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Diabetes + Endocrine Flashcards

1
Q

Definition of Hypoglycaemia

A

Blood Glucose less than/ including 3mmol/L

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2
Q

Thyroid Hormone Normal pathway

A

TRH (hypothalamus)- TSH (ap)- Acts on thyroid- produces T4 + T3

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3
Q

Where is the thyroid gland located?

A

C5-T1, under laryngeal prominence

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4
Q

Describe what you would see in a section of the thyroid gland histologically

A

Follicular cells (cuboidal, containing enzymes- thyroid peroxidase and thyroxine sparing thyroglobulin)
Colloid- inside follicular cells where iodisation + conjugation occurs
C cells- Surround follicular cells- secrete calcitonin (Ca balance)

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5
Q

How does iodine enter the colloid?

A

Iodine enters apical membrane via Na/I symporter and enders the colloid via pendrin

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6
Q

Function of Calcitonin

A

Secretion from thyroid C Cells, decreases blood level of calcium and increases levels in bone by binding to osteoclasts (bone breakdown)= osteoporosis
It also lowers the blood phosphorus level when that rises above normal. Calcitonin opposes the effects of parathyroid hormone, which acts to increase the blood level of calcium

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7
Q

Describe the process of formation of T4 + T3

A

Tyrosine is initially iodinated (iodine ionised to form iodide) (tyrosine peroxidase) to either form MIT (monoiodotyrosine) or DIT (diiodotyrosines) these are then conjugated via thyroid peroxidase (which contains free tyrosine residues) and added together-
MIT + DIT= T3
DIT + DIT= T4
these are stored back in follicular cells until given signal from anterior pituitary (TSH) to be exocytosed into the plasma

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8
Q

How are T4 + T3 stored in the plasma?

A

Bound in the plasma to thyroid binding globulin (TBG) or in serum (small amount)

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9
Q

What does thyroid binding globulin (TBG) have a higher affinity for?

A

T4 resulting in it having a higher half life (6days) than T3 (1day)

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10
Q

How is T4 converted to T3?

A

Converted via deiodinase enzymes in response to need of the tissue

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11
Q

Feedback of thyroid hormone

A

T4 and T3 negatively feedback on both the hypothalamus (TRH) and AP (TSH) to reduce/ increase production

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12
Q

What inhibits thyroid regulation?

A

Glucocorticoids (from Zona Fasiculata of the adrenals eg./ cortisol) stops production of TSH- T4+T3 + conversion of T4-T3
Somatastain (GHIH- Hypo) stops production of TSH- T4/T3

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13
Q

How is a goitre produced?

A

Over action of the gland via
Increase of trophic action of TSH on follicular cells
Overactivity as an autoimmune response eg./ Graves Disease

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14
Q

What is the function of Thyroid Hormone?

A

It bonds to nuclear receptor of target cells to alter trancription and translation (protein synthesis) -

  1. Inc. Metabolic Rate and promote Thermogenesis
  2. Inc hepatic gluconeogensis
  3. Inc lipolysis
  4. Foetal Brain Development
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15
Q

What is thyroxine?

A

T4

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16
Q

What is T3?

A

triiiodothyroxine (active form)

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17
Q

Is thyroid Hormone anabolic or catabolic?

A

Anabolic as it is permissive to Growth Hormone

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18
Q

Causes of Hypothyroidism (myxoedema)

A
  1. Aquired
    Hashimotos- autoimmune destruction
    Iodine Deficency
    Atrophic- autoimmune lymphocytes infiltration
    2.Congenital
    Developmental (agenesis,maldevelopment) Dyshormonogenesis
  2. Iatrogenic
    Post Op/ Radioactive Iodine
    Radiotherapy
    Anti-Thyroid Drugs
  3. Chronic Iodine Deficiency
  4. Post-subactute Thyroditis (post-partum)
  5. Secondary- Pituitary tumour, Craniopharyngeoma, sheehan’s syndrome (post partum haemorrhage)
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19
Q

Symptoms of Hypothyroidism

A

SLOW METABOLISM

  1. Dec metabolic rate (lethargy) + Heat Gain= Weight Gain
  2. Dec protein synthesis= brittle nails + thin/dry skin
  3. NS slow speech + reflex + congition
  4. Dec HR + contractions (bradycardia)
  5. Puffy face, large tongue, hoarseness + come (severe)
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20
Q

What is hypothyroidism?

A

Too little T4 and T3 production, catabolic

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21
Q

What is hyperthyroidism (thyrotoxicosis)?

A

Excess production of thyroid hormone, anabolic

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22
Q

Causes of hyperthyrooidism

A
  1. Graves Disease- 40-60, autoimmune, antibodies mimic TSH= continues thyroid gland stimulation (TSH low)
  2. Toxic Multinodular Goitre- elderly
  3. Secondary- Thyroid Adenoma- rare, producing T3 + T4
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23
Q

Symptoms of Hyperthyroidism

A

INC METABOLISM

  1. Inc metabolic rate + Heat= Weight Loss
  2. Inc protein synthesis/ catabolism= muscle weakness
  3. NS Paranoia, Anxiety + hyper excitable reflexes
  4. Increase HR + contractions (palpitations)
  5. Bowel Infrequency, Light periods
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24
Q

What is congenital hypothyroidism?

A

reduction in foetal neurological development can be caused by a maternal deficiency in iodine

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25
Q

Signs of Hypothyroidism?

A

Goitre- If Graves DIsease
Thyroid Eye Disease- Staring due to orbital oedema
Puffy eyes, large tongue, hoarseness

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26
Q

Where is a diffuse goitre seen?

A

Graves disease (hypo) or hashimotos (hyper)

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27
Q

Where is a nodular goitre seen?

A

Adenomas
Carcinoma
Multinodular Goitre

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28
Q

Tests for Hypothyroidism?

A
  1. T4 and TSH (don’t need T3 as doesn’t add any extra information)
    - Primary- Inc TSH, Dec T4 + T3
    - Subclinical (compensated)- Inc TSH, normla T4+3
    - Secondary- Dec TSH, Dec T4 + T3
  2. Thyroid Autoantibodies (+ve in autoimmune)
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29
Q

What test would you ask for if you suspected a thyroid disease was secondary to an autoimmune condition?

A

Thyroid Antibodies- Antithyroid Peroxidase in Graves Disease and hashimotos

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30
Q

What test would you ask for if you suspect a thyroid disease secondary to a carcinoma?

A

Serum thyroglobulin

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31
Q

What test would you do to determine activity of areas of the thyroid gland? What could this show?

A

Isotope scan, could show a secreting tumour

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32
Q

Tests for Hyperthyroidism?

A

T3, T4 and TSH= decrease (due to -ve feedback) TSH (unless pituitary adenoma) and an Inc T4 (some will also have raised T3)

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33
Q

Where is the adrenal gland?

A

Situated superior/ ontop of kidneys (suprarenal)

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34
Q

What is the venous drainage of the Right Kidney?

A

Direct drainage via R adrenal vein into the aorta

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35
Q

What is the venous drainage of the Left Kidney?

A

Indirect drainage via left adrenal vein- L renal vein- vena Cava

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36
Q

What are the 4 layers of the Adrenal Gland?

A
  1. Inner most- Adrenal Medulla
  2. Zona Reticularus
  3. Zona Fasiculata
  4. Zona Glomerulosa
    5 Capsule
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37
Q

What is the function of the innermost layer of the adrenal gland?

A

The Adrenal Medulla is a modified sympathetic ganglion (derived from neural crest tissue) and secretes caticholamines

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38
Q

What is the adrenal medulla derived from?

A

Neural Crest cells

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39
Q

Name the 3 catecholamines?

A

Epineprine, Noreprinephrine + dopamine

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40
Q

What does the 2nd layer of the adrenal gland secrete?

A

The Zona Reticularus secretes sex steroids- not main site but all 3 produced here

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41
Q

What all the 3 sex steroids?

A

Estrogen, testosterone + progesterone

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42
Q

What does the 3rd layer of the adrenal gland secrete?

A

The Zona Fasiculata secretes glucocorticoids involved in maintaining plasma glucose

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43
Q

What is the biggest layer of the adrenal gland?

A

Zona Fasiculata (glucocorticoids)

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44
Q

What is the most important glucocorticoid?

A

Cortisol

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45
Q

What does the 4th layer of the adrenal gland secrete?

A

Zona Glomerulosa secretes mineralcorticoids involved in regulation of Na and K

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46
Q

Where are all steroid hormones derived from?

A

Cholestrol

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47
Q

What enzyme is require to produce cortisol (Glucocorticoid, ZF) and Aldosterone from cholesterol?

A

21- hydroxylase

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48
Q

Example of a mineralocorticoid?

A

Aldersterone (derived from corticosterone)

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49
Q

What is the prehormone of the sex steroid called? What affects its levels?

A

DHEA, declines with age (especially in menstrual women)

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50
Q

What enzymes are required to produce mineralcorticoids?

A

Progesterone, DHT

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51
Q

What happens congenitally if a defect in 21-hydroxylase enzyme?

A

Cortisol and aldosterone not produced= congenital hyperplasia, so all cholesterol is converted to DHT (sex steroids)= malformed genitalia

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52
Q

Cortisol normal pathway

A

CRH (hypo)- ACTH (ap)- Cortisol (adrenal cortex)

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53
Q

What happens to CRH + ACTH if defect with 21- hydroxylase

A

No production of Cortisol results in removal of the -ve feedback mechanism= Inc CRH- ACTH secretions= Enlargment
Is still -ve feedback from ACTH to hypothalmus

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54
Q

What increases production of CRH and ACTH?

A 
Stress
Alcohol
Caffine
Lack of Sleep
disinhibit hypothalmic-pituitary adrenal axis. Alcohol also depresses hypothalmus + depresses -ve feedback (further increasing CRH + ACTH)
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55
Q

What is the function of cortisol?

A

Glucocorticoid from Zona Fasiculata alters gene transcription and translation (protein synthesis) to influence glucose metabolism

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56
Q

What does cortisol bind to?

A

Cortisol Binding Globulin

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57
Q

What is the release pattern of cortisol?

A

Cicadian Rhythm, follows ACTH (but stays longer as longer half life) peaks at 6-9am due to stress of getting up. Fluctuates in response to stress stimuli, lowest at night

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58
Q

Functions of cortisol? Glucocorticoid action

A
  1. Glucogneogenesis- permissive to glycogen as stimulates formation of gluconeogenic enzymes in liver
  2. Proteolysis- stimulate breakdown of protein in muscle tissue
  3. Lipolysis- in adipose tissue (free FAs)
  4. Decrease insulin sensitivity of muscle and adipose tissue so brain is primary metaboliser
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59
Q

What happens in the presence of excess cortisol?

A

Excess is diabetogenic= Cushings Disease (adrenal diabetes)- chronic glucocorticoid excess, loss -ve feedback and circadian rhythm.
Cortisol is catabolic= tissue breakdown- weakness skin muscle + bone
Sodium Retension- Hypertension + HF
Insulin Antagonism- Diabetes Mellitus

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60
Q

Insulin treatment of Adrenal Diabetes (Cushings)

A

Doesn’t respond well to insulin as excess cortisol decreases sensitivity of tissues to insulin (require it for uptake)

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61
Q

Functions of cortisol? Non-Glucocorticoid pattern

A
  1. -ve affect on Ca balance= decrease absorption from gut; inc secretion from kidneys; inc bone resorption= osteoporosis
  2. Impair mood/ cognitive function
  3. permissive effects on norepinephrine
  4. Immune suppression- decrease circulation lymphocyte count
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62
Q

What is the difference between Cushings Disease and Syndrome?

A

Corticosteriods EXCESS (cortisol, androgens)
Cuchings Syndrome- First degree (Adrenals) Tumour of the Adrenal Cortex. Chief cause is steroids. Therefore is ACTH Independent.
Cushings Disease- Second Degree (AP- INC ATCH production) ACTH Dependent

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63
Q

Symptoms of Cushings

A

Inc Weight
Depressive/ Low mood
Gonadal Dysfunction- Irregular Periods, Hirutism, Amorrhea, Erectile dysfunction, acne, virilization (occasionally)
Recurent Achilles tendon rupture

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64
Q

Signs of Cushings

A 
Lay down extra adipose especially face and back of neck
Wasting of extremities
Plethoric (red faced), brusing
Muscle atrophy 
Oestoporosis 
Infection prone/ poor healing
Oedema
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65
Q

What is hypersecretion of Cortisol Known as?

A

Cushings, iatrogenic

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66
Q

Test for Cushings

A

CANT use random plasma cortisol (fluctuates during day due to different stress factors)
CANT use imaging to locate over functioning area as can have incidental findings. MRI doesn’t pick up all as small.
1. Overnight dexamethasone suppression and test serum cortisol (should be suppressed- if not= CS)
2. 48h dexamethasone suppression test
3. Can localise lesion by testing plasma ACTH- none-adrenal tumoour- Brain CT
Need a 24hour cortisol urine sample

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67
Q

Treatment of Cushings

A

Disease- Remove pituitary adenoma
If medication- remove
Syndrome- If cancer adrenoectomy + radiotherapy + adrenergic drug replacement

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68
Q

What happens as a result of increased Aldersterone secretion?

A

Stimulates Na retention (water follows) + K depletion= Inc BV and BP

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69
Q

What happens as a result in decreased Aldersterone secretion?

A

Stimulates Na secretion (water follows) + K increased in cells= Dec BV and BP

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70
Q

What is the function of Aldersterone?

A

Aldosterone is a mineralocorticoid (Zona Glomérule) and is essential for Na and K balance in the plasma

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71
Q

What is Addisons Disease?

A

Destruction of the adrenal cortex= glucocorticoid (cortisol) + minercorticoid (aldersterone) deficency
Decrease in secretion of ALL steroid hormones= Primary Adrenal Insufficiency

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72
Q

How can Addisons be differentiated from Anorexia Nervosa?

A

K is decreased in anorexia but inc in addisons

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73
Q

What causes Addisons disease?

A 
Autoimmunity (destruction + other autoimmune eg./ thyroid, T1DM, premature ovarian failure)
Infection eg./ TB, Fungus related HIV
Invasion eg./ Adrenal Mets
Congenital 
Infarction
Iatrogenic- prolonged steroid therapy
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74
Q

What sites commonly metastasise to the adrenals?

A

Lung, Breast + Kidney

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75
Q

What are the symptoms of Addisons Disease?

A

lean, tan, tired, tearful, anorexia, flu-like
depression, psychosis
abdominal pain, vomiting, diarrhoea, salt cravings (aldosterone suppressed)
Pigmented palmar creases + buccal mucosa

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76
Q

What tests would you do to determine a diagnosis of addison’s disease?

A
  1. Na + K levels (dec Na and inc K)
  2. Glucose (decreased)
  3. ACTH
  4. U+Es
  5. Random Cortisol (>700= not Addisons, <700 Adrenal Status Uncertain) SO not definite diagnosis
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77
Q

How do you treat Addisons Disease?

A
  1. Replace steroids- Hydrocortisone (daily)
  2. Give miner corticoids to correct postural hypotension (due to dec Na and inc K= loss of water)- Fludrocortisone
    NOTE: cant abruptly stop steriods
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78
Q

What is Adrenal/ Addisonian Crisis?

A

Vomiting, Low BP, High Pulse

Levels of hormones produced by the adrenal glandgradually dropping dramatically low

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79
Q

What is Hyperaldosteronism?

A

Inc in production of mineralcorticoids (aldosterone)

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80
Q

What is the cause of hyperaldosteronism?

A
  1. Aldosterone- producing adenoma (Conns Syndrome)

2. Bilateral Adrenocortical Hyperplasia/ carcinoma

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81
Q

What are the symptoms of Hyperaldosteronism?

A

Asymptomatic (often)

Hypokalemia, Weakness (quadrapesis in extreme), Cramps, Parathesia, polyuria, polydipsia, Inc BP (sometimes)

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82
Q

What is the treatment of hyperaldosteronism?

A

laparoscopic adrenalectomy

Spirolactone (control BP and hypokalaemia)

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83
Q

What are the tests for hyperaldosteronism?

A

U +E s
Renin
Aldosterone

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84
Q

What is pheochromocytoma?

A

Catecholamine producing tumour (adrenal medulla)

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85
Q

What are the tests for pheochromocytoma?

A

White Cell Count

Plama for free met adrenaline and normetadrenaline

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86
Q

What is the treatment for pheochromocytoma?

A

Surgery

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87
Q

What kind of hormone is growth hormone?

A

Peptide Hormone

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88
Q

What are peptide hormones initial agents?

A

Preprohormone- Prohormone- Active form

eg./ Preproinsulin-Proinsulin- Insulin + C peptidase (used as a marker of insulin levels in the body)

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89
Q

Soluability of peptide hormones?

A

Polar + water soluble (lipophilic) so can travel freely in the blood but need receptors to enter cells

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90
Q

Soluability of Steroid Hormones?

A

Non-polar + non-water soluble (lipophobic) so travel in the blood bound to plasma proteins (constant reservoir) eg./ Albumin but can diffuse through cell membranes easily when unbound

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91
Q

Growth Hormone normal pathway to increase production

A

GHRH/ Somatostatin (hypo)- More GH/ somatotrophin (ap)- liver + other tissues

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92
Q

Growth Hormone normal pathway to decrease production

A

GHIH/ Somatostatin (hypo)- Less GH/ somatostatin (ap)- liver + other tissues

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93
Q

What does GH have a permissive affect on?

A

Thyroid Stimulating Hormone (ap). Needs this permissive action to work. If not= diabetes/ hypothyroidism

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94
Q

What affects does GH have on the body?

A
  1. Inc gluconeogenesis (produce glucose from proteins/AAs)
  2. Reduce ability of insulin to stimulate glucose uptake by muscle and adipose tissue (less stored- more used)
    3.Make adipocytes more sensitive to lipolytic stimuli (inc FFA)
  3. Inc muscle, liver + adipose tissue AA uptake + protein synthesis= anabolic
  4. Stimulate precondrocytes- condrocytes (cells secrete + become responsive to IGF-1- cell division= cartilage + bone growth)
    It is anabolic like glucose but works to break stores down instead of build them up
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95
Q

Is GH more like insulin of cortisol?

A

It’s anabolic so more like insulin (cortisol breaks down protein= catabolic) but works to break stores down instead of build them up

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96
Q

What is IGF-1

A

Growth Hormone with insulin like receptors and hypoglycaemic properties (brings down BG)

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97
Q

Is growth hormone diabetogenic?

A

Yes, increased levels of GH= Inc BG (breaks down stores)- leads to pancreas releasing large amounts of insulin to combat hyperglycemia= T2DM like syndrome

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98
Q

When are the biggest growth periods in relation to GH?

A

Infancy- episodic

Puberty- Androgens + oestrogen spikes in GH secretion + IGF-1. Terminates growth by fusing epithelial plates

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99
Q

What increases GH secretion?

A

Random bursts and well as response to specific stimuli-
- Stress Stimuli (infection, psychological)
- Delta Sleep (deep sleep released for neuronal + bone growth)
measure over a 24hr period
However IGF 1 secretion is relatively constant

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100
Q

When is IGF-11 secreted and what is its purpose?

A

Secreted during foetal development- for foetal growth

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101
Q

What decreases GH secretion? (inc GHIH-somatostatin secretion)

A
  1. Free plasma glucose
  2. FFA
  3. REM (light) sleep
  4. Cortisol (catabolic)- not related to GHIH release but INHIBITS GHRH
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102
Q

What are the Growth Hormones?

A

GH, IGF-1, Thyroid Hormones, Glucocorticoids + Insulin

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103
Q

At what stage of growth is TH most important?

A

At birth- determines ossification, teeth

NOTE: can’t be born with a lack of thyroid (get from mum) but can develop post-natally

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104
Q

At what stage of growth is GH most important?

A

During foetal development (10mnths)

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105
Q

At what stage of growth are Androgens + Oestrogens most important?

A

Puberty, enhance GH release + stop growth by fusing epiphyseal growth plates

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106
Q

What congenital defect occurs is loose maternal thyroid hormone?

A

Cretanism (retardant of growth) as also loose permissive action on IGF-1 + GH

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107
Q

What is Thyroid Hormone permissive to?

A

IGF-1 + GH

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108
Q

What does hypersecretion of GH cause?

A
  1. Gigantism- inc in GH due to pituitary tumour BEFORE epiphyseal plates close
    Acromeagly- inc in GH due to pituitary tumour AFTER epiphyseal plates close
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109
Q

What is acromegaly?

A

Inc in GH secretion after epiphyseal plates has fused due to pituitary tumour so grow outwards/ in extermities

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110
Q

What are the symptoms of acromegaly?

A

Headache, Sweating, curling hair, spade like hands and feet, coarse facial features (thick lips + tongue)

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111
Q

What are the signs of acromegaly?

A

may present with ketoacidosis, excessive sweating

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112
Q

What are the tests for acromegaly?

A

Glucose, Calcium + Phosphate
Serum GH +IGF-1 give OGTT (insulin usually surpassed in high glucose levels but not in acromegaly)
MRI scan pituitary fosssa

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113
Q

What is the treatment of acromegaly?

A
  1. Trans-sphenoidal Surgery
  2. Somatostatin Anologues
  3. GH antagonist
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114
Q

How is hypo(under)secretion of GH caused?

A
  1. GHRH deficency
  2. GH secreting cells abnormal/ unresponsive
  3. Laron Dwarfism- organ not responding to GH
  4. Precicous Puberty (grow plates fuse early)
  5. Mutation eg./ Pygmies impares IGF-1
  6. Hypothyroid- Retain infantile features due to a loss of the permissive action of GH + IGF-1 + TH= dec bone growth, neurological deficit, inc fat storage
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115
Q

What is the function of somatostatin?

A

Peptide hormone (polar + lipophilic) produced by the hypothalmus + pancreatic D cells surpasses insulin and glucagon + inhibits activity of GI tract

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116
Q

What type of hormone is glucagon?

A

Peptide (polar, lipophillic) so travels in plasma easily but needs receptors/ carriers to enter cells

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117
Q

What is the function of glucagon?

A

Acts on liver to increase plasma glucose conc.

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118
Q

What is the action of glucagon?

A

G-protein coupled receptors linked to cAMP phosphorylates specific liver enzymes

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119
Q

What is Glycogenolysis?

A

Glycogen- Glucose (liver)

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120
Q

What is Gluconeogenesis?

A

TAGs- Free FAs + Glycerol(adipose)= Glucose (liver)

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121
Q

What is the secretion of Glucagon?

A

Constant but when BG is less than 5.6mM (4.2-6.3 normal) then it increases

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122
Q

What is the normal range for blood glucose?

A

4.2-6.3 mM

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123
Q

What would increase the production of glucagon?

A
  1. Drop in BG levels
  2. Inc AA levels
  3. Sympathetic Innervation (epinephrine)
  4. Cortisol ( catabolic- permissive to gluconeogensis)
  5. Stress, exercise, infection
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124
Q

What would decrease the production of glucagon?

A
  1. Inc in BG levels
  2. Free FA + ketones
  3. Insulin
  4. Somatostatin (GHIH)
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125
Q

How are ketone bodies made?

A

B-Oxidation in the liver

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126
Q

What is lipogenesis?

A

Excess glucose- fat stores (TAG in liver + adipose tissue) Insulin stimulates this

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127
Q

What is glycogenesis?

A

Excess glucose- glycogen stores

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128
Q

What is the pancreas made up of?

A

99% Exocrine- Enzymes + NaHCO3- alimentary canal

1%- Endocrine hormones produces in Islets of Langerhans

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129
Q

What kind of cells are in the Isley of Langherans and what do they secrete?

A

alpha- Glucagon
beta- insulin
gama- somatostatin (GHIH)
F- pancreatic polypeptide

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130
Q

What kind of hormone is insulin?

A

Peptide hormone (polar + lipophilic)

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131
Q

What is the purpose of insulin?

A

To stimulate glucose uptake into muscle and adipose tissue (lipogenesis) ONLY hormone that lowers BGL

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132
Q

What is the function of the GLUT 4 transporter?

A

Insulin moves GLUT4 transporters from the cytoplasm to cell surface to allow glucose to enter

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133
Q

What is the function of the GLUT 1 transporter?

A

GLUT 1 + GLUT 3 allow basal glucose uptake in other tissues eg./ Brain, Kidney + RBC

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134
Q

What is the function of the GLUT 3 transporter?

A

GLUT 1 + GLUT 3 allow basal glucose uptake in other tissues eg./ Brain, Kidney + RBC

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135
Q

What is the function of the GLUT 2 transporter?

A

B Cells in pancreas and liver- liver takes up glucose as insulin activates hexokinase (dec BG)- favours movement into cells

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136
Q

What is the half life of insulin?

A

5 minutes

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137
Q

How is insulin degraded?

A

Degraded by the liver and kidneys via endocytosis in a destroyed by protease/ recycled

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138
Q

What is Diabetes Mellitus?

A

Loss of control of BG levels (large, sweet urine)

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139
Q

What is T1DM caused by?

A

Autoimmune destruction of pancreatic B(beta) cells due to genetic and environmental influences (destroys ability to produce insulin)

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140
Q

What is important to remember when giving a patient a peptide hormone?

A

Can’t be given orally (so not to be broken down by the GI tract)

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141
Q

What are the signs of T1DM?

A 
Thirst- polydipsia
Toilet- polyuria
Tired
Thinner- weight loss
Infection
Blurred vision
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142
Q

What level of finger prick glucose test indicated diabetes?

A

Finger prick glucose greater than 11mmol/L

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143
Q

What is and what are the signs for Diabeticketoacidosis?

A

Liver can’t recognise glucose, muscle can’t use it so looks for another energy source eg./ ketones- acidosis (pH<7.1)
Nausea/ Vommiting
Abdominal pain
Ketotic breath
Drowsiness- Coma
Rapid, deep, sighing breaths, tachycardia

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144
Q

What is a normal level of blood ketones?

A

less 0.6 mmol/L

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145
Q

What levels put you at a small risk of DKA? How do you correct this?

A

Ketone plasma of 0.6- 1.4

Drink sugar free liquid and correct insulin dose

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146
Q

What can out you at a medium risk of DKA?

A

1.5- 2.9 mmol/L- contact diabetes team

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147
Q

What plasma ketone level is classified as DKA?

A

Greater/ equal to 3 mol/L

URGENT

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148
Q

How do you treat DKA?

A

In small risk levels drink sugar free liquids + correct insulin dose.
In DKA give IV saline, K, insulin + (maybe: antibiotics)

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149
Q

What pH is acidosis?

A

less than pH 7.1= death

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150
Q

What is T2DM caused by?

A

Peripheral tissues become insensitive to insulin (insulin resistance in muscle and fat) + are damaged by lipotoxcitiy and glucotoxcitiy

  1. Abnormal response of insulin receptors
  2. Reduction in insulin receptor numbers
  3. High sugar and animal fat diet
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151
Q

Does obesity cause T2DM?

A

No, in order to have T2DM must have abnormal genes coding for inability to up regulate insulin (needed when a diet gets fattier) therefore a susceptible individual can put on 1 stone or 10 and this could still be an issue

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152
Q

How do you treat T2DM?

A
  1. Diet and exercise
  2. Metformin
  3. Sulfonyurea
  4. Thiazolianedione
  5. DPP-IV inhibitor
  6. SGLT-2 inhibitor
  7. Insulin (prevent hyperglycaemia)
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153
Q

Complications of T1DM

A 
Microvascular
Retinopathy
Neuropathy
Nephropathy
Macrovascular (CV Disease)
Stroke, MI, PVD
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154
Q

Complications of T2DM

A 
Cognitive dysfunction
lethargy
coma
convulsions
permanent brain damage- death
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155
Q

What risk factors contribute to T1DM?

A

HLA, B8+15, DR3+4 (genes)
Environment
Chemicals
Viral Infection (viral molecules on surface of pancreatic B cells)

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156
Q

What risk factors contribute to T2DM?

A

Insulin resistance
Inability to secrete high levels of insulin, pancreas (genes)
High BMI
Weight in abdomen/ momentum (males + post-menopausal women)
Environment (inc food, dec exercise)
Age (>30 if Maori/Asian, >40 if European)
Big birth weight (>4kg)

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157
Q

Complications of poor control in diabetes

A

Large vessel (arteries) + small vessel (arterioles + capillaries) disease- accelerated atherosclerosis

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158
Q

What is the blood glucose levels for hypoglycemia?

A

Low Bg of less than 4mmol/L

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159
Q

What is normalglycaemia?

A

glucose level of 5mmol with low diabetic/ CV risk

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160
Q

What is intermediate hyperglycaemia?

A

Fasting glucose- 6.1-7
OGTT- greater 7.8- 11mmol/L
HbA1c- 42-47 mol/L

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161
Q

What is hyperglycemia?

A

Significantly increased risk of diabetic/ CV complications
Fasting glucose greater than 7
OGTT- greater 11.1 mol/L
HbA1c- greater than 48mmol/L

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162
Q

What is Maturity Onset Diabetes in the Young (MODY)?

A

Autosominal dominat gene defect which leads to impart B cell function comes in 2 forms-

  1. Glucokinase Mutations- child onset, stable hyperglycaemia (don’t put on insulin as levels are stable)
  2. Transcription Factor Mutations- adolescent onset, progressive hyperglycemia, B cells don’t secrete insulin well
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163
Q

What is gestational diabetes?

A

inc in insulin resistance during pregnancy
family history of T2 (risk of getting it later)
neonatal problems

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164
Q

What is diabetes insipidous?

A

Reduced ADH secretion (posterior pituitary) so stops water reabsorption/ Kidneys don’t respond to ADH= pee lots

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165
Q

What is the endocrine system?

A

Secretion of hormones from cells/ tissues in a gland that travel in the blood to target organs DISTAL from site of synthesis

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166
Q

Describe Neural Communication

A

LOCAL- Action within a synaptic cleft

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167
Q

Where do Paracrine hormones act? Give an example of one

A

LOCAL action eg./ Histamine

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168
Q

Where to Autocrine hormones act? Give an example of one

A

SAME cell eg./ Cytokines

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169
Q

Where do Exocrine hormones act? Give an example of one

A

Glands- External environment eg./ Sweat, Saliva + Bile

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170
Q

Do endocrine glands have ducts?

A

No. They are packets of cells with secretary granules which are vascular and ductless

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171
Q

Where do endocrine hormones act?

A

DISTAL to site made, act of cell

  • Membranes
  • Cytoplasm
  • Inside (if lipophilic)
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172
Q

What are neuroendocrine hormones?

A

Mix between endocrine + nervous function

Nerves release hormones- blood- Targets

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173
Q

Is an endocrine response specific?

A

Travels in blood so technically can reach anywhere in the body however is still specific as only target cells have specific receptors

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174
Q

Can a hormone have a different function at different sites?

A

Yes as all target cells will have the same receptor
eg./ Insulin causes inc glucose uptake in skeletal muscle + adipose tissue
Insulin causes inc glycogenesis and dec gluconeogenesis in the liver

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175
Q

What systems is endocrine embedded in?

A

Reproductive, Renal, (GIT + Lung have diffuse endocrine cells)

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176
Q

In what areas is the endocrine system a system in it’s own right?

A

Thyroid gland, Parathyroid Gland, Adrenal gland, Pituitary Gland, Pancreas, Hypothalmus

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177
Q

Describe the simple pathway of endocrine hormones

A

Travel in blood to DISTAL target site

Cell/ Group of cells- excretion into blood- distal targets- bind to receptors- effect

178
Q

What range do endocrine hormones act in?

A

Picamolar range (10⁻9, 10⁻12) M, gives high receptor affinity the smaller (eg./ 12 has a better receptor affinity than 9)

179
Q

How is an endocrine glands production terminated?

A

Via negative feedback from product production

180
Q

What are peptide/protein hormones? Give an example

A

Peptide Hormones are chains of AAs

eg./ TRH (3AAs), FSH (glycoprotein-long), Insulin

181
Q

When are peptide hormones synthesised?

A

Synthesised (before need) and stored

182
Q

How are peptide/ protein hormones synthesised?

A
  1. Preprohormone produced via mRNA + ribosomes (inactive)
  2. Cleaved in rER
  3. Prohoromones (smaller, inactive)
  4. Packaged into vesicles in golgi + proteolytic enzymes)
    = Active hormone + fragments
183
Q

What changes prohormones (inactive) to their active form?

A

Proteolytic Enzymes

184
Q

Are both active peptide hormone + its fragments released into serum?

A

Yes, release via passive cosecretion

185
Q

How is insulin best measured in serum? Why is this better than it’s active form?

A

It is the fragments instead of the active form secreted that is measure (C-peptide instead of insulin) as it is metabolised slower. Additionally gives ability to distinguish synthetic insulin (diabetic injections) from pancreatic production

186
Q

What are steroid hormones? Give an example

A

Steroid hormones are lipids derived from cholesterol
eg./ Gonads- Testosterone, Estrogen, Progesterone
Placenta- hCG, sex steroids
Kidneys- Vit D3
Adrenal Cortex- Corticosteriods

187
Q

When are steroid hormones synthesised? Why is this the case?

A

Synthesised when needed

No storage available as lipophilic (lipid soluble) so can’t be retained

188
Q

How are steroid hormones transported?

A

They are hydrophobic (not water soluble) so transported via binding carrier proteins eg./ Albumin

189
Q

How are steroid hormones taken up by cells?

A

Receptors inside cells (cytoplasm, nuclear receptors) allow steroid hormones to bind to DNA
Activates/ Represses 1st genes= genomic effet
Controls protein synthesis

190
Q

What is the advantage of steroid hormones?

A

Slower response- persists for longer than peptide hormones

Control protein synthesis

191
Q

Explain the mechanism fo signal transduction in peptide hormones

A

Hydrophillic/ Lipophobic peptide Hormones bind to a G-Protein coupled receptor (fast acting) OR Tyrosine- Kinase linked receptor (slow). Phophorylation here changes cellular activity
Enter cell via ion channels/ 2nd messenger system

192
Q

What are amine hormones?

A

Derived from the amino acid tyrosine
eg./ catecholamines, thyroxin and triiodothyronine (t4 +T3)
Have properties common to both peptide and steroid hormones

193
Q

When are amine hormones synthesised?

A

Produced + stored before use (storage mechanism depends on type)

194
Q

What is the solubility of amine hormones?

A

Some polar (eg./ catecholamines so travel in blood + easily excreted) some protein bound (eg./ Thyroid so travel bound to proteins ad take longer to excrete)

195
Q

What is the solubility of peptide/ protein hormones?

A

Polar and water soluble (hydrophilic), can travel freely in the blood

196
Q

What is the solubility of steroid hormones?

A

Generally non-polar and require carried proteins eg./ Albumin to travel in the blood

197
Q

How are lipophilic (steroid + some amine) hormones transported in serum?

A

Ratio of Free Hormones: Hormone Plasma Complex kept in serum by the law of mass action- as steroid hormones is taken up (diffusion) more is released from the carrier

198
Q

How do you calculate Total Plasma Hormone?

A

Free Hormone (small, diffuse going to target tissue) + Hormone Plasma Complex (what’s bound)

199
Q

How is the ratio of Free Hormones: Hormones Plasma Complex (steroid/ amine hormones) determined?

A

It is determined by excretion (kidney) and metabolic transformation (liver) and should remain dynamic (moving but the same ratio) in health

200
Q

What affects kidney excretion in terms of FH: HPC?

A

1/2 life, how easily excreted a substance is
eg./ Catecholamines (amines) + Peptide Hormones are excreted easily and have short plasma half life
BUT Steroid + Thyroid (amines) Hormones take hours/ days to excrete and metabolise as protein bound

201
Q

How is Hormone secretion controlled?

A

Hormones Secretion is controlled via

  1. -ve feedback loop
  2. Neural Feedback Loop
  3. Sensitivity
  4. Permissive Effects
202
Q

How does the -ve feedback loop control hormone secretion?

A

Production of product feeds back onto effector to stop production
eg./ Dec plasma Ca- Production of PTH- blood stream- bone + kidney- Inc serum Ca- feedback to inhibit PTH secretion

203
Q

How does the Neural Feedback Loop control hormone secretion?

A

Trigger- Neuronal cells in adrenal medulla release hormones into BS (eg./ adrenaline)

204
Q

How does sensitivity control hormone secretion?

A

Prolonged exposure to dec hormone plasma= Inc regulation of number of receptors on target tissue (inc sensitivity)

Prolonged exposure to inc hormone plasma= Dec regulation of number of receptors on target tissue (dec sensitivity)
eg./ GH dec no. of insulin receptors (diabetic-like)

205
Q

How does Excessive Growth Hormone give a diabetogenic like syndrome?

A

Inc GH levels= Dec number of insulin recpetors (diabetic-like syndrome)

206
Q

How do Permissive Effects control hormone secretion?

A

presence of 1 hormone enhances the effects of another

207
Q

Give an example relating to TH + a Catecholamine of permissive action

A

Thyroid Hormone- No FA synthesis
Epinephrine- small amount of FA synthesis via lipogenesis
TH + Ep= Large amount of FA release via lipogenesis

208
Q

How are hormone levels best measured?

A

Most hormones are release in short bursts/ certain times so 24hr monitoring is essential

209
Q

In relation to endocrine disease what does HYPERPLASIA result in?

A

Increased number + Increased secretory activity of cells

210
Q

In relation to endocrine disease what does ATROPHY result in?

A

Diminution of cells due to lack of stimulation

211
Q

What causes tissue damage?

A

Inflammation, Infarction, Trauma, Compression, Tumour, Autoimmune Disease

212
Q

What are the 2 types of neoplasm?

A

Adenoma and Carcinoma

213
Q

What is the difference between the 2 subtypes of neoplasm?

A

Adenoma- Functioning/ Non-Functioning benign tumour

Carcinoma- 1yr/ Metastatic tumour

214
Q

How many parathyroid glands are there?

A

4

215
Q

What do parathyroid gland produce? In response to what?

A

Chief cells produce PTH in response to dec ionised Ca

216
Q

What is the action of the parathyroid gland?

A

Regulate plasma Ca2+

217
Q

What causes hyperparathyroidism?

A 
Solitary Adenoma (MEN1)
Hyperplasia of glands
Parathyroid Cancer (rare)
218
Q

What is the common presentation of hyperparathyroidism?

A

Weak, tired, depressed, thirsty, dehydrated but polyuric, RENAL STONES (+ abdominal pain), PANCREATITIS, ULCERS (duodenal/ gastric)

219
Q

Describe the mechanism of PTH secretion

A

ECF Ca2+ change- Calcium Sensing Receptor (CaSR)- Transmit levels to parathyroid chief cells- inc/ dec of PTH sectrion

220
Q

When is PTH levels elevated and what happens as a result?

A

Dec plasma Ca2+= Inc PTH levels- mediates conversion of Vit D to active form

221
Q

When is PTH levels decreased and what happens as a result?

A

Inc plasma Ca2+= Dec PTH levels- Promote reabsorption of Ca from renal tubules + bone

222
Q

How is Vitamin D from the diet converted into its active form?

A

VitD- LIVER- Vit D 25-hydroxylase (inactive)- KIDNEY- 25(OH)VitD1⍺hydroxylase- PTH- 1,25(OH)2VitD (active)

223
Q

Where is vitamin D converted to its active form?

A

In the kidney (inactive precursor comes from liver) where PTH acts on it

224
Q

What is an autoimmune disease?

A

Clinical disorders characterised by tissue/ organ damaged mediated through abhorrent immunological mechanisms mediated against autoantigens

225
Q

What factors affect an individuals susceptibility to an autoimmune disease?

A 
Initialing Event eg./ Infection
Genetic Susceptibility 
Environmental Factors
Hormonal Factors
Immune Regulatory Factors
226
Q

How is an autoimmune reaction precipitated?

A

Autoreactivity

  • Antibody medicated
  • Cellular Mediated
  • Complement Mediated
  • Phagocytes, Cytokines, Natural Killer Cells
227
Q

What is the difference between a humoral and cellular reaction?

A

Humoral- B Cells

Cellular- T Cells

228
Q

What are autoimmune polyendocrine syndromes?

A

Defined autoimmune clusters affecting 2 or more organs

229
Q

What HLA Hapatotypes are involved in polyendocrine autoimmune disease?

A

HLA- B8, DR3

Disease results in inappropriate expression of Class 2 HLA molecules on epithelial cells and circulating antibodies

230
Q

What are the 3 types of polendocrine autoimmune disease and what are they defined by?

A

T1- Adrenal + Parathyroid (chronic candida infections of mucus membranes/ nails)
T2- Adrenal +Thyroid (+ T1DM)
T3- Thyroid + T1DM + Gastric (atrophic gastritis)/ Non- Endocrine (SLA)

231
Q

What is Diabetes Insipidus?

A

Cause by problems with inappropriate ADH secretion/ its receptor. 4 types

232
Q

How do you test for diabetes insidious?

A

Urinalysis +fluid depravation tests

233
Q

What are the 4 types of diabetes insipidus

A

1) central diabetes insipidus
2) nephrogenic diabetes insipidus
3) dipsogenic diabetes insipidus
4) gestational diabetes insipidus.

234
Q

What is the difference/ similarities between diabetes mellitus and diabetes insipidus?

A

DI- kidney problem
DM- Pancreatic Problem
People with diabetes insipidus have normal blood glucose levels; however, their kidneys cannot balance fluid in the body.
Both have symptoms of polyuria and polydipsia

235
Q

What is HYPORESPOSIVENESS in the endocrine system?

A

Reduced responsiveness in a target cell

236
Q

What is HYPERRESPONSIVENESS in the endocrine system?

A

Increased response to target cell (permissive effects)

eg./ TH, Adrenaline, Mediated Lipolysis

237
Q

Where is the pituitary gland located?

A

Sella Tunica

238
Q

How many cell types are found in the AP?

A

3

239
Q

How is the AP connected to the hypothalmus?

A

Portal System

240
Q

What is another name for the AP + what does it secrete?

A

Adenohypophysis- true endocrine tissue

241
Q

What is bigger AP or PP?

A

AP (makes up 2/3rds of the gland)

242
Q

What is another name for the PP + what does it secrete?

A

Neurohypophysis- secretes neurohormones

243
Q

What is the difference in cellular origin between the AP and PP?

A

AP- Epithelial Origin

PP- Neural Tissue Origin

244
Q

What factors affect the activity of the hypothalmus?

A 
Cold
Stress
Hydration
Metabolism
Exercise 
Time
Sleep
Pregnancy/ Breast-Feeding
Puberty/ Menstrual Cycle
245
Q

Where is the hypothalmus and what is its function?

A

Located at the base of the brain below the thalmus

Is an integrating centre of endocrine systems

246
Q

What connects the hypothalamus to the pituitary?

A

Infindibulum (stalk)

247
Q

How do neurosecretory hormones travel from the hypothalamus to the anterior pituitary?

A

Release from Median Eminence (nerve cell terminal)

Travel via Hypothalmal Hypophyseal Portal System to AP

248
Q

What does the Anterior Pituitary Secrete?

A

Releasing/ Inhibiting trophic hormones that stimulate/ inhibit hormone production at distal sites

249
Q

What are trophic hormones?

A

Neurohormones released from the Anterior Pituitary released into capillaries that govern release of other hormones from distal sites

250
Q

How do neurosecretory hormones travel from the Hypothalamus to the Posterior Pituitary?

A

Travel via axons of hypothalamic neurones to PP- Released into blood

251
Q

What is the difference in travel mechanisms of neurohormones from the Hypothalamus to the Anterior Pituitary and Posterior Pituitary?

A

Neurohormones travel via the hypothalamic hypophyseal portal system to the anterior pituitary where trophic stimulating/ inhibiting hormones are released in respsonse
Neurohormones travel via the axons of the hypothyroid into the PP causing a release in to blood stream

252
Q

What hormones are produced by the posterior pituitary?

A

Vasopressin (ADH) + Oxytocin (mature hormones)

253
Q

What neurones in the Posterior Pituitary synthesise its hormones?

A

Magnocellular Neurones synthesise Vasopressin (ADH) + Oxytocin

254
Q

What is the function of Vasopressin (ADH)? Give its triggers and actions

A

Regulates water balance
TRIGGERED- Inc plasma osmolarity/ Dec in plasma volume (BP)
ACTION- Kidney Collecting Ducts= Inc water reabsorption
Vascular Smooth Muscle- Constrict to INc BP

255
Q

What BV does parasympathetic innervation act on?

A

Parasympathetic Innervation does not cause dilation thought the body as most blood cells in the body don’t have parasympathetic innervation aside from salivary glands, gastrointestinal glands, and genital erectile tissue where vasodilation occurs

256
Q

What is the function of oxytocin? Give its triggers and action

A

Milk ejection + Uterine Contraction
TRIGGERS- Labour (babies head at cervix); Suckling
ACTION- Contract smooth muscle, eject milk, childbirth

257
Q

Where are the ‘mature hormones’ in the body synthesised?

A

Posterior Pituitary- Vasopressin/ ADH (water balance) + Oxytocin (milk ejection + uterine contraction)

258
Q

What hormones does the Hypothalmus produce that act on the Anterior Pituitary?

A 
PRH
Dopamine
TRH
CRH
GHRH + GHIH
GnRH
259
Q

What hormones are produced from the Anterior Pituitary? ( in response to hypothalamic discharge)

A 
FLAGTOP
F: Follicle Stimulating Hormone
L: Luteinizing Hormone
A: ACTH
G: Growth Hormone
T: Thyroid Stimulating Hormone
O: MSH - melanOcyte stimulating hormone
P: Prolactin
260
Q

What hormones from the hypothalmus cause release of prolactin?

A

PRH, Dopamine, TRH

261
Q

What is the function of prolactin? Where does it act?

A 
Prolactin is produced from the Anterior Pituitary in response to PRH, TRH and Dopamine.
It DIRECTLY (not trophic) acts on breast tissue to induce lactation
262
Q

What hormones from the hypothalamus cause release of thyroid hormones (T4+T3)

A

TRH (hypothalamus)- TSH (ap- thyrotropin)- Thyroxine + Triiodothyrodine (thyroid)

263
Q

What hormones from the hypothalamus cause release of Cortisol?

A

CRH(hypothalamus)- Adrenocorticotrophic Hormone (ap)- Cortisol Release (liver)

264
Q

What causes release of Growth Hormones?

A

GHRH/ GHIH(hypothalmus)- GH/Not (ap)- Liver

265
Q

How is feedback used to control anterior pituitary release?

A

Stimuli- Hypothalamus- AP release- Trophic Hormone (blood stream) SHORT LOOP FEEDBACK- Endocrine Gland- Response LONG LOOP FEEDBACK

266
Q

What is a primary endocrine disorder?

A

A defect in the cell that secretes the hormone (ie. in the endocrine gland)

267
Q

What is a secondary endocrine disorder?

A

A defect in the pituitary resulting in too little/ too much trophic hormones being produced

268
Q

What is a tertiary endocrine disorder?

A

A defect in the hypothalmus

269
Q

What is a pituitary adenoma?

A

Cancer of the pituitary gland (secondary endocrine disorder) if functioning will produce excess hormone
= Prolactinoma- galatorhhea, menstral issues
GH Secreting- acromegaly, gigantism
ACTH Secreting- Cushings Disease

270
Q

What hormones Increase Blood Glucose levels?

A 
STENGG
Somatotropin (growth hormone)
Thyroid hormones (thyroxine and triiodothyronine)
Epinephrine
Norepinephrine
Glucagon
Glucocorticosteroids (cortisol)
Immunoglobulins
271
Q

What is Adrenal Failure?

A 
Unexplained hypoglycaemia (Dec Cortisol= Dec glucocorticoids)
There is a disproportion between severity of illness, circulatory collapse, hypotension + dehydration
\+ other endocrine features eg./ Hypothyroidism, body hair loss, amenorrhoea
272
Q

What affect does adrenal enzyme defect of 21-hydroxylase deficiency result in for babies, girls + boys?

A

Congenital Adrenal Hyperplasia
Babies- neonatal salt losing crisis
Boys- pseudo-precoscoius puberty
Girls- Ambiguous Genitalia, Hirsutism

273
Q

What is the synacthen test?

A

Used to confirm an Addions Diagnosis
Bloods- ACTH + Cortisol
+ Give tetracosactrin (IM/IV)
More blood for cortisol (rule out 21-HD)

274
Q

What do the results of the Syncthen Test show?

A

If-

  1. Impaired cortisol but ATCH normal= Primary Adrenal Failure
  2. Impaired ACTH= secondary adrenal failure
275
Q

What are the causes of hypo secretion of the adrenals?

A

Addisons Disease
Adrenal Enzyme Defect of 21-hydroxylase enzyme
Adrenal Failure
Acute meningococcal septicaemia

276
Q

How do you treat hypo function of the adrenal glands

A
  1. Glucocorticoid Replacement eg./ Hydrocortisone (2/3 doses per day)
  2. Mineralocorticoid Replacement eg./ Flucortisone (steroid) to correct postural hypotension
277
Q

What percussion has to be taken when prescribing high dose steroids over a prolonged period of time in Adrenal Hypofunction?

A

CANNOT STOP ABRUPTLY
Double hydrocortisone in illness/ distress
Add 5/10mg if intense exercise
Give IM injector incase vomitting/ diarrhoea stops oral injestion

278
Q

What hormones cause hypertension?

A 
Cortisol
Aldosterone
Thyroxine
Prolactin
Parathyroid
279
Q

What are the causes of Cushings Disease + Syndrome?

A

C. Syndrome- Primary, ACTH Independent- Adrenal Tumour eg./ Adenoma/ Carcinoma; Corticosteriod Therapy eg./ for asthma or IBS

C. Disease- Secondary, ACTH Dependent- Pituitary Tumour (most common); Ectopic ACTH Secretion eg./ lung carcinoma

280
Q

What is Primary Hyperaldosteronism?

A

Excess production of aldosterone (independent of the RAAS) causing an increase in Na and Water retension

281
Q

What are the symptoms of primary hyperaldosteronism?

A

Hypertension
Hypokalemia/ Alkalosis (if not on diuretics)
Sodium (mildly raised/ normal)
Weakness (quadriparxsis), Cramps, Paraesthiae, polyuria, polydipsia

282
Q

What causes Primary Hyperaldosteronism?

A
  1. Conns Syndrome (solitary aldosterone-producing adenoma)

2. Bilateral Adrenocortical Hyperplasia

283
Q

How can you test for Primary Hyperaldosteronsim?

A

Plasma Aldosterone: Renin (PA:PRA) should have a repressed renin and inc aldosterone
If >20 Primary Hyperaldosteronsim
If <20 Secondary/ Essential Hypertension
24hr urine aldosterone + urinary sodium (over 4 days of salt loading)
2. CT/ MRI of adrenals
3. Adrenal Venous Sampling (if CT inconclusive)- if adenoma the one side will have increased aldosterone secretion as compared with the other

284
Q

What is the most common cause of Increased Blood Pressure + Decreased Plasma K?

A

Renal Artery Stenosis is the most common cause (Hyperaldosteronism eg./ Conns Syndrome must also be considered)

285
Q

What is a Pheochromocytoma?

A

Rare catecholamine (adrenal medulla eg./ noradrenaline) producing tumour arising from sympathetic paraganglia cells in the adrenal medulla

286
Q

What causes Pheochromocytoma?

A 
Persistent Hypertension (stress= Inc in catecholamines)
Tumours- Inherited eg./ MEN2
287
Q

What is the classic triad of symptoms for Pheochromocytoma?

A

Episodic Headache, Sweating + Tachycardia
(suspect if BP hard to control/ episodic)
Symptoms may be precipitated by stress, exercise or abdominal pressure

288
Q

How do you treat Pheochromocytoma?

A

Catecholamine Tumour

Surgery (NOTE use ⍺blockers instead of βBlockers unless Heart disease or tachycardia)

289
Q

What extra care has to be taken in pregnancy with regards to thyroid function?

A

Thyroid function must be kept in high/ normal range to avoid cretinism

290
Q

How would you treat hypothyroidism?

A

Levothyroxine (T4) (don’t add Liothyroxine- T3 as harder to get and no benefit of combined therapy)
50mcg/day- 100mcg/day increasing dose until
Primary- TSH Normal
Secondary T4 in normal range

291
Q

What groups must you be cautious in when prescribing hypothyroid treatment?

A

Levothyroxine (T4)

  1. Pregnancy
  2. Ischaemic HD (25mcg/day)
  3. Post Partum Thyroditis- Withdraw
  4. Myxodema Coma- RARE, EMERGENCY IV T3 (liothyroxine)
292
Q

What clinical emergency can result from extreme hypothyroidism?

A

Myxodema Coma- rare, emergency, give IV T3 (liothyroxine)

293
Q

What is subclinical hypothyroidism? What are the indications of treatments?

A 
Mildly High TSH but normal T4
Treat if
1. TSH >10
2. TSH >5 + +ve autoantibodies
3. TSH Inc + Symtoms
294
Q

What can over-treatment of hypothyroidism cause?

A

Levothyroxine (T4) over treatment can cause osteoporosis + Atrial Fibrillation

295
Q

What treatment would you give for hyperthyroidism (thyrotoxicosis)?

A
  1. Anti-Thyroid Drugs via titration eg./ Carbimizole OR Block- Replace eg./ Carbimizole + Thyroxine simultaneously (stop Iatrogenic Hypothyroidism)
  2. Radioiodine- High Dose Alblative (hypo common, cant use in pregnancy)
  3. Steroids eg./ B Blockers for symtoms
  4. Surgery- Thyroidectomy
296
Q

What nerve do you have to watch out for during a thyroidectomy?

A

Recurrent laryngeal nerve

297
Q

What is subclinical Hyperthyroidism?

A

TSH Supressed but normal T3+T4, same treatment

298
Q

What can cause a Goitre?

A 
Autoimmune- Graves + Hashimotos
Thyroditis- de Quervanans, Reidels 
Physiological- Puberty, Pregnancy
Iodine Deficency
Dyshormogenesis
299
Q

What types of Goitre do you get?

A

Mulitnodular
Diffuse
Cystic

300
Q 
A Pt presents with-
dry and flaking skin
Puffy eyes + lips
Brittle hair
And a swelling neck
What is your clinical diagnosis and what tests would you run to determine this?
A

Hypothyroidism- Autoimmune (goitre) so Hashimotos/ Atrophic

Test- TSH + T4 + Thyroid Autoantibodies

301
Q 
A Pt presents with-
Weight Loss
Staring Appearance
Thin Hair
Lid Lag
Excessive Sweating
What is your clinical diagnosis and what tests would you run to confirm this?
A

Hyperthyroidism

Test- TSH + T4 + Thyroid Autoantibodies (rule in/out Graves Disease)

302
Q 
A Pt presents with-
Increased Weight
Mood Change
Mooned Face + Buffalo Neck Lump
Bruising
What is your clinical diagnosis and what tests would you run to confirm this?
A

Cushings
Test- 24 urinary free cortisol, overnight dexamethasone suppression
MRI (some)

NOTE:Inc Weight + Mood change could also be hypothyroidism

303
Q 
A Pt presents with-
Weight Loss
Tan
Tired
Emotional
Spouts of dizziness
What is your clinical diagnosis and what tests would you do to confirm this?
A

Addisons Disease

Tests- Na, K, glucose, uremia + synacthen test (ACTH + Cortisol)

304
Q

What investigations would you carry out fr a presenting complaint of a solitary thyroid nodule/ multinodular goitre with a dominant nodule?

A

TFTs
Isotope Scanning- ‘Hot Nodule’ if low TSH
US- Differentiate between benign and malignant
FNA
Chest + Thoracic inlet x-ray- if large retrosternal extensions

305
Q

What is the most common type of cancer of the thyroid?

A

Papillary Cancer

306
Q

How is papillary cancer of the thyroid identified and what can cause it?

A

Cause- BRAF Mutation, Ionizing Radiation Exposure
Idenitfiable- psomma bodies (histology), multifocal + local lympth spread.
Good Prognosis

307
Q

Describe Follicular cancer of the thyroid gland?

A

A single lesion associated with lung + bone mets

Good prognosis if resectable

308
Q

Describe Anaplastic Adenoma of the thyroid

A 
Agressive, locally invasive
Poor prognosis (as doesn't respond to RI)
NOTE: Can give external RI
309
Q

What cancer of the thyroid gland has an autoimmune association? How is it treated?

A

Hashimotos- Lymphoma (rare)

External RT and CT

310
Q

Where does medullary cancer of the thyroid come from? What serum marker if found? How is it treated?

A

Parafollicular C cells (MEN2A/B association)
Inc Calcitonin
Treat- total thyroidectomy (no RI)

311
Q

What cancers are found in the thyroid?

A 
Papillary (most common)
Follicular (lung/ bone)
Medullary (C cells)
Anaplastic
Lymphoma (hashimotos)
312
Q

How would you treat a papillary/ follicular cancer of the thyroid?

A

Total Thyroidectomy
High dose RI
Long term suppression of thyroxine
Thyroglobulin (follow up)

313
Q

What is Graves Disease?

A

Autoimmune (humoral) Hyperthyrodism
Peak 20-40 years
Hyperplasia + Hyperfunction of the gland causes enlargement= Goitre
Thyroid Eye Disease common (opthalmopathy)

314
Q

Describe the autoimmune presentation of Graves Disease

A 
Autoantibodies bind to TSH receptor- SITUMLATORY (Inc Cell activity + number)= Inc TSH= Inc Metabolic Rate in the thyroid and eyes (ocular fibroblasts have TSH receptor)
Is Humoral (some T cell involvement also)
315
Q

What is Hasimotos Thyroditis

A 
Autoimmune Hypothyroditis (destruction of thyroid epithelial cells)
Peak 45-60 years
316
Q

Describe the autoimmune presentation of Hashimotos Thyroditis

A

Humoral (goitre) + Cellular (tissue destruction, hyperfunction)
Invasion- cytokine production- cytokine + antibody mediated destruction- circulating autoantibodies to thyroglobulin + thyroid peroxidase (stops T4 + T3 production)
NOTE: Initial enlargement of gland due to over-compensation (hurtle cell change) but destructive process leads to failure of gland

317
Q

Histologically, what does Hashimotos Thyroditis look like under the microscope?

A

Intense infiltrate of plasma cells + hurtle cell change (follicular cells trying to put out TH to keep body in balance)

318
Q

How does a mulitnodular goitre form?

A

Iodine Deficenecy/ Goitrens- Impared synthesis of T3 + T4- Inc TSH levels- Hypertrphy + Hyperplasia

319
Q

What is a toxic nodular goitre?

A

Area no longer responding to TSH stimulation

320
Q

Describe the epitope pathway in thyroid autoimmune disease

A 
TSH- Metabolic Epitopes
Stimulating Ab- Graves, Hashimotos, goitre
Blocking Ab- Myxoedema (Hypothyroidism)
TSH- Growth Epitopes
Stimulating Ab- Graves
Blocking Ab- Myxodema
321
Q

What is Hyperprolactinaemia?

A

Caused by pituitary hyperfunction (prolactin) due to

  1. Physiological- pregnancy, lactation + stress
  2. Pathological- Prolactinoma, Stalk Compression
  3. Pharma- Dopamine Antagonists/ depleting agents, oestrogen, antidepressants
322
Q

What diseases can pituitary hyperfunction cause?

A

Acromegaly/ Gigantism (depending on growth plate fusion/ age)
Cushings
Hyperprolactinaemia
Micro/Macroprolactinomas

323
Q

What are Microprolactinmas?

A

Related to pituitary hyperfunction, <10mm lesion
Galatorrhea, Amenorrhea, infertility
Give Dopamine Agonist

324
Q

What are Macroprolactinomas

A

Related to pituitary hyperfunction >10mm lesion
lose visual acuity + Visual Fields, diplopia
Give dopamine agonist

325
Q

What can cause pituitary hypofunction?

A

Cranial Diabetes Insipidus
Tumour Compression eg./ carinopharyngioma
Trauma
Infection eg./ TB, Sarcoid, Sheehans Syndrome

326
Q

What is Cranial Diabetes Insipidus?

A

Hypofunction of the pituitary causes decreased ADH (no water regulation, inc urine passing)
Test via water deprivation test
Clinically- Weight gain, Depression, Dec libido, menstral problems, decreased growth (kids)

327
Q

What is the common presentation of a growing pituitary lesion?

A 
Bitemporal Hemianopia (stopping fibres crossing over)
Push on internal carotids- falls, fits, faints, strokes
CN presentation- Occulomotor, trochlear, opthalmic, abducent, maxillary
328
Q

How do you treat hypersecretion of the pituitary gland?

A

Gigantism/ Acromeagly, Cushings, Hyperprolactnaemia, Macro/Microprolactinoma
Dopamine Agonists- Prolactinoma
Somatostatin+ GH Receptor Analogues- Acromegaly

329
Q

How do you treat hyposecretion of the pituitary lgland?

A

Cranial Diabetes Insipidus, tumour, trauma + infection

Cortisol, T4, Sex Steroids, GH, Desmopressin (replace AP function)

330
Q

How would you treat a tumour of the pituitary gland?

A

Transphenoid Surgery

Radiotherapy (slow acting + destroying, can cause hypopituitarism)

331
Q

What are the 5 roles Calciums has in the body?

A
  1. Signalling- Ca ions used for exocytosis of synaptic vesicles eg./ insulin release; neurotransmitters; hormones; contraction of muscle fibres; alter enzyme function.
  2. Blood Clotting- Component of clotting cascade
  3. Apoptosis (programmed cell death)
  4. Skeletal Strength (calcium wrapped in bone)
  5. Membrane Excitability (Ca decreases Na permeability)
332
Q

How do changes in body calcium levels affect membrane excitability?

A

Hypocalcaemia- Inc neuronal Na permeability- hyperexcitation of neurones= tetany + asphyxiation (if spreads to larynx ad respiratory muscles)

Hypercalcaemia- Dec neuronal Na permeability- reducing excitability + depressing neuromuscular activity (cardiac arrhythmia)

333
Q

What can high levels of calcium in the body cause?

A

Hypercalcaemia- Dec neuronal Na permeability- reducing excitability + depressing neuromuscular activity
=cardiac arrhythmia

334
Q

What can kow levels of calcium in the body cause?

A

Hypocalcaemia- Inc neuronal Na permeability- hyperexcitation of neurones
= tetany + asphyxiation (if spreads to larynx ad respiratory muscles)

335
Q

What is calcium stored as in bone?

A

Hydroxyapatate

336
Q

How is calcium compartmentalised in the body?

A

99% bone (as hydroxyapatite- storage)

  1. 9% Intracellular (mitochondria + SR)
  2. 1% Extracellular (1/2 bound to albumin and globulin, 1/2 free and physiologically active)
337
Q

How is calcium found in the blood?

A

0.1% to TBC is in the plasma
40% is bound to proteins eg./ albumin(more) + globulin (high affinity due to +ve/-ve interactions)
50% free + physiologically active
10% in complex anions (sulphate, lactate, cal.carb etc)

338
Q

What happens to pH + Ca binding during hyperventilation?

A

long + deep= loose C02
Dec CO2= Dec H+= Alkalosis
Alkalosis encourages H+ bound to protein to dissociate freeing up binding sites for Ca
=Inc binding capacity of plasma proteins for Ca= HYPOcalcemia

339
Q

What happens to pH + Ca binding during hypoventilation?

A

Short + shallow= retain CO2
Inc CO2= Inc H+= Acidosis
Acidosis displaces some of Ca bound to protein
=Dec binding capacity of plasma proteins for Ca so more free in plasma= HYPERcalcemia

340
Q

How does pH relate to plasma Ca+ conc.?

A

Increase in pH (alkalosis)= Hypocalcemia

Decrease in pH (acidosis)= Hypercalcemia

341
Q

What is the role of osteoblasts?

A

Blasts are Bone Building- highly active and lay down a collagen extracellular matrix- calcified

342
Q

What are osteocytes and what is their role?

A

Differentiated osteoblasts (bone building)- are in established bone, less active and regulate osteoblast + osteoclast activity

343
Q

What is the role of osteoclasts?

A

Osteoclasts mobilise bone + secrete H+ (decrease pH= dissolves Calcium salts and produce proteyltic enzymes to digest ECM)

344
Q

What role do osteoclasts have in Ca regulation?

A

Osteoclasts secrete H+, when reaches pH4 calcium salts are dissolved- releasing free Ca+ into the plasma

345
Q

What role does PTH have in calcium homeostasis?

A

Inc plasma Ca via-

  1. Stimulates osteoclasts= Inc release of Ca from bone
  2. Inhibits osteoblasts (bone building)= reduced Ca going into bone
  3. Inc renal excretion of phosphate- stops Ca being deposited into bone
  4. Stimulates kidney to produce calcitriol (vitD)- promote Ca absorption at gut + kidney
346
Q

What is the function of PTH are where does it come from?

A

Released from the parathyroid gland (4 glands posterior to thyroid, although can have different distribution in some people)
Essential for life and regulates free plasma Ca

347
Q

What is the function of Calcitriol in calcium homeostasis?

A

Increase Plasma Ca via- Actively transporting Ca from intestinal lumen to the blood
Dec plasma Ca- Inc PTH- Inc calcitriol- Inc Ca (intestine)
Inc plasma Ca- Inhibit PTH- Inc osteoblast deposition + Ca in faeces

348
Q

What is calcitriol and where do we get it from?

A

Active form of Vitamins D3 (activated from liver- kidney via PTH)
Get inactive form (in liver) from diet, endogenous precursors, prolactin (lactating women)

349
Q

What do Calcitriol levels depend on?

A

Amount Ingested (diet)
Vit D Deficient- low levels so less Ca absorbed
Pregnancy/ Lactation/ Growth- high levels

350
Q

What is calcitonins role in calcium homeostasis?

A 
Decrease plasma Ca
produced by parafollicular cells (thyroid)
Binds to osteoclasts (stops action)
Inc renal excretion
NOTE: overridden by PTH
351
Q

What is cortisol role in calcium homeostasis?

A 
Dec Plasma Ca
Glucocorticoid (ZF of adrenal cortex, maintain plasma Glucose)
Inhibits osteoblasts
Inc renal excretion
Dec intestinal reabsorption
In high levels can cause osteoporosis
352
Q

What is insulins role in calcium homeostasis?

A

Inc Plasma Ca
Dec bone formation
Antagonises cortisol
NOTE: Diabetics may have significant bone loss due to this action

353
Q

What is oestrogen’s role in calcium homeostasis?

A

Dec plasma Ca

Promotes bones formation (osteoblasts)

354
Q

What is a common bone condition associated with post-menopausal women?

A

Osteoporosis is a common condition post-menopausal due to decreased oestrogen production (oestrogen usually works to decrease plasma Ca levels)

355
Q

What is GH role in calcium homeostasis?

A

Dec plasma Ca

Stimulates bone formation (constant)

356
Q

What is prolactins role in calcium homeostasis?

A

Inc Plasma Ca

Promotes Ca absorption from the gut by stimulating synthesis of calcitriol

357
Q

What hormones promote increase in plasma calcium levels?

A

PTH
Calcitriol
Prolactin
Insulin

358
Q

What hormones promote uptake/ excretion of Ca (less in plasma)

A

GH
Estrogen
Cortisol
Calcitonin

359
Q

What are common reasons for someone to become Vit D deficient?

A 
Age
Sunlight
Decreased gut absorption
Darker Skin
Lots of clothing
Kidney Issues (stop Vit D activation)
Bad Diet- not enough oily fish, eggs, milk, cereals etc
360
Q

What are the main dietary sources of calcium?

A

Diary, Green leafy veggies, soya, bread, fish bones (sardines)

361
Q

What is the normal rage of serum calcium?

A

2.2-2.6 mmol/L

362
Q

How is levels of free plasma calcium calculated from a blood sample?

A

Increase in Albumin= Dec in free Ca

Adjust Ca by 0.1 mmol/L for each 5g/L reduction in Albumin after 40g/L

363
Q

What is the definition of HYPOcalcemia

A

Serum calcium <2.20 mmol/L

364
Q

What are the 3 most common causes of hypocalcemia?

A
  1. Low PTH- hypoparathyroidism
  2. High PTH- secondary hyperparathyroidism (in response to hypocalcemia)
  3. Drugs eg./ calcitonin, fluoride, phenytonin
365
Q

What is the common clinical presentation of hypocalcemia?

A

Spasms (Trousseaus sign)
Perioral Parathesia
Anxious, Irritable
Seizures
Muscle Tone (inc SM)= colic, wheeze, dysphagia
Orientation Impared/ Confusion
Dermatitis
Impetigo Herpetiforms (pustles in pregnancy, rare + serious)
Chvosteks Signs (cover of mouth twitches whne facial nerve is tapped at parotid)
Choreoathetosis, Cataract
Cardiomyopathy (long QT interval= arrhythmia, HF, oedema)

366
Q

What is Chvosteks sign?

A

See in hypocalcemia- cover of mouth twitches whne facial nerve is tapped at parotid

367
Q

What is Trousseaus sign?

A

Carpopedeal spasms- BP cuff when inflated causes the wrist and fingers to flex, clenching together (when chronic becomes a Parkinsonium like syndrome)

368
Q

A patient presents with-
Spasms
Seizures
Confusion
Rash
And is positive for both Chvostek + Trousseaus sign
What is your likely diagnosis and how would you confirm this?

A

Hypocalcemia
Check serum calcium (normal 2.20-2.60mmol/L) + adjust for albumin (remove 0.1 for every 5g change from 40)
Check PTH (can also check PO4 in urine as PTH reduces its absorption)
If PTH
HIGH- (appropriate)
check urea (normal- check via D- low= deficiency, high= pseudohypoparathyrodism/ calcium deficiency)
+ creatinine (high= renal failure)
LOW/ NORMAL (inappropriate)
Check Mg (Low= Mg Deficiency, Normal= hypoparathyroidism/ calcium sensing receptor defect)

369
Q

What is pseudohypoparathyrodism?

A

Childhood presenting disorder where a target organ (eg./ kidney or bone is unresponsive to PTH)
= hypocalcemia, hypophosphatemia + Inc in PTH

370
Q

What is pseudo-pseudohypoparathyrodism?

A

Albrights hereditary osteodystrophy= obesity, short stature.

Tend not to have calcium/ PTH abnormailities

371
Q

What are the 3 valued stages of hypercalcemia?

A

<3.0mmol/L- Asymptomatic (no need for urgent correction)
3.0-3.5mmol/L- May be well tolerated (if symptomatic then treat)
>3.5mmol/L- Urgent correction (dysarrythmia + coma risk)

372
Q

How do you treat hypocalcemia?

A
  1. Mild (asymptomatic >1.9mmol/L) give oral Ca (repeat after 24hrs if post thryrodectomy), Vit D (if deficient), if low mg (stop drugs + replace)
  2. Severe (Symptomatic/ <1.9mmol/L) Medical Emergency- IV calcium gluconate bolus + ECG monitoring
373
Q

What are the causes of hypercalcaemia?

A
  1. Malignancy eg./ bone mets, myeloma, Pthr Cancer
  2. Primary Hyperparathyrodism
  3. Inherited eg./ multiple endocrine neoplasm
  4. Medication eg./ Thiazide type diuretics, lithium excess, vit A
  5. Renal failure, vit D intoxication
  6. Wegners, Sarcodosis, Acromeagly
374
Q

What are the clinical manifestations of hypercalceamia?

A

BONES- muscle weakness, bone pain, osetoporosis, ectopic calcification
STONES- polyuria, polydipsia, pancreatitis, renal stones/ failure
GROANS- abdominal pain, vomiting, constipation
Psychic MOANS- anorexia, depression, confusion
+ Hypertension, shortened QT interval, bradycardia

375
Q 
A Pt presents with-
Muscle weakness
Polyuria
Polydipsia
Abdomina Pain and vomiting
Confusion
And on investigation-
Hypertension
bradycardia
shortened QT Interval
What is your likely clinical diagnosis and what investigations would you like to carry out?
A
  1. Plasma Calcium + Albumin levels (>2.60, remember to exclude albumin)
  2. Plasma PTH
    LOW (appropriate)- malignancy possible so check albumin (d), ph (alkalosis), PO4 (I) + K (d)
    HIGH/ Normal (inappropriate)- primary hyperparathyroidism ,tertiary hyperparathyrodism (renal failure), hypocalciuric hypercalcaemia (familial) 3.check 24 calcium urine if HH suspected
  3. Abdominal Imagine- calculi
  4. Isotope bone scan (mets)
  5. Alkaline Phosphate- look for increased bone turnover in mets, sarcoidosis, thyrotoxicosis + lithium poisoning
376
Q

How would you treat hypercalcaemia?

A

Medically- IV fluids + biphosphates/ calcitonin. Cinacalet (mimics effect of Ca on Ca sensing receptors)
Surgical indications- symtoms, serum calcium 0.25 above upper limit (2.85mmol/L), Osteoporosis, eGFR<60/ kidney stones, <50 y/o

377
Q

What waist circumference in men and women is linked to comorbities?

A

Men >102cm

Women > 88cm

378
Q

What are dietary allowances?

A

Quaintitive guidelines for essential macro + micro nutrients to prevents nutritional deficiencies

379
Q

What are dietary goals?

A

Quantitive national targets for selected macro and micro nutrients to prevent long term disease (national level not individual)

380
Q

What are dietary guidelines?

A

Broad targets aimed at an individual to promote nutritional wellbeing (macro+micro) can be quantitive/ qualitative

381
Q

What are dietary reference values?

A

estimates amount of energy + nutrients needed by different HEALTHY groups in society

382
Q

What is the target for glycaemic control in T1DM?

A

48mmol/L (6.5%)

383
Q

What does stress do to BGL?

A

Increases BGL via adrenaline + noradrenaline (acute) and cortisol (chronic)

384
Q

Why is behaviour defined as idiosyncratic?

A

People do different things for different reasons

385
Q

What type of obesity- apple or pear distribution- is associated with worse cardiovascular risk?

A

Apple distribution

386
Q

What are the common effects of obesity?

A

CV Disease
Restrictive lung disease, sleep apnoea, corona artery disease, hypertension, cardiomyopathy, corpulmonale, mental abnormality, infertility, varicose veins, DVT, osteoarthritis

387
Q

How is obesity best managed?

A
  1. Lifestyle Changes
  2. Medication
  3. Bariatric Surgery- Gastric Band/ Roux en Y gastric bypass
388
Q

What is insulins function in the body?

A

Produces by Beta cells of the endocrine pancreas in repose to increased blood glucose levels.
It increases fat, proteins synthesis + glycogenesis

389
Q

What happens when BG drops and how does the body respond to this in terms of insulin secretion?

A

Drop BG- metabolism slows- ATP low- Katp channels open (K out)- hyper polarisation- V gated Ca channels closed- insulin NOT secreted

390
Q

What happens when BG drops and how does the body respond to this in terms of insulin secretion?

A

Drop BG- enters pancreatic cells via GLUT- metabolism increased- ATP high- Katp channels closed- Inc K so depolarisation- V gated Ca channels open= insulin vesicle exocytosed into circulation

391
Q

Once glucose is brought inside a cell by insulin how is it kept there?

A

Phosphorlyated= glucose6phosphate

392
Q

How does insulin act on muscle and adipose tissue?

A

Insulin stimulates mobilisation of GLUT4(cytoplasm)- migrates-(membrane) to move glucose in
NOTE: when insulin stimulationGLUT4 transporters return to cytoplasmic pool

393
Q

Other tissues don’t use insulin as an uptake mechanism (muscle and adipose tissue do) but use GLUT transporters. What are these transporters and where is their action?

A

GLUT4= Muscle + Adipose
GLUT 1+ 3= Kidney, Brain, RBC
GLUT2= B cells in pancreas and liver

394
Q

What function does the liver have with regards to insulin and glucose transport?

A

Insulin activates hexokinase- favours glucose movement into hepatocytes via GLUT2

395
Q

What does the liver do to glucose in the post absorptive state?

A

Fasted state, drop BGL

It synthesises glucose (glucogenolysis, gluconeogensis, lipogenesis, permissive to GH, INc K into cells= Inc ATP)

396
Q

Why are diabetics at risk of arrythmias?

A

Drops in BGL mean the liver increases K entry to cells (stimulate KNaATPasew)=Inc ATP levels but can cause hypokalemia= arrythmia

397
Q

If you want to stop a hypo would you give glucose IV or orally?

A

Insulin response is higher to a bolus than an IV load as when passing through the digestive tract glucose does not only act on Beta Cells of the pancreas but vagal stimulation + incretin effects (increase blood insulin levels)

398
Q

What has a longer half life insulin or glucagon?

A

Insulin- 5mins

Glucagon- 5-10mins

399
Q

What is the action of glucagon?

A

Needed when glucose is gone (dec BGL)
Inc gluconegensis
Inc glycogenolysis

400
Q

How are pancreatic islet cells involved in the autonomic nervous system?

A

Parasympathetic- INc insulin in anticipatory stage of digestion
Sympathetic- glucose mobilisation (Inc glucagon, Inc epinephrine, inhibits insulin)

401
Q

What is the function of somatostatin in regards to blood glucose levels?

A

Peptide hormone released from D cells of the pancreas + via hypothalmus (GHIH)
Inhibits activity of GI tract (slow absorption of nutrients-prevents peaks in plasma conc.)
Suppresses insulin + glucagon
CLINICALLY- pancreatic secreting tumours, develop diabetic symptoms until tumour is removed

402
Q

What is Diabetes Mellitus?

A

Loss of control of BG levels
Starvation in the midst of plenty
Large volumes of sweet tasting urine (excess glucose inc plasma osmolarity)

403
Q

What effect does exercise have on glucose and insulin concentrations?

A

Glucose levels into skeletal muscle increase (even without insulin- insulin INDEPENDENT inc in GLUT4 channel numbers with regular exercise)
Inc insulin sensitivity of muscle

404
Q

How can early stage T2DM be headed off?

A

Regular exercise as this encourages insulin INDEPENDENT increase in GLUT4 channel numbers

405
Q

How does the brain adapt in times of starvation?

A

Originally- cortisol makes brain primary metaboliser by stopping insulin action on muscle and adipose tissue
Dramatic loss- brain uses ketone bodies (via free FA broken down by b-oxidation in the liver) to spare protein

406
Q

What are the 4 types of diabetes?

A
  1. Immune mediated B cell destruction
  2. Insulin resistance
  3. Genetic defects (MODY)
  4. Gestational
407
Q

What can cause secondary diabetes mellitus?

A
  1. Pancreatic issues eg./ surgery, cancer, trauma, pancreatitis
  2. Cushings Disease, Acromeagly, Phaechromacytoma, hyperthyroidism, Pregnancy
  3. Congenital lipodystrophy
  4. Drugs eg./ corticosteroids
408
Q

How does T2DM usually present?

A

Asymptomatic/ Symptoms of complications common
Same symptoms as T1DM- polyuria, polydipsia etc
+ Not ketotic
Usually overweight
low grade infection eg./ thrush common

409
Q

What is HbA1c and why is it tested in diabetes? What are contraindications for use?

A

Glycated Haemoglobin- gives indication of glucose levels over last 8-12 weeks (doesn’t require fasting)
Contraindications- anything that changes haemoglobin levels (eg./ anaemia, haemorrhage, pregnancy current or recent, renal or pancreatic damage, HIV, corticosteriod use

410
Q

How is glucose taken from a meal into the blood stream?

A

Eat Meal- Inc Glucose levels- Stimulates B cells to release insulin- Inc Gl uptake by cells- Dec glucose in serum
Therefore, spike in glucose levels returned to normal glycaemia is routine after eating a meal

411
Q

What are the symptoms of hypoglycaemia? How is this measured?

A

Edinburgh Hypoglycaemic Scale
Based on
Autonomic- Sweating, Palpitations, Shaking + Hunger
Neurological- Confusion, Drowsiness, Speech Difficulty + Incoordination
General Malaise- Headache + Nausea

412
Q

What can cause hypoglycaemia?

A

Diabetes Link- too much/ inappropriate timing of insulin injections/ sulfynoea
Inadequate Food/ Fasting
Exercise
Alcohol
Warfrin/ NSAIDS
Post-Prandial- After Gastric/ Bariatric surgery (dumping syndrome)

413
Q

How do you treat hypoglycaemia?

A

Simple CHO (oral sugar + long acting starch eg./ toast)
If oral unavailable- 50% IV glucose + 0.9% saline flush (prevent phlebitis)
If Oral + IV not available- 1mg glucagon IM

414
Q

What is the aetiology of T1DM?

A
  1. Genetic + Environment
  2. Islet inflammation/ Lymphocyte Infiltration/ B Cell Damage
  3. Release of (non-tolerated) B cell autoantigens/ Structural modification of BCell autoantigen
  4. Sensitisation of auto reactive TCells to islet cell antigens + Inappropriate HLA expression on islet cells
  5. Tell regognisition of autoantigen + BCell destruction
415
Q 
A Pt presents with-
New onset Nightime Wetting
Weight Loss
And napping at nursery
What is your clinical diagnosis?
How would you confirm this?
What are your next steps in Pt treatment if your diagnosis is confirmed?
A

Type 1 Diabetes Mellitus (could be type 2 as share symptoms but due to young onset more likely to be type 1)
Immediate finger prick glucose is required- if >11mmol/L
Telephone specialist team (as at risk of DKa if >14mmol/L)

416
Q

What are the 2 types of insulin? What circumstances are they used?

A

Rapid Short Acting Insulin- doesn’t need to dissociate. Used at meal times in association with amount of carbohydrate eaten
Basal Long Acting/ Soluable Insulin- take 30mins before eating,

417
Q

What are the 3 possible insulin regimes for T1DM?

A
  1. Biphasic Regimen 2x Daily- 1 Rapid Acting + 1 Intermediate acting (bb+bt) In T1DM good control/ T2DM
  2. QDR Regimen 3x Daily- Rapid Acting + Intermediate Acting + Long acting analogue (bedtime) in flexible lifestyle T1DM (adjust dose for lifestyle + exercise)
  3. One daily (before bed) long acting insulin
    Its trained via DAFNE (autonomy)
418
Q

What meal advice is used for Pts with diabetes?

A 
Avoid missing meals
eat 5 fruit and veg a day
2 portions of oily fish a week
salt <6g (1tbsp) per day
include more beans and lentils
avoid saturated fats
AVOID foods with a high glycaemic index (rapid glucose release eg./ fizzy drinks) opt for ones with a low glycemic index (eg./ wholegrain rice)
419
Q

What eating disorders are associated with diabetes?

A

Diabulemia= poor glycemic control, Recurrent DKa, Insulin omission
High mobility + High mortality

420
Q

What affect does alcohol have on diabetes?

A

Alcohol= BGL to rise/ fall

Eat before and after, don’t have more than 2-3 units at a time. DONT take insulin (hypo risk)

421
Q

Why is smoking more risky on diabetes?

A

Already risk of microvascular disease

422
Q

What can happen to diabetics when using illicit drugs?

A

DKA, seizures, hypo/hypertension

423
Q

How should an insulin regime be altered when exercising?

A

Reduce insulin taken before and after (so more in serum to be taken up by working muscle/ less risk of hypo)
Eat more carbs

424
Q

What precautions must diabetics taken when driving?

A

Can’t drive for 45mins after hypo
Inform DVLA if on insulin (can drive G2-bus/lorry but strict)
Check BGL within 2 hrs of starting driving + 2hr when driving

425
Q

Diabetes + Work?

A

Disability Discrimination Act

BUT exceptions eg./ police, armed forces

426
Q

Diabetes + Holidays?

A

Insurance, Fluids, avoid gastroenteritis, hand luggage insulin

427
Q

What drugs increase insulin release?

A

Sulphonylureas
DPPIV Inhibitors
Therefore is a hypoglycaemic risk

428
Q

What drugs increase secretion of glucose?

A

SGLT2 inhibitors

429
Q

What drugs increase insulin action?

A

thiazididiones

430
Q

What vitamin levels would you need to monitor when prescribing metformin to a diabetic?

A

Vitb12 (as it can cause malabsorption)

431
Q

How do you reduce the risk of microvascular complications in a diabetic?

A 
HbA1c to 53mmol/L
BP < 130/80
Smoking cessation
Statin Therapy
Lifestyle Changes
432
Q

What is diabetic retinopathy? What are the stages + signs? How do you treat it?

A

Microvascular Disease cause by poor glycaemic control
Production of new vessels in the retina- bleeding/ blurring of vision
1. Background- microaneurysms + haemorrhages + hard exudates (lipid deposits)
2. Pre-proliferative retinopathy- cotton wool spots (infarcts), haemorrhages, venous bleeding
3. Proliferative Neuropathy- New vessel formation
4. Maculopathy
5. Cataracts
Rubeosis Iris- new vessel formation in the iris
TREAT: Laser photocoagulation, vitrectomy (removal of vitreous humour)

433
Q

What is diabetic nephropathy?

A

Microalbuminuria (urine dipstick -ve for protein but urine: creatinine >3mg/mol
Early renal disease
Increased connective tissue around capillaries eg./ Kimmelsteil Wilson (around glomerulus)

434
Q

What affects does poorly controlled diabetes have macrovascularly? How does this occur?

A

Accelerates atherosclerosis via glucose attachement to LDLs (can’t be removed by liver- hyperlipidemia)

435
Q

How does diabetic foot disease present? How is it investigated? How is it treated?

A
  1. Neuropathy- Decreased Sensation- stocking distribution, absent ankle jerks, burning pain/ numbness. Clinical investigation. Treat via feet protection + gabapentin (if pain)
  2. Ischaemia- loose feet pulses (doppler+ angiography)
  3. Ulceration- painless, punched out ulcer. Treat via screening, footwear
  4. Bony Deformity- eg./ Charcots Foot (loss of pain sensation leads to mechanical stress on the ankle joint) Investigate via xray. Treat via bed rest.
  5. Infection- swabs, blood culture needed
436
Q

What is mono neuritis multiplex?

A

CN 3, 4 + 6, acute onset

treat- immunosuppression (eg./ corticosteroids)

437
Q

What is amyotrophy?

A

Painful wasting of quadriceps + pelvifemorad muscles

438
Q

What is autonomic neuropathy?

A

Erectile Dysfunction- Viagra + Prostyglandins
Postural Hypotension- NSAIDS, Flucortison
Urine Retension- if severe catheterise

439
Q

What is the most flexible insulin regimen?

A

A basal-bolus insulin regimen (usually requiring a minimum of 4 injections per day) offers more flexibility to patients with Type 1 diabetes than twice daily insulin.

440
Q

Should insulin be stopped in a T1DM with an acute ilness that stops eating?

A

Insulin should NEVER be discontinued during acute illness in patients with Type 1 diabetes even if he/she is unable to eat.

GI (6 decks)

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