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GP - General Practice > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Define Diabetes Mellitus

A

Endocrine disorder characterised by lack of insulin or the increased resistance to insulin

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2
Q

Define Type 1 and Type 2 Diabetes.

A

Type 1 (age <30): Autoimmune disease characterised by the destruction of islet cells responsible for the production of insulin

Type 2 (Age >65):
Progressive disease resulting from reduced insulin secretion AND increased insulin resistance.

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3
Q

Which type of diabetes is associated with weight loss?

A

1

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4
Q

Which type of diabetes is associated with Diabetic ketoacidosis?

A

1

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5
Q

What is metabolic syndrome?

What are the features of metabolic syndrome?

A

Metabolic syndrome is a cluster of features that occur together increasing the risk of heart disease, stroke, and T2DM
1) Abdominal obesity (<40inch male, <35 inch female)
2) BP >130/85 or on BP meds
3) Fasting glucose >5.6
4) High TGs
5) Low HDL

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6
Q

Which type of diabetes is associated with LADA - Latent autoimmune disease in adulthood?

Define LADA
When should you suspect LADA?

A

Type 2 DM (6-10% of patients with T2DM develop this)

LADA is a latent autoimmune disease characterised by Anti-GAD antibodies and is associated with increased risk of insulin dependence and ketoacidosis (basically think of them becoming type 1)

Suspect if either:
1) T2DM
2) Absence of metabolic syndrome features
3) Uncontrolled hyperglycemia despite oral medical management.
4) other autoimmune diseases (Thyroid, pernicious anaemia)

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7
Q

What is MODY?
When should you suspect?
How is it diagnosed?

A

Maturity-Onset Diabetes of the Young
Patients <25yo with family hx of diabetes.

Diagnosed via genetic testing of HNF1-alpha (main one). (also HNF1beta, HNF4alpha, glucokinase)

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8
Q

Give 5 RF for T2DM

A

1) Age >65
2) Obesity
3) Past medical hx of GDM or macrosomia (7x)
4) Pancreatic Disease (Pancreatic Ca, surgery, pancreatitis, CF, Haemochromatosis)
5) Endocrine: Cushing’s thyrotoxicosis, phaechromocytoma, acromegaly.
6) Drugs: Steroids
7) Anti-glutamic acid decarboxylase (LADA)
HNF1alpha (MODY)
8) Fam Hx of diabetes
9) Ethnic (south asians/afrocarribean)

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9
Q

Why is HbA1c superior?

A

Blood glucose may be temporarily raised during acute illness, steroid use, after trauma etc.. HbA1c tests the % of hemoglobin that is glycated due to exposure to glucose in the blood.

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10
Q

Give 3 tests used in the diagnosis of diabetes.

Give the ranges of each test for Normal, pre-diabetes, and diabetes

A

Fasting glucose:
Normal <6
Pre-diabetic 6-7
Diabetes: 7+

OGTT - 1hr post-prandial
Normal <7.8
Pre-diabetic 7.8-11
Diabetes >11

HbA1c
Normal <42%
Pre-diabetic 42-48%
Diabetes >48

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11
Q

Explain the diagnostic algorithm for Diabetes

A
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12
Q

What is the diagnostic definition of pre-diabetes?

How would you manage a patient with pre-diabetes? (not in depth)

A

Fasting Glucose 6-7
OGTT 7.8-11
HbA1c 42-48%

These people are at risk of developing full-blown diabetes => should begin lifestyle changes now to prevent diabetes.

=> Management is followup w/annual Fasting glucose/HbA1c + Lifestyle modifications

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13
Q

How can diabetes present?

A

Acute: Ketoacidosis (mostly Type 1 and LADA Type 2) or hyperosmolar non-ketotic coma

Subacute: Weight changes, polydipsia, polyuria, lethargy, recurrent infections, visual disturbances, paraesthesia

Chronic: Complications of diabetes (nephropathy, neuropathy, eye disease, skin changes, diabetic foot)

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14
Q

State the 9 complications of Diabetes

A

1) Hypoglycemia
2) Recurrent UTIs
3) Diabetic Nephropathy
4) Cardiovascular
5) Skin changes
6) Eye disease (retinopathy)
7) Diabetic neuropathy
8) Diabetic Foot
9) Depression

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15
Q

What are the symptoms of hyperglycemia

What are the symptoms of hypoglycemia

A

Hyper: Polydispsia, Polyuria, urinary frequency, weight changes, lethargy

Hypo: Polyphagia, sweating, tremor, lightheadedness, fits/seizures, altered GCS/coma, tachycardia

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16
Q

How would you manage a hypoglycaemic episode?

A

3x oral glucose tablets/sugar drink/glucogel (babies) followed by complex carbs

If cannot because unconscious, IM 1mg glucagon followed by IV 10% glucose/dextrose followed by complex carbs

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17
Q

There are 2 scenarios whereby IM glucagon would be much less effective. What are they?

A

Patient is drunk
Patient is starved

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18
Q

A patient has just been diagnosed with diabetes requiring insulin. What would you tell them with regards to hypoglycaemic episodes and their prevention (Give 5)

A

Prevention:
1) Advise on pattern of checking before exercise and after meals
2) Importance of adherence to insulin/meds and alter insulin to match needs
3) Explain the signs of hypoglycaemia to look out for them: Polyphagia, sweating, tremor, lightheadedness, fits/seizures, altered GCS/coma, tachycardia
4) Reduce alcohol intake as that may induce “starvation: and hence reduced effectiveness of IM glucagon
5) Blood sugar diary: Assess frequency of testing and control of sugar levels
6) Glucagon kit. Advise family members of signs of hypoglycemia and how to safely administer IM glucagon injection

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19
Q

Why do diabetics get recurrent UTIs?

A

Weakened immunity + Diabetic nephropathy exacerbates renal failure and causing scarring especially in uncontrolled cases. This leads to papillary necrosis and hence increased risk of UTIs

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20
Q

Diabetes is the most common cause of end-stage renal failure. Diabetes causes the progressive loss of renal function. How does this affect
GFR
BUN
Protein
BP

A

Progressive loss of renal function (reduced GFR, increased BUN, proteinuria and BP)

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21
Q

What investigations would you conduct to rule out or screen for evidence of diabetic nephropathy?

A

1) ACR/PCR (albumin-creatinine ratio) (>70-refer)
2) eGFR (<30-refer)
Conduct these annually and refer to renal physician for Renal US if CKD grade 4/5 (eGFR<30) or ACR > 70
3) Folic acid/B12 (pernicious anaemia)

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22
Q

How is ACR (albumin-creatinine ratio obtained)?

A

Urine

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23
Q

How would you specifically manage a patient with diabetic nephropathy in GP practive?

A

1) Optimise blood glucose control: adherence, adjust dose, consider insulin pump
2) Prevent renal damage: Reduce dosages and avoid nephrotoxic drugs. Adjust doses of medication dependent on renal elimination
3) Treat BP: ACE inhibitor/ARD, Atorvastatin
4) Supplements: Vitamin B12 and Folic acid

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24
Q

What are the cardiovascular complications of Diabetes?

A

Remember metabolic syndrome with the increased risk of T2DM (this), stroke MI, PVD (atherosclerosis)

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25
Q

How would you medically manage atherosclerosis?

A

Plaques => lipid and platelets => Statin therapy and antiplatelet therapy

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26
Q

What is Vitiligo?

A

Patches of skin losing pigment

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27
Q

State 5 skin complications of Diabetes

A

1) Vitiligo
2)Predisposition to infection (candidiasis) => Neuropathic and ischaemic ulcers
3) Xanthoma/Xanthalasma
4) Necrobiosis Lipoilica (small dusky-red nodule on shin that become yellow-brown in colour before ulcerating)
5) Acanthosis Nigricans
6) Diabetic Cheiroarthropathy (Skin thickening ver dorsum of hand causing restricted mobility)
7) Diabetic Dermopathy (pigmented scars over shins)

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28
Q

State the 3 main eye complications of diabetes

A

Blurred vision
Cataract
Retinopathy

Others include: optic neuropathy, retinal vein occlusion and ocular nerve palsies

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29
Q

Poor control in diabetes is the main cause of eye complications such as blurred vision and Cataracts. What are the 2 types of cataracts that are a result of poorly controlled diabetes.

How would you manage it?

A

Juvenile Cataracts (more common) which can develop over days

Senile cataracts can occur very early (on average 10 years earlier than juvenile)

Cataract surgery

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30
Q

95% of T1DM and 60% of T2DM will have retinopathy. 20-40% of T2DM will have retinopathy at diagnosis, 5-10% of which are sight-threatening. What is the pathophysiology of Retinopathy?

A

Small retinal vessels become blocked (atherosclerosis) or swollen (aneurysm) => ischaemia => Inflammation => leaky exudate formation, oedema, haemorrhages, and angiogenesis (new immature vessels quickly to regain supply)

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31
Q

Diabetic retinopathy is the most common cause of blindness in people of working age (18-65). How is diabetic retinopathy classified/staged?

A

Non-proliferative: Microaneurysms, haemorrhages, venous bleeding (graded by number of microaneurysms)

Proliferative: + angiogenesis/new vessel formation (graded by how close they are to optic disc)

Maculopathy: + Involvement of macula => macular oedema

Retinal detachment: Severe complication due to haemorrhages of abnormal vessel formation => scarring and fibrosis

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32
Q

How would you assess for diabetic neuropathy

A

Neuropathic ulcers
Paraesthesia
Pain
Erectile dysfunction

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33
Q

What are the 2 main causes of diabetic foot ulcers?

A

Peripheral vascular disease: Atherosclerosis causing reduced flow => increased pain (ischemic) and predisposition to infection and ucleration
Peripheral neuropathy: Reduced sensation -> increased risk of unknown breach (and reduced sensation of pain from ischaemia) => ulceration and goes longer unnoticed.

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34
Q

What is Charcot’s arthropathy and give the 2 defining features on exam

A

AKA Charcot’s foot
Neuropathic foot damages due to trauma secondary to loss of pain sensation
Abnormal foot shape/foot deformity
Joint deformity and rigidity

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35
Q

What is this?
What is it used for?

A

Monofilament
Tests for peripheral neuropathy by assessing sensation

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36
Q

Briefly go over the history and examination of a patient presenting for their annual diabetic foot check.

A

Incorporate this to any hx and exam concerning diabetes
Hx: Assess
1) Foot problems since last review
2) Knowledge of foot care and self-care behaviours
3) Visual or mobility problems affecting self-care
4) Hx of numbness, paraesthesia, burning

Examination:
1) Foot shape, deformity, joint rigidity (Charcot’s Arthropathy/foot)
2) Skin condition: fragility, cracking, ulceration, shiny skin, absence of hair (vascular component so same as PVD)
3) Monofilament sensitivity: Testing for sensation

+ ABPI

37
Q

How would you differentiate between Vascular and Neuropathic ulcers

A

Vascular: Cool foot, absent pulses, reduced ABPI, located in webspaces, painful, and clearly defined (punched out)

Neuropathic: Warm, pounding pulses, normal ABPI, located at pressure points!!, painless, irregular/less delienated

38
Q

You perform ABPI on a diabetic patient and notice that there are absent pulses but a normal ABPI. What does this indicate?

A

Calcifications are present which make the artery stiffer. The calcifications are retaining BP but the weakened or absent pulses from atherosclerosis remain

39
Q

How would you educate a patient about footcare in diabetes

A

Ensure that
1) Daily examination of the feet for problems including sensation, swelling, colour change, breaks in skin!! and to seek medical attention if any occur
2) Wear well-fitting shoes and avoid walking bearfoot
3) Hoisery (if ABPI >0.8)
4) Daily washing and careful drying for hygeine
5) Observe lesion if healing properly, otherwise seek medical attention

40
Q

How would you manage a diabetic patient presenting with skin changes associated with PVD and paraesthesia of the foot?

A

Conservative:
1) Supervised exercise program (>2h/week for 3 months) with advice to exercise to the point of maximal pain
2) Foot care via regular chiropody/podiatry
3) Educate about foot care:
a) Daily examination of the feet for problems including sensation, swelling, colour change, breaks in skin!! and to seek medical attention if any occur
b) Wear well-fitting shoes and avoid walking bearfoot
c) Hoisery (if ABPI >0.8)
d) Daily washing and careful drying for hygeine
e) Observe lesion if healing properly, otherwise seek medical attention
4) Optimize diabetic control
5) Optimise vascular RF via RF reduction:
- Reduce intake of fats. avoid saturated fats, low cholesterol diet
+
- Smoking cessation
- Reduce weight (5-10%)
- Regular exercise (150 moderate, 75 high)
- Reduce alcohol intake (<14)
- Reduce salt intake (<6g/day)
- Mediterranean diet: Increase fruit and veg intake (>5/day), fish >2/week
- Reduce caffeine

41
Q

A patient has just been diagnosed with T2DM.
How often will they need to be reviewed?
What is included in that review?

A

6-monthly review:
1) Update on recent life events, new sx, and difficulties with management
2) Review
a) Blood sugar diary
b) Labs: HbA1c, lipid profile, BP, U&E, eGFR, ACR
c) LIfestyle - Dietary behaviours, physical activity, smoking
d) Adherence and injection technique
e) Complications (incl examination) => Hypoglycemic episodes, any infections, skin changes, visual problems + Fundoscopy, Neuropathy (tingling), Foot care, Depression screening

42
Q

A diabetic diet does not need to include expensive diabetic products. A diabetic diet is just a healthy diet. What dietary advice would you give a patient?

A

Aim for 5-10% weight loss
>50% of calories need to be a fibre-rich diet with minimum saturated fat and refined carbs by avoiding ready-made foods etc…
Spread food intake throughout the day to prevent hypoglycemia
Avoid alcohol

43
Q

Diabetes is a chronic condition that requires self-care no matter how well controlled it is in clinic. A patient has just been diagnosed with T2DM. What education would you provide to this patient including lifestyle advice

A

1) General knowledge about
a) The complications of diabetes and how to access diabetic service.
b) Equipment information and administration of medications
c) Problems with pregnancy (miscarriage, Preterm labour, IUGR, macrosomia, NTD, heart…)

2) Diet:
Aim for 5-10% weight loss
>50% of calories need to be a fibre-rich diet with minimum saturated fat and refined carbs by avoiding ready-made foods etc…
Spread food intake throughout the day to prevent hypoglycemia
Avoid alcohol

3) Exercise: Exercise increases insulin sensitivity and reduces BP => reduces most complications. Aim for 150 minutes of moderate exercise/week or 75 high intensity. (or 30 minutes 5/week)

4) Immunisation with annual influenza vaccine and pneumococcal
5) Psychological support, counselling services
6) Smoking and alcohol cessation

44
Q

The medical management of diabetes involves lifestyle changes, hypoglycemic meds, non-hypoglycemic meds, and insulin. Give 3 examples of medications that are non-hypoglycemic used in the treatment of diabetes and 3 hypoglycemic

A

Non-hypoglycemics:
Metformin
DPP4i (Linagliptin)
Pioglitazone

Hypoglycemics:
Sulfonylureas (Glicazine)
SGLT2i (only introduced in triple therapy)
GLP-1 mimetics (Exenatide)

45
Q

What is the indication for GLP-1 mimetics in the management of diabetes?

When it is indicated, what 2 other drugs are prescribed with it?

A

T2DM that has HbA1c >58 despite being on triple therapy AND patient does not wish to go on insulin

Triple therapy with Metformin + Sulfonylurea + GLP1-mimetic

46
Q

What is the aim of diabetic management (in terms of HbA1c)

What is the threshold to begin medical management of diabetes?

What is the threshold to escalate medical management

A

<48 if lifestyle controlled or 1 non-hypoglycemic medication (metformin, DPP4i/linagliptin, pioglitazone

<53 if Hypoglycemic meds or any combination

Medical management begins once the individual is diabetic (HbA1c >48) and is escalated if HbA1c >58 despite current therapy (same at every step)

47
Q

Metformin is not associated with hypoglycemia and is only effective if some endogenous insulin is produced. Its side effects include GI disturbances and impaired B12 absorption with long-term use => Pernicious anemia.
What is the typical starting dose? What is the regimen?
What is it’s mechanism of action?
When should it be stopped?
What is 2nd line to it? Give an example

A

Metformin 500mg TDS. This is then increased monthly until control achieved (<48)

It suppresses gluconeogenesis and increases peripheral glucose utilisation.

As metformin relies on renal excretion, it must be stopped/avoided if eGFR<30. Go for DPP4i (Linagliptin)

48
Q

DPP4i, or dipeptidyl peptidase 4 inhibitor is a non-hypoglycemic medication used in the treatment of T2DM.
Give an example
What is it’s mechanism of action?

A

Linagliptin
Inhibits breakdown of GLP-1 (which promotes insulin secretion by giving negative feedback to glucagon - glucagon-like peptide) => reduces serum glucose.

49
Q

Pioglitazone is a non-hypoglycemic medication used in the treatment of T2DM by reducing peripheral insulin resistance. In the case that these non-hypoglycemic drugs are not sufficient, Hypoglycaemic drugs such as Sulfonylureas and GLP-1 mimetics may be used. Give an example of each and their mechanism of action

A

Sulfonylureas: Glicazine
Augments insulin secretion

GLP-1 Mimetic: Exenatide
Promotes insulin secretion by giving negative feedback to glucagon - glucagon-like peptide) => reduces serum glucose. (same as DPP4i as that just inhibits the breakdown of GLP1 => effect lasts longer)

50
Q

Give an example of a long-acting insulin

A

Insulin Detemir or Glargine

51
Q

Give an example of rapid acting insulin
When should these be taken

A

Lispro taken before meals

52
Q

What is an intermediate-acting insulin?

A

NPH (type containing protamine) Neutral Protamine Hagedorn
Answer: Isophane (which is an example of an NPH)

53
Q

How is insulin administered?
What are the risks of insulin administration (4)?

A

Deep Subcutaneous injections into upper arm, thigh, buttocks, or abdomen

Risks:
Hypoglycemia
Lipodystrophy:
Ecchymosis
Infection
Needle-stick injury
(additional info)
It is advised to teach the patient the technique and allow them to demonstrate it back.
Advise monitoring via blood sugar diary
Provide contact telephone
Teach glucagon kit.
Advise adjustments of dose when starting to achieve acceptable levels.
Fasting >10 => increase by 6-8 units
Fasting 8-10 => increase by 4-6
6-8 => increase by 2-4

54
Q

What is Lipodystrophy?

A

Fat atrophy and hypertrophy with repeat injections in same place => keep changing location of injection

55
Q

What is the first line medical management of T1DM?

A

Insulin with multiple daily injection boluses

1) Basal insulin therapy is long-acting insulin => Insulin Detemir or Glargine
2) Before meals, Rapid acting insuling => Insulin Lispro

Those with BMI >25, + Metformin

56
Q

What is the Full medical management of Type 2 diabetes with its escalations?

A

Refer to goals of HbA1c <48 vs <53 and escalation if HbA1c >58 despite current therapy (same at every step)

1) If pre-diabetic (<48) => lifestyle advice only
2) Once diabetic (48+) => Monotherapy with Metformin or other non-hypoglycemic drugs (DPP4i, Pioglitazone)
3) Dual Therapy: Metformin + any other medication
4) Triple therapy: Metformin + any 2 other medications (here including SGLT2i)
5) Insulin OR Metformin + Sulfonylurea + GLP-1 mimetic

Note that if metformin is not tolerated or eGFR <30, replace with DPPi4 (Linagliptin)

57
Q

What is the Insulin Regimen for T2DM

A

Once triple therapy has failed (>58 despite), Metformin is continued and either:
a) Intermediate-acting insulin => Isophane (NPH) OD/BD
b) Long-acting insulin => Insulin Detemir/glargine

58
Q

What is the indication for an insulin pump

A

T1 or T2DM on insulin >12yo with poor adherence leading to unpredictable shifts in glucose levels
+ HbA1c >69 mmol/mol

59
Q

What is your advise to a newly diagnosed patient with diabetes with regards to exercise

A

Exercise increases insulin sensitivity (reduces resistance)
Reduce your insulin dose before exercise to prevent a hyperglycemic episode
Or take 1-2 glucose tablets before exercise and check levels after

60
Q

What is your advice to a diabetic patient currently suffering from an intercurrent illness e.g. diarrhoea

A

Continue insulin as usual but check more frequently. Monitoring is crucial with an intercurrent illness.
If Type 1 diabetic, ensure regular checks of ketone levels and to attend hospital if feeling unwell

61
Q

Give the Full management plan for a T1DM patient

A

Conservative:
1) General knowledge about
a) The complications of diabetes and how to access diabetic service.
b) Equipment information and administration of medications
c) Problems with pregnancy (miscarriage, Preterm labour, IUGR, macrosomia, NTD, heart…)

2) Diet:
Aim for 5-10% weight loss
>50% of calories need to be a fibre-rich diet with minimum saturated fat and refined carbs by avoiding ready-made foods etc…
Spread food intake throughout the day to prevent hypoglycemia
Avoid alcohol

3) Exercise: Exercise increases insulin sensitivity and reduces BP => reduces most complications. Aim for 150 minutes of moderate exercise/week or 75 high intensity. (or 30 minutes 5/week)

4) Immunisation with annual influenza vaccine and pneumococcal
5) Psychological support, counselling services
6) Smoking and alcohol cessation

Medical:
Insulin with multiple daily injection boluses

1) Basal insulin therapy is long-acting insulin => Insulin Detemir or Glargine
2) Before meals, Rapid acting insuling => Insulin Lispro

Those with BMI >25, + Metformin

62
Q

Give the full management plan for a T2DM patient

A

Conservative:
1) General knowledge about
a) The complications of diabetes and how to access diabetic service.
b) Equipment information and administration of medications
c) Problems with pregnancy (miscarriage, Preterm labour, IUGR, macrosomia, NTD, heart…)

2) Diet:
Aim for 5-10% weight loss
>50% of calories need to be a fibre-rich diet with minimum saturated fat and refined carbs by avoiding ready-made foods etc…
Spread food intake throughout the day to prevent hypoglycemia
Avoid alcohol

3) Exercise: Exercise increases insulin sensitivity and reduces BP => reduces most complications. Aim for 150 minutes of moderate exercise/week or 75 high intensity. (or 30 minutes 5/week)

4) Immunisation with annual influenza vaccine and pneumococcal
5) Psychological support, counselling services
6) Smoking and alcohol cessation

Medical: Refer to goals of HbA1c <48 vs <53 and escalation if HbA1c >58 despite current therapy (same at every step)

1) If pre-diabetic (<48) => lifestyle advice only
2) Once diabetic (48+) => Monotherapy with Metformin or other non-hypoglycemic drugs (DPP4i, Pioglitazone)
3) Dual Therapy: Metformin + any other medication
4) Triple therapy: Metformin + any 2 other medications (here including SGLT2i)
5) Insulin OR Metformin + Sulfonylurea + GLP-1 mimetic

63
Q

A diabetic patient presents with uncontrolled diabetes. What factors may lead to this?

A

Exclude any intercurrent illness
Check blood sugar diary
Consider diet
Check insulin administration, ensuring sites are not scarred or hypertrophic
Consider psychosocial factors
If all fails, there may be an underlying change in insulin resistance/sensitivity

64
Q

You conduct TFTs on a patient. What are the typical results of a patient with hyperthyroidism? Hypothyroidism?

A

Hyperthyroidism: reduced TSH and raised T4
Hypothyroidism: increased TSH, reduced T4

65
Q

What is meant by subclinical Hypothyroidism? (answer based on TFTs)

A

Raised TSH but normal T4

66
Q

What would it mean if TSH and T4 are both low?

A

Pituitary failure

67
Q

You conduct TFTs on a patient and results show low TSH and raised T4. Give the causes

What are the features of hyperthyroidism?

A

Causes:
1) Grave’s disease
2) Toxic nodular goitre
3) Thyroiditis
4) Amiodarone

Features:
Increased metabolism: Heat insensitivity, increased sweating, increased appetite despite weight loss, diarrhoea, palpitations, Brittle/fine hair
Bonus: HTN with widened pulse pressure, tachycardia, atrial fibrillation.

Increased movement: Tremulousness (hand tremor), excessive sweating (warm clammy skin)

Increased mentation: Increased anxiety, insomnia, depression

Women: Hypomenorrhoea
Elderly: Confusion,
Eyes: Exompthalmos, lid lag, double vision
Syncope

68
Q

What is the management of Hyperthyroidism as a GP?

A

Refer to endocrinology

69
Q

How is syncope a feature of hypo and hyperthyroidism

A

A.fib from hyper
Hypotension from Hypo

70
Q

What is the role of beta blockers in the management of thyroid disease

A

Used in hyperthyroidism for symptom control until anti-thyroid therapy takes effect

71
Q

What is the surgical management of hyperthyroidism?

What are the indications?

What are specific risks associated with this surgery?

A

Partial or Total thyroidectomy.

Reserved for patients with large goitres or who decline radioactive iodine or in patients that have had unsuccessful previous treatment

Recurrent laryngeal nerve injury (hoarse voice)
Damage to parathyroid glands => Hypercalcaemia (trousseau and Chvostek’s sign

72
Q

How would you manage a patient presenting with Hyperthyroidism

A

1) Give patient education and refer to endocrinology at presentation
2) Carbimazole
3) Radioactive Iodine
4) Surgery (partial/total thyroidectomy)
+ Beta blocker for symptom control until anti-thyroid therapy takes effect

73
Q

What is the mechanism of action of Carbimazole?

What must you warn patients about when prescribing this medication

A

Inhibits synthesis of thyroid hormone

Agranulocytosis is the major risk factor. Patients should be warned to stop medication and seek urgent help if they develop sore throat or signs of infection

74
Q

A patient is on Carbimazole with uncontrolled thyroid disease. What is the next step?

A

Radioactive Iodine or Surgery (partial/total thyroidectomy) if they refuse

75
Q

A patient is on Carbimazole with uncontrolled thyroid disease. They opt for radioactive iodine therapy.

What should the patient be warned about before starting radioactive iodine therapy?

What are the long term risks?

A

Patients should be warned that it takes 3-4 months for the effects to become apparent.
+ Stop Carbimazole 4 days prior and 3 days after iodine therapy.
+ Advise against pregnancy with 4 months after treatment

Most patients end up hypothyroid years later.

76
Q

What is the most common cause of Hyperthyroidism?

A

Grave’s Disease

77
Q

Grave’s disease is the most common cause of hyperthyroidism. It is associated with smoking.
What is the pathophysiology behind it?

What are the clinical features of Grave’s disease (including exam findings)

A

Autoimmune antibodies (LT) to TSH receptors prevent their down-regulation

Clinical features:
Signs and sx of hyperthyroidism - Increased metabolism: Heat insensitivity, increased sweating, increased appetite despite weight loss, diarrhoea, palpitations
Bonus: HTN with widened pulse pressure, tachycardia, atrial fibrillation.

Increased movement: Tremulousness (hand tremor), excessive sweating (warm clammy skin)

Increased mentation: Increased anxiety, insomnia, depression

Women: Hypomenorrhoea
Elderly: Confusion,
Eyes: Exompthalmos, lid lag, double vision
Syncope

Exam:
Diffuse goitre
Grave’s opthalmopathy
Pretibial Myxoedema
Thyroid acropachy (swelling of finger + Clubbing)
Retrosternal expansion
Thyroid bruit

78
Q

What is thyroid acropachy

A

rare (0.3%)
Thickening of the extremities associated with hyperthyroidism with the characteristic triad of
1) Clubbing
2) Digital and feet swelling
3) New bone formation

79
Q

What is Pre-tibial Myxoedema?
Is the oedema pitting or non-pitting?

A

Thickening and welling of skin over tibia. It is waxy and shiny + colour ranges from pink to brown.

It is non-pitting oedema

80
Q

A patient presents with a large goitre on examination. You conduct blood tests showing raised TSH but low T4. What is the most likely diagnosis?

A

Hashimoto’s thyroiditis

81
Q

Give the top 3 causes of hypothyroidism

A

1) Post- Radioactive Iodine therapy
2) Post- Thyroidectomy
3) Hashimoto’s thyroiditis (Anti-TPO)

82
Q

What are the signs and symptoms of hypothyroidism?

A

Signs:
1) Goitre (Hashimoto’s)
2) Slow reflexes
3) Non-pitting oedema => Myxoedema of the face. eyelids…systemic

Symptoms: (just opposite of hyper)
Depression
fatigue, lethargy
General malasie
Increased weight
Constipation
Cold intolerance
Hair loss
Anhydrosis (dry skin and hair)
Hoarse voice (a/w thyroidectomy)

83
Q

Myxoedema is a feature of both hypo and hyperthyroidism.
Define myxoedema
How would you differentiate

A

Myxoedema is the widespread thickening and non-pitting swelling of the skin as a result of thyroid dysfunction
In both they are non-pitting oedema (definition of myxoedema). In pre-tibial myxoedema (from Grave’s disease), it is localized to the shin => Pre-tibial. In hypothyroidism it is systemic => widespread mostly to the face, eyelids, and feet

84
Q

When someone presents as always being tired what tests will you always order?

A

FBC (anemia) and TFTs (hypothyroidism)

85
Q

What is the management of Hypothyroidism including followup

A

Patient education

<65 and healthy: 50-100mcg Levothyroxine OD
>65 or heart disease: Start at 25mcg levothyroxine (Consider beta blocker propanalol if heart disease)

For both, followup every 4 weeks to adjust dose until Euthyroid, then checks annually

86
Q

What genotype is associated with T1DM?

A

HLADR3/4

87
Q

What is meant by widened pulse pressure?
Where is it seen?

A

widened difference between systolic and diastolic pressure
Seen in hyperthyroidism. Hypo would have normal or narrow
Think of asian guy who takes tablets for thyroid and he had a very wide pulse pressure as well as very anxious

88
Q

What is the treatment of subclinical hypothyroidism?

A

Raised TSH but normal T4
It is not treated unless patient is symptomatic or infertile
Then start Etroxin 25mg

GP - General Practice (15 decks)

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