Endocrine Flashcards

1
Q

why diabetes mellitus associated with loss of urine

A

Glucose in blood plasma exceeds the ability of the kidneys to resorb it back into the blood again so it goes into the urine. Osmotically draws liquid out so increased loss of urine, causing increased thirst

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2
Q

Difference between diabetes type 1 and 2

A

1=autoimmune destruction of Pancreatic Beta cells in islets of Langerhann so don’t produce enough insulin.
2= metabolic. combination of insulin resistance (increased glucose so have become de-sensitised) and relative lack of insulin to do its job properly

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3
Q

how is glucose stored

A

-glucose from diet is converted to glycogen (glycogenesis) by insulin and stored in muscles and liver

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4
Q

Which type of diabetes is insulin dependent. which is more common. what age is type 1 likely to manifest

A

type 1 insulin dependent - always needs insulin to treat
type 2 more common
10-14 years old

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5
Q

other than type 1 and type 2, what other causes of diabetes

A

gestational in pregnancy
secondary to other condition (Cushing’s syndrome or removing pancreatic cancer)
chronic kidney disease

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6
Q

symptoms of diabetes mellitus. Difference between type 1 and 2 manifestations

A

Both cause:
-polynuria - pass lots of urine
-polydipsia - drinks lots more to make up for urine loss
-weight loss - cells don’t take up glucose
-blurred vision - eye dehydration. (blood has higher osmotic pressure)

Type 2 - symptoms less rapid and dramatic. may be asymptomatic and find out during blood test. Can have increased infection such as candida or UTI.

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7
Q

how is type 2 diabetes diagnosed with the oral glucose tolerance test. what are the normal and abnormal values

A

-measure glucose level when fasted
-then give 75g of glucose
-measure glucose level after 2 hours
-in diabetes, glucose levels for both will be high

When fasted:
-normal <6.1 mmol/l
-diabetes >7.0
After 2 hours of glucose:
-normal <7.8
-diabetes >11.1

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8
Q

How glycated haemoglobin test is used to diagnose diabetes. Normal, pre-diabetic and diabetic levels

A

-Glycated hemoglobin [HbA1c] is a form of hemoglobin in RBCs that is chemically linked to a sugar
- RBCs last 120 days in the circulation so HbA1c level is a measure of the average blood glucose over several weeks
-Normal= <42 mmol/mol
-prediabetic = 42-47
-diabetic = ≥ 48

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9
Q

3 variations that type 2 diabetics can manage their diabetes

A
  1. Diet alone
  2. Diet plus drugs
  3. Diet plus insulin
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10
Q

Which hormones raise blood glucose, which lowers

A

-Raises= glucagon, cortisol, adrenaline, growth hormone
-lowers = insulin

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11
Q

does food, starvation, illness, stress, exercise, hypoglycaemic drugs cause increased or decreased blood glucose

A

-Increased= food, stress (increased cortisol), illness
-Decreased= hypoglycaemic drugs, insulin, exercise (uses up glucose for energy), starvation

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12
Q

Action of gliptens and glutides for type 2 diabetes. Name drugs

A

-increase insulin secretion [insulin secretagogues]
-sulphonylureas eg. gliclazide - oral
-DPP4 inhibitors eg. sitagliptin, vildaglipin - oral
-GLP-1 binders eg. exanetide, liraglutide - injected

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13
Q

Action of metformin (biguanides) for diabetes. side effects

A

-sensitises body to effects of insulin to improve its action (instead of getting body to produce more) -insulin sensitiser
-most common drug for type 2
-it can stimulate weight loss
-first choice for overweight patients
-can cause taste disorders

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14
Q

How alpha glucosidase inhibitors and guar gum work

A

-delay carbohydrate abdorption
-increase glucose loss in the urine
-associated with thrush
-rarely used
-can be used by cardiologists for patients with fluid overload

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15
Q

where to inject insulin. why it is not given orally.

A

Because insulin is broken down by digestive enzymes, it cannot be taken in pill form. Instead, it is delivered with a syringe into subcutaneous tissue where it can be absorbed into the blood
The layer of fat on the stomach, hips, thighs, buttocks and backs of the arms are common sites for injecting insulin.
-injected via needles or pens. Also can use pumps and inhalers

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16
Q

Explain short acting, long acting and biphasic insulin types. when they are taken.

A
  1. Short acting= injected right before meal. Peak insulin within an hour. [eg. soluble]
  2. Long/intermediate acting = taken a few hours before a meal. Insulin level long and slow, in blood for up to 12-24 hours. [eg. isophane]
  3. Biphasic = a mixture of a short-acting insulin with an intermediate-acting insulin. Can be used to cover mealtime and basal insulin requirements, and are often used twice a day
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17
Q

Name examples of insulin names and brands

A

-fast-acting= soluble [actrapid, humulin S], aspart [Novarapid], Lispro [Humalog], gluisine
-long-acting= isophane [insulatard, humulin l], glargine [Lantus], detemir [Levemir]
-biphasic= mixtard, humulin M3, Novomix 30, humalog Mix25

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18
Q

When is twice daily insulin injected. and the type of drug used

A

2x fast acting (soluble), 2x long acting (isophane insulin)
-injection initially before breakfast = 1 of each
-injection before dinner = 1 of each

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19
Q

Explain the basal-bolus insulin regime. what type of insulin used and when injected

A

-allows more flexibility for when you eat
-check insulin level before they eat and adjust the amount of insulin they need to inject in accordance with the amount of carbohydrate they are going to eat
-Long acting (eg. isoprene), given once a day.
-Then use short-acting (soluble) right before they eat

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20
Q

3 acute complications of diabetes (rapid onset)

A
  1. Hyperosmolar hyperglycaemic state
  2. Ketoacidosis
  3. Hypoglycaemia - complication of treatment
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21
Q

What is ketoacidosis. which diabetes it is likely to occur in. symptoms

A

-acute complication (12-24hrs) of type 1 diabetes, due to forgetting insulin or intercurrent illness
-hyperglycemia, osmotic diuresis
-low sugar stores to use as energy so the body starts breaking down fats at a high rate. The liver processes the fat into a fuel called ketones, which causes the blood to become acidic
-Fast, deep breathing (trying to rid of acid)
-Dry skin and mouth. Thirst
-Flushed face.
-Fruity-smelling breath -like nail varnish remover
-Headache. Dehydration
-Muscle stiffness or aches.
-Being very tired. Confusion. Drowsiness
-Nausea and vomiting.

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22
Q

What is a Hyperosmolar hyperglycaemic state. which type of diabetes it occurs in. symptoms

A

-acute complication of type 2
-similar to ketoacidosis, but goes on for a few days rather than hours.
-happens when your blood glucose levels are too high for a long period, leading to urine loss, severe dehydration and confusion. HHS requires immediate medical treatment.

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23
Q

Name 2 chronic diabetic complications associated with eyes

A
  1. Diabetic retinopathy: damaged retinal blood vessels, causing micro aneurysms and sometimes microhaemorrhages. Usually asymptomatic if at periphery of eye, but if at centre of vision then noticeable
  2. Sub-hyaloid haemorrhage in eye: localized detachment of vitreous from the retina caused by accumulation of blood. Jagged lower border as blood moves down by gravity. Can lead to loss of vision when it takes place in the macular area.
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24
Q

Name 3 chronic diabetic complications associated with feet/ hands

A

1-Diabetic neuropathy: Numbness and tingling of hands and feet due to damaged nerves due to high glucose, or damaged vessels. Skin becomes thickned on feet and no good blood supply so becomes necrotic
2-Diabetic foot: damaged vessels can cause claudication of legs and feet (poor circulation and numbness)
3. Diabetic cheiroarthopathy: occurs in those with diabetic neuropathy. glucose binds to proteins and collagen. Loss of feeling in feet, fingers won’t fully straighten, damaged motor neves in hands

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25
Q

Name chronic diabetic complications associated with macrovasculature

A

-atherosclerosis, causing…
1. Peripheral - gangrene, claudication of hand and feet
2. Coronary - angina, MI
3. cerebral - strokes, TIA

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26
Q

How diabetes can affect the kidneys

A

-nephropathy: impaired kidney function. poorly controlled diabetes can cause damage to blood vessel clusters in your kidneys that filter waste from your blood. This can lead to kidney damage and cause high blood pressure

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27
Q

How to treat retinopathy, nephropathy, neuropathy, peripheral vascular disease and foot ulcers associated with diabetes

A
  • Retinopathy – laser photocoagulation (burns out bits of ischemic retina)
  • Nephropathy – ACE inhibitors, dialysis & transplantation
  • Neuropathy – advice about foot care. Amputation if necessary
  • PVD – bypass surgery, angioplasty with stents or amputation
  • Foot ulcers – chiropody, protection from pressure, good footwear & surgery
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28
Q

What blood glucose level is hypoglycaemia

A

<4 mmol/L

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29
Q

What are the warning and established symptoms of hypoglycaemia

A

1-Warning symptoms= adrenergic symptoms due to excess adrenaline to counteract.
-tremor, anxiety, palpitations, hunger, dry mouth

2-Established symptoms= neuroglycopenic symptoms due to brain not getting enough glucose/ energy.
-appear drunk
-confusion
-aggression
-slurred speach
-inco-coordination
-coma
-convulsions
-irreversible brain damage
-death

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30
Q

Treatment options for hypoglycaemia if conscious and unconscious

A

-establish diagnosis by checking blood glucose <4
-oral glucose tablets or drink (10-20g)
-buccal hypostop gel for uncooperative patient

If unconscious:
-subcutaneous glucagon 1mg
-IV glucose 20-30ml 50% (dextrose)

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31
Q

what type of patients will glucagon not work if they are hypoglycaemic

A

-doesn’t work for anorexic or severe starvation as no glucose stores
-liver disease - cirrhosis prevents glucagon from working

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32
Q

why important to inject glucose IV rather than subcutaneously

A

glucose is acidic so if went in subcutaneous tissues it may cause blackness of skin

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33
Q

how to inject glucagon (the form it is in and why. and where to inject) When is it used

A

Comes as dry powder to be drawn up with diluent – (as poor shelf life in solution)
Injected IM into outer thigh
-used for hypoglycaemic

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34
Q

Treatment of diabetic ketoacidosis and hypersomolar hyperglycaemic state

A
  • Medical emergency
  • IV insulin infusion
  • IV rehydration and electrolyte replacement
  • Treat underlying cause
  • Secondary prevention – educating the patient about what to do next time

-hyperosmolar is same as DKA but slower correction and thromboprophylaxis (use heparin) to reduce risk of nephropathy, thrombosis

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35
Q

What a dentists should do with diabetic patients

A
  • Ask about diabetes history
  • Check control and usual treatment
  • Check for relevant complications
  • List first in morning – minimise disruption to routine. Advise them to eat as normal
  • Check glucose before and after procedure, be prepared to treat hypoglycaemia
  • Give a mid-morning snack before leaving surgery
  • Remember increased infection risk with diabetic patients

inhaled insulin (rare) can cause dry mouth
soluble insulin may cause pain and swelling of salivary glands (although rare)

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36
Q

What sort of procedure require fasting. What should diabetic patients do

A

-endoscopy
-do procedure first on list, early in morning
-don’t take insulin or breakfast
-give breakfast and treatment immediately after

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37
Q

What is a GKI infusion and when it is used

A

-intravenous treatment for diabetic patients for major or longer procedure or under GA
-contains glucose, potassium and insulin
-Monitor glucose hourly – adjust insulin content of bag to keep between 6 and 12

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38
Q

Definition of gym steroids, steroid medication and biochemical steroids. what are the 5 steroid hormones

A
  1. Gym: synthetic analogues of testosterone to increase muscle
  2. Meds: hydrocortisone (eg. prednisolone) are synthetic analogues of cortisol for immunsupression
  3. Biochemical: steroids hormones derived from cholesterol and secreted in the blood (testeosterone, estrogen, preogesterone, cortisol, aldosterone)
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39
Q

Difference between the anterior and posterior pituitary (how it is connected to hypothalamus, what tissue it is composed of, what is does)

A

-Anterior pituitary= connected to hypothalamus by blood vessels. Composed of glandular tissues. Synthesises the hormones it secretes (FSH, LH, GH, TSH, ACTH, prostacyclin)

-Posterior pituitary =works via neuronal control (releases ADH and oxytocin) It stores hormones synthesised by the hypothalamus. Composed of neuronal tissue

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40
Q

Explain the hypothalamic pituitary axis

A

-The hypothalamus regulates the pituitary gland, involved in feedback cycles which determine what the other glands do
-Hypothalamus releases hormones which travel to the pituitary gland via pituitary stalk.
-Pituitary hormones are released into the general circulation.
-Hormones act on target organ (adrenal cortex, thyroid, liver, gonads, mammary gland,) and the glands produce hormones
-Once this hormone passes back to the hypothalamus, it downregulates it ensuring the appropriate amount is released (negative feedback)

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41
Q

which glands have their own nerve supply and not determined by hypothalamic pituitary hormone release.

A

adrenal medulla and cortex (adrenaline, aldosterone), parathyroid (PTH), pancreas (insulin, glucagon)

42
Q

how the following hormones are controlled: adrenaline from adrenal medulla, PTH from parathyroid, aldosterone from adrenal cortex, insulin and glucagon from pancreas

A

-Adrenaline = CNS
-PTH = plasma calcium
-Aldosterone = plasma volume via kidneys (renin, angiotensin)
-Insulin and glucagon = plasma glucose

43
Q

Name hormones released from adrenal medulla and cortex. Gonads. A and B cells of pancreas. Thyroid.

A

Cortex= cortisol, aldosterone, estrogen, testosterone
Medulla = adrenaline, catecholamines
A cells = glucagon
B cells = insulin
Thyroid = T3 (triiodothyronine), T4 (thyroxine), calcitonin
Ovaries= progesterone
Testes= testosterone

44
Q

4 cause of endocrine disease

A
  1. autoimune destruction of gland, so lack of particular hormone (eg. diabetes)
  2. Autoimmune stimulation of gland, so increased production (eg. Grave’s)
  3. Destruction of gland due to surgery, cancer, TB)
  4. Tumor formation pressing on structure- hyper secretion or hypo secretion
45
Q

What is Cushing’s syndrome. causes

A

-hypercortisolism - too much cortisol
-due to corticosteroid use, pituitary tumour (increased ACTH), adrenal tumor (increased cortisol)

46
Q

Diagnosis and treatment of Cushing’s syndrome

A
  • Blood test – measure cortisol levels (but wide range as cortisol levels are constantly changing – after food, after stress)
  • Raised urine or serum cortisol
  • Fails to suppress with dexamethasone
  • ACTH levels
  • Imaging of pituitary/adrenals

Treatment usually surgical – adrenalectomy or hypophysectomy. Or metyrapone as it blocks cortisol synthesis

47
Q

Symptoms of Cushing’s syndrome

A

-Moon face – cortisol increases adipose tissue
-Buffalo hump
-Abdominal obesity
-Proximal muscle weakness – cortisol causes muscle breakdown
- stretch marks, Thin skin
-Easy Bruising
-Osteoporosis
-Hirsutism (androgenic) = females grow man like hair
-Hypertension – retaining sodium and water = oedema
-Raised blood glucose level (can cause secondary diabetes)

48
Q

What is Addison’s disease. causes

A

-autoimmune destruction of adrenal cortex, causing adrenal insufficiency.
-Decreased cortisol and aldosterone
-insufficiency also due to prolonged corticosteroid therapy, TB, surgical removal, pituitary failure causing lack of ACTH, adrenal tumours

49
Q

Symptoms of Addison’s disease. oral manifestation and how this occurs

A

-fatigue, depression, weak, handgrip and limbs
-weight loss, loss of appetite, increased thirst
-dizzy when standing due to drop in BP
- increased pigmentation of skin folds, buccal mucosa and scars, due to melanin which is a by-product from excess ACTH (due to insufficient adrenal gland)
-vitiligo = destruction of melanocytes

50
Q

What endocrine disease is associated with increased pigmentation of buccal mucosa

A

Addison’s disease

(less cortisol = more ACTH = stimulated melanocytes)

51
Q

Symptoms of adrenal crisis and when it is caused

A

If someone with Addison’s disease has major infection/ illness/ injury, surgery, undergoes GA, when their body is unable to produce enough hormones during stress. This causes…
-vomitting, dehydration, weak, confused
-hypotension (low aldosterone so lose salt and water so decreased blood volume and BP)
-hypoglycameia
-electrolyte disturbances - low Na and K
-feeble rapid pulse
-anorexia, nausea, severe abdominal pain

52
Q

Diagnosis of Addison’s disease

A

-low cortisol level
-ACTH levels - high if primary adrenal failure as it builds up, low if pituitary failure
-adrenal antibodies
-low serum Na and high K (due to low aldosterone)

53
Q

Treatment for Addison’s disease and acute adrenal crisis

A
  • Hydrocortisone (= cortisol, the main glucocorticoid)
  • Fludrocortisone (synthetic mineralocorticoid)

Crisis= lay flat, call for help, ABCDE approach
- IV fluids of electrolytes and glucose
-200mg hydrocortisone (or 4mg/kg for child)

54
Q

What is hyperthyroidism and its causes

A

-excess T3 and T4 made by thyroid, usually due to thyroid abnormality.
-thyroid adenoma (nodules in gland)
-multinodular goitre (enlarged gland, usually benign)
- excess TSH caused by Grave’s disease (80% of causes)
-lack of iodine = increased TSH = enlarged thyroid = hyperthyroidism

55
Q

Signs and symptoms of hyperthyroidism

A

-increased metabolic rate:
* Feels hot. Increased HR
* Sweaty palms
* Weight loss
* Increased appetite
* Poor sleep
* Diarrhoea
* Tremor
* Tachycardia/atrial fibrillation
* Goitre – lump at front of neck
* Graves eyes: bulging eyes (Exophthalmos)
- Adrenaline causes lid retraction
- Eye movement restriction
- Finger clubbing sometimes

56
Q

Diagnosis of hyperthyroidism

A

Diagnosed by raised T4 and T3
suppressed TSH
Thyroid stimulating antibodies
Thyroid scan
Radio-iodine - thyroid takes up iodine. measure the amount of radioactivity in the thyroid gland

57
Q

What is Grave’s disease. symptoms

A

an autoimmune condition where your immune system mistakenly attacks your thyroid which causes it to become overactive.

-an enlarged thyroid gland, called a goiter in the neck
-buldging eyes
-weight loss, despite an increased appetite.
-rapid or irregular HR.
-nervousness, insomnia, fatigue.
-tremor, muscle weakness.
-sweating or trouble tolerating heat.
-frequent bowel movements.
- Adrenaline causes lid retraction
- Eye movement restriction
- Finger clubbing sometimes

58
Q

Treatment of hyperthyroidism (and grave’s disease)

A
  1. Surgical thyroidectomy
  2. Anti-thyroid drugs (carbimazole, propulthiouracil)
  3. Beta-blockers for symptom control (will suppress the adrenergic side effects i.e. reduce tremor/ sweating/ tachycardia).
  4. Radioactive iodine – iodine taken up by thyroid so this keeps the treatment localised to the thyroid gland
59
Q

How hypothyroidism can be caused. What TSH levels will be

A

-lack of T4 and T3, with increased TSH as it builds up (unless it is due to pituitary disease so would be low)
-due to autoimmune destruction of thyroid, surgical removal of gland, radio-iodine treatment, pituitary disease

60
Q

Treament of hypothyroidism

A

levothyroxine

61
Q

Features of hypothyroidism

A
  • Feels cold, cold intolerance
  • Dry skin, thin hair
  • Slow, tired, confused
  • Slow pulse
  • Weight gain
  • Poor appetite, muscle aches
  • Sluggish bowels - constipation
  • Infertility
  • Myxoedema - tissues filled with fluid, under-eye bags, coarse facial feature, croaky voice
62
Q

Diagnosis of hypothyroidism

A

Low T4 and T3, high TSH
thyroid autoantibodies

63
Q

What is acromegaly and cause

A

-excess growth hormone by pituitary gland (after puberty)
- due to pituitary tumour secreting GH

64
Q

Features of acromegaly

A

-Enlarged hands, feet, jaw (malocclusion), skull (change in hat, shoes, dentures, rings fit)
-Coarse facial features as cartilage grows– nose, brow, tongue
-Thick skin/lips – soft tissue grows
-Arthritis – includes TMJ
-Hypertension
-Hyperglycaemia (insulin resistance)
-Headache due to pituitary tumour
-Bitemporal hemianopia due to compression of optic chiasm by the tumour

65
Q

How is acromegaly diagnosed

A

High GH level, that does not suppress with glucose
High IGF-1 made by liver
Pituitary MRI scan
Visual field testing

66
Q

What is Hyperparathyroidism. what causes it

A

-an over-active parathyroid causing hypercalcaemia.
-High PTH stimulates release of calcium from stores in the bones into the bloodstream. This increases bone destruction
-caused by parathyroid adenoma, vitamin D excess, cancer

67
Q

Lack of what nutrients can cause hypocalcaemia

A

vitamin D

68
Q

Features of hypercalcaemia. Findings on a DPT

A
  • Often asymptomatic or non-specific
  • Stones, bones, abdominal groans and psychic moans
  • Dry eyes and mouth
  • Thirst and polyuria - inability to concentrate urine (cause of mild diabetes insipidus)

-reduced cortical width of mandible, loss of lamina dura

69
Q

Diagnosis of hyperparathyroidism. treatment

A

-high plasma calcium with raised PTH. But low PTH in secondary hypercalcaemia
-imaging of glands
-treated by surgical removal as treatments not as good

70
Q

Hypoparathyroidism cause

A

Underactive parathyroid gland, causing hypocalcaemia
-due to autoimmune destruction or damage to the glands during thyroid surgery

71
Q

Features of hypoparathyroidism

A

tingling and paraesthesia
cramps and tetany (muscle spasms due to low calcium)

72
Q

Diagnosis and treatment of hypoparathyroidism

A

Low plasma calcium, low PTH (but will be high if hypocalcaemia is due to vitamin D deficiency)

treated by vitamin D analogues

73
Q

What endocrine disease causes TMJ arthritis, malocclusion or altered denture fit

A

acromegaly - excess growth hormone

74
Q

effects of cortisol. what disease is caused by excess amount

A

-lowers blood calcium
-triggers glucagon release, increasing blood glucose. Also glycogenolysis
-supresses immune system
-enhances lipolysis
-lower at night due to low brain activity
-stress response

-cushing’s syndrome

75
Q

Effects of aldosterone

A

it is released in response to fluid loss and low BP
-It retains water and Na in kidney so increases blood volume and increases BP and cardiac output

76
Q

what are the effects of T4 and T3

A

growth and maturation, brain development, increases oxygen consumption, increased HR, protein breakdown, gluconeogenesis, increased metabolic rate, lipolysis
-increases cholesterol, a starting molecule for steroid hormones

77
Q

How is thyroxine (T4), trim-iodothyronine (T3) produced in HPA axis. How calcitonin produced. How iodide controls hormones

A

-Hypothalamus (TRH) – Anterior pituitary (TSH) – Thyroid gland (T3/4)
-calcitonin produced by C cells of the thyroid gland
-production dependant on iodide ions. Ions stored as thyroglobulin in plasma then undergoes proteolysis to release hormones

78
Q

Is T3 or T4 more potent

A

T3.
T4 undergoes transformation to T3 in tissues

79
Q

Causes of cretinism. symptoms

A

term for someone with congenital hypothyroidism. Affects growth, must be treated early to allow growth of body and brain
-due to hypothyroidism from autoimmune or surgical destruction, congenital thyroid problem, Hashimoto’s thyroiditis, hypothalamic or pituitary dysfunction
-round face, pot belly, weird hair, profound learning disabilities

80
Q

Action of thioamides. drug names.

A

Carbimazole/ propulthiouracil = THIOAMIDES
- anti-thyroid drugs for treating hyperthyroidism
* Prevent incorporation of iodine into T3 and T4
* Propylthiouracil also stops conversion of T4 to T3
-carbimazole most common. propylthiouracil only used if intolerant and is first choice in 1st trimester of pregnancy

81
Q

Unwanted effects of thioamide meds and iodine

A

Thioamides:
-Agranulocytosis – reduction in WBCs (immunocompromised. So my causes candidiasis)
-Hives
-Hepatitis
-Arthralgia - joint stiffness
-Taste disturbances

Iodine:
-Hypersensitivity reactions (angioedema)
-Hypothyroidism
-damage to salivary glands

82
Q

How calcitonin affects osteoclasts. What is it used to treat

A

-influences calcium and phosphate metabolism
-Decreases blood calcium = hypocalcaemia and hypophosphataemia by inhibiting osteoclasts
-treats hypercalcaemia and Paget’s

83
Q

Why avoid adrenaline in uncontrolled hyperthyroidism

A

Epinephrine and other vasoconstrictors in local anesthetic drugs cause cardiovascular stimulation, and hyperthyroid patients can develop dysrhythmias, tachycardia, and thyrotoxic crisis when administered these drugs.

84
Q

2 possible drug interactions with insulin

A
  • NSAIDs produce hypoglycaemia and should be used with caution
  • Systemic steroids antagonise the hypoglycaemic effect of insulin
85
Q

Action of sulphonylureas. Indications and contraindication. oral manifestation

A

-encourage insulin secretion, so don’t work on type 1 as B cells don’t function properly
-for those not overweight or cannot take metformin

lichenoid eruptions, erythema multiforme and oral neuropathy

86
Q

Action of biguanides

A

-. sensitised body to effects of insulin to improve its action. decrease gluconeogenesis, decreasing blood glucose
-only used in type 2 as only acts in the presence of insulin
-first choice in overweight patients
-eg. metformin

87
Q

How the combined pill works

A

exogenous oestrogen and progesterone taken to target the negative feedback system of their production so secretion and ovulation is inhibited. Mimics the pregnant state so no fertilisation
* Oestrogen inhibits FSH release from pituitary so prevents ovarian follicle development
* Progesterone inhibits LH from pituitary and thickens the cervical mucus so passage of sperm to ovum is difficult
* Combined pill most effective

88
Q

What hormone the implant contains and the morning after pill

A

-implant = progesterone only
-morning after pill = oestrogen only

89
Q

When is a progesterone pill used, why oestrogen would be contraindicated

A

overweight/ high BP/ predisposition to venous thrombosis

90
Q

How oral contraceptives affect dentistry and the mouth

A
  • Increased inflammation due to increased circulating hormones
  • Increase in gingival crevicular fluid
  • Gingival pigmentation
  • Appear to increase the incidence of dry socket
  • Increases severity of oral aphthous ulceration related to menstruation
  • May increase post-operative pain
91
Q

what antibiotic interacts with oral contraceptives

A

enzyme-inducers eg. rifampicin. None that dentists prescribe

92
Q

Do 1) organ transplant or 2) adrenal suppressed patients need steroid cover for simple gingival surgery under LA

A

no, but monitor blood pressure throughout, and if starts to drop (suggesting Addisonian crisis) then give steroids if need be- 100-200mg hydrocortisone cover

93
Q

Prevention of acute adrenal crisis

A
  • Knowledge
  • History of patient
  • Educating patients
  • If in doubt ask for advice
  • Consider whether treatment would be safer in a hospital unit
  • Spare medication carried by patient
  • Emergency hydrocortisone injection
  • Medic alert bracelet / letter from GMP with instructions
94
Q

What to do with a patient with primary adrenal insufficiency undergoing major dental procedure under LA (eg. difficult surgical extraction) or under GA

A

-double dose (up to 20mg) hydrocortisone the day before treatment and for 24 hours after
-OR 100-200mg hydrocortisone IM 30 mins before procedure, or IV instantly with treatment

95
Q

what Stevens Johnson syndrome can present with. 2 drug classes that is associated with it

A

erythema multiforme
antihistamine and diuretics

96
Q

what is raised in Willson’s syndrome

A

RAISED COPPER CAUSING HEPATITIS

97
Q

AUTOIMMUNE DISEASE CAUSING SEVERE VASCULITIS AND MOUTH ULCERS

A

Behcet’s disease

98
Q

signs and symptoms of pituitary tumor

A

Problems with eyesight, including vision loss.
High blood pressure.
High blood sugar.
Bone loss.
Heart problems.
Problems with thinking and memory
Acromegaly

99
Q

What conditions can cause Raynaud’s

A

Lupus (systemic lupus erythematous)
Scleroderma.
CREST syndrome (a form of scleroderma)
Buerger disease.
Sjögren syndrome.
Rheumatoid arthritis.

100
Q

Causes of myxoedema coma

A

extreme complication of long-standing hypothyroidism
anaesthesia, barbiturates, b blockers, directs, lithium, phenytoin