyroid (T3+T4)

160
Q

Thyroid Hormone Circulation (2)

A

TBG has higher affinity for T4 (6 day 1/2 life) than T3 (1 day 1/2 life)
There is 50x more T4 than T3 in plasma but TH receptors inside cells have a much higher affinity to T3 so it is more physiologically active

161
Q

Thyroid Hormone Regulation (6)

A

TRH released from hypothalamus in response to stimuli, eg. cold/exercise/pregnancy
TRH stimulates ant. pituitary to release TSH
Thyroid hormones are subsequently released from the thyroid gland
-ve feedback: high levels of thyroid hormones in blood inhibit TRH + TSH release
Somatostatin inhibits TSH
Glucocorticoids inhibit TSH

162
Q

Thyroid Hormone Function (5)

A

TH binds to nuclear receptors in target cells and change transcription and translation to alter protein synthesis
Raises metabolic rate and promotes thermogenesis
Increased proteolysis
Increased
lipolysis
Stimulates growth hormone receptor expression

163
Q 
Hyperthyroidism
Primary hyperthyroidism (3)
A 
Grave's Disease (2/3 cases, typical age 40-60) 
Toxic multinodular goitre (usually in elderly, nodules secrete TH) 
Toxic adenoma (solitary nodule producing T3 + T4)
164
Q 
Hyperthyroidism 
Secondary hyperthyroidism (3)
A

TSH secreting pituitary adenoma
Gestational thyrotoxicosis
B-hCG secreting tumour

165
Q

Hyperthyroidism

Symptoms (10)

A 
Diarrhoea 
Weight loss 
Increased appetite 
Sweats 
Overactive 
Heat intolerance 
Palpitations 
Tremor 
Irritability 
Oligomenorrhoea +/- infertility
166
Q

Hyperthyroidism

Signs (8)

A

Pulse: fast/irregular
Warm, moist skin
Fine tremor
Palmar erythema
Thin hair
Lid lag (eyelid lags behind eyes descent as patient watches your finger slowly descend
Lid retraction (exposure of sclera above iris)
Goitre, thyroid nodules or bruit depending on the cause

167
Q

Hyperthyroidism

Specific Grave’s Disease signs (3)

A

Eye disease: exopthalmos (protruding eye), proptosis (eyes protrude beyond orbit), opthalmoplegia
Pretibial myxoedema: oedematouus swellings above lateral malleoli
Thyroid acropachy: extreme manifestation with clubbing and painful finger and toe swelling

168
Q

Hyperthyroidism

Investigations (7)

A

Primary hyperthyroidism: low TSH, high T4/T3
Secondary hypothyroidism: high TSH, high T4/3
ESR: high
Ca: high
LFT: high
Technetium 99 isotope scan: increased uptake in Grave’s disease, decreased uptake in thyroiditis (which causes hypothyroidism but there may be a thyrotoxic phase first)
Check thyroid antibodies

169
Q

Hyperthyroidism

Treatment (4)

A

B-blocker for symptom control
Anti-thyroid medication: carbimazole (can either do titration based on TFTs o do block-replace by adding in thyroxine)
Radioiodine (most become hypothyroid post treatment, must avoid pregnant women and children)
Thyroidectomy (could damage recurrent laryngeal nerve- hoarse voice)

170
Q

Hyperthyroidism

Complications (4)

A

Heart failure
Angina
AF
Thyroid storm: extreme manifestation of thryotoxicosis often precipitated by intercurrent factors eg. infection, abrupt withdrawal of antithyroid medication, causes hyper-pyrexia, tachycardia and reduced GCS

171
Q

Hypothyroidism

Aetiology (6)

A

Primary atrophic hypothyroidism (autoimmune hypothyroidism)
Hashimoto’s thyroiditis (autoimmune hypothyroidism, goitre)
Iodine deficiency
Post thyroidectomy or radioiodine treatment
Drugs: carbimazole, amiodarone, lithium
Secondary hypothyroidism: hypopituitarism (not enough TSH)

172
Q

Hypothyroidism

Symptoms (7)

A 
Lethargy 
Low mood 
Cold intolerance 
Weight gain 
Constipation 
Menorrhagia 
Reduced memory/cognition
173
Q

Hypothyroidism

Signs (6)

A 
Slow reflexes 
Dry hair/skin 
Cold hands 
Goitre 
Bradycardia 
Severe hypothyroidism: myxoedema (subcutaneous tissue swelling, usually around eyes and dorsum of hand- can cause carpal tunnel syndrome)
174
Q

Hypothyroidism

Investigations (4)

A

Primary: High TSH , low T4/T3
Secondary: Low TSH, low T4/T3
Thyroid antibodies: anti-thyroid peroxidase antibodies
FBC: macrocytic anaemia

175
Q

Hypothyroidism

Treatment (1)

A

Levothyroxine

176
Q

Thyroid Eye Disease

Pathology (1)

A

Autoimmunity leads to inflammatory response and periorbital oedema

177
Q

Thyroid Eye Disease

Symptoms (6)

A 
Eye discomfort 
Grittiness 
Increased tear production 
Diplopia 
Reduced acuity 
Afferent pupillary defect (optic nerve compression)
178
Q

Thyroid Eye Disease

Signs (6)

A

Exopthalmos (appearance of protruding eyes)
Proptosis (eyes protrude beyond orbit- look from above)
Conjunctival oedema
Corneal ulceration
Papilloedema
Loss of colour vision

179
Q

Thyroid Eye Disease

Treatment (3)

A

Treat hypo/hyper-thyroidism
Mild: artificial tears, elevation of head when sleeping to reduce periorbital oedema
Moderate-severe: IV methylprednisolone, surgical decompression, eyelid surgery

180
Q

Thyroid Lumps

Differentials (2)

A

Benign: diffuse goitre, multinodular goitre (de Quervain’s), subacute lymphocytic thyroiditis, follicular adenoma, thyroid cyst
Malignant: thyroid cancer (10% of solitary thyroid nodules are malignant)

181
Q

Thyroid Lumps

History (3)

A

Features of lump: swelling, tenderness, onset
Associated symptoms: hypo/hyperthyroidism, pressure symptoms
Past or family history of thyroid problems or autoimmune disease

182
Q

Thyroid Lumps

Examination (2)

A

Features of hypo/hyperthyroidism
Lump: diffuse goitre, multinodular goitre, solitary thyroid nodules (cyst, adenoma, malignancy, discrete nodule or multinodular goitre)

183
Q

Thyroid Lumps

Investigations (5)

A

TFT + thyroid autoantibodies
CXR + thoracic inlet view: for retrosternal goitres and mets
USS: solid, cystic, complex or part of a group of lumps
Radionuclide scan: hypofunctioning suggests malignancy, hypoerfunctioning suggests adenoma
FNAC

184
Q

Thyroid Lumps

Complications of Thyroid Surgery (4)

A

Airway obstruction (haemorrhage/oedema)
Recurrent laryngeal nerve palsy (right > left)
Hyperparathyroidism
Thyroid storm

185
Q

Thyroid Lumps

Goitre (4)

A

Aetiology: iodine deficiency, autoimmune, hereditary
Simple, multinodular, diffuse and painless (may have mass effect- dysphagia, stridor, SVC obstruction)
Multinodular usually euthyroid but may be subclinical hyper

186
Q

Thyroid Lumps

De Quervain’s thyroiditis (5)

A 
Aetiology: viral URTI, autoimmune 
Pathology: thyrotoxicosis --> hypothyroid --> euthyroid 
Diffuse painful goitre 
Reduced iodine uptake 
Self-limiting
187
Q 
Thyroid Lumps 
Follicular adenoma (2)
A

Benign solitary thyroid nodules, may cause pressure symptoms

Do hemithyroidectomy as clinical and diagnostic tests can’t tell if benign/malignant

188
Q

Thyroid Cancer

Aetiology (5)

A

Papillary (60%): 20-40y/o, node and lung mets
Follicular (25%): 40-60y/o, F>M, haematogenous spread to bone and lungs
Medullary (5%): 1/3 familial (MEN2) and occur in young, can occur sporadically in 40-50y/o
Anaplastic (rare): F>M, >60y/o, rapid growth and aggressive with spread
Lymphoma (5%): F>M, mucosal associated lymphoid tissue (MALT) associated with good prognosis

189
Q 
Thyroid Cancer
Risk factors (6)
A 
Solitary thyroid nodule 
Solid thyroid nodule 
Male 
Cold thyroid nodule 
MEN2
Radiation exposure
190
Q

Thyroid Cancer

Signs + symptoms (3)

A

Painless neck mass
Cervical lymphadenopathy
Compression symptoms (dysphagia, stridor, SVC obstruction)

191
Q

Thyroid Cancer

Investigations (7)

A 
TFT 
Thyroid autoantibodies 
USS neck 
CXR
Radionuclide scan 
FNAC 
Tumour markers: Tg (papillary/follicular), calcitonin (medullary)
192
Q

Thyroid Cancer

Treatment (2)

A

Thyroidectomy +/- node clearance

Chemoradiotherapy for lymphoma

193
Q 
Parathyroid Physiology 
Calcium distribution (4)
A

Bone 99%
Intracellular 0.9%
ECF 0.1%
Plasma: 2.2-2.6 (tight limits; plasma conc. takes precedence over bone storage)

194
Q 
Parathyroid Physiology 
Bone cells (3)
A

Osteoblasts: bone building cells that lay down a collagen extracellular matrix which is calcified
Osteocytes: differentiated osteoblasts which regulate osteoblast and osteoclast activity
Osteoclasts: responsible for bone resorption

195
Q 
Parathyroid Physiology 
Vitamin D (1)
A

Converted in the liver then the kidneys to calcitriol (steroid hormone secreted in response to increased PTH)

196
Q 
Parathyroid Physiology 
Calcitriol roles (3)
A

Increased calcium gut absorption
Increased calcium renal reabsorption
Stimulates osteoclasts

197
Q

Parathyroid Physiology

Functions of calcium (5)

A 
Cell signalling 
Blood clotting 
Apoptosis 
Skeletal strength 
Regulation of membrane excitability
198
Q

Parathyroid Physiology

Hypocalcaemia (1)

A

Increased neuronal Na permeability causing hyper excitation and tetany

199
Q

Parathyroid Physiology

Hypercalcaemia (1)

A

Reduced neuronal Na permeability, reducing hyperexcitability and depressing neuromuscular activity

200
Q

Parathyroid Physiology

Definition of parathyroid hormone (1)

A

Polypeptide hormone produced and released by parathyroid glands in response to reduced free calcium in the plasma

201
Q

Parathyroid Physiology

Actions of parathyroid hormone (3)

A

Stimulates osteoclasts to increase calcium and phosphate resorption in bone leading to an increase in the plasma
Inhibits osteoblasts
Increased calcium reabsorption at the kidney tubules and thus decreasing urinary excretion

202
Q

Parathyroid Physiology

Negative feedback of parathyroid hormone (1)

A

Increased levels of plasma calcium inhibit PTH causing a shift to greater osteoblast deposition and less osteoclast resorption

203
Q

Parathyroid Physiology

Definition of calcitriol (1)

A

Steroid hormone produced by liver and then kidneys from dietary vitamin D in response to increased levels of PTH

204
Q

Parathyroid Physiology

Actions of calcitriol (4)

A

Bind to receptors in intestine, bone and kidney
Increased calcium absorption from gut via active transport system
Mobilises calcium stores by stimulating osteoclast activity
Facilitates renal absorption of Ca

205
Q

Parathyroid Physiology

Calcitonin (3)

A

Peptide hormone produced by medullary cells in the thyroid gland in response to increased plasma calcium concentration
Binds to osteoclasts to inhibit bone resorption
Increases renal excretion of calcium

206
Q

Hypercalcaemia

Aetiology (7)

A

Parathyroid mediated: primary hyperparathyroidism, MEN
Non-parathyroid mediated: malignancy, vitamin D deficiency, sarcoidosis
Medications: thiazide diuretics, lithium
Hyperthyroidism
Acromegaly
Phaeochromocytoma
Adrenal insufficiency

207
Q

Hypercalcaemia

Signs + symptoms (6)

A

Bones: pain, osteopenia, osteoporosis, muscle weakness
Stones: renal stones
Neuro: reduced concentration, confusion, fatigue
Cardio: shortening of QT interval, tachycardia, hypertension
Pancreatitis
Features of malignancy eg. lymphadenopathy

208
Q

Hypercalcaemia

Investigations (4)

A

Bone profile: increased calcium, albumin, phosphate, vitamin D3, alk phos
Parathyroid hormone: normal/high (inappropriate)- primary hyperparathyroidism, low (appropriate)- malignancy, drug causes
Myeloma screen
ECG: short QT

209
Q

Hypercalcaemia

Treatment (4)

A

Rehydration: 0.9% saline 4-6L over 24h with monitoring for fluid overload, consider dialysis for severe renal failure
IV bisphosphonates: after rehydration zolendronic acid over 15 mins
Calcitonin if poor response to bisphosphonates
Parathyroidectomy if acute presentation and severe hypercalcaemia when poor response to other measures

210
Q

Primary Hyperparathyroidism

Aetiology (3)

A

Solitary adenoma (80%)
Hyperplasia of all parathyroid glands (20%)
MEN1 (causes parathyroid hyperplasia/adenoma)

211
Q

Primary Hyperparathyroidism

Pathology (1)

A

PTH oversecretion causes increased resorption, hypophosphataemia and hypercalcaemia

212
Q

Primary Hyperparathyroidism

Signs + symptoms (4)

A

Often asymptomatic with raised Ca on routine tests
Signs related to high Ca: weak, tired, depressed, thirsty, renal stones, abdo pain, pancreatitis and ulcers
Bone resorption effects of PTH can cause pain, fractures and osteopenia/osteoporosis
High BP

213
Q

Primary Hyperparathyroidism

Investigations (8)

A 
High Ca 
High PTH (or inappropriately normal) 
Low PO4 (unless in renal failure) 
High alk phos (from bone activity) 
High 24h urine Ca 
X-ray: osteosis fibrosa cystica (severe resorption causes sub periosteal erosions, cysts, pepper pot skull) 
DEXA: exclude osteoporosis 
Abdo ultrasound: renal calculi
214
Q

Primary Hyperparathyroidism

Treatment (2)

A

Mild: increase fluid intake to prevent stones

Surgical excision of all 4 glands or the adenoma if high serum/urinary calcium, osteoporosis, renal calculi

215
Q

Secondary Hyperparathyroidism

Aetiology (3)

A

Disease outside of the parathyroid glands causes all of the parathyroid glands to become enlarged and hyperactive
Kidney failure
Vitamin D deficiency

216
Q

Secondary Hyperparathyroidism

Investigations (2)

A 
Low Ca
High PTH (appropriately)
217
Q

Secondary Hyperparathyroidism

Treatment (3)

A

Correct causes
Phosphate binders
Vitamin D

218
Q

Tertiary Hyperparathyroidism

Aetiology (2)

A

Occurs after prolonged secondary hyperparathyroidism, causing glands to act autonomously having undergone hyperplastic/adenomatous change
Renal failure

219
Q

Tertiary Hyperparathyroidism

Investigations (2)

A

High Ca

Really high PTH (inappropriately- unlimited by feedback control)

220
Q

Hypocalcaemia

Aetiology (3)

A 
Low PTH (hypoparathyroidism): autoimmune, post-surgical (thyroidectomy/parathyroidectomy) 
High PTH (secondary hyperparathyroidism): vit D deficiency, pseudohypoparathyroidism, renal disease 
Drugs: bisphosphonates, calcitonin
221
Q

Hypocalcaemia

Signs + symptoms (5)

A 
Neuromuscular irritability (tetany): paraesthesia, muscle twitching, Chovstek's sign (facial nerve tapped at masseter muscle = facial muscle on same side contracts momentarily due to nerve hyperexcitability), Trosseau's sign (carpal spasm due to ulnar nerve excitation occurs when sphygmanometer is elevated above systolic pressure) 
Prolonged QT 
Hypotension 
Papilloedema 
Extrapyramidal signs, Parkisonism
222
Q

Hypocalcaemia

Investigations (5)

A

ECG
Low Ca
PTH low/normal (inappropriate): magnesium deficiency or hypoparathyroidism
PTH high (appropriate): renal failure, vit D deficiency, pseudohypoparathyroidism
Magnesium

223
Q

Hypocalcaemia

Treatment (2)

A

Mild: oral calcium tablets, calcitriol for vit D deficiency
Severe: IV calcium gluconate

224
Q

Primary Hypoparathyroidism

Pathology (1)

A

PTH secretion is reduced due to gland failure, leading to low Ca and high phosphate

225
Q

Primary Hypoparathyroidism

Signs + symptoms (1)

A

Hypocalcaemia

226
Q

Primary Hypoparathyroidism

Investigations (6)

A 
Low PTH 
Low Ca 
High phosphate 
Normal alk phos
Normal vit D 
ECG: prolonged QT
227
Q

Primary Hypoparathyroidism

Treatment (2)

A

Calcium supplements

Calcitriol

228
Q 
Pseudohypoparathyroidism 
Pathology (1)
A

Genetic failure of target cell to respond to PTH

229
Q 
Pseudohypoparathyroidism
Signs (4)
A

Short metacarpals
Round face
Short stature
Reduced IQ

230
Q 
Pseudohypoparathyroidism
Investigations (3)
A

Low Ca
High PTH
Normal/high alk phos

231
Q

Pseudopseudohypoparathyroidism (1)

A

Same as pseudohypoparathyroidism but with normal biochemistry

232
Q

Multiple Endocrine Neoplasia

Definition (1)

A

Autosomal dominant functioning hormone producing tumours in multiple organs

233
Q

Multiple Endocrine Neoplasia

MEN-1 (5)

A

Tumour suppressor gene
Mutations present 40-60y/o
Parathyroid hyperplasia/adenoma (high Ca)
Pancreas endocrine tumours (eg. insulinoma)
Pituitary prolactinoma or GH secreting tumour (acromegaly)

234
Q

Multiple Endocrine Neoplasia

MEN-2 (5)

A

Ret proto-oncogene (tyrosine kinase receptor)
Testing for ret mutations now allows for prophylactic thyroidectomy before neoplasia occurs
Thyroid: medullary thyroid carcinoma
Adrenal: phaeochromocytoma
Hypercalcaemia less common than in MEN-1 but parathyroid hyperplasia does still occur

Med Student Finals (23 decks)

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