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YR3 HUD > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What cells does glucose bind to?

A

RBC and nerve cells

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2
Q

What are the hypoglycemic and hyperglycemic drugs we need to be aware of?

A

Hypoglycemic = insulin

Hyperglycemic = glucagon, growth hormone, catecholamines, cortisol

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3
Q

What cell is insulin made in?

A

Beta cells of islets of langerhan in the pancreas

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4
Q

Why do catecholamines raise blood sugar levels?

A

Released in response to stress to raise blood glucose for fight or flight response

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5
Q

What is the aetiology of type 1 diabetes?

A

Autoimmune condition causing destruction to pancreatic beta cells OR removal of pancreas

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6
Q

Are these conditions part of type 1 or type 2 diabetes?

1) Occurs in younger people
2) Weight loss is common
3) No links to HLA
4) Oral hypoglycemics is the treatment

A

1) 1
2) 1
3) 2
4) 2

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7
Q

What are the main symptoms of hyperglycemia?

A 
Increasing frequency of passing urine
Increases thirst
Weight loss
Fatigue 
Fat/protein breakdown
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8
Q

If a patient has a blood glucose of 7mmol/l after fasting, what does this suggest?

A

> 6.7mmol/l suggets diabetes

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9
Q

What are the 4 main oral hypoglycemics given?

A
  1. Sulphonylureas
  2. Glibenclamide
  3. Tolbutamide
  4. Biguanides
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10
Q

Why may we given a mixtard of insulin injections to a type 1 diabetic?

A

Mixture of short and long acting insulin yo try and smooth out peaks and troughs

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11
Q

What are the 4 main tests for blood glucose?

A
  1. Finger prick : do this in emergencies
  2. Urine tests : glucose appears in urine when levels are high
  3. Lab tests : accurate but takes hours for result
  4. HBA1C - measures glycosylated haemoglobin for long term monitoring
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12
Q

What oral hypoglycemic commonly causes a hypoglycemic emergency?

A

Sulphonylureas

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13
Q

What are some reasons why hypoglycemic attacks happen?

A
  • Patient does not eat before appointment
  • Liver and kidney failure stopping gluconeogenesis
  • Excess alcohol inhibits gluconeogenesis
  • Insuliomonas producing excess insulin
  • Addison disease (low steroid level so less increase in blood glucose)
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14
Q

What signs and symptoms suggest a hypoglycemic attack?

A
  • Hunger, sweating, increase in temperature
  • Fear and aggression
  • Altered peripheral sensation
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15
Q

If a patient having a hypo goes unconscious, what do we give them?

A

50% 50ml dextrose IV or glucagon 1mg intramuscular

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16
Q

Why does a ketoacidosis occur?

A

Occurs in someone who is an unknown diabetic or a diabetic missing medication.

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17
Q

What are the main ketones produced in ketoacidosis?

A

Acetate, acetoacetate and butyrate

18
Q

What are the main complications to the blood vessels during diabetes?

A

Macrovascular : accelerates atheroma leading to MI and stroke risk

Microvascular:
Retinopathy - leading to blindness
Nephropathy - renal failure
Neuropathy - nerve damage causing tingling to peripheries

19
Q

What is the dental relevance of diabetes?

A
  • Infection : reduced polymorph function. May need antibiotic cover
  • Oral candidiasis and dry mouth : poor infection control and reduction in saliva
  • Periodontal disease and uncontrolled diabetes : reduction in defence mechanism, increase glucose in crevicular fluids
  • Under GA: move to short acting insulin to gain stronger control, sliding scale needed
  • Book early appointments and make sure patient eats before
20
Q

What hormones are produced in the adrenal cortex?

A

STERIODS!

Fasciculata - mineralocorticoids (aldosterone)

Glomerulosa - glucocorticoids (coristol)

Reticularis - sex hormones

21
Q

What are the main roles of glucocorticoids?

A
  • Hyperglycemic molecule (increase blood sugar level)
  • Increase protein breakdown
  • Sensitise the arterioles to noradrenaline action
  • Increase urine production (inhibits ACTH which works on kidney to allow water uptake)
22
Q

What controls glucocorticoid release from the adrenal cortex?

A
  • Hypothalamus releases corticotrophic release hormone to anterior pituitary
  • Anterior pituitary releases ACTH which causes adrenal cortex to release cortisol
23
Q

What controls glucocorticoid release from the adrenal cortex?

A
  • Hypothalamus releases corticotrophic release hormone to anterior pituitary
  • Anterior pituitary releases ACTH which causes adrenal cortex to release cortisol
24
Q

What is caused by too many glucocorticoids?

What are the two reasons this may happen?

A

Cushings disease or syndrome

Disease = EXCESSIVE ACTH produced from pituitary adenoma, ACTH producing tumour

Syndrome = problem with adrenal cortex producing too many glucocorticoids

25
What are the clinical features of Cushing disease?
- Fat face and thin limbs - Red complexion as cortisol causes vasodilation - Moon face due to fat deposits - Purple striae on abdomen and thighs - Pigmentation areas around wounds and scars
26
What will we see for the investigations for cushings?
- High urinary cortisol levels - Lack of suppression of cortisol produced when cortisol is given - High ACTH in cushing disease - Chest X ray looking for tumours on adrenal glands
27
How is Cushings managed?
- Surgical removal of pituitary - Metyrrapone drug to inhibit cortisol release - Pituitary radiation when surgery fails - Reduce the number of steroids given orally
28
What happens in an Addisonian Crisis?
Excess steroid given by mouth for some time to gain control of inflammatory conditions such as RA and MS If drug is withdrawn too quickly, their own endogenous methods cannot pick up cortisol fast enough In a stressful position, they cannot produce adequate cortisol to match adrenaline levels to facilitate vascular shunting (getting blood from gut to lungs&heart&muscles) in fight or flight response They cannot shunt blood from gut via vasoconstriction - everything then tends to dilate Shunting from 5L of blood from a shunted circulation to an open circulation has a CATASTROPHIC EFFECT!!! This leads to blood pressure falling and heart rate rises to compensate More of the blood circulation opens up = blood pressure falls lower and heart rate rises faster Patient collapses into coma due to heart not being able to keep up OR heart is going so fast it enters atrial fibrillation leading to cardiac arrest
29
What system is aldoestone driven by and what does it do?
Renin - angiotensin system Causes sodium reabsorption in the distal convoluting tubule
30
What happens in Conns syndrome?
High aldosterone = too much sodium reabsorption Secondary hypertension
31
How will an investigation tell the difference between primary and secondary conns syndrome?
Primary = high sodium levels in blood Secondary = low sodium in blood (increase in stimulation of renin angiotensin system)
32
What is acromegaly?
Growth hormone produced in excess in adulthood when lots of growth plates in limbs have fused. Leads to abnormally large hands, feet, forehead and mandible.
33
How is the production of thyroxine controlled?
This is made under the control of the hypothalamus via thyrotrophin releasing hormone. The hypothalamus via TRH induces the anterior pituitary to release thyroid stimulating hormone. This then arrives at thyroid to induce release of T3 (tri-iodothryonine) and T4 (thyroxine). This exerts tissue affects and gives a negative feedback loop to hypothalamus.
34
What are the main causes of hypothyroidism?
1)Atrophic autoimmune hypothyroidism = antibodies to thyroid gland leading to fibrosis and atrophy Associated with SLE and rheumatoid arthritis 2) Hashimotos Thyroiditis Antibodies attacking thyroid gland leading to atrophy of gland. Regeneration leads to goitre production 3) Iatrogenic causes - usually after surgery for hyperthyroidism to become hypothyroid and then be managed 4) Iodine deficiency - in the diet or malabsorption, thyroid swells and it needs iodine from blood supply to make thyroid hormones 5) Dsyhormonogenesis : inherited condition producing inactive and ineffective thyroxine
35
How much thyroxine do we give to those with hypothyroidism?
50-200mg daily
36
What are the common causes of hyperthyroidism?
1) Graves disease (auto antibody IgG class antibody against the TSH receptors, antibody binds and simulates T3 and T4). IgG molecule is called long acting thyroid simulator. Tends to lead to thyroid eye signs. 2) Solitary toxic nodules - single nodule grows on the thyroid gland casing it to become enlarged and produced more thyroxin. Drugs aren’t successful 3) Toxic multi nodular goitre - more than one nodule on the thyroid gland. Drugs aren’t successful 4) De Quervain’s thyroiditis - painful swelling of the thyroid gland triggered by a viral infection. Typically accompanied by fever, malaise and neck pain.
37
What is the management of hyperthyroidism?
Drug - carbimazole 10-20mg two times a day - inhibits formation of thyroid hormones, 2) Beta blockers to gain control over the sympathetic symptoms 3) Radio iodine - concentrated in the thyroid gland and leads to radiotherapy here - hard to control but good to suppress thyroxine release 4) Surgery to remove parts of the thyroid gland - Subtotal thyroidectomy is a surgical procedure, in which the surgeon leaves a small thyroid remnant in situ to preserve thyroid function, thereby preventing lifelong thyroid hormone supplementation therapy.
38
Why can hyperthyroidism cause dysphagia?
Goitre on the thyroid gland can press on oesophagus
39
Why may someone have hyperparathyroidism?
Increase secretion of parathyroid hormone in response to low serum calcium.
40
What is the difference between primary, secondary and tertiary parathyroidism?
Primary = adenoma producing parathyroid hormone Secondary = parathyroid hormone increasing due to gut malabsorption of calcium Tertiary = hyper plastic parathyroid gland develops autonomy and becomes self regulating

YR3 HUD (23 decks)

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