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Human Disease > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Definition of diabetes mellitus

A
  • Clinical syndrome associated with chronic hyperglycaemia

- Results from relative insulin deficiency, peripheral tissue insulin resistance or both

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2
Q

Which hormones control blood sugar levels? Where are they released and what is their effect?

A

-Insulin
Decreases blood sugar levels
Released in hyperglycaemic conditions, inhibited in hypoglycaemic conditions
Produced in B cells of the islets of Langerhans

-Glucagon
Increase blood sugar levels
Released in hypoglycaemic conditions, inhibited in hyperglycaemic
Released from a cells of the Islets of Langerhans

-Cortisol
Steroid hormone of glucocorticoid class
Increases blood sugar levels
Released in stress and hypoglycaemic conditions
Released from zona fasciculta of the adrenal cortex in the adrenal gland
Promotes gluconeogenesis

-Catecholamines eg adrenaline
Released in hypoglycaemic conditions, stress response and increase in sympathetic acitvity
Increases blood sugar levels
Released from the adrenal medulla

-Growth hormones
Increases blood sugar levels
Released from pituitary gland
Promotes gluconeogenesis

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3
Q

How does hyperglycaemia typically develop

A
  • Imbalance of glucose homeostatic hormones

- For example, lack of insulin or excess of glucagon/cortisol and catecholamines

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4
Q

Two types of diabetes and definition

A

-Type 1 Diabetes
Insulin-Dependent Diabetes Mellitus
Results from an autoimmune destruction of the pancreatic B cells
Process occurs in genetically susceptible individuals
Autoantibodies directed against insulin
Association with other organ-specific autoimmune diseases
Sometimes secondary to pancreatitis or pancreatectomy, crushings dx or acromegaly, drugs eg steroids and thiazide diuretic

-Type 2 diabetes
Non-insulin dependent type diabetes
Environmental factors such as central obesity trigger the disease in genetically susceptible individuals
-B cell mass reduced by 50% so hyperglycaemia arrises by inadequate insulin secretion and peripheral tissues that become insulin resistant

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5
Q

Different between IDDM and NIDDM

in terms of
Epidemiology, onset, habitus, weight loss, serum insulin, ethnicity, fam history, aetiology and clinical

A 
-Epidemiology
Younger pts (10-20) for Type 1
Older pts (40+) for Type 2

-Onset
Acute for T1
Chronic for T2

-Habitus
Lean for T1
Obese for T2

-Weight loss
Usual for T1
V.rare for T2

-Serum insulin
Low/absent in T1
Normal at rest in T2

-Ethnicity
Often European in T1
Anyone in T2

-Fam history
Uncommon in T1
Frequent in T2

-Aetiology
Autoimmune/viral in T1??
No evidence of immune related in T2

-Clinical
Always require insulin (insulin deficient) in T1
Diet/oral hypoglycaemics as partial insulin deficient they occasionally need insulin in T2

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6
Q

Symptoms of hyperglycaemic

A
  • Excess blood glucose beyond renal re-absorption limit so enters unine and:
  • Osmotic diuretic leads to polyuria and thirst as excess fluid and electrolytes lost by the diuretic effect
  • Weight loss, lethargy, fluid depletion and fat/protein breakdown as cells cant use glucose

In IDDM, weight loss may be the first symptom

  • Blurred vision
  • Ketoacidosis

In NIDDM, clinical features also include:

  • obesity
  • lichen planus, oral candidosis
  • CV disease
  • neuropathy
  • retinopathy
  • renal disease

Onset longer with milder signs and symtpoms in older cases
Youngsters can present with a shorter history

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7
Q

Diagnosis diabetes

A

-A random blood glucose finger-prick test of >11mmol/l is clear cut diabetes
If random is <8, then diabetes in unlikely
-A fasting blood glucose finger prick test of >6.7mmol/l is clear cut diabetes
If fasting is <5.5mmol/l then diabetes is unlikely

If unsure, you can do an equivocal test: Glucose tolerance test
-75g of glucose given orally after an overnight fast
-BG measured at the end of the fast and 2 hours after the glucose
-At the end of the fast:
A BG of >6.7mmol/l suggests diabetes
A BG of <6.7 suggests either normal or impaired glucose tolerance
-2 hours after the glucose:
A BG of >10 suggests DM
A BG of 6.7-10 suggests impaired glucose tolerance
A BG of <6.7 suggests normal

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8
Q

Management of hyperglycaemic patients

A
  • Control and alleviate symptoms of hyperglycaemia
  • Achieve best control of blood glucose as near normal as possible
  • Minimize long term complications
  • Multi-disciplinary team including diabetologist, GMP, dietician, community nurses and GDP
  • Improve gingival health

-Specific treatment for IDDM:
Hyperglycaemia controlled with insulin
3 types of insulin:
Actrapid- fast acting (onset 15-60 mins duration 4-6hrs)
Monotard- intermediate acting (12-24hrs) or long acting (>24hrs)
Mixtard- mixture of long and shorting insulins

-Specific tx for NIDDM:
Dietary control- help and encourage pts to lose weight
Oral Hypoglycaemics as shown below:
Sulphonylureas-increase B cell insulin secretions and reduce peripheral resistance to insulin action
Glibenclamide
Tolbutamide
Boguandines- MOST COMMON (METFORMIN)- decreases gut absorption and increases peripheral tissue insulin sensitivity. It also does not increase apetite so good for the obese. But may cause diarrhoea and lactic acidosis

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9
Q

Measuring control of blood glucose levels

A

-Fingerprick glucose:
Read by test strips or digital readout glucometer

-Urine dipstix:
Crude as glucose only appears in urine if blood glucose exceeds the renal threshold of that individual
Info often out of date as well because urine lags behind blood

-Lab serum glucose
More accurate
Gives accurate level at the time of test
But have to wait a while cus youre sending it off

-HbA1c
Long term control review is useful measure of average control over life of Hb molecule (6 weeks)

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10
Q

Examples of diabetic emergencies

A

-Acute Hypoglycaemia
-Diabetic Ketoacidosis
Both can lead to hypoglycaemic coma

Also diabetic collapse is an emergency

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11
Q

Acute Hypoglycaemia definition and causes

A
  • Type 1 diabetic becoming hypoglycaemic
  • Blood glucose<2.2mmol/l
  • Frequent complication of insulin therapy

-Sometimes a problem with sulphonylurea drugs
-Liver and renal failure jeopardises hepatic and renal cortical gluconeogenesis
-Excess alcohol inhibits hepatic gluconeogenesis
-Insulinomas produce an excess hormone
-Addison’s disease leads to low cortisone production which impairs gluconeogenesis
-Self-management problem:
Pt must match insulin dose to dietary intake
If pts vomits or skips meal then normal insulin dose can lead to relative overdose and hypoglycaemic risk

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12
Q

Signs and symptoms of acute hypoglycaemia

A
  • Increased sympathetic tone
  • Causes hunger, sweating, pallor and tachycardia
  • Personality changes such as aggression, peripheral tingling and altered sensations
  • Fits, hemiparesis and ultimately coma will supervene
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13
Q

What kind of pts are most at risk to acute hypoglycaemia and why

A
  • Those with autonomic neuropathy

- They lose early warning signs such as sweating, pallor and hunger

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14
Q

Investigations of acute hypoglycaemia

A
  • Finger prick blood glucose AND lab serum glucose

- But tx begins while awaiting the results

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15
Q

Tx for acute hypoglycaemia

A

-If patient is conscious, rapid ingestion of sugar is essential

-If pt is unconcious then IV glucose can be given (50ml 50% dextrose)
or glucagon (1mg through an intramuscular injection)
Never give glucagon twice

  • Should be followed by in-patient care aimed at sustained glucose supply
  • To match relative insulin excess
  • Constant blood glucose monitoring
  • Until the cause of hypo is identified and rectified
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16
Q

If you think a pt has collapsed because of hyperglycaemia but not 100% sure what should you give the pt

A

Dextrose
NEVER GIVE INSULIN IF IN DOUBT

Extra glucose does fuck all if hyperglycaemic but in hypoglycaemia it can become a fatality

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17
Q

Complication of diabetes

A
  • Poorer control and earlier onset reduces life expectancy
  • Main causes of death over 50 include heart disease, atheroma, stroke, peripheral vascular disease

-Macrovascular
Accelerated atheroma- additive with other large vessel disease risk factors (hypertensions, hyperlipidaemia and smoking)
Stroke (Ischaemic heart disease/MI or ischaemia limbs/gangrene)

-Microvascular (body wide but 3 main sites of danger)
1) diabetic retinopathy- blindness
2) diabetic nephropathy- renal failure
3) diabetic neuropathy- irreversible glove and stocking loss of peripheral sensation
autonomic system failures eg impotence, loss of joint and position sense

-Infection
Poorly controlled diabetes reduces polymorph function so can lead to increased risk of UTI and skin infections

-Skin
Lipodermatosclerosis- fatty lumps at repeatedly over used injection sites
Necrobiosis liopoidica diabeticorum= red waxy brown deposits on the shins
Granuloma annulare= fleshy nodules over extensor surfaces of the fingers

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18
Q

Diabetic ketoacidosis

A

Dont understand this need to look it up

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19
Q

Special circumstances of DM

A

-If pregnant
Poorly controleld diabetic women run greater risk of congenital defects in pregnancy

-If undergoing surgery
Smooth diabetic control minimizes the risk of hypo/hyperglycaemic infections
Provides the best control/balance to starvation and body’s catabolic response to surgery

For IDDM:
First on op list
Convert long to short acting insulins 1-2 days before
5% dextrose/insulin given during surgery and until normal eating is resumed
Either by infusions or a sliding scale

For NIDDM:
Convert long to short acting drugs prior to surgery date
Consider IV regimes if procedure too long or wont allow post op eating

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20
Q

Dental Relevance of Diabetes Mellitus

A
  • Increased incidence of caries and other dental infections
  • Predisposed to oral candidasis
  • Periodontal disease
  • Xerostomia
  • Sialosis
  • Oral hypoglycaemia may be associated (lichenoid reactions)
  • Peripheral mononeuropathy may present in the facial and oropharyngeal area
  • Timings of appointments is important to minimize risk of a hypoglycaemic event occuring
  • Dental procedure may be complicated by long-term medical problems of diabetes including ischaemic heart disease, chronic renal failure and autonomic and peripheral neuropathy
  • Avoid appointments at the end of the day in case a complication occurs
  • routine tx under LA should be undertaken so that completion of the dental procedure and recovery occurs before a meal is due
  • For GA, appropriate referral to a specialist center is necessary
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21
Q

Adrenal gland functional parts and respective functions

A

-Adrenal medulla (inner)= involved in catecholamine (adrenaline) production

-Adrenal Cortex (outer) consists of 3 parts:
zona glomerulosa- aldosterone
zona fasciculata- glucocorticoids (cortisol)
zona reticularis- sex hormones

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22
Q

Functions of glucocorticoids and what is the main glucocorticoid

A
  • Increase protein catabolism
  • Increase gluconeogenesis
  • Increase glycogenolysis
  • Sensitize arterioles to noradrenaline action which is vital to blood pressure maintenance

-Cortisol is the main glucocorticoid

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23
Q

How is glucocorticoid secretion regulated

A
  • Higher centres lead to increased secretion of CRF from hypothalamus
  • Leads to increased ACTH from the anterior pituitary gland
  • CRF release has a circadian rhythm which is minimal at midnight and peaks at 8am

-ACTH leads to increased production and release of cortisol from the cortex of the adrenal gland

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24
Q

Outline syndromes related to glucocorticoid secretions

A
  • Deficiency of ACTH is a sign of secondary adrenal insufficiency (suppressed production of ACTH due to an impairment of pituitary gland or hypothalamus)
  • Addison’s syndrome occurs when adrenal gland production of cortisol is chronically deficient (primary adrenal insuficiency), leading to chronically elevated ACTH levels
  • Cushing’s syndrome occurs in prolonged exposure to glucocorticoids such as cortisol
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25
Q

Cushing’s disease v Cushing’s syndrome

A
  • Cushing’s syndrome encompasses all the signs and symtpoms due to prolonged exposure to glucocorticoids such as cortisol
  • Many causes including medication (most commonly) and due to a pituitary adenoma (2nd most common)
  • If the cause is related to an increase in ACTH (often caused by a pituitary adenoma), then it is known as Cushing’s disease
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26
Q

Cushing’s syndrome definition and aetiology

A

-Persistant and inappropriately high plasma cortisol levels

  • Most commonly caused by exogenously supplied steroid eg. asthma, Rh A and MS (medications)
  • Cushing’s disease is different- refers to glucocorticoid excess secondary to inappropriate ACTH secretion only (often due to a pituitary adenoma)

-Can also be ACTH-independent such as an adrenal adenoma or adrenal carcinoma, which would secrete more cortisol independent of ACTH levels

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27
Q

Relation of alcohol and Cushing’s syndrome

A
  • Sometimes alcohol can mimic Cushing syndrome clinically and biochemically
  • Named pseudo-cushings syndrome
  • Pathogenesis not understood
  • Resolves on cessation of alcohol
28
Q

Clinical features of Cushing’s Syn

A
  • Obesity- fat centrally distrubuted, trunk, abdomen and buffalo hump on nek
  • Plethoric complex and thin skin which bruises easily
  • Moon face
  • Purple striae on abdomen breasts and thighs
  • Pigmentation (melanin if ACTH dependent)
  • Depression
  • Muscular weakness
29
Q

Investigations of Cushing’s Syndrome

A
  • Raised plasma cortisol (loss of circadian rhythm so often high during night)
  • Raised urinary cortisol
  • Plasma ACTH is low/undetectable in ACTH independent disease (for example in adrenal adenomas)
  • CXR/Bronchoscopy/CT scan to find the tumour
30
Q

Management of Cushing’s Syndrome

A
  • Surgical removal of pituitary adenoma if Cushing’s disease
  • Metyrrapone inhibits cortisol release in the short-term
  • Pituitary irradation can be used as salvage for impossible or failed surgery but risk of irradiating entire pituitary gland rather than just the anterior. Also have to compensate for other hormones
  • Iatrogenic cushings disease (too much steroids) responds to reduction/cessation of the steroid. Immunosuppresive doses of steroid reduced with steroid saving stratagies
31
Q

Dental Relevance of Cushing’s syndrome

A
  • Prone to infections
  • Poor wound healing
  • Pts may be diabetic
  • Bruise easily
  • Depression/anxiety
  • Hypertensive
  • Emotionally labile
  • Visual loss if Cushing’s disease
  • Immunosupression possible
32
Q

Definition of Addison’s Syndrome and distinguishing between Addison’s Disease along with aetiology of each

A
  • Long-term endocrine syndrome associated with hypoadrenalism
  • Adrenal glands do not produce enough glucorticoids (cortisol)

-If caused specifically by the destruction of the adrenal cortex (eg. post partem haemorrhage in which the adrenal gland is destroyed) then it is known as Addison’s Disease
-Addison’s syndrome is much more common:
Caused by suppression of steroid production by exogenous therapeutics
80% are autoimmune

-If tx stops suddenly or is not increased to cover illness or stress then the pt is unable to make their own steroid

33
Q

Clinical features of Addison’s Disease and worse case

A
  • Insidious development of lethargy, anorexia and weight loss
  • Postural hypotension
  • Hyperpigmentation of buccal mucosa, skin creases and scars (excess ACTH stimulates melanocytes)

-Can present as an Addisonian Crisis:
Where inadequate levels produce a hypotensive crash
Leads to vomiting, abdominal pain, low Na, high K, hypoglycaemia, hypovolaemic shock with no bleeding

34
Q

Addisonian Crisis/Adrenal Crisis definition, clinical features and management

A
  • Constellation of symptoms
  • Vomiting, abdominal pain, low Na, high K
  • Results of either previously undiagnosed Addison’s disease or a process suddenly affecting adrenal function
  • Leads to a hypotensive crash
  • Remember cortisol sensitizes arterioles for noradrenaline action
  • Steroids are important for vasoconstriction
  • In a fight or flight symptoms, if there is no cortisol, there is no vasoconstriction of the GI system and skin
  • Blood goes everywhere in the body as there is no vasoconstriction anywhere
  • Leads to a hypovolaemic shock where the volume of blood is inadequate to fill expanded vascular tree

-Urgent treatment involves cortisone supplements, and saline on IV

35
Q

Investigations of Addison’s Syndrome

A 
-Serum Chemistry
Na low
K raised 
Urea Up
Hypoglycaemia
  • Adrenal auto-antibodies may be present
  • CXR may show evidence of tuberculosis, for example calcified nodes and adrenals

-Short Synacthen Test (synthetic ACTH): blood taken for baseline plasma cortisol then 250 iv and take cortisol levels at 30 and 60 minutes
Adreno-cortical insufficiency excluded if basal cortisol >170nmol/l or if rises are greater than 330 and 690nmol/l at the time intervals

36
Q

Management of Addison’s Syndrome

A

-Supplementation for life
Hydrocortisone 20mg orally in the morning and 10mg at night to mimick the circadian rhythm
Fludrocortisone every morning which is a synthetic mineralcorticoid

During stresses, additional supplementation may be essential

37
Q

Secondary Hypoadrenalism definition and cause

Difference in clinical findings

A
  • Hypothalmic pituitary axis disease
  • Basically the pituitary gland releases less ACTH
  • Leading to lack of cortisol production from the adrenal gland
  • Clinical features identical to Addison’s syndrome but no pigmentation as ACTH levels are low
  • Long term steroid therapy required
38
Q

Dental Relevance of Addisonian patients

A

-oral pigmentation is often the first sign
Light brown to black on buccal mucosa
Only if ACTH levels are high, so not in secondary hypoadrenalism patients

-Patients require steroid cover prior to treatment
100-200mgl of hydrocortisole iv if short procedure. Multi dose if longer

-Hypotensive or fainting episodes may occur on alighting from the dental chair
BP and IV access if mandatory

-Increased susceptibility to oral infection

39
Q

Mineralocorticoids definition and where do they work. Most common mineralocorticoid and where is it released

A
  • Steroid hormones that promote renal sodium reabsorption and potassium excretion
  • Via Na/K exchange pumps in the distal convoluted tubule
  • Vital in regulation of extracellular fluid volume and blood pressure
  • Aldosterone is the most important mineralocorticoid
  • Released from zona glomerulosa of adrenal cortex
  • Secretion is principally independent of ACTH
  • Driven primarily by the renal Renin-Angiotensin system
  • Increased by low plasma Na or low BP
  • High K stimulates aldosterone secretion directly
40
Q

Explain the control of aldosterone secretion

A
  • Low blood pressure or low sodium concentration stimulates release of angiotensinogen into the circulation by the liver
  • Renin cleaves angiotensinogen into angiotensin 1
  • ACE converts angiotensin 1 into angiotensin 2
  • Adrenal glands release aldosterone, leading to increased sodium retention and an increase in blood pressure
41
Q

Definition of Conn’s Syndrome and causes

A
  • Hyperaldosteronism
  • Excess aldosterone
  • Primary- due to adrenal adenoma or hyperplasia, leading to excess fluid retention (Where sodium goes water follows), hypokalaemia and secondary hypertension

-Secondary hyperaldosteronism caused by excess stimulation through the renin-angiotensin axis

42
Q

Examples of endocrine systems causing hypertension

A

Excess renin production
Renal A.stenosis or renin secreting tumour
Excess aldosterone production
Adrenal adenoma or hyperplasia
Excess production of other steroids such as in Cushing’s
Excess catecholamines

43
Q

Investigations of Conn’s syndrome

A
  • Serum K low
  • Serum Na high in primary, but low in secondary
  • Alkalosis
  • Serum aldosterone level high in primary but in secondarym the plasma renin is increased
  • Ct/MRI to show adrenal masses
44
Q

Management of Conn’s syndrome

A
  • Surgical resection of an adenoma

- Hypertension from hyperplasia can be combatted using spironolactone (aldosterone antagonist)

45
Q

Definition of Congenital adrenal hyperplasia

A
  • Congenital defect in steroid synthesis
  • Leads to low cortisol levels
  • aldosterone levels in severe cases
  • Hypotension
46
Q

Growth hormone role and release. Control. What happens if u have too much/little

A
  • Secreted by the adenohypophysis in the anterior pituitary
  • GHRF in hypothalamus leads to release of GH from anterior pituitary. Negative feedback mechanism
  • Effects are mediated via Insulin like Growth Factor 1 which is synthesised in the liver
  • GH deficiency in kids produces a dwarf (short stature with proprtionate trunk and limbs)
  • Excess GH in kids leads to gigantism

-In adults hypoproduction GH is silent clinically but maybe some evidence of reduction of well-being and mental work capacity

47
Q

Definition of acromegaly and cause

A
  • Growth hormone excess in adulthood
  • Typically produced from a benign anterior pituitary acidophil adenoma
  • Rarely from excessive GHRF release
48
Q

Clinical features of acromegaly

A
  • Enlarging head, hands and feet as these are the only limbs that can still grow in adulthood
  • Gloves and shoes dont fit
  • Chin enlarges, dentures too small
  • Some patients may notice headaches and visual field defects as pituitary adenoma presses on the optic chiasm
49
Q

Investigations of acromegaly

A
  • Glucose tolerance test as 25% of acromegalics have diabetic tolerance test
  • Elevated serum GH and IGF1
  • Lateral skill radiographs abnormal
  • CT/MRI shows the tumour in sella turcica
  • Visual field defects
50
Q

Management of acromegaly

A
  • Untreated acromegaly leads to reduced survival
  • Most deaths result from heart failure, coronary artery disease (diabetes link) and hypertension related causes

-Surgery to remove pituitary tumour
-Often use Deep x ray therapy as difficult to ensure tumour free resection margins
-Radiotherapy
-Drug:
Octreotide- long acting somatostatin analogue
Controls difficult cases and can shrink inoperable tumours to resectable proportions
Bromocriptine is reserved for the elderly and frail

51
Q

Describe the control of the thyroid system

A
  • Under control of the hypothalamus (via TRF/TRH Thyrotropin releasing hormone)
  • Anterior pituitary gland then releases Thyroid Stimulating Hormone (TSH)
  • This directly drives thyroxine (T4) and tri-iodothyronine (T3) to the circulation from thyroid gland
  • Plasma T3/T4 levels are negative feedback controlled
  • Most circulating T3 is produced by peripheral conversion of T4
52
Q

Tests to check for hyper/hypothyroidism

A

-Thyroid function tests:
Serum [TSH] and [T3]/[T4] are diagnostic
-Women are 5 times more often affected than men

53
Q

Hypothyroidism definition and causes

A
  • Underreactive thyroid
  • Does not produce enough thyroid tissues
  • Typically due to a primary disease of the thyroid tissue (TSH up, T3/T4 low)
  • Rareley due to a hypothalumus-pituitary axis disease (TSH low, T3/T4 low)

1) Atrophic Autoimmune Hypothyroidism
- Most common aetiology
- Autoantibodies and lymphoid infiltrate of the gland leads to fibrosis and atrophy

2) Hashimoto’s Thyroiditis
- Antimicrosomal antibodies producing atrophic change with regeneration producing a goitre. Pts can be hypo, eu or initially hyperthyroid

3) Iatrogenic
- After surgery/radio iodine therapy for hyperthyroidism 40% of cases become hypothyroid

4) Iodine deficiency (Goitre)
- Swiss Alps and South American diets can be iodine deficient

5) Dyshormonogenesis
- Rare inherited conditions cause by genetic enzyme encoding errors
- Produces defective and innefective thyroxine

54
Q

Clinical features of hypothyroidism

A
  • Hard to diagnose in elderly
  • Cold peripheries
  • Mental slowness
  • Normocytic/macrocytic anaemia
  • Hypercholesterolaemia
  • Hyponatraemia
  • Hypothermia
  • Oedema
  • Mild obesity
55
Q

Management of Hypothyroidism

A

-Lifelong replacement therapy with thyroxine (50-200mcg po daily)
-Assess efficacy and adjust dose on:
Clinical resolution of symptoms
Thyroid function tests (TSH low and normalised T3/T4)

-Severe hypothyroidism can produce dramatic symptoms such as hypothermia, hypoventilation and cardiac failure, untimately ending in confusion and coma
Depression also common

56
Q

Hyperthyroidism definition and aetiology

A
  • Overactive thyroid gland
  • Affects 2-5% of all women

1) Grave’s Disease:
- Most common cause
- IgG autoantibody against TSH receptors stimulate thyroxine production
- Associated with all clinical signs and symptoms but especially with the thyroid eye signs

2) Solitary Toxic Nodules
- Responsible for 5% of all cases
- Prolonged remission is rarely induced by drug therapy

3) Toxic Multinodular Goitre
- Common in elder women
- Drug therapy rarely successful

4) De Quervain’s Thyroiditis
- Secondary to inflammation
- Transitional hypethyroidism
- Fever, malaise and neck pain

57
Q

Clinical features of hyperthyroidism

A

-If grave’s disease, eye signs, pretibial myxoederma, thyroid achropachy (clubbing/swollen fingers/ and periosteal new bone formation)

-Graves Eye signs
Exopthalmos arrises from antibody mediated retro orbital inflammation and oedema
-Proptosis limits eye movements and causes lid lag and corneal scarring as the eyelids cannot close properly
-OAPs often present with atrial fibrillation or heart failure

58
Q

Differential diagnosis of hyperthyroidism and how to rule it out

A
  • Reto orbital tumour

- CT/MRI may be needed

59
Q

Investigations of hyperthyroidism

A

-Thyroid function Tests
-T3 and T4 raised
-If only T3 elevated, then T3 toxicosis
TSH is supressed

60
Q

Management of Hyperthyroidism

A

Carbimazole 10-20mg

  • Inhibits formation of thyroid hormones
  • Mild immunosuppressive powers
  • Can totally block thyroid with increased dose and replace with thyroxine

-B Blockers
Used to control sympathetic symptoms

-RadioIodine
Concentrates in the gland
Localised radiotherapy
Indicated if relapse afer drug treatment

Surgery

  • Subtotal thyroidectomy should IN Patients previously rendered euthyroid
  • Antithyroid gland should be replaced with potassium iodide before surgery to inhibit thyroid hormone release and reduce the vascularity of the gland
61
Q

Goitre

A
  • Swelling of the neck
  • More common in women than men
  • Can be painful and cause dysphagia
  • May be physiological (puberty, pregnancy)
  • Or pathological (Grave’s)

Investigations include:
TFTs
Work out if hypo/hyperthyroid
Radiograph thoracic inlet

62
Q

Hyperparathyroidism definition

A
  • PTH acts with vitamin D to defend serum ionised calcium
  • Negative feedback of serum calcium
  • Increased secretion of parathyroid
63
Q

Causes of hyperparathyroidism

A

-Primary
Unstimulated PTH excess by adenoma inappropriate to serum calcium level
Perhaps due to renal stones, bone disease, peptic ulcers secondary to hypercalcaemia or psychiatric symptoms secondary to hypercalcaemia

-Secondary
PTH hypersecretion develops in response to gut malabsorption of Ca or Chronic Renal Failure Ca losses

-Tertiary
Develops when a secondary hyperplastic parathyroid gland develops autonomy
Adenoma no longer simply compensating for calcium losses

64
Q

Clinical features of hyperparathyroidism

A
  • Little to see
  • Porosis of bone on X ray
  • Skull and osteoclast masses can erode dental roots
65
Q

Investigations of Hyperparathyroidism

A
  • Serum Ca up
  • Phosphates down
  • Increased alkaline phosphatase indicating bone resorption
  • Serum PTH elevated in face of high Calcium is diagnostic
  • Hypercalciuria
66
Q

Tx for hyperparathyroidism

A
  • Ct/MRI the adenoma
  • Neck ultrasound
  • All 4 glands must be identified as multiple adenomas can arise

Human Disease (19 decks)

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