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A-CCC > GP- Endocrinology > Flashcards

GP- Endocrinology Flashcards

1
Q

Obesity BMI classifications

A
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2
Q

Management of obesity

A
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3
Q

Criteria of qualification for taking orlistat

A
  • BMI of 28 kg/m^2 or more with associated risk factors (like HTN and T2D), or
  • BMI of 30 kg/m^2 or more
  • continued weight loss e.g. 5% at 3 months
  • orlistat is normally used for < 1 year
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4
Q

Criteria for qualification for taking liraglutide in obesity

A
  • person has a BMI of at least 35 kg/m²
  • prediabetic hyperglycaemia (e.g. HbA1c 42 - 47 mmol/mol)
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5
Q

Orlistat side effects

A

faecal urgency/incontinence and flatulence
fatty or oily stools

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6
Q

Liraglutide side effects

A

nausea and diarrhea

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7
Q

When is bariatric surgery recommended by NICE?

A

Essentially NICE recommend that very obese patients (e.g. BMI 40-50 kg/m^2 etc) are referred early for bariatric surgery, particularly if they have other conditions that may be caused by it (e.g. type 2 diabetes mellitus, hypertension), rather than it being a ‘last resort’.

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8
Q

Types of bariatric surgery

A
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9
Q

medical causes of obesity

A
  • Genetic syndromes associated with hypogonadism (for example Prader-Willi syndrome and Laurence-Moon-Biedl syndrome).
  • Hypothalamic damage (for example due to a tumour, trauma, or surgery).
  • Polycystic ovary syndrome.
  • Growth hormone deficiency.
  • Cushing’s syndrome.
  • Hypothyroidism.
    Medications, including :
  • Pizotifen.
  • Beta-blockers.
  • Corticosteroids.
  • Lithium.
  • Antipsychotics — especially atypical antipsychotics.
  • Anticonvulsants — sodium valproate, gabapentin, vigabatrin.
  • Antidepressants — tricyclics, mirtazapine, monoamine oxidase inhibitors (MAOIs).
  • Insulin — when used in the treatment of type 2 diabetes.
  • Oral hypoglycaemic drugs — sulphonylureas, thiazolidinediones (glitazones).
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10
Q

risk factors for obesity

A
  • Age — in the 2015 Health Survey for England, the highest obesity levels were reported in the 55–64 age group [NHS Digital, 2017].
  • Peri-and menopause.
  • Prior pregnancy, although this association is confounded by contributing cultural, environmental, and socioeconomic factors.
  • Sleep deprivation.
  • Less formal education.
  • Low socioeconomic status.
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11
Q

Complications of obesity

A

Obesity is one of the leading causes of death and disability worldwide. Overweight and obesity are associated with the following:
* An increased risk of developing (or exacerbation of) a number of chronic diseases and conditions, including:
* Type 2 diabetes.
* Coronary heart disease.
* Hypertension and stroke.
* Asthma.
* Depression.
* Metabolic syndrome.
* Dyslipidaemia.
* Cancer.
* Gastro-oesophageal reflux disease (GORD).
* Gallbladder disease.
* Reproductive problems.
* Osteoarthritis and back pain.
* Obstructive sleep apnoea.
* Breathlessness.
* Psychological distress.
* Decreased life expectancy

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12
Q

type 1 diabetes presentation

A

Features of diabetic ketoacidosis (DKA):
* abdominal pain
* polyuria, polydipsia, dehydration
* Kussmaul respiration (deep hyperventilation)
* acetone-smelling breath (‘pear drops’ smell)
* altered consciousness
* hypotension
* nausea and vomiting

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13
Q

Investigations in type 1 diabetes

A
  • urine should be dipped for glucose and ketones
  • fasting glucose and random glucose (see below for diagnostic thresholds)
  • HbA1c is not as useful for patients with a possible or suspected diagnosis of T1DM as it may not accurately reflect a recent rapid rise in serum glucose
  • C-peptide levels are typically low in patients with T1DM
  • diabetes-specific autoantibodies are useful to distinguish between type 1 and type 2 diabetes (see below)
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14
Q

Antibodies specific to type 1 diabetes

A
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15
Q

Diagnostic criteria for type 1 diabetes

A

If the patient is symptomatic:
* fasting glucose greater than or equal to 7.0 mmol/l
* random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.

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16
Q

Distinguishing between type 1 and type 2 diabetes

A
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17
Q

Diagnose type 1 diabetes on clinical grounds in adults presenting with hyperglycaemia, bearing in mind that people with type 1 diabetes typically (but not always) have one or more of:

A

ketosis
rapid weight loss
age of onset below 50 years
BMI below 25 kg/m²
personal and/or family history of autoimmune disease

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18
Q

Consider further investigation in adults that involves measurement of C peptide and/or diabetes specific autoantibody titres if:

A

type 1 diabetes is suspected but the clinical presentation includes some atypical features (for example, age 50 years or above, BMI of 25 kg/m² or above, slow evolution of hyperglycaemia or long prodrome)

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19
Q

Type 1 diabetes management: monitoring and drugs

A
  • Subcutaneous insulin
  • Monitoring dietary carbohydrate intake
  • Monitoring blood sugar levels upon waking, at each meal and before bed
  • Monitoring for and managing complications, both short and long term
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20
Q
  • A basal bolus regimen involves a combination of:
A
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21
Q

Blood glucose targets in type 1 diabetes

A

5-7 mmol/l on waking and
4-7 mmol/l before meals at other times of the day

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22
Q

Hba1c should be monitored how often?

A

every 3-6 months

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23
Q

adults with type 1 diabetes should have a target of HbA1c level of

A

48 mmol/mol (6.5%) or lower

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24
Q

how often should you self monitor blood glucose in type 1 diabetes and when?

A
  • recommend testing at least 4 times a day, including before each meal and before bed
  • more frequent monitoring is recommended if frequency of hypoglycaemic episodes increases; during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding
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25
Q

Type of insulin used in type 1 diabetes

A
  • offer multiple daily injection basal–bolus insulin regimens, rather than twice‑daily mixed insulin regimens, as the insulin injection regimen of choice for all adults
  • twice‑daily insulin detemir is the regime of choice. Once-daily insulin glargine or insulin detemir is an alternative
  • offer rapid‑acting insulin analogues injected before meals, rather than rapid‑acting soluble human or animal insulins, for mealtime insulin replacement for adults with type 1 diabetes
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26
Q

When should metformin be used in type 1 diabetes?

A

NICE recommend considering adding metformin if the BMI >= 25 kg/m²

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27
Q

Short term complications of type 1 diabetes

A
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28
Q

Long term complications of type 1 diabetes

A
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29
Q

Pathophysiology of DKA

A

DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

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30
Q

pathophysiology of ketogenesis

A
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31
Q

The most common precipitating factors of DKA are

A

infection, missed insulin doses and myocardial infarction

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32
Q

Features of DKA

A

The patient will present with symptoms of the underlying hyperglycaemia, dehydration and acidosis:

  • Polyuria
  • Polydipsia
  • Nausea and vomiting
  • Weight loss
  • Acetone smell to their breath (“pear drop smell”)
  • Dehydration and subsequent hypotension
  • Altered consciousness
  • Symptoms of an underlying trigger (i.e. sepsis)
  • Kussmaul respiration (deep hyperventilation)
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33
Q

Diagnostic criteria for DKA

A
  • Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
  • Ketosis (i.e. blood ketones > 3 mmol/l)
  • Acidosis (i.e. pH < 7.3)
  • bicarbonate < 15 mmol/l
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34
Q

Main principles of management DKA

A
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35
Q

slower infusion may be indicated in young adults (aged 18-25 years) as they are at greater risk of…

A
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36
Q

JBDS potassium guidelines when treating DKA

A
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37
Q

DKA resolution is defined as:

A
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38
Q

both the ketonaemia and acidosis should have been resolved within …… if this hasn’t happened the patient requires:

A

both the ketonaemia and acidosis should have been resolved within 24 hours. If this hasn’t happened the patient requires senior review from an endocrinologist

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39
Q

Complications may occur from DKA itself or the treatment:

A
  • gastric stasis
  • thromboembolism
  • arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
  • iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
  • acute respiratory distress syndrome
  • acute kidney injury
  • children/young adults are particularly vulnerable to cerebral oedema following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment but can present at any time. If there is any suspicion a CT head and senior review should be sought
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40
Q

Type 2 diabetes simplified pathophysiology

A
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41
Q

T2DM RF

A

Non-modifiable risk factors:

Older age
Ethnicity (Black African or Caribbean and South Asian)
Family history

Modifiable risk factors:

Obesity
Sedentary lifestyle
High carbohydrate (particularly sugar) diet

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42
Q

T2DM presentation

A
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43
Q

Pre diabetes diagnostic criteria

A

Pre-diabetes is an indication that the patient is heading towards diabetes. They do not fit the full diagnostic criteria but should be educated about the risk of diabetes and lifestyle changes.

An HbA1c of 42 – 47 mmol/mol indicates pre-diabetes.
or fasting glucose of 6.1 to 6.9

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44
Q

Diagnostic criteria for T2DM: if symptomatic, and if asymptomatic

A

The HbA1C sample is typically repeated after 1 month to confirm the diagnosis (unless there are symptoms or signs of complications).

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45
Q

Conditions where HbA1c may not be used for diagnosis:

A

haemoglobinopathies
haemolytic anaemia
untreated iron deficiency anaemia
suspected gestational diabetes
children
HIV
chronic kidney disease
people taking medication that may cause hyperglycaemia (for example corticosteroids)

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46
Q
  • A fasting glucose greater than or equal to ….but less than … mmol/l implies impaired fasting glucose (IFG)
A

A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)

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47
Q

Impaired glucose tolerance (IGT) is defined as

A

Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

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48
Q

Which dietary advice is given to patients with type 2 diabetes

A
  • encourage high fibre, low glycaemic index sources of carbohydrates
  • include low-fat dairy products and oily fish
  • control the intake of foods containing saturated fats and trans fatty acids
  • limited substitution of sucrose-containing foods for other carbohydrates is allowable, but care should be taken to avoid excess energy intake
  • discourage the use of foods marketed specifically at people with diabetes
  • initial target weight loss in an overweight person is 5-10%
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49
Q

How often to check hba1c

A

every 3-6 months until stable, then 6 monthly

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50
Q

HBAI1c target if:
just lifestyle management,
lifestyle plus metformin, includes any drug which may cause hypoglycaemia (e.g. lifestyle + sulfonylurea),
Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%)

A
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51
Q

Initial drug therapy for type 2 diabetes: first line management

A
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52
Q

Table summary of first line drug management of diabetes

A
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53
Q

SGLT-2 inhibitors should also be given in addition to metformin in type 2 diabetes if any of the following apply:

A
  • the patient has a high risk of developing cardiovascular disease (CVD, e.g. QRISK ≥ 10%)
  • the patient has established CVD
  • the patient has chronic heart failure
  • metformin should be established and titrated up before introducing the SGLT-2 inhibitor
  • SGLT-2 inhibitors should also be started at any point if a patient develops CVD (e.g. is diagnosed with ischaemic heart disease), a QRISK ≥ 10% or chronic heart failure
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54
Q

T2DM first line manageemnt if metformin is contraindicated:

A
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55
Q

If the HbA1c has risen to… mmol/mol (7.5%) then further treatment is indicated.

A

58

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56
Q

Further drug therapy if HbA1c targets are not met table summary

A
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57
Q

Second line therapy T2DM

A

Dual therapy - add one of the following:
metformin + DPP-4 inhibitor
metformin + pioglitazone
metformin + sulfonylurea
metformin + SGLT-2 inhibitor (if NICE criteria met)

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58
Q

Third line therapy T2DM

A

If a patient does not achieve control on dual therapy then the following options are possible:
* metformin + DPP-4 inhibitor + sulfonylurea
* metformin + pioglitazone + sulfonylurea
* metformin + (pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT-2 if certain NICE criteria are met
* insulin-based treatment

59
Q

Further therapy in T2DM if third line therapy didn’t work

A
60
Q

How to start insulin as a further drug therapy in type 2 diabetes

A

metformin should be continued. In terms of other drugs NICE advice: ‘Review the continued need for other blood glucose-lowering therapies’

61
Q

Which insulin type should be started for further therapy in type 2 diabetes

A

NICE recommend starting with human NPH insulin (isophane, intermediate-acting) taken at bed-time or twice daily according to need

62
Q

Type 2 diabetes risk factor modification: blood pressure targets if age less than 80 and if age more thsan 80

A

same as non-diabetic
ACE inhibitors first line

63
Q

If type 2 diabetes and black, which blood pressure medication do you offer

A

ARB is preferred if the patient has a black African or African–Caribbean family origin

64
Q

Antiplatelet and lipids risk medication advice in type 2 diabetes

A

Antiplatelets
should not be offered unless a patient has existing cardiovascular disease

Lipids
following the 2014 NICE lipid modification guidelines only patients with a 10-year cardiovascular risk > 10% (using QRISK2) should be offered a statin. The first-line statin of choice is atorvastatin 20mg on

65
Q

GLP1 memetics examples

A

Liraglutide and exanatide

66
Q

GLP1 memetics MOA

A

increase insulin secretion and inhibit glucagon secretion

67
Q

Advantages of GLP1 memetics

A

hey typically result in weight loss, in contrast to many medications such as insulin, sulfonylureas and thiazolidinediones. They are sometimes used in combination with insulin in T2DM to minimise weight gain.

68
Q

How is exenatide administered?

A

Exenatide must be given by subcutaneous injection within 60 minutes before the morning and evening meals. It should not be given after a meal.

69
Q

One the main advantages of liraglutide over exenatide

A

it only needs to be given once a day.

70
Q

NICE criteria for adding a GLP1 drug

A
71
Q

The major adverse effect of GLP-1 mimetics

A

nausea and vomiting.
The Medicines and Healthcare products Regulatory Agency has issued specific warnings on the use of exenatide, reporting that is has been linked to severe pancreatitis in some patients.

72
Q

dipeptidyl peptidase-4, DPP-4 inhibitors examples

A

Vildagliptin, sitagliptin

73
Q

DPP4 MOA

A

increase levels of incretins (GLP-1 and GIP) by decreasing their peripheral breakdown

74
Q

DPP4 effect of weight

A

NONE

75
Q

DPP4 inhibitors SE

A

constipation, vomiting, nausea, diarrhoea, dyspepsia, gastritis, and gastro-oesophageal reflux (common).
Acute pancreatitis (uncommon)

76
Q

Sulfonylurea MOA

A

increasing pancreatic insulin secretion and hence are only effective if functional B-cells are present.
On a molecular level they bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells.

77
Q

Sulfonylurea common SE

A
  • hypoglycaemic episodes (more common with long-acting preparations such as chlorpropamide)
  • weight gain
78
Q

Sulfonylurea rare SE

A
  • hyponatraemia secondary to syndrome of inappropriate ADH secretion
  • bone marrow suppression
  • hepatotoxicity (typically cholestatic)
  • peripheral neuropathy

Sulfonylureas should be avoided in breastfeeding and pregnancy.

79
Q

Sulfonylureas examples

A

glicazide
glimepiride
glipizide
tolbutamide

80
Q

SGLT2 inhibitors MOA

A

reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.

81
Q

SGLT2 inhibitors examples

A

Examples include canagliflozin, dapagliflozin and empagliflozin.

82
Q

SGLT2 SE

A
  • urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
  • normoglycaemic ketoacidosis
  • increased risk of lower-limb amputation: feet should be closely monitored
83
Q

SGLT2 inhibitors effect on weight

A

weight loss

84
Q

Pioglitazone drug class

A

Thiazolidinediones

85
Q

Thiazolidinediones MOA

A

agonists to the PPAR-gamma receptor and reduce peripheral insulin resistance.
The PPAR-gamma receptor is an intracellular nuclear receptor. It’s natural ligands are free fatty acids and it is thought to control adipocyte differentiation and function.

86
Q

Thiazolidinediones side effects

A
  • weight gain
  • liver impairment: monitor LFTs
  • fluid retention - therefore contraindicated in heart failure. The risk of fluid retention is increased if the patient also takes insulin
  • recent studies have indicated an increased risk of fractures
  • bladder cancer: recent studies have shown an increased risk of bladder cancer in patients taking pioglitazone (hazard ratio 2.64)
87
Q

Thiazolidinediones effect on weight

A

weight gain

88
Q

Pioglitazone is contraindicated in which patients?

A

contraindicated in heart failure. The risk of fluid retention is increased if the patient also takes insulin

89
Q

Metformin SE

A

Gastrointestinal side effects
Lactic acidosis

90
Q

Insulin side effects

A

Hypos

Weight gain

91
Q

What are the 2 different types of diabetic neuropathy?

A

Peripheral neuropathy
GI autonomic neuropathy

92
Q

Peripheral neuropathy features/definitions

A

Diabetes typically leads to sensory loss and not motor loss.
Sensory loss typically results in a ‘glove and stocking’ distribution, with the lower legs affected first due to the length of the sensory neurons supplying this area.
Painful diabetic neuropathy is also a common problem in clinical practice.

93
Q

First line treatment of peripheral neuropathy

A

Diabetic neuropathy is now managed in the same way as other forms of neuropathic pain:
* first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin
* if the first-line drug treatment does not work try one of the other 3 drugs
* tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
* topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
* pain management clinics may be useful in patients with resistant problems

94
Q

Gastrointestinal autonomic neuropathy features and management

A

Gastroparesis
* occurs secondary to autonomic neuropathy
* symptoms include erratic blood glucose control, bloating and vomiting
* management options include metoclopramide, domperidone or erythromycin (prokinetic agents)

Chronic diarrhoea
* often occurs at night

Gastro-oesophageal reflux disease
* caused by decreased lower esophageal sphincter (LES) pressure

95
Q

diabetic neuropathy symptoms for both types

A
96
Q

specific conditions in diabetic nephropathy??

A
  • glomerulosclerosis
  • pyelonephritis
97
Q

macrovascular complications in diabetes

A
98
Q

Diabetic nephropathy screening

A
  • all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
  • should be an early morning specimen
  • ACR > 2.5 = microalbuminuria
99
Q

Diabetic nephropathy management

A

dietary protein restriction
tight glycaemic control
BP control: aim for < 130/80 mmHg
ACE inhibitor or angiotensin-II receptor antagonist
* should be start if urinary ACR of 3 mg/mmol or more
* dual therapy with ACE inhibitors and angiotensin-II receptor antagonist should not be started

control dyslipidaemia e.g. Statins

100
Q

Diabetic nephropathy pathology signs

A

Kimmelstein-Wilson nodules are acellular nodules in the mesangium of the glomerulus, and suggest diabetic nephropathy.

Diabetic kidney biopsies may also show thickening of the basement membrane of the tubules and peritubular capillaries.

101
Q

4 stages of diabetic nephropathy

A

hyperfiltration, microalbuminuria, macroalbuminuria, end stage renal failure

102
Q

Diabetic nephropathy symptoms

A
103
Q

Diabetic nephropathy brief pathophysiology

A
104
Q

how are thryoid problems classified?

A

Hypothyroidism may be classified as follows:
* primary hypothyroidism: there is a problem with the thyroid gland itself, for example an autoimmune disorder affecting thyroid tissue (see below)
* secondary hypothyroidism: usually due to a disorder with the pituitary gland (e.g.pituitary apoplexy) or a lesion compressing the pituitary gland
* congenital hypothyroidism: due to a problem with thyroid dysgenesis or thyroid dyshormonogenesis

Whilst there are a number of causes thyrotoxicosis the vast majority are primary in nature. Congenital thyrotoxicosis is not seen and secondary hyperthyroidism is rare, account for less than 1% of cases.

105
Q

Causes of hypothyroidism and thyrotoxicosis summarised in a table

A
106
Q

Hypothyroidism vs thyrotoxicosis summary table of features

A
107
Q

summary table of investigation and results for the different thyroid disorders

A

The principle investigation is ‘thyroid function tests’, or TFTs for short:
* these primarily look at serum TSH and T4 levels
* T3 can be measured but is only useful clinically in a small number of cases
* TSH levels are more sensitive than T4 levels for monitoring patients with existing thyroid problems and are often used to guide treatment

108
Q

3 main types of thyroid autoantibodies that can be tested for in thyroid disease

A
  • Anti-thyroid peroxidase (anti-TPO) antibodies
  • TSH receptor antibodies
  • Thyroglobulin antibodies

There is significant overlap between the type of antibodies present and particular diseases, but generally speaking TSH receptor antibodies are present in around 90-100% of patients with Graves’ disease and anti-TPO antibodies are seen in around 90% of patients with Hashimoto’s thyroiditis.

Other tests include:
* nuclear scintigraphy; toxic multinodular goitre reveals patchy uptake

109
Q

summary of treatment for thyroid disease

A

This clearly depends on the cause. For patients with hypothyrodism thyroxine is given in the form of levothyroxine to replace the underlying deficiency.

Patients with thyrotoxicosis may be treated with:
* propranolol: this is often used at the time of diagnosis to control thyrotoxic symptoms such as tremor
* carbimazole: blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production. Agranulocytosis is an important adverse effect to be aware of
* radioiodine treatment

110
Q

causes of primary hypothryroidism

A
111
Q

causes of secondary hypothyroidism

A

Secondary hypothyroidism is often associated with a lack of other pituitary hormones, such as ACTH, referred to as hypopituitarism. This is rarer than primary hypothyroidism, and may be caused by:

  • Tumours (e.g., pituitary adenomas)
  • Surgery to the pituitary
  • Radiotherapy
  • Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
  • Trauma
112
Q

presentation of hypothyrodism

A

The features that are universal to all causes of hypothyroidism include:

  • Weight gain
  • Fatigue
  • Dry skin
  • Coarse hair and hair loss
  • Fluid retention (including oedema, pleural effusions and ascites)
  • Heavy or irregular periods
  • Constipation

Iodine deficiency causes a goitre.

Hashimoto’s thyroiditis can initially cause a goitre, after which there is atrophy (wasting) of the thyroid gland.

113
Q

levothyroxine drug class, MOA, how it is titrated and monitored

A
114
Q

most common cause of hypothyrodism in developing world

A

iodine deficiency

115
Q

most common cause of hypothyrodism in the developed world

A

Hashimoto’s thyroditis

116
Q

causes of hyperthyroidism

A

The causes of hyperthyroidism can be remembered with the “GIST” mnemonic:

G – Graves’ disease
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule
T – Toxic multinodular goitre

117
Q

Thyroiditis causes

A

Thyroiditis (thyroid gland inflammation) often causes an initial period of hyperthyroidism, followed by under-activity of the thyroid gland (hypothyroidism). The causes of thyroiditis include:

  • De Quervain’s thyroiditis
  • Hashimoto’s thyroiditis
  • Postpartum thyroiditis
  • Drug-induced thyroiditis
118
Q

Presentation of hyperthyroidism

A
119
Q

graves’ disease features

A

Graves’ disease has specific features relating to the presence of TSH receptor antibodies:

  • Diffuse goitre (without nodules)
  • Graves’ eye disease, including exophthalmos
  • Pretibial myxoedema
  • Thyroid acropachy (hand swelling and finger clubbing)
120
Q

Solitary toxic nodule definition and treatment

A
121
Q

De Quervain’s thyroiditis definition, its 3 phases and treatment

A
122
Q

Thyroid storm definition, presentation and treatment

A
123
Q

First line drug for hyperthyroidism, how it is taken and the one important rare side effect

A

TOM TIP: Both carbimazole and propylthiouracil can cause agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections. A sore throat is a key presenting feature of agranulocytosis. In your exams, if you see a patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.

124
Q

second line drug used for hyperthyrodism including side effects

A

Propylthiouracil is the second-line anti-thyroid drug. It is used in a similar way to carbimazole. There is a small risk of severe liver reactions, including death, which is why carbimazole is preferred.

also risk of agrunolocytosis just like carbimazole

125
Q

third line treatment for hyperthyroidism and rules for taking it

A
126
Q

treatment for symptoms of hyperthyrodism

A

Beta blockers are used to block the adrenalin-related symptoms of hyperthyroidism. Propranolol is the usual choice, as it non-selectively blocks adrenergic activity (as opposed to something like bisoprolol, which is more selective).

Beta blockers do not treat the underlying problem but control the symptoms, while definitive treatment takes time. They are particularly useful in patients with thyroid storm.

127
Q

definitive treatment option for hyperthyrodism

A

Surgery is a definitive option. Removing the whole thyroid gland (thyroidectomy), or the toxic nodules, effectively stops the excess thyroid hormone production. Patients will be hypothyroid after a thyroidectomy, requiring life-long levothyroxine.

128
Q

Hyperthyroidism is

A

Hyperthyroidism is where there is over-production of the thyroid hormones, triiodothyronine (T3) and thyroxine (T4), by the thyroid gland.

129
Q

Thyrotoxicosis refers to

A

Thyrotoxicosis refers to the effects of an abnormal and excessive quantity of thyroid hormones in the body.

130
Q

Primary hyperthyroidism is due to

A

Primary hyperthyroidism is due to thyroid pathology. The thyroid is behaving abnormally and producing excessive thyroid hormone.

131
Q

Secondary hyperthyroidism is due to

A

Secondary hyperthyroidism is due to pathology in the hypothalamus or pituitary. The pituitary gland produces too much thyroid-stimulating hormone, stimulating the thyroid gland to produce excessive thyroid hormones.

132
Q

Subclinical hyperthyroidism is

A

Subclinical hyperthyroidism is where the thyroid hormones (T3 and T4) are normal and thyroid-stimulating hormone (TSH) is suppressed (low). There may be absent or mild symptoms.

133
Q

Graves’ disease is

A

Graves’ disease is an autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism. These TSH receptor antibodies, produced by the immune system, stimulate TSH receptors on the thyroid. This is the most common cause of hyperthyroidism.

134
Q

Toxic multinodular goitre (also known as Plummer’s disease) is

A

Toxic multinodular goitre (also known as Plummer’s disease) is a condition where nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones. It is most common in patients over 50 years.

135
Q

Exophthalmos (also known as proptosis) describes

A

Exophthalmos (also known as proptosis) describes the bulging of the eyes caused by Graves’ disease. Inflammation, swelling and hypertrophy of the tissue behind the eyeballs force them forward, causing them to bulge out of the sockets.

136
Q

Pretibial myxoedema is

A
137
Q

Goitre refers to

A

Goitre refers to the neck lump caused by swelling of the thyroid gland.

138
Q

Hyperparathyroidism refers to

A

Hyperparathyroidism refers to raised parathyroid hormone.

139
Q

basic physiology of parathyroid hormone

A
140
Q

The symptoms of hypercalcaemia

A

The symptoms of hypercalcaemia can be remembered with the “stones, bones, groans and moans” mnemonic:

  • Kidney stones
  • Painful bones
  • Abdominal groans (constipation, nausea and vomiting)
  • Psychiatric moans (fatigue, depression and psychosis)
141
Q

Primary hyperparathyroidism cause, investigation results and treatment

A

Primary hyperparathyroidism is caused by uncontrolled parathyroid hormone production by a tumour of the parathyroid glands. This leads to a raised blood calcium (hypercalcaemia). Treatment is to remove the tumour surgically.

142
Q

Secondary hyperparathyroidism cause, investigation results and treatment

A

Secondary hyperparathyroidism is where insufficient vitamin D or chronic kidney disease reduces calcium absorption from the intestines, kidneys and bones. This result in low blood calcium (hypocalcaemia).
The parathyroid glands react to the low serum calcium by excreting more parathyroid hormone. The serum calcium level will be low or normal, but the parathyroid hormone will be high.
Treatment is to correct the underlying vitamin D deficiency or chronic kidney disease (e.g., renal transplant).

143
Q

Tertiary hyperparathyroidism cause, investigation results and treatment

A

Tertiary hyperparathyroidism happens when secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated. Hyperplasia (growth) of the parathyroid glands occurs as they adapt to producing a higher baseline level of parathyroid hormone. Then, when the underlying cause of the secondary hyperparathyroidism is treated, the baseline parathyroid hormone production remains inappropriately high. In the absence of the previous pathology, this high parathyroid hormone level leads to the inappropriately high absorption of calcium in the intestines, kidneys and bones, causing hypercalcaemia. Treatment is surgically removing part of the parathyroid tissue to return the parathyroid hormone to an appropriate level.

144
Q

Primary vs secondary vs tertiary hyperparathyroidism PTH and calcium results

A

A-CCC (9 decks)

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