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Week 11 > CC endocrine, thyroid & parathyroid > Flashcards

CC endocrine, thyroid & parathyroid Flashcards

1
Q

What are the specialised cells in the pancreas and what do they produce?

A

Islets of Langerhans: clusters of hormone-producing cells

  • Alpha cells: produce glucagon to raise BSL
  • Beta cells: Produce insulin to lower BSL
  • Delta cells: Produce somatostatin for regulatory functions
  • PP cells: produce pancreatic peptide another regulatory function
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2
Q

List some other hormones that can affect BGL

A
  • Cortisol: Catcholamines
  • Growth Hormone
  • Thyroid Hormone
  • Human placental lactogen
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3
Q

How is the Tyrosine Kinase Second Messenger activated?

A

1) The insulin receptor is associated with tyrosine kinase (enzyme) in the cytosol
2) bidding of insulin activates the second messenger which phosphorylates intracellular proteins
3) cascade of events
4) Responses:
- uptake of glucose
- fatty acids
- amino acids
- various anabolic reactions

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4
Q

What molecular function does insulin play on a cells membrane?

A
  • Insulin binds to a receptor on the cell membrane
  • Signal transduction cascade results in activation of the GLUT 4 transporters
  • The GLUT 4 binds to the cell membrane allowing glucose to enter the cell
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5
Q

What are the effects of insulin on CARBS?

A
  • Increases cellular uptake of glucose
  • Increases glycolysis (ATP production)
  • Liver: increases storage of glucose as glycogen
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6
Q

What are the effects of insulin on PROTEINS?

A
  • decreases gluconeogenesis
  • glucose used over AA’s as a source of ATP
  • increases cellular uptake of AA;s
  • increases protein synthesis
  • Lack of insulin: AA’s are used as a fuel source
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7
Q

What are the effects of insulin on FATS?

A
  • decreases gluconeogensis
  • Glucose used over fats as a source of ATP
  • Adipose tissue: increases conversion of glucose to fat (storage)
  • Lack of insulin: fatty acids used as a fuel source
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8
Q

How does glucagon affect its target tissue?

A

by the cyclic AMP second messenger system

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9
Q

What is the main affect of glucagon on the liver?

A
  • Glycogenesis: breakdown of glycogen to glucose
  • Glycogenesis: synthesis of glucose form noncarbohydrate molecules ie. fattys acids, AA’s
  • release of glucose by hepatocytes
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10
Q

What is the secondary affect of glucagon on the liver?

A
  • Lowers blood levels of AA’s

- Sequestration of AA’s triggers gluconeogensis

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11
Q

What is Diabete Mellitus?

A

A clinical syndrome characterised by hyperglycaemia, due to either an absolute or relative insulin deficiency

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12
Q

What are the ranges of sugar in mol/L for diabetic patients?

A

If random blood sugar levels are > 11.1 mmol/L
If fasting sugar levels are >7 mol/L
HvA1c > 6.5%

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13
Q

What is type 1 diabetes?

A

An ABSOLUTE deficiency of insulin

“ Insulin dependent diabetes mellitus (IDDM) “

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14
Q

What is type 2 diabetes?

A

A RELATIVE deficiency of insulin
“ Non-Insulin dependent diabetes mellitus (NIDDM) “
Either problem with secondary messenger system or receptors become

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15
Q

What is secondary diabetes?

A 
Diabetes cause by a known pathology
- Pancreatic disease ie Cystic Fibrosis
- Latrogenic: Corticosteriods
- Conditions with excessive insulin-antagonists:
GH
Cortisol
Thyroid Hormone
Pregnancy (human placental lactogen)
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16
Q

What are the two hypothesis’ for type 1 diabetes

A

Autoimmunity:
85% of T1DM= circulating antibodies to islet cells (B, A, D)
hyperglycaemia only occurs after 90% of islet cells have been destroyed
T1DM= absolute deficiency

Combined Hypothesis:
A virus triggers the autoimmune response in a genetically vulnerable patient

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17
Q

What are the five risk factors of Type 2 diabetes

A

1) Genetic
2) Obesity
3) Metabolic syndrome
4) Smoking: 30-40% higher than non smokers
5) Age 70% in population over 50

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18
Q

What role does Obesity play in T2DM?

A

Excessive nutrients (glucose and FA) act as stressors for insulin-sensitive tissues: adipose, liver, mm

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19
Q

What molecules do adipose tissue produce and how does it affect insulin receptors?

A

Adipose tissue produces cytokines
in T2DM the cytokines interact with insulin receptors
Responce:
- Causes cell to be less responsive to insulin
- linked to damaging the beta cells of the pancreas

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20
Q

How do insulin receptors vary with weight?

A
  • Obese= decrease in insulin receptor density

- Weight loss= increased concentration of insulin receptors

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21
Q

How does T2DM develop?

A

Initially: hyperinsulaemia to prevent the appearance of diabetes for years

Eventually: Beta cells which produce the hyperinsulaemia start to dysfunction. This results in insulinpaenia

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22
Q

What are some clinical features of T1DM?

A
  • Really dramatic
  • Despite hyperglycaemia: Polyphagia, weight loss, fatigue
  • Polyuria
  • Polydipsia, cracked lips, tachycardia, hypotension
  • Glycosuria: excess sugar in the urine –> vulvitis and balanitis
  • Gluconeogensis results in mm wasting and weakness

TRIAD: Polyphagia, polyuria, polydipsia

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23
Q

What are some clinical features of T2DM?

A

hyperglycaemia and glycosuria can lead to:

  • skin infections and boils
  • recurrent UTI’s
  • Vulvitis, balanitis
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24
Q

What are some chronic complications of T2DM?

A
  • diabetic vascular disease (angina)
  • diabetic neuropathy (snubness/tingling)
  • diabetic foot: Gangreen
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25
Q

What is the level at which neurological Sx of hypoglycaemia occur?

A

Glucose is the fuel source of the brain

Neuro SSx arise when BGL is <2.5mmol/L

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26
Q

what are some factors that can precipitate hypoglycaemia

A
  • Not recognising SSx because you’re asleep
  • Inappropriate use of insulin/meds
  • Missing or delaying meals
  • Excessive exercise
  • Alcohol
  • Other comorbidities: malabsorption or endocrine disorders
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27
Q

What are some Central Nervous System clinical presentations of hypoglycaemia?

A
  • drowsiness
  • confusion
  • speech difficulties
  • inability to concentrate
  • headache or fatigue
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28
Q

What are some Autonomic Nervous System clinical presentations of hypoglycaemia?

A
  • sweating
  • trembling
  • palpitations
  • getting hungry
  • anxiety
  • nausea/ vomiting
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29
Q

Management strategies on hypoglycaemia

A
  • patient education on SSx
  • portable monitoring system
  • adjustment of insulin regime
  • oral glucose (jelly beans)
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30
Q

What are some possible symptoms of a sever hypoglycaemic attack?

A
  • coma
  • convulsions
  • brain damage
  • stroke
31
Q

What is the cause of a Diabetic Ketoacidosis?

A
  • Fatty acids are used when there is no glucose available (over a long time days)
  • excessive catabolism of fatty acids creates ketones
  • The accumulation of ketones have the ability to decrease the pH of environments (making it more acidic)
32
Q

What symptoms would someone present with if having a Diabetic Ketoacidosis attack?

A
  • Any form of stress can precipitate ketoacidosis
  • SSx related to hyperglycaemia: dehydration, frequent urination, nausea/vom
  • Acetone breath: sweet ‘fruity’ smell
  • Respiratory compensation: increased RR, Kussmaul respiration which is deep laboured breathing
  • mental disturbances ranging from inattention –> coma
  • Peripheral vasodilation leading to low BP and dangerously low body temp (hypothermia)
33
Q

Management for Diabetic Ketoacidosis

A
  • IV drip for rehydration
  • replacement of electrolytes
  • Carefully titrated insulin
34
Q

What is diabetic vascular disease an umbrella term for?

A

Its an umbrella term for a range of blood vessel pathologies

35
Q

What are the two major complications from diabetic vascular disease?

A

1) Diabetic Macroangiophathy (athlerosclerosis) AMI, PVD, Stroke
2) Diabetic Microangiopathy (arteriolosclerosis) retinopathy, neuropathy

36
Q

What is diabetic Retinopathy?

A

A common cause of blindness due to damaged blood vessels in the retina
Cotton wool spots, neurovascularisation

37
Q

What does diabetic neuropathy affect?

A
  • It mainly effects the PNS
  • Thickened basement membrane of intra-neural capillaries
  • Axonal degeneration
  • Patchy demyelination –> to degeneration
38
Q

SSx of diabetic Neuropathy

A

Sensory Polyneuropathy:

  • “glove and stocking” impairment (reflex and vibration) of sensory modalities
  • Paraesthesia, pain and ataxia

Motor Neuropathy:

  • generalised mm wasting and weakness
  • Amyotrphy: progressive weakness and wasting of hip girdle mm

Monone neuropathy: involvement of a single peripheral nerve (ie Ptosis)

Autonomic neuropathy: SNS, PNS, visceral afferents

39
Q

Why is foot trauma and ulceration common in diabetic patients?

A
  • Peripheral neuropathy
  • peripheral vascular disease effect the feet
  • hyperglycaemia and ketosis decrease the immune response to protect the peripheries
40
Q

What are some oral hypoglycaemic agents?

A

Exogenous Insulin
- Biguanides: Metformin- first line therapy
- Sulphonylureas: beta cells to make more insulin
- Thiazolidinediones: increase insulin sensitivity
- Alpha-Glucosidase Inhibitors: reduce digestion of carbs to decrease BGL
Other: Exenatide- promote insulin secretion and inhibit glucagon secretion

41
Q

What are some lifestyle modifications T2DM patients can take?

A

LIFESTYLE MODIFICATION

  • early cases: weight-loss and diet modification
  • frequent small meals
  • foods with low glycemic index (GI)
  • limit calorie and fat intake
  • alcoholic considerations
42
Q

What is the structure of the thyroid gland?

A

2x lateral lobes

1x isthmus

43
Q

what are the veins and arteries of the thyroid gland?

A

sup and inf thyroid arteries
sup, middle and inf thyroid veins
Over-activity of the glands can cause a bruit

44
Q

What is the molecular structure of the thyroid gland?

A
  • hollow, spherical follicles

- followed by a ring of follicular cells supported by a basement membrane

45
Q

What do the follicular cells secrete and what is its role?

A
  • thyroglobulin- a glycoprotein that is the precursor of the thyroid hormones (T3/4)
  • it is stored in the follicular lumen suspended in gel called colloid
    for regulating metabolism
46
Q

What are parafollicular cells (C cells)?

A

They secret Calcitonin which has a minor effect on storage of calcium in the bones

47
Q

What is the pathway from the hypothalamus –> cellular response, of thyroid hormone?

A
  • Hypothalamus: Thyrotrophin releasing hormone (TRH)
  • Ant Pituitary: Thyroid stimulating hormone (TSH) eg Thyrotropin
  • TSH binds to receptors on follicular cells
  • leads to release of thyroid hormone
  • synthesis of more thyroglobulin to restock colloid
48
Q

How does T3/4 circulate around the body?

A
  • Majoirty: Bound to thyroxine-binding globulins (TBG’s) and Albumin
  • Minority: as free molecules
49
Q

What effects can the thyroid hormones have on bodily functions?

A
  • Gene transcription associated with glucose oxidation: increase heat production and increase basal metabolic rate
  • Catecholamine-like effects: increase normal cardiac function and maintenance of BP
  • Regulates normal development and functioning: NS, Muscle System, digestive, reproductive, integumentary
50
Q

What is simple (nontoxic) goitre?

A

An enlargement of the thyroid gland where euthyroid function is maintained (levels of thyroid hormone are normal)

51
Q

What are the two different classification for simple (nontoxic) goitre?

A

Based on uniformity of the goitre:

  • Simple Diffuse Goitre: uniform enlargement of the thyroid
  • Simple multi nodular goitre: enlargement with nodule formation
52
Q

What is the aetiology (cause) of simple (nontoxic) goitre?

A

The leading cause if iodine deficiency

  • Ant pit –> Higher levels of TSH are recreated to maintain normal T3/4 levels
  • this results in hyperplasia of follicular cells

Other causes:

  • Ingestion of goitrogens (lithium, smoking)
  • Pregnancy
  • Use of OCP
  • Early stage of Hashimoto’s thyroiditis
53
Q

What are some clinical features of Simple Diffuse Goitre

A
  • women age 15-24
  • pregnant women
  • soft and symmetrical goitre
  • neck tightness on swallowing
  • no tenderness or bruit
54
Q

What are some clinical features of Simple Multi-nodular Goitre

A
  • goitre can become very enlarged
  • haemorrhage into nodule= pain, swelling

compression of mediastinal structures ie oesophagus or trachea:

  • cough
  • stridor
  • dysphagia
  • oedema
55
Q

What are some management strategies of goitre?

A
  • High-dose iodine supplements for children (won’t effect adults)
  • partial thyroidectomy for compressive symptoms (high recurrence rate)
56
Q

What is Hypothyroidism?

A
  • A deficiency in T3/4 having a negative impact on metabolism.
  • If a child has it, it creates a development/intellectual disability ‘cretinism’
  • In adults it leads to general slowing of body functions
57
Q

What are the three different classification of hypothyroidism?

A

1) Primary hypothyroidism: due to failure of the thyroid
- most common: Hashimoto’s thyroiditis (autoimmune disorder)
- Other: iatrogenic (due to treatment of overactive thyroid), congenital, iodine deficiency

2) Secondary: due to TSH deficiency
- causes: pituitary adenoma or surgery

3) Tertiary: Due to TRH deficiency
- hypothalamic dysfucntion

58
Q

What is Hashimoto’s thyroiditis?

A

An autoimmune disorder characterised by lymphocyte-mediated inflammation and fibrosis (autoimmune disease)

59
Q

What are some precipitating factors of Hashimoto’s thyroiditis?

A
  • high dose iodine supplementation
  • exposure to radiation
  • certain drugs: lithium, aminodarone
60
Q

What is Chronic Lymphocytic Thyroiditis?

A

The secretion fo IgG autoantibodies

  • some direct against thyroglobulin
  • other directed against thyroid peroxidase

Early disease: Goitre
Late disease: Thyroid atrophises

61
Q

How TSH produced T3/4

A

43 min mark

62
Q

What are the clinical features of hashimotos

A
  • Goitre: neck-tightness, with without compress

Reduced metabolic rate:

  • cold
  • weight gain
  • Xanthelasma formation (periorbital region)
  • Constipation

Glycosaminoglycan (GAG) accumulation
Proteoglycans normally found in the ECM around CT cells
GAGS accumulate in various tissues due to reduced rate of protein breakdown
Pale, Puffy face

GAG accumulation can increase angina and hypertension due to GAG near arteries causing squishing

63
Q

Management of hashimotors

A

Thyroid replacement therapy

maintain euthyroid state (add)

64
Q

What is thyrotoxicosis

A

A clinical state arising from thyroid hormone in excess

Toxic state produced by too much thyroid hormone usually arising from hyperthyroidism but not always the case
(accidentally taking levothyroxine eg children)

65
Q

Classification of the 3 thyrotoxicosis

A
  • Toxic diffuse goitre (graves disease)
  • Toxic multi nodular goitre
  • Toxic solitary nodule
66
Q

Risk factors of Graves disease

A

autoimmune disorder causing thyroid excess

age 20-40 (women > men)

Risk factors:

  • genetic
  • major stresses –> autoimmune response
  • high dose iodine supplementation increases risk
  • possible E.Coli infection mimicking TSH
67
Q

Pathophys of Graves

A
  • Autoantibodies that are directed against TSH receptors called TSHrAbs
  • These antibodies bind to follicular cell receptors and cause more T3/4 to be release
  • Promotion of T3/4 secretion of follicular cells causing goitre
68
Q

Clinical features of Graves disease

A
  • Thyroid is 2-3x normal size
  • +/- bruits over the gland
  • Metabolic rate: increase heat, weight loss, increase sweating
  • GIT manifestation: increase hunger and thirst, hyperdefecation, diarrhoea
  • Cardiorespiratory: palpations, atrial fib, exacerbation of asthma
  • Neuro: nerbousness, emotional lability, psychosis, tremor, hyper-reflexia, muscle weakness/proximal wasting
  • Repro: menstural irregularities, loss of libio

Occular changes: GAG accumulation= extraoccular mm swelling and exophthalmos
- lid retraction, corneal ulceration, conjunctivitis, excess lacrimation, diplopia, decreased visual acuity

Skin changes: GAG can accumulate in the skin Pretibial skin myxoedema (& marked thickening of overlying skin)

69
Q

Management of Graves

A
  • Antithyroid drugs: like PTU decrease thyroid peroxidase
  • Beta blockers: CVD symptoms
  • Radioactive thyroxine: treatment of choice (except in pregnancy)
  • Surgery: thyroidectomy (partial or full)
    Risk for hypothyroidism, damage to laryngeal nerves
  • Post-treatment hypothyroidism is common
70
Q

Risk factors for Thyroid Cancer

A
  • exposure to ionising radiation
  • Fam Hx
  • Benign thyroid disease
    eg thyroid adenoma
71
Q

What are the possible types of thyroid cancer?

A

Most common: Papillary Carcinoma (80%)
Begins as a solid nodule –> spreads through the glands, lymphatics, trachea and even lungs

Other types:

  • Follicular Carcinoma
  • Medullary Carcinoma
  • Anaplastic Carcinoma
72
Q

Clinical presentation of Thyroid Cancer

A
  • Recent onset of a nodule or an enlarging nodule which is firm on palpation and non-tender
  • Larger tumours can cause neck discomfort or pressure-related issues Dysphagia, hoarseness, Horner’s syndrome

3% of patients present with symptoms of metastatic spread:

  • Cervical lymph node enlargement
  • Spread into the trachea, lungs
73
Q

How is Thyroid cancer Managed ?

A

hemi- or total thyroidectomy
followed by radioactive iodine to abate any remaining issues

prognosis is usually excellent, possible complication is laryngeal nerve damage and damage to parathyroid glands

Week 11 (2 decks)

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