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Phase 2A > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Define obesity

A

Abnormal or excessive fat accumulation which poses a risk to health.
BMI > 30.

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2
Q

What are some potential consequences of obesity ?

A
  • Type II Diabetes
  • Hypertension
  • Coronary artery disease
  • Stroke
  • Osteoarthritis
  • Gout
  • Obstructive sleep apnoea
  • Carcinoma (breast, endometrium, colon, prostate)
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3
Q

What are 5 risk factors for obesity

A
  • Hypothyroidism
  • Hypercortisolism
  • Corticosteroid therapy
  • Diet high in sugar and fats
  • High alcohol intake
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4
Q

What is leptin and its action?

A

A hormone released by adipocytes which switches off appetite and stimulates the immune system. Leptin levels in the blood increase after eating and decrease after fasting.

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5
Q

What is ghrelin and its action?

A

A hormone released by endocrine cells of the stomach which stimulates growth hormone release and appetite. Blood levels are high when fasting and fall after eating.

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6
Q

What is the action of insulin?

A
  • suppresses hepatic glucose output (decreases glycogenolysis and gluconeogenesis)
  • increases glucose uptake into muscle and fat
  • suppresses lipolysis and muscle breakdown
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7
Q

What is the action of glucagon?

A
  • increases hepatic glucose output (increases glycogenolysis and gluconeogenesis)
  • reduce peripheral glucose uptake
  • stimulate peripheral release of gluconeogenic precursors (glycerol, AAs) - increases lipolysis and muscle breakdown
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8
Q

What other hormones have counterregulatory effects similar to glucagon?

A

adrenaline
cortisol
growth hormone

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9
Q

What is diabetes mellitus?

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia.

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10
Q

How does DM cause morbidity and mortality?

A
  • Acute hyperglycaemia (leads to diabetic ketoacidosis and hyperosmolar hyperglycaemic state if untreated)
  • Chronic hyperglycaemia leading to tissue complications
  • Side effects of treatment - hypoglycaemia
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11
Q

What random plasma glucose level with symptoms indicates diabetes mellitus?

A

> 11mmol/l

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12
Q

What fasting plasma glucose value indicates diabetes mellitus?

A

> 7mmol/l

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13
Q

What is GTT and what are the fasting and 2hr values that indicate diabetes mellitus?

A

GTT = Glucose tolerance test
GTT (75g glucose) fasting > 7mmol/l
or 2hr value >11mmol/l (repeated on 2 occasions)

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14
Q

What is HbA1c and what value is associated with diabetes mellitus?

A

HbA1c = glycated haemoglobin, a form of haemoglobin used to measure the average haemoglobin-associated glucose in blood over the last three months, HbA1c >48mmol/mol (6.5%) is seen in patients with diabetes mellitus

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15
Q

What are the types of diabetes mellitus?

A
  • Type I
  • Type II
  • Maturity onset diabetes of youth (MODY)
  • Pancreatic diabetes
  • Endocrine diabetes (result of acromegaly/cushings)
  • Malnutrition related diabetes
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16
Q

What is Type I diabetes?

A

An insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction.

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17
Q

What is the cause of Type I diabetes?

A

Beta cells express HLA (human leukocyte antigen) which activates a chronic cell mediated immune process leading to chronic ‘insulitis’ and consequently insulin insufficiency

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18
Q

What are the risk factors for T1 Diabetes?

A
  • HLA DR3 and DR4 and islet cell antibodies
  • Other autoimmune diseases
  • Environmental infections (e.g. viruses)
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19
Q

What is the typical presentation/symptoms of Type I DM?

A

Young lean pt
- polydipsia
- nocturia/polyuria
- glycosuria
- polyphagia (excessive eating) + weight loss
- excessive tiredness

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20
Q

What is the treatment for T1DM?

A

Basal Bolus Insulin
- basal = longer acting to maintain stable insulin levels throughout day
- bolus = faster acting, 30 mins preprandial to give “insulin spike”

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21
Q

What is diabetic ketoacidosis?

A

Result of too much gluconeogenesis so that glucose is converted to ketone bodies which are acidic. Caused by poorly managed T1 DM or from infection/illness

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22
Q

What are the signs of diabetic ketoacidosis?

A

T1DM symptoms +…
- Kussmaul breathing (deep laboured breaths to compensate for increased CO2)
- Pear drop breath (breath smells fruity due to ketones)
- Reduced tissue turgor, hypotension + tachcardia

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23
Q

What are the diagnostic blood concentrations of ketones, glucose and acid in DKA?

A

Ketones >3mmol/l
Random plasma glucoe >11.1mmol/l
pH<7.3 or <15mmol HCO3-

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24
Q

What is the treatment for DKA?

A
  • in an emergency ABCDE
  • 1st line always fluid (dehydration is most likely cause of death)
  • then insulin (+ glucose and postassium)
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25
Q

What are the potential complications of DKA?

A
  • cerebral oedema
  • adult respiratory distress syndrome
  • thromboembolism
  • aspiration pneumonia (drowsy/comatose patients)
  • death
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26
Q

Why can insulin treatment for DKA cause hypokalaemia and why is this dangerous?

A

insulin decreases potassium levels in the blood by redistributing K+ into the cells via increased Na/K pump activity causing low serum K+ levels –> hypokalaemia
low levels of K+ can cause arrhythmia, weakness (as the heart and muscles can struggle to contract)

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27
Q

What is Type II Diabetes Mellitus?

A

Insulin resistance and impaired insulin secretion due to a combination of genetic predisposition and environmental factors (obesity and lack of physical activity)

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28
Q

What are the risk factors for T2DM?

A

genetic link, smoking, obesity, sedentary lifestyle

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29
Q

What is the pathophysiology of T2DM?

A

Peripheral insulin resistance (e.g. malfunctional insulin intracellular activation pathway) leads to decrease GLUT4 receptor expression + minor destruction of pancreatic islets.
This results in hyperglycaemia with increased insulin demand from depleted beta cell population.

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30
Q

What is the typical presentation and symptoms of T2DM?

A

Obese, hypertensive, older patient
- persistant hyperglycaemia
- polydypsia
- nocturia + polyuria
- glycosuria
- blurred vision
- recurrent infections
- tiredness
- acanthosis nigiricans (dark pigmentation of skin folds) suggesting insulin resistance

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31
Q

What are IGT and IFG?

A

IGT = Impaired Glucose Tolerance
IFG = Impaired Fasting Glycaemia
Conditions of slightly elevated blood glucose but not high enough to be classed as diabetic so are called prediabetic states

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32
Q

What are the FPG and OGTT values in IGT?

A

FPG >/= 6mmol/l
2hr OGTT 7.8-11mmol/l

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33
Q

What are the FPG and OGTT in IFG?

A

FPG 6.1-6.9mmol/L
2hr OGTT <7.8mmol/l

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34
Q

What is the treatment for T2DM?

A
  • Lifestyle changes (weight loss, exercise, diet changes)
  • medications to control BP, blood glucose + lipids
  • Metformin (1st line)
  • DPP-IV inhibitors (vildagliptin, sitagliptin)
  • GLP analogues (exenatide, liraglutide)
  • SGLT-2 inhibitors (empagliflozin, canagliflozin)
  • Sulphonylureas (gliclazide, glibenclamide)
  • Thiazolidinediones (pioglitazone)
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35
Q

What is the action of metformin?

A

improves action of insulin in reducing blood glucose

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36
Q

What is the action of GLP-1 analogues?

A

They extend the duration of GLP-1 which is a gut hormone that stimulates insulin release and reduces appetite. GLP-1 analogues extend the duration of GLP-1 action and so lower blood glucose and help to reduce weight and cardiovascular disease.

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37
Q

What is the action of DPP-IV inhibitors?

A

DPP-IV is an enzyme which destroys incretin, a hormone which helps the body reduce blood glucose. DPP-IV inhibitors stop the destruction of incretin and so help lower blood glucose however the effect is not highly significant and has no effect on CVD or weight.

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38
Q

What is the action of SGLT2 inhibitors?

A

They inhibit the sodium glucose transporters in the renal proximal tubules, blocking the reabsorption of glucose and so increasing glucose excretion and lowering blood glucose levels.

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39
Q

What are the actions of sulphonylureas?

A
  • Stimulate insulin release by binding to beta-cell receptors
  • improve glycaemic control at the expense of significant weight gain
    *risk of hypoglycaemia
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40
Q

What are the actions of thiazolinediones?

A
  • Bind to the nuclear receptor PPARy and activate genes concerned with glucose uptake and utilisation and lipid metabolism
  • improve insulin sensitivity
  • need insulin for therapeutic effect
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41
Q

What is MODY?

A

Maturity-onset diabetes of the young
- includes several forms of diabetes with monogenetic defects of beta-cell function (impaired insulin secretion)
- usually manifesting as mild hyperglycaemia at a young age and inherited in an autosomal-dominant manner

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42
Q

What is C-peptide and why is it measured?

A

A peptide which connects the alpha and beta pro-insulin chains. It is measured to show whether there is insulin being produced by the body or only synthetic insulin in the blood.

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43
Q

What is permanent neonatal diabetes?

A

Inability to produce insulin caused by mutations in the genes encoding the beta cell ATP sensitive potassium channel (Kir6.2 and SUR1). They prevent closure of the channel so insulin cannot be secreted.

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44
Q

What is maternally inherited diabetes and deafness (MIDD)?

A

Mutation in mitochondrial DNA which causes loss of beta cells and presents similarly to Type 2 diabetes.

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45
Q

What is lipodystrophy?

A

Selective loss of adipose tissue associated with insulin resistance, dyslipidaemia, hepatic steatosis (fatty liver disease), hyperandrogenism, PCOS

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46
Q

What is hypoglycaemia?

A

abnormally low blood glucose

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47
Q

What are the symptoms of hypoglycaemia?

A

dizziness, feeling faint, loss of consciousness

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48
Q

What is the treatment for hypoglycaemia?

A

IV glucose

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49
Q

What are the most common causes of hypoglycaemia?

A
  • result of the sulfonylureas (stimulate insulin production + secretion) or insulin used to treat diabetes
  • non-diabetic causes = liver failure, Addison’s disease (adrenal insufficiency)
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50
Q

What is HHS?

A

Hyperosmolar Hyperglycaemic state - often precipitated with infection

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51
Q

What are the symptoms of HHS?

A

urination,
thirst
nausea
dry skin
disorientation and, in later stages, drowsiness and a gradual loss of consciousness.

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52
Q

How is HHS diagnosed?

A
  • heavy glycosuria
  • increased plasma osmolarity (>30mmol/L) w/ hyperglycaemia
  • No ketonuria/hyperketonemia
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53
Q

What is the treatment for HHS?

A
  • First insulin with potassium + glucose
  • then IV fluid (0.9% saline)
  • LMWH (low molecular weight heparin) to anticoagulate patient as they have thicker blood
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54
Q

How is insulin introduced in T2DM?

A

Basal insulin initially followed by prandial insulin when necessary

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55
Q

What is pre-mixed insulin?

A

Both basal and prandial components in a single insulin preparation which can cover insulin requirements through most of the day.

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56
Q

What is level 1 hypoglycaemia?

A

Alert value:
Plasma glucose <3.9 mmol/l and no symptoms

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57
Q

What is level 2 hypoglycaemia?

A

Serious biochemical:
Plasma glucose <3.0 mmol/l

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58
Q

What is the difference between non-severe and severe symptomatic hypoglycaemia?

A

With non-severe hypoglycaemia the patient can self-treat and cognitive function is only mildly impaired whereas with severe there is impaired cognitive function to require external help to recover.

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59
Q

What are the symptoms of developing hypoglycaemia?

A

Autonomic - palpitations, trembling, sweating, anxiety, hunger
Neuroglycopenic - difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking, dizziness
Non-specific - nausea, headache

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60
Q

What is impaired awareness of hypoglycaemia?

A

Following several hypoglycaemic episodes the body’s sensitivity to hypoglycaemia is reduced and the protective mechanisms of inhibiting insulin secretion, releasing glucagon and adrenaline are impaired so there is increased risk of severe hypoglycaemia.

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61
Q

What are the causes of hypoglycaemia?

A
  • long term diabetes
  • tight glycaemic control with repeated episodes of non-severe hypoglycaemia
  • increasing age
  • use of drugs (prescribed, alcohol)
  • sleeping (reduced ability to produce protective measures e.g. adrenaline)
  • increased physical activity
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62
Q

What are the effects of hypoglycaemia on the body?

A

Brain - cognitive dysfunction, blackouts, seizures, comas, psychological effects
Musculoskeletal - fails, accidents, driving accidents, fractures, dislocations
Heart - increased risk of myocardial ischaemia, cardiac arrhythmias
Circulation - inflammation, blood coagulation abnormalities, haemodynamic changes, endothelial dysfunction

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63
Q

What are the 5 steps for treatment of hypoglycaemia?

A
  1. Recognise symptoms
  2. Confirm need for treatment if possible (blood glucose <3.9 mmol/l is the alert value)
  3. Treat with 15g fast-acting carbohydrate to relieve symptoms
  4. Retest in 15 mins to ensure blood glucose >4.0 mmol/l and re-treat if needed
  5. Eat a long-acting carbohydrate to prevent recurrence of symptoms
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64
Q

What are the consequences of hypocalcaemia?

A
  • parasthesia
  • muscle spasm (hands and feet, larynx, premature labour)
  • seizures
  • basal ganglia calcification
  • cataracts
  • ECG abnormalities (long QT interval)
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65
Q

What is the calculation for corrected calcium?

A

corrected calcium= total serum calcium + 0.02*(40 - serum albumin)

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66
Q

What is Chvostek’s sign?

A

Tap over the facial nerve, look for spasm of facial muscles which indicates hypocalcaemia

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67
Q

What is Trosseau’s sign?

A

Inflate the blood pressure cuff to 20 mmHg above systolic for 5 mins.
Positive result for hypocalcaemia is carpopedal contraction of hand and wrist.

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68
Q

What is the difference between primary and secondary hypoparathyroidism?

A

Primary is decreased PTH secretion due to gland failure whereas secondary is commonly caused by surgical removal of the parathyroid gland (often accidental).

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69
Q

What are 2 syndromes associated with hypoparathyroidism?

A
  • Di George
  • HDR/Barakat Syndrome
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70
Q

What are the 4 clinical manifestations of hypoparathyroidism?

A
  • twitching facial muscles
  • muscle pains or cramps
  • tiredness
  • mood changes (feeling irritable, anxious, depressed)
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71
Q

What are the causes of hypoparathyroidism?

A
  • surgical
  • genetic
  • syndromes
  • radiation
  • autoimmune
  • infiltration
  • magnesium deficiency
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72
Q

What is pseudohypoparathyroidism?

A

resistance to parathyroid hormone resulting in short stature, obesity, round facies, mild learning difficulties, subcutaneous ossification

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73
Q

What are the symptoms of hypercalcaemia?

A
  • thirst
  • polyuria
  • nausea
  • constipation
  • confusion => coma
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74
Q

What are the chronic consequences of hypercalcemia?

A
  • renal stones
  • ECG abnormalities (short QT)
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75
Q

What are the 2 main causes of hypercalcaemia?

A

90% of cases:
- malignancy
- primary hyperparathyroidism

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76
Q

What are the less common causes of hypercalcaemia?

A

Two CHIMPANZEES

Thyroid disorders
Calcium supplements
Hyperparathyroidism
Iatrogenic
Milk-alkali syndrome
Paget’s disease
Adrenal insufficiency (Addisons)/Acromegaly
Neoplasm

Zollinger-ellison
Excessive vitamin D
Excessive vitamin A
Sarcoidosis

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77
Q

What is the difference between primary and secondary hyperparathyroidism?

A

Primary hyperparathyroidism is caused by direct alterations to the parathyroid gland e.g. cancer
Secondary is caused by physiologically elevated PTH due to reduced calcium levels

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78
Q

What is tertiary hyperparathyroidism?

A

Occurs after prolonged secondary hyperparathyroidism due to structural changes in the gland (indicated by elevated blood calcium levels)

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79
Q

What are the consequences of primary hyperparathyroidism?

A

Bones (osteitis fibrosa cystica, osteoporosis), stones (kidney), groans (confusion) + moans (constipation, acute pancreatitis)

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80
Q

What are the actions of parathyroid hormone?

A
  • increased bone resorption (increased calcium levels)
  • increased reabsorption of calcium and excretion of phosphate in the kidney
  • increased synthesis of vitamin D (increased calcium absorption from gut)
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81
Q

When are changes in PTH appropriate/inappropriate?

A

Appropriate when maintain calcium balance.
Inappropriate when causing calcium imbalance.

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82
Q

What is hypercalcaemia of malignancy?

A

High calcium levels in the body caused by tumour secretion of parathyroid gland

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83
Q

Which hormones are secreted by the hypothalamus?

A
  • GHRH & Somatostatin
  • GnRH
  • CRH
  • TRH
  • Dopamine
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84
Q

Which hormones are secreted by the pituitary?

A
  • GH
  • LH & FSH
  • ACTH
  • TSH
  • Prolactin
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85
Q

What is the difference between Cushing’s syndrome and Cushing’s disease?

A

Cushing’s syndrome = Clinical manifestation of pathological hypercortisolism from any cause
Cushing’s disease = pathological hypercortisolism caused by tumour of pituitary gland

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86
Q

What is the typical presentation of Cushing’s syndrome?

A
  • central obesity
  • supraclavicular fullness
  • facial rounding + plethora (swelling)
  • violaceous striae (often across stomach)
  • proximal muscle weakness
  • thinning of the skin
  • dorsocervical fat pads (lump at back of neck)
  • ## acne
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87
Q

What is the pathophysiology of cushing’s syndrome?

A

The clinical manifestations of Cushing’s syndrome result from excess exposure of tissues to cortisol.

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88
Q

What are the normal effects of cortisol in the body?

A
  • regulates the body’s stress response (maintains high alert levels produced by adrenaline and triggers glucose release for fast-release energy)
  • helps control the body’s use of fats, proteins and carbohydrates
  • suppresses inflammation
  • regulates blood sugar (counterbalances effect of insulin by releasing stored glucose)
  • regulates blood pressure (increased cortisol results in increased BP and vv.)
  • helps to regulate circadian rhythm (cortisol is low in the evening and peaks in the morning before you wake up)
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89
Q

What are 5 complications of Cushing’s syndrome?

A
  • diabetes mellitus
  • dyslipidaemia (changes in blood lipid concentrations)
  • metabolic bone disease
  • hypertension
  • immune suppression
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90
Q

What are risk factors for Cushing’s syndrome?

A
  • adrenal adenoma
  • adrenal carcinoma
  • pituitary adenoma
  • exogenous corticosteroid use (decreases ACTH)
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91
Q

What are the treatments for cushing’s syndrome?

A

1st line: transsphenoidal pituitary adenomectomy
- post-surgical corticosteroid or non-corticosteroid replacement therapy

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92
Q

What is used as a marker of an underactive thyroid?

A

elevated TSH levels

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93
Q

What are 5 disease of the pituitary?

A
  • Benign pituitary adenoma
  • Craniopharygioma (epithelial tumour)
  • Trauma
  • Apoplexy / Sheehans
  • Sarcoid / TB
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94
Q

What are the potential ways that pituitary tumours cause disease?

A
  1. Pressure on local structures e.g. optic nerves
    - bitemporal hemianopia
    - headaches
  2. Pressure on normal pituitary
    - hypopituitarism
  3. Functioning tumour
    - Prolactinoma
    - Acromegaly and gigantism
    - Cushing’s disease
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95
Q

What are the symptoms of prolactinomas?

A
  • galactorrhoea
  • amenorrhoea
  • infertility
  • loss of libido
  • visual field defect
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96
Q

What is used to treat prolactinomas?

A

Dopamine agonist e.g. cabergoline or bromocriptine

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97
Q

What thelarche?

A

Breast development, the first visible change of puberty, induced by estrogen

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98
Q

What is adrenarche?

A

Maturation of the adrenal gland where a specialized subset of cells arises forming the androgen-producing zona reticularis.
Results in mild advancement of bone age, axillary hair, oily skin, mild acne and body odour.

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99
Q

What is the incidence of precocious puberty?

A

1 in 5,000-10,000
90% patients female

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100
Q

What is precocious puberty?

A

Thelarche and increased growth velocity before age 8 in girls and genital development in boys before age 9.

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101
Q

What are the two forms of precocious puberty?

A
  1. Gonadotrophin-dependent precocious puberty (GDPP; due to premature activation of the hypothalamo-pituitary-gonadal axis)
  2. Gonadotrophin-independent precocious puberty (GIPP; due to autonomous secretion of sex steroids)
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102
Q

Define hyperthyroidism

A

Excess of thyroid hormones in the blood

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103
Q

What are the 3 mechanisms for developing hyperthyroidism?

A
  1. Overproduction of thyroid hormone
  2. Leakage of preformed hormone from the thyroid
  3. Ingestion of excess thyroid hormone
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104
Q

What are 6 causes of hyperthyroidism?

A

common
- Graves disease (75-80% of cases)
- Toxic multinodular goitre
- Toxic adenoma

less common
- congenital hyperthyroidism
- non-autoimmune hereditary thyroiditis
- subacute thyroiditis (De Quervain’s)re

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105
Q

Which 4 medications can cause drug-induced hyperthyroidism?

A
  • Iodine
  • Amiodarone
  • Lithium (rare)
  • Radiocontrast agents
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106
Q

What are the clinical features of hyperthyroidism?

A
  • weight loss
  • tachycardia
  • hyperphagia
  • anxiety
  • tremor
  • heat intolerance
  • sweating
  • diarrhoea
  • lid lag + stare
  • menstrual disturbance
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107
Q

What is Graves’ disease?

A

AN autoimmune condition where the immune system attacks the thyroid gland causing to become overactive.

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108
Q

What are the Graves’ specific signs of hyperthyroidism?

A
  • diffuse goitre
  • thyroid eye disease (infitrative)
  • pretibial myxoedema
  • acropathy
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109
Q

What is goitre?

A

Swelling at the front of the neck due to a swollen thyroid gland

110
Q

What is MNG?

A

Multinodular goitre

111
Q

What is the clinical sign specific to adenomas of hyperthyroidism?

A

solitary nodule

112
Q

What are the steps taken to investigate hyperthyroidism?

A
  • Thyroid function test (TFT)
  • Diagnose underlying cause
  • Clinical history - physical signs for diagnosis
  • Supporting investigations- thyroid antibodies, isotope uptake scan
113
Q

What are the results of TFTs in primary hyperthyroidism?

A

Elevated free T4 and T3, suppressed TSH

114
Q

What are the results of TFTs in secondary hyperthyroidism?

A

Elevated free T3 and T4 as well as inappropriately high TSH

115
Q

What is the treatment for hyperthyroidism?

A
  • Anti-thyroid drugs (course or long-term) –> carbamazepine, propothiouracil
  • Radioiodine ^131I
  • surgery (partial, subtotal thyroidectomy)
116
Q

What are thionamides?

A

Antithyroid drugs which reduce synthesis of new thyroid hormone.
They do no treat the underlying causes of hyperthyroidism but immune modifying effects are seen (decrease IL-6) and reduction in antibody titres.

117
Q

What are the names of 3 thionamides?

A
  • Carbimazole
  • Propylthiouracil (PTU) - used particularly in pregnant women
  • Methimazole
118
Q

What are the side effects of thionamides?

A

Common = rash
Uncommon = arthralgia (joint stiffness), hepatitis, neuritis, thrombocytopoenia, vasculitis
- usually occur within the first few months and resolve after stopping drug
- the most serious side effect is agranulocytosis which occurs in 0.1% to 0.2%

119
Q

What type of surgery is implicated for Graves’ disease and MNG?

A

Near total thyroidectomy

120
Q

What type of surgery is implicated for toxic adenoma?

A

Near total thyroidectomy or Lobectomy

121
Q

Define hypothyroidism

A

Abnormally low thyroid hormone levels

122
Q

What is the physiological cause of primary hypothyroidism?

A

Absence/dysfunction of thyroid gland

123
Q

What condition is the cause of most cases of primary hypothyroidism?

A

Hashimoto’s thyroiditis

124
Q

What is Hashimoto’s thyroiditis?

A

An autoimmune disease which causes the immune system to attack the thyroid gland resulting in permanent hypothyroidism

125
Q

What are the symptoms of Hashimoto’s thyroiditis?

A
  • goitre
  • tiredness
  • weight gain
  • muscle weakness
126
Q

What are the physiological causes of secondary and tertiary hypothyroidism?

A

Secondary - pituitary disfunction
Tertiary - hypothalamic dysfunction

127
Q

What are the causes of primary hypothyroidism?

A
  • Hashimoto’s thyroiditis
  • ^(131)I therapy
  • Thyroidectomy
  • Postpartum thyroiditis
  • Thyroiditis
  • Drugs
  • Iodine deficiency
  • Thyroid hormone resistance
128
Q

Which drugs can cause hypothyroidism?

A
  • Iodine (inorganic or organic)
  • Iodide
  • Iodinated contrast agents
  • Amiodarone
  • Lithium
  • Thionamides
  • Interferon-a
129
Q

What are the causes of hypothyroidism in children/neonates?

A
  • Thyroid agenesis
  • Thyroid ectopia
  • Thyroid dishormonogenesis
  • Resistance to thyroid hormone
  • Isolated TSH deficiency
130
Q

What are the clinical features of hypothyroidism?

A
  • Fatigue
  • Weight gain
  • cold intolerance
  • Constipation
  • Menstrual disturbance
  • muscle cramps
  • Slow cerebration (thinking)
  • Dry, rough skin
  • Periorbital oedema
  • Carotenaemia
  • Oedema
131
Q

What are the investigations for primary hypothyroidism?

A

Elevated TSH and usually low free T4 and T3

132
Q

What are the investigations for secondary/tertiary hypothyroidism?

A

TSH inappropriately low for reduced free T4/T3 levels

133
Q

What is the treatment of choice for hypothyroidism?

A

Synthetic Levothyroxine (T4)
- in primary dose is titrated until TSH normalises
- in secondary T4 is monitored as TSH will remain low

134
Q

What is the prevalence of hyperthyroidism?

A

2.5%

135
Q

What is the prevalence of hypothyroidism?

A

5%

136
Q

What is the prevalence of goitre?

A

5-15%

137
Q

Which antibodies are found in almost all patients with autoimmune hypothyroidism?

A

Thyroglobulin and thyroid peroxidase (TPO)
* also present in 75% of Graves’ patients

138
Q

How much more likely are women to develop thyroid autoimmune diseases?

A

5-10 times

139
Q

What are the risk factors for thyroid autoimmunity?

A
  • female sex (onset of disease also common postpartum)
  • HLA-DR3 and other immunoregulatory genes contribute
  • stress
  • smoking
  • high iodine intake
140
Q

What are 5 autoimmune diseases associated with thyroid autoimmunity?

A
  • T1 diabetes mellitus
  • Addison’s disease
  • Pernicious anaemia
  • Vitiligo
  • Myasthenia gravis
141
Q

What is thyroid associated opthalmopathy?

A

Swelling in extraocular muscles most likely due to an autoantigen in the muscles that cross reacts with a thyroid antigen.
Present in most Graves’ and some autoimmune hypothyroidism patients

142
Q

What is goitre?

A

Palpable + visible thyroid enlargement with a variety of causes.
- Commonly sporadic or autoimmune
Not associated specifically with hypo or hyperthyroidism

143
Q

What is the prevalence of hypothyroidism during pregnancy?

A

2-3%

144
Q

How does hypothyroidism affect pregnancy if untreated?

A
  • low birth weight
  • preterm delivery
  • neonatal goitre
  • neonatal respiratory distress
145
Q

How does hypothyroidism affect the pregnancy with inadequate treatment?

A
  • gestational hypertension and pre-eclampsia
  • placental abruption
  • post-partum haemorrhage
146
Q

What is the prevalence of hypertension in pregnancy?

A

0.1-0.4%

147
Q

What causes 90% of hyperthyroidism in pregnancy?

A

Graves’ disease

148
Q

How does hyperthyroidism effect pregnancy?

A
  • IUGR (intrauterine growth restriction)
  • Low birth weight
  • Pre-eclampsia
  • Preterm delivery
  • Risk of stillbirth
  • Risk of miscarriage
149
Q

What are the treatments for hypertension in pregnancy?

A
  • symptomatic treatment e.g. B blockers are safe to use (propanolol)
  • anti-thyroid medication (PTU or carbimazole)
  • surgical interventions
150
Q

Which thyroid drugs increase or decrease thyroid hormone secretion?

A

Iodide, amiodarone, lithium (rare increase)

151
Q

What are the types of thyroid carcinoma?

A
  • Papillary (70%)
  • Follicular (25%)
  • Anaplastic (worst prognosis)
  • Medullary cell
  • Lymphoma
152
Q

What are the signs of thyroid carcinoma?

A
  • Thyroid nodules (esp. if hard and irregular
  • hoarseness (indicating recurrent laryngeal involvement)
153
Q

What are the diagnostic tests used for thyroid carcinoma?

A
  • Fine needle aspiration biopsy
  • TFTs
  • Thyroid ultrasound
154
Q

What is the treatment for thyroid carcinoma?

A
  • papillary + follicular -> thyroidectomy or radiotherapy
  • anaplastic -> palliative surgery + chemoradiation
155
Q

Define diabetes insipidus

A

An absolute or relative inability to concentrate urine resulting from an absolute or relative deficiency of arginine vasopressin (also known as ADH) or from resistance to its action in the renal collecting ducts.

156
Q

What is the prevalence of diabetes insipidus?

A

1 in 25000

157
Q

What are the symptoms of DI?

A
  • Polyuria
  • Polydipsia
  • Hypernatraemia
  • lethargy
  • confusion
  • coma
  • severe dehydration
158
Q

What are the two types of diabetes insipidus?

A

Central/Cranial DI - absolute or relative deficiency of AVP.
Nephrogenic DI - renal insensitivity or resistance to AVP.

159
Q

What are the causes of AVP deficiency (cranial DI)?

A

Acquired causes:
- idiopathic
- tumours - craniopharyngioma, germinoma, mets
- trauma
- infections - TB, encephalitis, meningitis
- vascular - aneurysm, infarction, Sheenan’s, sickle cell
- inflammatory - neurosarcoidosis, Langerhan’s histiocytosis, Guillain Barre, Granuloma

Primary causes:
Genetic - DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, deafness)/wolfram syndrome, autosome dominant rarely autosomal recessive
Developmental - septo-optic dysplasia

160
Q

What are the causes of AVP resistance (nephrogenic diabetes insipidus)?

A

Familial (rare):
- X-linked V2 receptor defect
- Autosomal AQP-2 defect

Acquired:
- osmotic diuresis (e.g. diabetes mellitus)
- drugs (e.g. lithium, demeclocycline, tetracycline)
- chronic renal impairment
- post-obstructive nephropathy
- metabolic (e.g. hypercalcaemia/hypokalaemia)
- renal infiltration (e.g. amyloid)

161
Q

What investigations are used to diagnose diabetes insipidus?

A
  • water deprivation test (no fluid intake for 8hrs, pts with DI will continue to produce large volumes of dilute urine when normally people would only produce a small amount of concentrated urine)
  • vasopressin test (pt given injection of vasopressin, if this stop them producing urine DI likely to be caused by AVP shortage (cranial DI), whereas if they continue to produce urine it suggests the problem is with the kidney’s response to AVP (nephrogenic))
  • MRI - used if cranial DI is suspected to check whether there is damage to the hypothalamus or pituitary gland
162
Q

What is the management for cranial DI?

A
  • treat any underlying condition
  • desmopressin (high activity at V2 receptor) - comes in tablet, nasal spray and injection forms
163
Q

What is the management for nephrogenic DI?

A
  • treat underlying cause
  • thiazides - increase H2O loss at DCT encouraging sodium uptake + H2O retention ->concentrated urine and increased water retention
164
Q

What is the serum sodium associated with hyponatraemia?

A

<135 mmol/l

165
Q

What is a normal serum sodium?

A

135-144mmol/l

166
Q

What are the symptoms of hyponatraemia?

A

Moderate:
- headache
- irritability
- nausea/vomiting
- mental slowing
- unstable gait/falls
- confusion/delirium
- disorientation

Severe:
- stupor/coma
- convulsions
- respiratory arrest

167
Q

What are the serum sodium values associated with mild, moderate and severe hyponatraemia?

A

Mild - 130-135mmol/l
Moderate - 125-129mmol/l
Severe <125mmol/l

168
Q

What are the investigations used in diagnosing hyponatraemia?

A
  • plasma + urine osmolality
  • urinary Na+
  • glucose
  • TFT’s
  • +/- assessment of cortisol
  • assessment of underlying causes e.g. chest imaging
169
Q

What are the three types of hyponatraemia?

A
  1. Hypervolemic - very large increase in total body water with insufficient increase in total body sodium
  2. Hypovolemic - small decrease in water with large decrease in sodium ions
  3. Euvolemic - increase in water (but no oedema) with normal sodium
170
Q

What are 3 conditions associated with hypervolemic hyponatraemia?

A
  • congestive heart failure
  • cirrhosis
  • nephrotic syndrome
    (result of oedema)
171
Q

What are 3 causes of hypovolemic hyponatraemia?

A
  • diarrhoea + vomiting
  • medications such as diuretics
  • cerebral salt wasting
172
Q

What are 3 causes of euvolemic hyponatraemia?

A
  1. adrenal insufficiency
  2. drinking too much water (polydipsia) or beer (potomania)
  3. syndrome of inappropriate antidiuretic hormone secretion (SIADH)
173
Q

What are acute and chronic hyponatraemia defined as?

A

Acute = occurred over <48hrs
Chronic = occurred over 48hrs or more

174
Q

What is SIADH?

A

Syndrome of Inappropriate ADH secretion
- overdiagnosed cause of euvolemic hyponatraemia
- excess ADH => more water retention + compensatory sodium excretion to maintain euvolemia

175
Q

What are the causes of SIADH?

A

S - SCLC (small cell lung cancer)
I - infection/immunosuppression
A - abcesses
D - drugs (SSRIs, carbamazapine, sulphonylureas)
H - head trauma

176
Q

What are the symptoms of SIADH?

A

same as hyponatraemia
- vomiting, headache, decreased GCS (glasgow coma scale), muscle weakness
- very low sodium = seizures, nuerological complications, brainstem herniation

177
Q

Why does very low sodium cause brainstem herniation?

A
  • low Na+ mean increased compensatory water retention
  • water enters skull increasing intracranial pressure
  • causes hyponatraemic encephalopathy
  • this creates the risk of brainstem herniation through the foramen magnum (tentorial herniation)
178
Q

How is SIADH diagnosed?

A
  • low serum sodium and normal serum potassium
  • high urine osmolality
  • to confirm diagnosis give 0.9% saline -> with SIADH serum will fail to normalise whereas with sodium depletion sodium will normalise
179
Q

What is the treatment for SIADH?

A
  • fluid restrict and give hypertonic saline to concentrate blood
  • treat underlying cause (e.g. tumour excision)
  • chronic cases -> furosemide, vasopressin antagonist (tolvaptan), demeclocycline
180
Q

What is the managemtn of acute severe symptomatic hyponatraemia?

A
  1. IV 150ml of 3% saline or equivalent over 20 mins
  2. Check serum Na+
  3. Repeat twice until 5mmol/l Na+ increase
  4. After 5mmol/L increase:
    - Stop hypertonic saline
    - Establish diagnosis
    - Na+ 6 hourly for 1st 24 hours
    - Limit increase to 10mmol/l first 24 hour
181
Q

Define acromegaly

A

Rare, chronic disease caused by excessive secretion of growth hormone. Usually due to a pituitary somatotroph adenoma.

182
Q

What are the key features of acromegaly?

A
  • large extremeties
  • box jaw
  • vision changes (bitemporal hemianopia)
  • sleep apnoea
  • large interdental gaps
  • carpal tunnel syndrome
  • arthralgias
  • headache
  • hypogonadal features
183
Q

How is acromegaly diagnosed?

A

1st line screening
- IGF-1 serum level always increased (no low values)
Gold standard test
- oral glucose tolerance test (if normal, GH level should drop in response to increased glucose but in acromegaly the GH level will remain high)

184
Q

Which co-morbidities are associated with acromegaly?

A
  • hypertension + heart disease
  • sleep apnoea
  • cerebrovascular events and headache
  • arthritis
  • insulin-resistant diabetes
185
Q

What are the treatment options for acromegaly?

A
  • best option = pituitary surgery
  • medical therapy (dopamine agonists, somatostatin analogues, GH antagonist)
  • radiotherapy
186
Q

What is the primary treatment for all types of pituitary adenoma except prolactinoma?

A

Transphenoidal pituitary surgery

187
Q

What are 3 groups of medications used to treat acromegaly?

A
  • Dopamine agonists (cabergoline) - control GH secretion
  • Somatostatin analogues (ocreotide) - suppress GH secretion
  • Growth hormone receptor antagonists (pegvisomant) - selectively binds to GH receptors, blocking the binding of GH
188
Q

What is a prolactinoma?

A

Benign lactotroph adenomas which express and secrete prolactin.

189
Q

What are the local effects of prolactinomas (macro-adenoma)?

A
  • headache
  • visual field defect (bi-temporal hemianopia)
  • CSF leak (rare)
190
Q

What are the effects of excess prolactin?

A
  • menstrual irregularity/amenorrhoea
  • infertility
  • galactorrhoea
  • low libido
  • low testosterone in men
191
Q

What is the treatment for prolactinomas?

A
  • Dopamine agonists (carbergoline, bromocriptine) shrink tumour
192
Q

What are craniopharyngiomas?

A

Benign tumours which arise from squamous epithelial remnants of Rathke’s pouch (developmental stage of pituitary gland)

193
Q

What are the types of craniopharyngioma?

A

Adamantinous: cyst formation and calcification
Squamous papillary: well circumscribed

194
Q

What are the symptoms of craniopharyngiomas?

A
  • Raised ICP
  • Visual disturbances
  • Growth failure
  • Pituitary hormone deficiency
  • Weight increase
195
Q

What are Rathke’s cysts?

A

Single layer of epithelial cells with mucoid, cellular, or serous components in cyst fluid derived from remnants of Rathke’s pouch

196
Q

What are the presentations of Rathke’s cyst?

A

Headache and amenorrhoea, hypopituitarism and hydrocephalus

197
Q

What is a meningioma

A

Predominantly benign tumour of the meninges occurring at both cranial and spinal sites.

198
Q

What symptoms are associated with meningiomas?

A
  • Visual disturbance
  • Endocrine dysfunction
199
Q

What is Lymphocytic hypophysitis?

A

Inflammation of the pituitary gland due to an autoimmune reaction

200
Q

What are non-functioning pituitary adenomas/silent pituitary adenomas?

A

Usually benign tumours of the pituitary. Called non-functioning tumours as they do not secrete hormones however they can still cause symptoms due to pressure on the pituitary and surrounding structures. (headaches, visual disturbance, hypopituitarism)

201
Q

What condition is identified by raised TSH and low free T4?

A

Primary hypothyroidism

202
Q

What condition is characterised by low free T4 with normal or low TSH?

A

Hypopituitarism

203
Q

What condition is characterised by suppressed TSH with high free T4?

A

Graves disease (toxic)

204
Q

What 2 conditions are characterised by high free T4 and normal/high TSH?

A

TSHoma (very rare)
Hormone resistance

205
Q

What condition is characterised by low testosterone and raised LH/FSH?

A

Primary hypogonadism

206
Q

What condition is characterised by low testosterone or low LH/FSH?

A

Hypopituitarism

207
Q

What condition is characterised by low cortisol, high ACTH and poor response to Synacthen?

A

Primary Adrenal Insufficiency

208
Q

What can be a sign of adrenal insufficiency?

A

Low sodium and high potassium

209
Q

What is primary adrenal insufficiency?

A

Commonly known as Addison’s Disease, PAI is a disorder resulting from intrinsic diseases that affect the cortex of the adrenal glands, causing the impairment in the synthesis and secretion of all steroids.

210
Q

What are the common symptoms of PAI?

A
  • fatigue
  • anorexia
  • weight loss
  • hyperpigmentation
  • nausea, vomiting
  • abdo pain
211
Q

What are the risk factors for adrenal insufficiency?

A
  • female
  • adrenocortical autoantibodies
  • adrenal haemorrhage
  • autoimmune disease
  • coeliac disease
  • infections
  • cortisol-inhibiting drugs
212
Q

What are the primary investigations for PAI?

A
  • morning serum cortisol (<140nmols/l suggests PAI)
  • plasma ACTH (>12picomols/l suggests PAI)
  • U&E + FBC bloods (low Na, high K)
213
Q

What is the 1st line treatment for an adrenal crisis?

A
  • Intravenous hydrocortisone 100mg
  • Fluid resuscitation (Il N/saline 1hr)
  • Hydrocortisone 50-100mg 6 hourly
  • In primary AI start fludrocortisone 100-200ug once HC <50mg
  • WHen patient stable wean to normal replacement over 24-72hrs
214
Q

What are the sick day rules for adrenal insufficiency?

A
  • always carry 10x10mg tablets hydrcortisone
  • if unwell with fever or flu-like illness double steroid dose
  • if vomiting or increasingly unwell take emergency injection of hydrocortisone 100mg IM
  • go to emergency room/ring ambulance
215
Q

What are the actions of aldosterone?

A

increased Na+ reabsorption from the distal tubule
increased K+ secretion from the distal tubule
increase H+ secretion from the collecting ducts

216
Q

What is Conn’s syndrome?

A

Also known as primary hyperaldosteronism, Conn’s syndrome is a rare condition caused by overproduction of aldosterone by the adrenal glands.

217
Q

What are the possible causes of Conn’s syndrome?

A
  1. Adrenal Adenoma = aldosterone secreting tumour (most common cause)
  2. Bilateral adrenal hyperplasia
  3. Familial hyperaldosteronism
  4. Adrenal carcinoma
218
Q

What is secondary hyperaldosteronism?

A

Overproduction of aldosterone cause by excessive renin secretion. This is due to the blood pressure in the kidneys being lower than the BP of the rest of the body.

219
Q

What are the causes of secondary hyperaldosteronism?

A
  1. Renal artery stenosis (narrowing of renal artery)
  2. Renal artery obstruction
  3. Heart failure
220
Q

What are the renin:aldosterone ratios seen in primary and secondary hyperaldosteronism?

A

Primary: low renin, high aldosterone
Secondary: high renin, high aldosterone

221
Q

What investigations are done to diagnose hyperaldosteronism

A
  • renin/aldosterone ratio
  • plasma potassium (normal or low)
  • blood pressure (high)
  • blood gas (alkalosis)
  • CT/MRI (adrenal tumour)
  • Doppler/CTangiogram/MRA (rnal artery stenosis/obstruction)
222
Q

What is the treatment for hyperaldosternism?

A
  • Aldosterone antagonists e.g. eplerenone, spironolactone
  • treat underlying cause (e.g. adrenalectomy)
223
Q

What is the definition of hyperkalaemia?

A

Mild = 5.5-5.9 mmol/l
Moderate = 6.0-6.4mmol/l
Serum potassium >6.5mmol/l = MEDICAL EMERGENCY

224
Q

What are the main pathophysiological mechanisms which cause hyperkalaemia?

A
  • increased intake of potassium in association with decreased renal excretion
  • decreased cellular entry of potassium or increased exit of potassium from cells
225
Q

Which conditions can cause hyperkalaemia?

A
  • Acute kidney injury
  • Chronic kidney disease
  • Rhabdomyolysis
  • Adrenal insufficiency
  • Tumour lysis syndrome
226
Q

Which medications can cause hyperkalaemia?

A
  • Aldosterone antagonists
  • ACE inhibitors
  • Angiotensin II receptor blockers
  • NSAIDs
  • Potassium supplements
227
Q

What investigations are used to diagnose hyperkalemia?

A
  • U&E bloods
  • ECG (absent P waves, prolonged PR, tall tented T waves, wide QRS)
228
Q

What are the clinical signs of hyperkalaemia?

A

-non-specific symptoms like weakness and fatigue
- muscle weakness and flaccid paralysis
- fast irregular pulse
- myalgia
- depressed or absent tendon reflexes

229
Q

What is the treatment for hyperkalaemia?

A

If urgent: calcium gluconate (stabilise cardiac membrane)
Non urgent: insulin + glucose

230
Q

What are potassium levels signifying hypokalaemia?

A

Moderate <3.5 mmol/l
Emergency <2.5mmol/l

231
Q

What are the causes of hypokalaemia?

A
  • thiazides + loop diuretics (K+ excretion)
  • Conn’s syndrome
  • renal tubular acidosis 1+2
  • GI losses
  • decreased potassium intake
232
Q

What are the symptoms of hypokalaemia?

A

mild is usually asymptomatic
- muscle weakness
- myalgia
- tremor
- muscle cramps
- decreased intestinal motility + constipation
- abnormal heart rhythm

233
Q

What investigations are used to diagnose hypokalaemia?

A

U&E (decreased potassium)
ECG (small inverted T waves, prominent u waves, ST depression, PR prolongation)

234
Q

What is the treatment for hypokalaemia?

A

K+ replacement
Aldosterone antagonist (spironolactone)

235
Q

What are the ECG changes seen in hypokalaemia?

A

prolongation of the PR interval
T wave flattening and inversion
ST depression
prominent U waves (best seen in the precordial leads)

236
Q

What is a phaeochromocytoma?

A

Adrenal medullary tumour which secretes catecholamines (NAd, Adr)

237
Q

What are the symptoms of phaeochromocytoma?

A
  • headaches
  • diaphoresis (excessive sweating)
  • hypertension
  • pallor
  • tachycardia
238
Q

What are the investigations for phaeochromocytoma?

A
  • 24hr urine collection (for catecholamines, metanephrines, normetanephrines)
  • Serum free metanephrines and normetanephrines
239
Q

What is the treatment of phaeochromocytoma?

A
  • a-blocker first (e.g. phenoxybezmine)
  • then beta-blocker (e.g. atenolol) *prevents reactive vasoconstriction
  • if surgery possible, excise tumour
240
Q

What are the four main types of thyroid cancer?

A
  • follicular
  • anaplastic
  • medullary
  • papillary

FAMP (make up 98% of thyroid cancers)

241
Q

What is the most common age range to be diagnosed with thyroid cancer?

A

45-54

242
Q

What are the risk factors for developing thyroid cancer?

A
  • head and neck irradiation
  • female sex
  • genetic factors
243
Q

What is the most common pathophysiology of a papillary carcinoma?

A

Papillary carcinoma tends to spread to local lymph nodes

244
Q

How does anaplastic thyroid cancer spread?

A

Anaplastic thyroid cancer is a rare, aggressive, undifferentiated carcinoma with a high propensity for local invasion and metastatic spread

245
Q

What are the key presentations for thyroid cancer?

A
  • Presence of risk factors
  • Palpable thyroid nodule
246
Q

What are some symptoms of thyroid cancer?

A
  • Hoarseness
  • Tracheal deviation
  • Dyspnoea
  • Dysphagia
247
Q

What is the first-line investigation for thyroid cancer?

A

Normal TSH with reduced thyroid function

248
Q

What is the gold standard test for thyroid cancer?

A

Fine-needle biopsy

249
Q

What is a differential diagnosis for thyroid cancer?

A

a benign thyroid nodule

250
Q

How would you manage a follicular tumour?

A

Surgery followed by radioactive iodine ablation and suppression of TSH for most patients

251
Q

What is the management for a medullary tumour?

A

Total thyroidectomy

252
Q

What is the management for an anaplastic tumour?

A

Total thyroidectomy or chemo-/radiotherapy

253
Q

What is the management for a thyroid lymphoma?

A

Radio and chemotherapy

254
Q

What is the prognosis for a papillary/follicular carcinoma?

A

> 90% 10 year survival rate - medullary is slightly worse due to metastasis

255
Q

What is the prognosis for an anaplastic thyroid tumour?

A

Average survival of a few months after diagnosis

256
Q

What is the prognosis for a medullary tumour?

A

80% 5 year survival rate

257
Q

What is the prognosis for a primary thyroid lymphoma?

A

<50% 5 year survival rate

258
Q

What are the 6 hormones secreted by the anterior pituitary?

A

Adrenocorticotrophic hormone (ACTH)
Thyroid-stimulating hormone (TSH)
Luteinising hormone (LH)
Follicle-stimulating hormone (FSH)
Prolactin (PRL)
Growth hormone (GH)

259
Q

Which 2 hormones are secreted by the posterior pituitary?

A

Oxytocin
Vasopressin/Anti-diuretic Hormone (ADH)

260
Q

What are the effects of cortisol?

A
  • regulates stress response
  • manages metabolism of carbohydrates, fats and proteins
  • increases blood glucose
  • acts as an anti-inflammatory
  • regulates blood pressure
  • controls sleep/wake cycle
261
Q

What are the effects of aldosterone on the body?

A
  • increases salt and water retention
  • increases potassium excretion
  • involved in regulation of fats, carbohydrates and proteins
262
Q

What are the effects of thyroid hormone?

A

Regulation of metabolic rate
High levels of T3/T4 typically cause increases in:
- basal metabolic rate
- gluconeogenesis
- glycogenolysis
- protein synthesis
- lipogenesis
- thermogenesis

263
Q

What is the effect of parathyroid hormone?

A

3 main actions to increase calcium levels in the body:
- increase bone resorption
- increase calcium reabsorption in the kidney
- increase vitamin D synthesis

264
Q

What are the effects of vasopressin (ADH)?

A

Increased AQP2 expression in cortical collecting ducts
- leads to increased water reabsorption
- results in increased blood volume
Vasoconstriction of smooth muscle cells around blood vessels
- leads to increased BP

265
Q

What is the difference between hyperthyroidism and thyrotoxicosis?

A

hyperthyroidism = condition where the thyroid gland produces excess thyroid hormones

thyrotoxicosis = clinical syndrome resulting from tissue exposure to high levels of circulating thyroid hormone

266
Q

Why can insulin treatment for DKA cause hypokalaemia and why is this dangerous?

A

insulin decreases potassium levels in the blood by redistributing K+ into the cells via increased Na/K pump activity causing low serum K+ levels –> hypokalaemia
low levels of K+ can cause arrhythmia, weakness (as the heart and muscles can struggle to contract)

267
Q

Why can cerebral oedema occur in rehydration therapy for DKA?

A

if the blood is initially very concentrated, with corresponding high salt levels (hypernatremia) and is rapidly diluted with IV fluids (to hyponatremia) then osmotic shifts will occur
water will move from the blood into the tissues which in the brain causes swelling of structures in an enclosed space (skull)
swelling of the brain causes rapid deterioration, coma, and can be fatal
this is why correction of fluid deficit is recommended to be undertaken slowly in DKA, over 48 hours

268
Q

What is De Quervain’s thyroiditis?

A

also known as subacute granulomatous thyroiditis, it is a self-limited inflammation of the thyroid gland which usually follows a viral infection and causes rapid swelling of the thyroid

269
Q

What are the 4 phases of de quervain’s thyroiditis?

A

phase 1: lasts 3-6 weeks –> hyperthyroidism, painful goitre, raised ESR
phase 2: lasts 1-3 weeks –> euthyroid (normal function)
phase 3: weeks to months –> hypothyroidism
phase 4 –> thyroid structure and function returns to normal

270
Q

WHat is thyroid storm?

A

thyrotoxic crisis represents the severe end of the spectrum of thyrotoxicosis and characterised by compromised organ function

271
Q

What inhibits the release of GH?

A

somatostatin
high levels of glucose
dopamine

272
Q

What are the side effects of corticosteroids?

A

Cataracts
Ulcers
Striae, skin thinning
Hypertension, Hirsutism
Immunosuppression, Infections
Necrosis of femoral heads
Glucose elevation
Osteoporosis, Obesity
Impaired wound healing
Depression/mood changes

CUSHINGOID

Phase 2A (18 decks)

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