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Phase 4 Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Where is insulin secreted?

A

Pancreatic beta cells (islets of Langerhans)

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2
Q

What is the action of insulin? (2)

A

To increase cellular uptake of glucose, fatty acids and amino acids into the liver, adipose tissue and muscle.

Also promotes storage of nutrients in the form of glycogen, lipids and protein respectively.

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3
Q

Describe the synthesis of insulin (3)

A

Synthesised form precursor (proinsulin).

Proinsulin is cleaved by the endoplasmic reticulum into active form insulin and a C peptide fragment.

Both are stored in secretory granules in beta cells awaiting release by exocytosis.

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4
Q

What receptor (promoted by insulin) promotes glucose uptake on the cell surface of muscle and adipose tissue cells?

A

GLUT4

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5
Q

Describe 4 types of glucose transporter proteins. Which is the most common?

A

GLUT-1 - Allows basal non-insulin stimulated glucose uptake into cells.

GLUT-2 - Transports glucose into beta cells, allowing them to sense serum glucose concentrations (low affinity receptor - so require high conc of glucose)

GLUT-3 - Enables non-insulin mediated uptake of glucose into brain, neurones and placents

GLUT-4 - Mediates majority of peripheral action of insulin, promoting glucose uptake into muscle and adipose tissue (most common)

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6
Q

Where is the majority of insulin extracted and degraded?

A

In the liver (50%)

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7
Q

Define gluconeogenesis

A

Glucose synthesis

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8
Q

Describe the impact of insulin on the liver

A

Acts on hepatocytes to inhibit gluconeogenesis (glucose synthesis) and activate glycogenesis (formation of glycogen), resulting in glycogen storage within the liver.

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9
Q

Define glycogenesis

A

Glycogen synthesis

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10
Q

Define glycogenolysis

A

Glycogen breakdown

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11
Q

Describe the impact of insulin on muscle (3)

A

Post-prandial spike (after eating) in insulin acts on monocytes to increase glucose import and shifts muscle metabolism to primarily use glucose as an energy source.

Promotes amino acid import and protein synthesis in muscle and inhibits protein degeneration and metabolism.

Promotes potassium uptake into cells, thus preventing dangerous hyperkalaemia following a meal.

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12
Q

Describe glycogen

A

Mainly stored in liver and muscles. Accumulated in response to insulin and broken down into glucose by glucagon

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13
Q

What hormone is released in response to low glucose levels? Where is it released?

A

Glucagon.

Released by pancreatic alpha cells

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14
Q

Describe glucagon

A

Peptide hormone produced by alpha cells of the pancreas.

Increase concentration of blood glucose (counteracts insulin) by stimulating hepatic glucose production through the breakdown of glycogen.

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15
Q

Describe the function of glucagon and where it acts. (3)

A

Acts on the liver to;

Convert glycogen to glucose (glycogenolysis)

Forms glucose from lactic acid and amino acids (gluconeogenesis)

Stimulates lipolysis and muscle glycogenolysis and breakdown (increased ketogenesis)

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16
Q

What are normal blood glucose levels?

A

3.5-8.00 mmol/L

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17
Q

Define diabetes mellitus (2)

A

Describes a reduced responsiveness to endogenous insulin.

Described as a syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both

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18
Q

Describe the difference between type 1 and type 2 diabetes

A

Type 1 - An inability to synthesise insulin

Type 2 - The body becoming resistant to the effects of insulin.

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19
Q

Name 3 microvascular complications of diabetes

A

Retinopathy (blurred vision, cotton wool sports, macular oedema)

Neuropathy (pain - at night, numbness in feet and hands, paraesthesia)

Nephropathy (microalbuminuria)

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20
Q

Name 3 macrovascular complications of diabetes

A

Stroke

MI

Limb ischaemia

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21
Q

Give 4 secondary causes of diabetes

A

Pancreatic pathology (total pancreatectomy, chronic pancreatitis, haemochromatosis)

Endocrine disease (acromegaly, cushing’s disease, hyperthyroidism)

Drug induces (thiazide diuretics, corticosteroids)

Maturity onset diabetes of youth (MODY)

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22
Q

Define MODY. When does it present? (3)

A

Maturity onset diabetes of youth (MODY)

Describes an autosomal dominant form of type 2 diabetes.

Presents in <25 year olds with a positive family history.

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23
Q

Describe 3 types of MODY

A

MODY1 - Mutation in HNF4A (presents in neonates - macrosomia and hyperglycaemia)

MODY2 - Mutation in GCK (glycokinase - sensor of pancreatic b-cells)

MODY3 - Mutation in HNF1A (patients respond well to sulfonylurea treatment so don’t require insulin)

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24
Q

Define type 1 diabetes

A

Describes a disease of insulin deficiency caused by the autoimmune destruction of insulin producing pancreatic beta cells.

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25
Q

Mutations in which HLA genes are strongly linked to type 1 diabetes? (2)

A

HLA-DR3 and HLA-DR4

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26
Q

Name 4 autoantibodies involved in type 1 diabetes

A

Anti-GAD (most common)

Pancreatic islet cell Ab

Islet antigen 1Ab

ZnT8 (zinc transporter 8)

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27
Q

When is the peak incidence of type 1 diabetes?

A

Manifests during childhood, peak incidence around puberty)

<30 years old and tend to be lean

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28
Q

Give 4 risk factors for Type 1 Diabetes

A

Family history (HLA-DR3/DR4)

Autoimmune disease (autoimmune thyroid, coeliac disease, addison’s disease, pernicious anaemia)

Environmental factors (diet, coxsackie B4, vitamin D deficiency)

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29
Q

Describe the pathophysiology of type 1 diabetes

A

Autoimmune destruction of insulin producing beta cells > insulin deficiency > glucose cannot be taken up by cells > body resultantly responds as if were hypoglucaemic > liver compensates by increasing glycogenolysis (producing glucose and ketones) > glucose is excreted by kidney leading to glycosuria and ketouria > increase in glucose and ketone excretion pulls more water into urine leading to thirst and polyuria.

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30
Q

Describe symptom triad of type 1 diabetes (3)

A

Polyuria/nocturia

Polydipsia (thirst)

Weight loss

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31
Q

Give 3 additional clinical signs of type 1 diabetes

A

Early onset (childhood/adolescence)

Lead body physique/build

Acute onset of osmotic symptoms (polyuria/nocturia/polydipsia/weight-loss)

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32
Q

Name 3 additional presenting features of type 1 diabetes

A

Hunger (hyperphagia - due to lack of usable energy source i.e glucose)

Pruritis vulvae and balanitis (glucosuria increases infection risk)

Blurred vision (lens swelling due to increased uptake of glucose and water)

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33
Q

Give 6 investigations used to diagnose type 1 diabetes

A

Urine dipstick for glucose and ketones

Random plasma glucose (>11mmol/L - confirms diagnosis)

Fasting plasma glucose (>7mmol/L)

Oral glucose tolerance test (>11mmol/L)

Autoimmune markers (i.e Anti-GAD)

Fasting C-peptide (Byproduct of insulin generation - Low due to absence of insulin secretion)

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34
Q

Describe the diagnostic criteria for a symptomatic patient with ? Type 1 diabetes

A

Fasting plasma glucose >7mmol/L

Random plasma glucose >11mmol/L (or after 75g oral glucose tolerance test)

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35
Q

Describe the diagnostic criteria for an asymptomatic patient with ? type 1 diabetes

A

Fasting plasma glucose >7mmol/L

Random plasma glucose >11mmol/L (or after 75g oral glucose tolerance test)

ON TWO SEPERATE OCCASIONS

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36
Q

What is more common Type 1 Diabetes or Type 2?

A

Type 2 diabetes

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37
Q

Describe 5 differences between type 1 and type 2 diabetes

A

Age of onset - Type 1 <20 years, Type 2 >40 years

Speed of onset - Type 1 more acute (hours/days), Type 2 slower (weeks/months)

Weight of patient - Type 1 recent weight loss typical, Type 2 Obesity strong risk factor

Features - Type 1 features of DKA, Type 2 milder symptoms (polyuria, polydipsia)

Ketonuria - Type 1 common, Type 2 rare.

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38
Q

NICE recommend diagnosis Type 1 diabetes on clinical grounds in adults presenting with hyperglycaemia, bearing in mind that Type 1 diabetics also have one or more what features? (5)

A

One or more of;

Ketosis
Rapid weight loss
Age of onset <50 years
BMI below 25kg/m2
Personal and/or family history of autoimmune disease

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39
Q

What further test is recommended by NICE to diagnose Type 1 Diabetes?

A

Measurement of C-peptide and/or diabetes specific antibodies

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40
Q

How is type 1 diabetes managed? (4)

A

Multiple daily subcutaneous insulin injections

Monitor HbA1c every 3-6 months (target of >48mmol/L in adults)

Self-monitor blood glucose 4 times a day (before each meal and before bed)

Metformin (if BMI is >25kg/m2)

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41
Q

Describe the blood glucose targets for those being managed for type 1 diabetes

A

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

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42
Q

What complications can occur as a result of insulin treatment? And how can these be prevented?

A

Hyperglycaemia (due to not taking enough insulin)

Hypoglycaemia (due to taking too much)

Can use DAFNE (Dose Adjusted for Normal Eating) - Teaches patients how to adjust insulin doses relative to amount of carbohydrate they’re consuming.

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43
Q

DKA is more common in which form of diabetes?

A

Type 1 Diabetes

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44
Q

What is the most common management error leading to DKA?

A

Patients reducing/omitting insulin due to being unable to eat (nausea/vomiting).

Insulin should never be stopped, only adjusted.

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45
Q

Describe the pathophysiology of DKA (3)

A

Body responds as if were hypoglycaemic, stimulating ketogenesis

Uncontrolled peripheral lipolysis causes increase in free fatty acids > increases in Acetyl CoA results in excess ketone production.

Ketones are strong acids, so lower the pH of the blood, leading to metabolic acidosis.

Increased acidity of the blood impairs the ability of haemoglobin to bind to oxygen.

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46
Q

Give 4 symptoms of DKA

A

Breath/Urine smells like pear drops

Polyuria, Polydipsia, Dehydration (leading to AKI)

Vomiting/Severe weight loss

Hyperventilation/Breathlessness (Kussmaul’s respiration)

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47
Q

Define Kussmaul’s respiration. What complication of diabetes is it associated with? (2)

A

Associated with DKA

Describes paradoxical rise in JVP on inspiration or failure for appropriate fall of JVP with inspiration.

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48
Q

Give 3 diagnostic factors for DKA

A

Hyperglycaemia (blood glucose >11mmol/L)

Raised plasma ketones (Urine >2+ or >3mmol/L in blood)

Metabolic acidosis (plasma bicarbonate <15mmol/L, Blood pH <7.3)

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49
Q

What other features may be present on a blood test in patients with DKA?

A

Hyperkalaemia (acidosis promotes potassium efflux from cells) (Insulin can promote potassium influx into cells vis Na/H antiporter - sodium influx stimulates Na/K ATPase)

Raised urea and creatinine (renal failure)

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50
Q

How is DKA managed? (3)

A

Fluids - 0.9% Sodium Chloride +/- Potassium Chloride

Insulin - (IV infusion at 0.1unit/Kg/hour) (once blood glucose is <14mmol/L, 10% dextrose should be started in addition to 0.9% sodium chloride).

Long acting insulin should be continues, short-acting insulin should be stopped

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51
Q

How is DKA resolution defined? (3)

A

DKA resolution defined as;

pH >7.3 AND blood ketones <0.6mmol/L AND bicarbonate >15mmol/L

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52
Q

Give 5 complications of DKA

A

Gastric stasis

Thromboembolism (hyperglycaemia causes hyperviscosity -thicker blood)

Cardiac arrhythmias (due to hyper/hypokalaemia)

Acute respiratory distress syndrome

Acute kidney injury

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53
Q

Name 1 common trigger for DKA and how is causes DKA.

A

Infection

Increases epinephrine release > increases glucagon levels > results in gluconeogenesis and glycogenolysis > hyperglycaemia

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54
Q

Give 1 important complication of fluid resuscitation in DKA (especially in young patients). How may this present and why does this occur?

A

Cerebal oedema

Presents as; Low GCS, Incontinence, vomiting, resp symptoms; grunting, apnoea, tachypnoea

When fluids are given too quickly, the sudden drop in blood osmolarity can lead water to move into cerebral tissue, causing oedema

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55
Q

Describe type 2 diabetes

A

Describes diabetes mellitus forming from a combination of insulin resistance and less severe insulin deficiency.

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56
Q

Describe the epidemiology of type 2 diabetes (4)

A

Age - Patients tend to be > 40

Fitness - Patients tend to be overweight/obese

Ethnicity - Tends to be more prevelent in South Asian, African and Caribbean

Sex - More common in males

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57
Q

Give 4 risk factors for type 2 diabetes

A

Obesity/lack of exercise/calorie alcohol excess

Increasing age

Family history

Low birth weight (impairs beta cell development and function)

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58
Q

Describe the pathophysiology of type 2 diabetes

A

Insulin resistance likely occurs due to a defect in the translocation of GLUT4 to the membrane.

Established T2DM leads to hypersecretion of insulin by depleted beta cells. Resulting in high circulating levels of insulin.

Insulin blood levels increase due to increased glucose production from the liver (due to inadequate suppression of gluconeogenesis) and reduced glucose uptake by peripheral tissues (insulin resistance).

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59
Q

Why don’t type 2 diabetics tend to develop DKA?

A

As even a small amount of insulin can halt the breakdown of fat and muscle into ketones.

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60
Q

Define 2 states of pre-diabetes

A

Impaired glucose tolerance (IGT) - When blood glucose levels are elevated but they’re not high enough to be classified as diabetes

Impaired Fasting Glucose (IFG) - When blood glucose levels are elevated in a fasting state but they’re not high enough to be classified as diabetes.

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61
Q

Describe 4 macrovascular complications of Type 2 diabetes

A

Myocardial infarction (4x more common)
Stroke (2x more common)
Atherosclerosis (can lead to stroke, IHD or PVD)
Peripheral Vascular Disease (can lead to amputation)

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62
Q

Diagnostically define Impaired Glucose Tolerance (IGT) (2)

A

Fasting plasma glucose - <7mmol/L

Oral glucose tolerance test - >7mmol/L but <11mmol/L

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63
Q

Describe 4 symptoms of peripheral vascular disease secondary to type 2 diabetes

A

Diminished or absent pedal pulses

Coolness of feet

Poor skin and nails

Absence of hair on feet and legs

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64
Q

Diagnostically define Impaired Fasting Glucose (IFG)

A

Fasting Plasma Glucose - >6.1mmol/L but <7mmol/L

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65
Q

How can peripheral vascular disease be detected?

A

Detected via doppler ultrasound

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66
Q

How is type 2 diabetes diagnosed? (3)

A

Fasting plasma glucose >7mmol/L

Random plasma glucose >11.1mmol/L

HbA1c >48mmol/mol (diagnostic)

(must be fulfilled on 2 separate occasions if asymptomatic)

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67
Q

When may HbA1c not be used for diagnosis of Type 2 diabetes? (8)

A

Increase in HbA1c can be caused by increased red cell turnover, occurring in;

Haemoglobinopathies
Haemolytic anaemia
Untreated iron deficiency anaemia
Gestational diabetes
Children
HIV
CKD
Corticosteroid use

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68
Q

Describe the initial management of Type 2 Diabetes (3)

A

Assess cardiovascular risk (QRISK >10%)

If QRISK <10% - Metformin

If QRISK >10% or Pt has CVD, or Pt has chronic heart failure - Metformin + SGLT-2 inhibitor (Empagliflozin/Dapagliflozin)

*SGLT-2 inhibitors should be started at any point if patient develops CVD)

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69
Q

Describe risk factor management patient Type 2 diabetes (4)

A

Lifestyle and dietary changes
Blood pressure control - Ramipril (ACEi) or ARB (in Afro-Caribbean)
Hyperlipidaemia control - Statins (Atorvastatin if QRISK >10%)
Obesity control - Orlistat

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70
Q

When metformin be contraindicated? Why? (3)

A

Heart failure

Liver disease

Renal disease

Can induce lactic acidosis

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71
Q
A
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72
Q

Give 4 side effects of metformin

A

Gastrointestinal upset;

Anorexia
Diarrhoea
Nausea
Abdominal pain

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73
Q

What should be given as an initial management of type 2 diabetes if metformin is contraindicated? (2)

A

If patient has CVD disease/risk - SGLT-2 monotherapy

If patient does not have CVD disease/risk - DPP-4 inhibitor or pioglitazone or a sulfonylurea

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74
Q

Describe the treatment ladder for Type 2 diabetes (3)

A

1st line (monotherapy) - Metformin (+/- SGLT-2 inhibitor - depending on CVD risk)

2nd line (dual therapy) - Add; DPP-4 inhibitor OR Pioglitazone OR sulfonylurea OR SGLT-2 inhibitor

3rd line;
- Metformin + DPP-4 inhibitor + sulfonylurea
- Metformin + Pioglitazone + Sulfonylurea
- Metformin + (Pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGL-2 inhibitor
- Insulin based treatment

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75
Q

What is the 4th line treatment for type 2 diabetes?

A

Glucagon-like peptide (GLP analogues) - Exenatide + Liraglutide

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76
Q

Describe the HbA1c targets for patients on lifestyle or single drug treatments of Type 2 diabetes

A

Lifestyle - 48mmol/mol

Lifestyle + metformin - 48mmol/mol

Lifestyle + Sulfonylurea (can cause hypoglycaemia) - 53mmol/mol

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77
Q

What is the HbA1c target for type 2 diabetic already on 1 drug but HbA1c has risen to 58mmol/mol?

A

53mmol/mol

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78
Q

Describe the MOA of metformin (2)

A

Suppresses gluconeogenesis and glycogenolysis in liver

Increases cells’ sensitivity to insulin

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79
Q

Name and describe MOA of DPP4 inhibitors

A

Sitagliptin (gliptins)

Dipeptidyl peptidase 4 inhibitors. DPP4 usually breaks down incretin. Incretin stimulates insulin release facilitating decrease in blood glucose levels.

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80
Q

What can DPP4-inhibitors (gliptins) increase the risk of?

A

Pancreatitis

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81
Q

Name and describe the moa of sulfonylurea

A

Gliclazide

Stimulates insulin secretion from pancreatic beta cells by binding and blocking K+ channels > stimulates influx of calcium into beta cells > stimulates exocytosis of vesicles containing insulin.

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82
Q

When should sulfonylureas not be used?

A

In obese patients as can cause weight cain and fluid retention.

Can also cause hypoglycaemia if overused.

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83
Q

Name and describe MOA of SGLT-2 inhibitors

A

Empagliflozin and Dapagliflozin

Selective sodium glucose co-transporter 2 inhibitor

Blocks glucose reabsorption in the proximal tubule, promoting excretion of glucose in urine

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84
Q

Give 3 side effects of SGLT-2 inhibitors (Empagliflozin/Dapagliflozin)

A

DKA, Hypoglycaemia, Increased risk of Infection

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85
Q

Describe the MOA of poiglitazone

A

Increases cellular insulin sensitivity

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86
Q

Give 3 complications of pioglitazone

A

Increases risk of heart failure, bladder cancer and bone fractures

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87
Q

In who should pioglitazone be avoided? (4)

A

In patients with history of;

Bladder cancer
Heart Failure
Hepatic Impairment
DKA

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88
Q

How can diabetic nephropathy be diagnosed?

A

Urine Albimin:Creatinine ratio >3 indicated microalbuminuria

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89
Q

How is diabetic nephropathy treated? (2)

A

ACEi/ARBs (ramipril/candesartan)

Avoid metformin (contraindicated in renal disease)

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90
Q

Name symptoms of diabetic neuropathy (2-7)

A

Somatic symptoms;
Pain (worse at night)
Numbness (glove and stocking distribution - hands and feet)
Pareaesthesia

Autonomic symptoms;
Postural hypotension
Gastroparesis
Diarrhoea, constipation, incontinence
Erectile dysfunction

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91
Q

Describe a life threatening emergency associated with uncontrolled type 2 diabetes (3)

A

Hyperosmolar Hypeglycaemic State.

Characterised by marked hyperglycaemia, hyperosmolality and mild/no ketosis.

Important to distinguish from DKA as insulin therapy (Mx of DKA) can produce adverse effects of HHS

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92
Q

How is diabetic neuropathy managed?

A

1st line - Amitriptyline, Duloxetine, Gabapentin or Pregabalin

Tramadol can be used as a ‘rescue therapy’ for exacerbations of neuropathic pain

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93
Q

Give 3 risk factors for hyperosmolar hyperglycaemic state

A

Infection (most common) (particularly pneumonia)

Consumption of glucose rich fluids

Concurrent medications; thiazide diuretics or steroids

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94
Q

In who should amitryptiline be avoided?

A

In those with urinary retention (i.e BPH)

AmiDRIPtiline

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95
Q
A
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96
Q

Describe the pathophysiology of Hyperosmolar Hyperglycaemic State

A

Insulin levels decrease > Hepatic ketogenesis is inhibited but hepatic gluconeogenesis still occurs > Hyperglucaemia > osmotic diuresis > Loss of sodium and potassium > volume depletion and raised serum osmolairy > Hyperviscosity

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97
Q

Describe the clinical presentation of Hyperosmolar Hyperglycaemic State (4)

A

Osmotic symptoms (polyuria, polydipsia, weight loss)

Severe dehydration

Decreased level of consciousness

Stupor (near unconsciousness) or coma (rare)

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98
Q

What tests may be conducted to investigate ? Hyperosmolar Hyperglucaemic State (5)

A

Blood glucose - >30mmol/L, no ketones or acidosis (pH >7.3, bicarbonate >15mmol/L)

Hyperosmolality - >320mmol/Kg

Urine dipstick - Heavy glycosuria)

Hypovolemia

Hyperkalaemia/hypokalaemia

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99
Q

How is hyperosmolar hyperglycaemic state managed?

A

Slow rehydration - 0.9% saline +/- electrolyte replacement over 48 hours

Insulin - only if blood glucose is NOT falling by 5mmol/L following rehydration OR if NO ketonaemia present

Low Molecular Weight Heparin - Enoxaparin
(reduces risk of thromboembolism, stroke, MI)

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100
Q

What is the function of the thyroid?

A

Controls metabolism, growth and development.

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101
Q

What 3 hormones are produced by the thyroid?

A

T3 - Most active
T4 (thyroxine) - Less active but more abundant

Calcitonin (produced by parafollicular cells)

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102
Q

What molecule and process is required for the synthesis of thyroid hormones?

A

Iodine

Iodination of tyrosine molecules AND combination of two tyrosine residues.

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103
Q

Describe the Hypothalamic Pituitary Thyroid Axis

A

HPT axis regulates thyroid hormone synthesis

Neurones in the paraventricular nucleus of the hypothalamus release Thyrotropin Releasing Hormone (TRH).

TRH stimulates release of Thyroid Stimulating Hormone (THS) from the anterior pituitary.

TSH travels to thyroid gland and stimulates release of T3 and T4.

T3 and T4 negatively feedback to TSH and TRH.

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104
Q

From where is Thyotropin Releasing Hormone released?

A

Paraventricular Nucleus of the Hypothalamus

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105
Q

From where is Thyroid Stimulating Hormone produced?

A

Anterior pituitary

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106
Q

Describe the Wolff-Chiakoff effect. When is this useful clinically?

A

Describes an autoregulatory phenomenon in which thyroid hormone synthesis is inhibited irrespective of serum TSH levels, when excess iodine is ingested.

Useful clinically as pharmaceutical doses of iodine may be used to acutely reduce thyroid activity.

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107
Q

Name 3 types of thyroid disorders

A

Hyperthyroidism - Graves’ Disease (overactive thyroid)

Hypothyroidism - Hashimoto’s thyroiditis/Iodine deficiency (underactive thyroid)

Thyrotoxicosis (excessive amount of thyroid hormone in in the body)

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108
Q

Describe 2 types of goitre formation and describe when they’re seen?

A

Diffuse (Entire thyroid gland swells, is smooth to touch)
Associated with; Iodine deficiency, Graves’, Hashimotos, De Quervain’s

Nodular (lumpy - solitary or multinodular)
Associated with: adenoma/cyst, carcionma

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109
Q

What hormone is the basis of screening for possible thyroid disease?

A

TSH

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110
Q

What will circulating levels of TSH, T4 and T3 look like in primary hyperthyroidism?

A

Low TSH
High T4
High T3

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111
Q

What will circulating TSH, T3 and T4 levels look like in hypothyroidism?

A

High TSH
Low T3
Low T4

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112
Q

If TSH is raised, T3 is low and T4 is raised, what is the likely diagnoses? Why?

A

Deiodinase deficiency or euthyroid hypothyroxinaemia

Because T4 is converted into T3 by deiodinases. If these are deficient then T3 is unable to be generated.

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113
Q

Thyroid function tests - Name 3 antibodies that are useful for diagnosing autoimmune thyroid disease.

A

Anti-TPO antibodies (Graves’/Hashimoto’s)

Antithyroglobulin antibodies (Graves’/Hashimoto’s/Cancer)

TSH receptor antibodies (Graves’)

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114
Q

Thyroid function tests - What imaging tool is used to investigate thyroid nodules?

A

Ultrasound (can also be used for guided biopsy)

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115
Q

Thyroid function tests - Describe the use and purpose of a radioisotope scan

A

Used to investigate hyperthyroidism and thyroid cancers, providing functional information about the thyroid.

Radioactive iodine is given orally/IV. This is taken up by the thyroid.

The more active the thyroid cells, the faster the radioactive iodine will be taken up.

(e.g Graves will show diffuse uptake of radioactive iodine. Toxic multi-nodular goitre will show focal high uptake)

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116
Q

Define primary hyperthyroidism

A

Describes pathology of the thyroid itself, causing it to produce too much thyroid hormone

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117
Q

Define secondary hyperthyroidism

A

Occurs when the thyroid is producing too much thyroid hormone due to overstimulation from thyroid stimulating hormone (TSH).

May rise due to an issue with the pituitary or hypothalamus.

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118
Q

Give 5 causes of hyperthyroidism

A

Graves’ disease
Toxic Multinodular goitre
Solitary toxic adenoma/nodule
Amiodarone
Sub acute de Quervain’s thyroiditis

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119
Q

Describe Graves’ disease

A

Most common form of hyperthyroidism.

Graves’ disease describes an autoimmune disease characterised by the production of Thyroid Stimulating Immunoglobin (igG) from b lymphocytes.

Thyroid Stimulating Immunoglobin mimics TSH, binds to and activates TSH receptors on the thyroid cell membrane, stimulating synthesis of T3 and T4.

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120
Q

Give 5 risk factors for Graves’ disease

A

Female (biggest risk factor - common post-partum)

Genetic association (HLA-B8, DR2 and DR3)

Infection - E.coli contain TSH binding sites.

High iodine intake

Autoimmune disease (vitiligo, addisons, pernicious anaemia, myasthenia gravis, Type 1 diabetes)

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121
Q

Name 5 autoimmune diseases associated with Grave’s disease

A

Vitiligo

Addison’s disease

Pernicious anaemia

Myasthenia gravis

Type 1 diabetes

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122
Q

Give 5 clinical features of Graves’ disease

A

Sweating, weight loss, irritability

Palpitations/tachycardia/cardiac flow murmur

Diffuse (smooth) goitre

Heat intolerance

Graves orbitopathy (only occurs in Graves’)

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123
Q

How may Graves’ orbitopathy present? (3)

A

Presents in 25% of Graves’ patients

Results in retro-orbital inflammation and swelling of the extraocular muscles

May present as;
Upper eyelid retraction
Exophthalmos (protruding eye)
Optic neuropathy

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124
Q

Give 2 rare but distinct clinical signs of Graves’ disease

A

Pretibial myxoedema - Arises from excess hyaluronic acid leading to deposits of mucin under the skin. Presents as swelling and lumpiness in the lower legs (may be red)

Acropachy - Finger clubbing with erosion of the distal phalanges

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125
Q

What will thyroid function tests show in a patient with Graves’ disease?

A

Free TSH - Low
Serum T4/T3 - High
TSH receptor antibodies - Positive (highly specific)

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126
Q

What test can be used to identify Graves Orbitopathy?

A

MRI or CT

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127
Q

How is Graves’ disease initially managed?

A

Symptom control;
Beta blockers - Propranolol
Hydrocortisone (for Graves’ dermopathy)
IV Methylprednisolone (for Graves’ orbitopathy)

Antithyroid drugs;

First line - Carbimazole (continued for 12-18 months)

Second line - Propylthiouracil (used in pregnancy as Carbimazole is teratogenic)

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128
Q

If Graves’ patient relapses following Anti-Thyroid Drug treatment, what treatment is offered?

A

1st line - Radioiodine treatment

2nd line - Thyroidectomy

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129
Q

Give 1 complication of radioiodine therapy

A

Can lead to hypothyroidism resulting in patient requiring thyroxine replacement therapy (levothyroxine)

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130
Q

What is the major complication of Carbimazole?

A

Agranulocytosis (increases risk of sepsis)

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131
Q

Give 3 possible consequences of thyroidectomy

A

Can risk damaging the recurrent laryngeal nerve

Can cause parathyroidism

Patients become hypothyroid so require life-long thyroid replacement therapy.

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132
Q

Name and describe 2 treatment strategies for hyperthyroidism

A

Titration Regimen (12-18 months) - Dose of drug is reduced (every 1-2 months) with the aim of keeping the patient on the lowest dose required for normal thyroid function.

Block and replace - Give high dose carbimazole to stop thyroid producing T3/T4. When T3/T4 levels return to normal range, give levothyroxine replacement.

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133
Q

What is the MOA of Carbimazole?

A

Inhibits TPO from coupling and iodinating tyrosine residues.

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134
Q

In whom is Carbimazole contraindicated?

A

In pregnancy as it is teratogenic

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135
Q
A
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136
Q

Describe subclinical hyperthyroidism (2)

A

Describes a condition where there is low TSH levels but normal T3 and T4.

Most causes are iatrogenic, especially due to over treatment with levothyroxine (T4)

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137
Q
A
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138
Q
A
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139
Q

Describe Toxic Multinodular Goitre (4)

A

Describes hyperthyroidism in which nodules form on the thyroid gland, each producing excessive amounts of thyroid hormone.

2nd most common form of thyrotoxicosis

Primarily seen in elderly and in iodine deficient areas.

1st line - Radioactive iodine therapy (I-131)

140
Q

Describe De Quervain’s thyroiditis and it’s two phases. How is it treated? (3)

A

Occurs when a viral infection (i.e URTI)causes pain and inflammation in the thyroid.

Two phases;
A hyperthyroid phase followed by a hypothyroid phase.
(Occurs as TSH levels fall due to negative feedback from the hyperthyroid phase)

Treatment; NSAIDs and Beta blockers for symptomatic relief

141
Q

Name 3 drugs that can induce hyperthyroidism

A

Amiodarone (anti-arrhythmic drug) (Can cause both hyper and hypothyroidism.

Iodine

Lithium

142
Q

What blood results would you expect in a patient with De Quervain’s Thyroiditis? (T4, ESR, Uptake of Iodine-131)

A

T4 - Raised
ESR - Raised
Uptake of Iodine-131 - Reduced

143
Q

What effect can amiodarone have on the thyroid? How can each happen?

A

Can cause Hyperthyroidism (due to high iodine content)

Can cause hypothyroidism (as inhibits conversion of T4 to T3)

144
Q

Describe a Thyroid Storm (Aka thyrotoxic crisis)

A

Describes an acute, severe, life-threatening presentation of hyperthyroidism.

Usually precipitated by stress, infection, surgery or radioactive iodine therapy.

145
Q

How may a thyroid storm (thyrotoxic crisis) present? (3)

A

Pyrexia (raised body temp)
Tachycardia
Delerium/Coma

146
Q

How is thyroid storm (thyrotoxic crisis) treated? (4)

A

Oral Carbimazole
Oral Propranolol
Oral Potassium Chloride (acutely blocks release of T3/T4)
IV Hydrocortisone (inhibits peripheral conversion of T4 to T3)

147
Q

Describe hypothyroidism

A

Describes underactivity of the thyroid gland resulting in symptoms associated with a lack of thyroid hormone.

148
Q

What is the most common cause of hypothyroidism in the developing world?

A

Iodine deficiency

149
Q

What is the most common cause of hypothyroidism in the developed world?

A

Autoimmune/atrophic hypothyroidism - Hashimotos’

150
Q

Give 5 risk factors for Hypothyroidism

A

Iodine deficiency (developing world)

Autoimmune diseases (Hashimoto’s is the most common in the developed world)

Female

Turners’/Down’s syndrome

Drugs (amiodarone and lithium)

151
Q

Give 7 clinical features of hypothyroidism

A

Tiredness/sleepy/lethargic

Decreased mood/depression

Cold sensitivity

Weight gain

Constipation

Muscle weakness/myalgia

Menorrhagia (menstrual bleeding lasting >7 days)

152
Q

Using the acronym BRADYCARDIC, give clinical signs of hypothyroidism.

A
  • Bradycardia
  • Reflexes relax slowly
  • Ataxia (cerebellar)
  • Dry thin hair/skin
  • Yawning/drowsy/coma
  • Cold Hands/Low body temperature
  • Ascites (+/- pitting oedema in feet, hands, eye lids) (+/- pericardial or pleural effusion)
  • Round puffy face/double chin/obese
  • Defeated demeanour
  • Immobile
  • CCF – Congestive Cardiac Failure
153
Q

What hand pathology is associated with hypothyroidism?

A

Carpal Tunnel Syndrome

154
Q

What antibodies are raised in Hashimoto’s Thyroiditis?

A

Anti-TPO antibodies (raised in >90% of patients)

155
Q

How is hypothyroidism treated?

A

Young and healthy - Levothyroxine therapy

Elderly or Ischaemic heart disease - Low dose levothyroxine (as too much can precipitate angina or MI)

156
Q

Over-replacement of levothyroxine in hypothyroid patients can increase the risk of developing what?

A

Osteoporosis and atrial fibrillation

157
Q

Define Hashimoto’s thyroiditis

A

Most common cause of hypothyroidism in the developed world.

Characterised by the formation of antithyroid antibodies that attack thyroid tissue, causing lymphocyte infiltration, atrophy and progressive fibrosis, leading to decreased thyroid hormone production.

158
Q

Hashimoto’s thyroiditis is associated with the development of what?

A

MALT lymphoma (mucous associated lymphoid tissue)

159
Q

What will Thyroid Function tests show in a patient with Hashimoto’s thyroiditis?

A

High TSH

Low T3

Low T4

High Anti-TPO antibodies

160
Q

Name one complication of giving iodine supplementation to patients with iodine deficiency goitre

A

Can cause iodine-induced hyperthyroidism (aka Jod-Basedow Effect)

Occurs as some patients Wolff-Chaikoff effect due to impaired autoregulation.

161
Q

Describe Post-Partum Thyroiditis

A

Describes a short lasting (transient) episode of thyroid dysfunction occurring within the first year post-partum.

No presence of toxic nodule or TSH receptor antibodies.

Usually follows a pattern of hyperthyroidism/thyrotoxicosis followed by hypothyroid followed by euthyroid.

162
Q

What would thyroid function tests show in post partum thyroiditis?

A

Low TSH
High T4
High T3
Negative TSH antibodies

163
Q

When is it recommended to test TSH levels post partum?

A

Test 6-12 weeks post-partum, particularly in high risk populations and in patients experiencing postpartum depression, lactation difficulties or hyper/hypothyroidism.

164
Q

Name 1 complication of hypothyroidism and describe how it is treated

A

Myxoedema coma

Features;
Confusion/coma
Hypothermia
Cardiac failure
Hypoventilation/Hypoglycemia/Hyponatremia

Treatment;
IV/Oral T3
Glucose infusion
Gradual rewarming

165
Q

Are features of hyper/hypothyroidism seen in thyroid cancer?

A

No as they rarely secrete excess thyroid hormone.

166
Q

Name 5 types of thyroid cancers

A

Papillary (70%)

Follicular (20%)

Medullary (5%)

Anaplastic (rare)

Lymphoma (rare)

167
Q

Describe sub-clinical hypothyroidism

A

No obvious symptoms

TSH is raised but T3 T4 are normal

168
Q

Describe papillary thyroid carcinomas (3)

A

Most common type of thyroid carcinoma

Often seen in young females and have a good prognosis

Well differentiated and arise from thyroid epithelium

169
Q

How is sub-clinican hypothyroidism managed in relation to TSH levels?

A

If TSH is >10mU/L and T3/T4 is normal = Consider offering levothyroxine if TSH level is >10mU/L on 2 separate occasions 3 months apart.

If TSH is 5.5-10mU/L and T4 is normal =
If <65 consider offering 6 month trial of levothyroxine if; TSH level is 5.5-10mU/L on 2 separate occasions 3 months apart AND there are symptoms of hypothyroidism.

170
Q

Describe follicular thyroid carcinomas (3)

A

Usually present as a solitary thyroid nodule

Well differentiated and arises from thyroid epithelium

More likely than papillary to spread to lung/bone but usually has a good prognosis

171
Q

Describe medullary thyroid carcinoma (2)

A

Arises from parafollicular (c-cells) and secrete calcitonin

Associated with the hereditary condition (MEN-2) (multiple endocrine neoplasia type 2)

172
Q

Describe anaplastic thyroid carcinomas (3)

A

Very undifferentiated and arises from thyroid epithelium

Tend to be aggressive, spreading local quickly and has a poor prognosis.

Management is generally palliative.

173
Q

Medullary Thyroid Cancer is associated with MEN-2. What type of cancer is this associated with? How may this present?

A

Phaeochromocytoma

May present as poorly controlled hypertension.

174
Q

Describe the clinical presentation of thyroid cancer (4)

A

90% present as thyroid nodules

May present as cervical lymphadenopathy or with lung, cerebral, hepatic or bone metastases

Dysphagia

Hoarseness of voice (due to tumour compressing oesophagus/recurrent laryngeal nerve)

175
Q

Name 4 diagnostic tests used to diagnose thyroid cancer

A

Fine needle aspiration cytology biopsy

Thyroid Function tests (to assess hyper/hypothyroid)

Laryngoscopy (may show ispilateral paralysed vocal cord - suggestive of malignancy)

Circulating thyroglobulin (>90% if differentiated thyroid carcinomas secrete thyroglobulin)

176
Q

What may a fine needle aspiration cytology biopsy show for a papillary carcinoma? (3)

A

Orphan Annie eyes

Intranuclear holes and grooves

Pasmmoma bodies

177
Q

What may a fine needle aspiration cytology biopsy show for follicular thyroid carcinoma?

A

Hypercellularity (excess cells)

Microfollicles

Absence of colloid

178
Q

In which type of thyroid carcinoma would you see orphan annie eyes on cytology?

A

Papillary carcinoma

179
Q

What type of thyroid carcinoma commonly secretes calcitonin?

A

Medullary thyroid carcinomas

180
Q

How are papillary and follicular carcinomas treated? (4)

A

Total thyroidectomy
Node excision
Radioiodine therapy
Levothyroxine (Suppresses TSH which acts as growth factor for cancer)H

181
Q

How are medullary thyroid carcinomas treated?(3)

A

Thyroidectomy and lymph node removal
Levothyroxine (for replacement rather than suppression)
Vandetanib (2nd line) - Used for more aggressive cancers

182
Q

What class of drug is Vandetanib and what is it used to treat?

A

Tyrosine Kinase Inhibitor

Used to treat more aggressive/metastatic medullary thyroid cancers

183
Q

Define carcinoma

A

Describes malignant neoplasms of epithelial origin

184
Q

Name and define 2 subtypes of carcinomas

A

Adenocarcinoma - Develops from an organ or gland.

Squamous cell carcinoma - Develops from squamous epithelium

185
Q

Define sarcoma

A

Refers to malignant cancer that originates in supportive and connective tissues, such as; bone, tendons, cartilage, muscle or fat

186
Q

What is the benign and malignant name for Bone cancers

A

Osteoma and Osteosarcoma

187
Q

What is the benign and malignant name for cartilage cancers

A

Chondroma and Chondrosarcoma

188
Q

What is the benign and malignant name for smooth muscle cancers

A

Leiomyoma and leiomyosarcoma

189
Q

What is the benign and malignant name for skeletal muscle

A

Rhabdomyoma and Rhabdomyosarcoma

190
Q

What is the benign and malignant name for cancers of the membranous lining of body cavities?

A

Mesothelioma and mesothelial sarcoma

191
Q

What is the benign and malignant name for cancers of fibrous tissue?

A

Fibroma and Fibrosarcoma

192
Q

What is the benign and malignant name for cancers of blood vessels?

A

Hemangioma and Angiosarcoma/Hemangioendothelioma

193
Q

What is the benign and malignant name for cancer of adipose tissue?

A

Lipoma and Liposarcoma

194
Q

What is the benign and malignant name for cancer of primitive embryonic connective tissue?

A

Myxosarcoma

195
Q

Describe the adrenal glands

A

Adrenal glands are paired endocrine glands (retroperitoneal) situated over the medial aspect of the upper poles of each kidney.

They consist of an outer connective tissue capsule, a corted and a medulla.

196
Q

What are the adrenal glands neurologically innervated by?

A

Coeliac plexus and greater splanchnic nerves (T5 to T8)

197
Q

From where do the adrenal glands receive their blood supply? (3)

A

Superior adrenal artery (arises from inferior phrenic artery)

Middle adrenal artery (arises from abdominal aorta)

Inferior adrenal artery (arises from renal arteries)

198
Q

What veins drain blood from the adrenal glands? (2)

A

Right adrenal vein = Inferior Vena Cava

Left adrenal vein = Left renal vein

199
Q

What are the 3 regions of the adrenal cortex (from superficial to deep)

A

(GFR - Makes Good Sex)

Zona Glomerulosa

Zona Fasciculata

Zona Reticularis

200
Q

What does the zona glomerulosa produce?

A

Mineralocorticoids (such as aldosterone)

201
Q

What does the Zona Fasciculata produce?

A

Glucocorticoids (cortisol - corticosteroids)

202
Q

What does the Zona Reticularis produce?

A

Androgens

203
Q

What does the medulla of the adrenal gland produce? (2)

A

Contains chromaffin cells which secrete catecholamines (i.e adrenaline) into the blood in response to stress.

Also secrete enkephalins which function in pain control

204
Q

Describe the Hypothalamic-Pituitary-Adrenal Axis (4)

A

Corticotrophin Releasing Hormone (CRH) is secreted by the hypothalamus.

CRH acts on the anterior pituitary, secreting secretion of adrenocorticotrophic hormone (ACTH).

ACTH acts on the adrenal cortex, stimulating production of cortisol (glucocorticoid) and androgens.

Both negatively feed back to inhibit further secretion of CRH and ACTH

205
Q

Where in the adrenal gland is cortisol produced?

A

Zona Fasciculata

206
Q

With regards to cortisol, what happens physiologically in response to stress?

A

The amygdala sends stress signals to the hypothalamus.

This kickstarts the HPA axis

Leads to cortosol and adrenaline secretion

207
Q

Name 5 functions of cortisol

A

Increases blood pressure

Increases insulin resistance

Increases gluconeogenesis, lipolysis and proteolysis

Inhibits bone formation (increases risk of osteoporosis)

Inhibits inflammatory and immune responses

208
Q

Define Cushing’s Syndrome

A

Describes a disease of cortisol excess and loss of normal feedback mechanism of the HPA axis.

209
Q

Define Cushing’s Disease

A

Characterised by excess cortisol production resulting from inappropriate ACTH secretion from a pituitary adenoma.

210
Q

Give 2 ACTH dependent causes of Cushing’s

A

Cushing’s disease - Bilateral adrenal hyperplasia resulting from an ACTH secreting pituitary adenoma

Paraneoplastic Cushing’s Syndrome - Ectopic ACTH secreting tumour (Small lung cancer)

211
Q

Give 3 ACTH independent causes of Cushings

A

(More common than ACTH dependent causes)

Iatrogenic (most common cause is oral steroids - prednisolone)

Adrenal adenoma/cancer

Adrenal nodular hyperplasia

212
Q

What is the most common cause of Cushing’s Syndrome?

A

Use of Oral Corticosteroids (prednisolone)

213
Q

Give 6 clinical features of Cushing’s Syndrome

A

Swollen/Moon Face/

Weight gain (central obesity)/Purple striae/Buffalo Hump (far build up on back of neck)

Mood change (depression, lethargy, irritability)

Gonadal dysfunction (irregular menses, hirsutism, erectile dysfunction)

Infections

Increased BP

Premature osteoporosis or unexplained fractures

214
Q

What electrolyte disturbance can be seen in Cushing’s?

A

Hypokalaemia (leading to metabolic alkalosis)

215
Q

What is the 1st line screening test for Cushing’s? What are the findings?

A

Overnight (low-dose) dexamethasone suppression test.

Patients with Cushing’s do NOT have their morning cortisol spike suppressed.

Results = Elevated cortisol

216
Q

What other tests can be used to screen for Cushings? (2)

A

24hr urinary free cortisol (2 measurements required)

Bedtime salivary cortisol (2 measurements required)

217
Q

What is dexamethasone? What impact does dexamethasone have on the HPA axis?

A

A corticosteroid with high glucocorticoid activity, meaning it acts similarly to cortisol.

Dexamethasone negatively feeds back to the pituitary gland, decreasing ACTH release, resulting in a decrease in cortisol secretion from the Zona Fasciculata.

218
Q

What is the importance of the dexamethasone suppression test? (2)

A

In pathological hypercortisolism, the HPA axis is partially or entirely resistant to feedback inhibition by dexamethasone, so cortisol levels will be elevated.

The test allows us to confirm diagnosis of Cushing’s Syndrome AND understand whether the cause is primary or secondary

219
Q

What test allows us to diagnose Cushing’s Syndrome? What will the results show?

A

Low Dose (1mg) Dexamethasone Suppression Test.

Cortisol levels will remain high (as Cushing’s patients already have high circulating cortisol levels)

220
Q

What test identifies the cause of Cushings?

A

High dose (8mg) dexamethasone suppression test

221
Q

High dose dexamethasone suppression test results = Low Cortisol + Low ACTH.

What does this suggest?

A

AVTH secreting pituitary adenoma

222
Q

High dose dexamethasone suppression test results = High Cortisol + Low ACTH

What does this suggest?

A

Adrenal Cushing’s (Adrenal tumour producing excess cortisol)

223
Q

High dose dexamethasone suppression test results = High Cortisol + High ACTH

What does this suggest?

A

Paraneoplastic Cushing’s (ectopic source of ACTH - Small cell lung cancer/carcinoid tumour)

224
Q

What results would you get from a high dose dexamethasone suppression test for a patient with an ACTH Secreting Pituitary adenoma?

A

Low Cortisol + Low ACTH

If a ACTH secreting tumour is present, the high dose dexamethasone should be enough to inhibit it’s ACTH release.

225
Q

What results would you get from a high dose dexamethasone suppression test for a patient with a cortisol secreting adrenal gland tumour?

A

High cortisol + Low ACTH

The dexamethasone will have no impact on cortisol levels because the cortisol is being secreted from the adrenal glands irrespective of ACTH.

226
Q

What results would you get from a high dose dexamethasone suppression test for a patient with a paraneoplastic ACTH secreting tumour?

A

High Cortisol and High ACTH

Dexamethasone inhibits ACTH secretion from the pituitary but ACTH is being produced ectopically, so it’s level will remain high.

227
Q

How is Cushing’s syndrome treated?

A

Treat the cause;

Iatrogenic (corticosteroid use) - Stop medications

Cushing’s Disease;
- Trans-sphenoidal resection of causative pituitary tumour
- Bilateral adrenalectomy (removal of adrenal glands)

Adrenal adenoma/carcinoma;
- Adrenalectomy

228
Q

Give one complication of Bilateral Adrenalectomy

A

Nelson’s syndrome;

Increased skin pigmentation (due to increased ACTH) from an enlarging pituitary tumour as adrenalectomy will remove the negative feedback.

May also have intracranial compressive symptoms due to pituitary growth.

Will respond to pituitary radiotherapy.

229
Q

Where in the adrenal cortex is Aldosterone produced?

A

Zona Glomerulosa (outermost layer)

230
Q

What is the primary function of aldosterone? (3)

A

Acts on principle cells in the distal convoluted tubule and collecting duct.

Stimulates sodium reabsorption and potassium secretion.

Achieves this by increasing expression of sodium channels and sodium/potassium ATPase in the cell membrane.

231
Q

What system controls the production of aldosterone? Where is this located?

A

Renin-angiotensin system.

Responding to renin release by the juxtaglomerular cells of the afferent arterioles of the kidney.

232
Q

Describe the Renin-Angiotensin-Aldosterone System in relation to low blood pressure.

A

Low blood pressure is detected by juxtaglomerular cells in the afferent arteriole of the kidney, stimulating the release of renin.

Renin converts angiotensin (produced by the liver) to angiotensin I.

Angiotensin I is converted to Angiotensin II in the lungs by Angiotensin Converting Enzyme (ACE)

Angiotensin II stimulates release of aldosterone from zona glomerulosa.

Aldosterone stimulates expression of sodium channels and Na/K+ ATPases in the membranes of principle cells in the distal convoluted tubule and collecting duct.

This increases sodium reabsorption and potassium excretion.

Also works in conjunction with ADH to increase water reabsorption in the proximal convoluted tubule.

This eventually increases plasma volume, increasing blood pressure.

233
Q

Where is renin produced?

A

Kidney

234
Q

Where is angiotensin produced?

A

Liver

235
Q

Where is angiotensin I converted to angiotensin II? What enzyme catalyses this reaction?

A

In the Lungs

Catalysed by Angiotensin Converting Enzyme (ACE)

236
Q

Define Conn Syndrome (Primary Hyperaldosteronism)

A

Describes condition characterised by excess production of aldosterone independent of the renin-aldosterone system.

237
Q

What is Conn Syndrome (primary hyperaldosteronism) the most common cause of? Why?

A

Secondary Hypertension

Aldosterone promotes sodium reabsorption (and thus water reabsorption), thus increasing plasma volume and increasing blood pressure.

238
Q

What are the main physiological effects of Conn Syndrome (Primary Hyperaldosteronism)? (5)

A

Increased Sodium Reabsorption (DCT)
Increased Water Reabsorption (PCT)
Increased Potassium Secretion (DCT)
Increased Hydrogen Ion Secretion (CD)
Decreased Renin Release (due to negative feedback)

239
Q

When should Conn Syndrome be suspected?

A

Hypertension in patients;
- Under 30 with no family history
- Accelerated (malignant) hypertension
- Hypokalaemia before diuretic surgery
- Resistant to antihypertensive therapy (e.g >3 drugs)

Hypokalaemia

Alkalosis

Hypernatremia

240
Q

Give 2 causes of Primary Hyperaldosteronism

A

Adrenal adenoma (of zona glomerulosa) - Secreting excess aldosterone (Conn Syndrome) (2/3 of cases).

Bilateral adrenocortical hyperplasia (1/3 of cases).

241
Q

Give 4 features of primary hyperaldosteronism

A

Treatment resistant hypertension

Symptoms of hypokalaemia (muscle weakness, hypertonis, cramps, palpitations, constipation, light-headedness)

Nocturia/polyuria

Metabolic alkalosis

242
Q

What must primary hyperaldosteronism be differentiated from before initiating treatement?

A

Secondary hyperaldosteronism which arises when there is excess renin (and hence angiotensin II) which stimulates aldosterone release.

243
Q

How does secondary hyperaldosteronism occur? What can cause it?

A

Occurs when blood pressure in the Kidneys is disproportionally lower than the rest of the body, usually doe to reduced renal perfusion.

Causes include;
- Renal artery stenosis/Obstruction
-Accelerated hypertension
-Diuretics
-Heart Failure

244
Q

What is the most important diagnostic test for Primary Hyperaldosteronism?

A

Aldosterone:Renin Ratio

245
Q

What Aldosterone to Renin Ratio would you expect to see in a patient with Primary Hyperaldosteronism?

A

Increased Aldosterone and Decreased Renin

246
Q

What Aldosterone to Renin ratio would you expect to see in a patient with Secondary Hyperaldosteronism?

A

Increased Aldosterone and Increased Renin

247
Q

What may an ECG show in a patient with Primary Hyperaldosteronism? And Why?

A

May show features of hypokalaemia;

Small or inverted T waves
Prominent U waves
A long PR interval
Depressed ST segment

248
Q

What is the treatment for Conn’s Syndrome?

A

Laparoscopic Adrenalectomy

Spironolactone or eplerenone post-op to control blood pressure (aldosterone antagonists)

249
Q

What is the treatment for bilateral adrenal hyperplasia?

A

Oral spironolactone or amiloride

250
Q

Describe Addison’s Disease

A

Aka Primary Adrenal Insufficiency

Characterised by bilateral destruction of the entire adrenal cortex.

Results in Mineralocorticoid (aldosterone), Glucocorticoid (cortisol) and androgen (sex hormone) deficiency.

Eventually leads to an elevation of ACTH and CRH due to loss of negative feedback

251
Q

When is Addison’s disease usually first recognised?

A

Has an insidious nature so usually not recognised until an acute adrenal crisis develops.

252
Q

What is the most common cause of Addison’s disease in the UK?

A

Autoimmune adrenalitis (80% of cases)

253
Q

Give 5 other causes of Addison’s disease

A

TB (most common worldwide)
Adrenal metastases
CMV (in HIV patients)
Long term steroid use
Adrenal haemorrhage/infarction (meningococcal septicaemia)

254
Q

Give 6 symptoms of Addison’s disease

A

This Addison’s in all with unexplained abdominal pain or vomiting.

Lethargy/Depression
Anorexia/Weight loss
Posutral Hypotension (due to loss of aldosterone leading to hypovolemia)
Nausea/vomiting
Hyperpigmentation of the skin (due to increased ACTH > melanin)

255
Q

What test is used to diagnose Addison’s disease? What does it involve?

A

Synacthen test

Involves giving synthetic ACTH IM to stimulate the adrenal glands to produce cotrisol.

In healthy individuals, cortisol levels will rise in response to synacthen.

In Addison’s patients, there will be no increase in cortisol

256
Q

What will serum ACTH levels be like in a patient with primary adrenal insufficiency?

A

High

257
Q
A
258
Q

Define secondary adrenal insufficiency.

A

Most commonly caused by long term steroid use.

This leads to suppression of the pituitary-adrenal axis.

Characterised by a reduction in ACTH production.

Only becomes apparent on the withdrawal of steroids

259
Q

What will ACTH levels be like in a patient with secondary adrenal insufficiency?

A

Low

260
Q

What will serum electrolytes look like in a patient with primary adrenal insufficiency? (2)

A

Hyponatremia
Hyperkalaemia

261
Q

How is Addison’s Disease Managed?

A

Glucocorticoid and Mineralocorticoid replacement.

Combination of;
Hydrocortisone 20-30mg OD (given in 2/3 divided doses)
Fludrocortisone

262
Q

How should an Addison’s patient manage an intercurrent illness?

A

Double dose of glucocorticoid (hydrocortisone)

Continue with same dose of fludrocortisone

263
Q

What hormones are secreted by the hypothalamus to act on the anterior pituitary? (5)

A

Corticotrophin Releasing Hormone (CRH)
Thyrotropin Releasing Hormone (TRH)
Growth Hormone Releasing Hormone (GHRH)
Gonadotrophin Releasing Hormone (GnRH)
Dopamine

264
Q

How is an acute Addisonian crisis managed?

A

Resuscitation - IV saline + Hydrocortisone

265
Q

What triad is seen in Addisonian crisis? (Na, K, Glucose)

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

266
Q

What hormones are secreted by the anterior pituitary? (6)

A

Follicle Stimulating Hormone (FH)
Leutinising Hormone (LH)
Adrenocorticotropic Hormone (ACTH)
Thyroid Stimulating Hormone (TSH)
Prolactin
Growth Hormone (GH)

267
Q

Describe physiological effect of Thyrotropin Releasing Hormone on the body.

A

Thyrotropin-releasing hormone (TRH) → thyroid-stimulating hormone (TSH) → increases the release of T3 & T4 from thyroid → increased metabolism.

268
Q

Describe the physiological effect of Gonadotropin Releasing Hormone (GnRH) on the body.

A

-Gonadotropin-releasing hormone (GnRh) → lutenizing hormone (LH) & follicle stimulating hormone (FSH) → target gonads to increase oestrogen, progesterone & testosterone

269
Q

Describe the physiological effect of Growth Hormone Releasing Hormone (GHRH) on the body.

A

Growth-hormone releasing hormone (GHRH) → growth hormone (GH) → stimulates growth & protein synthesis

270
Q

Describe the physiological effect of Somatostatin (SST) on the body

A

Somatostatin (SST) → inhibits growth hormone (GH) → inhibits growth & protein synthesis

271
Q

Describe the physiological effect of Corticotropin Releasing Hormone (CRH) on the body.

A

Corticotropin-releasing hormone (CRH) -> adrenocorticotrophic hormone (ACTH) → increases cortisol production in the adrenal cortex from zona fasiculata

272
Q

Describe the physiological effect of Dopamine on the body.

A

Dopamine (DA) → inhibits prolactin → inhibits breast growth/development & milk production

273
Q

What is the difference between the anterior and posterior pituitary glands?

A

Anterior Pituitary Gland - Comprised of Glandular Tissue so is the hormone secreting part of the pituitary

Posterior pituitary - Contains axons that originate in the hypothalamus (an extension of the hypothalamus)

274
Q

Name 2 hormones produced by the posterior pituitary and state their function.

A

Vasopressin (ADH) - Promotes water reabsorption by stimulating expression of Aquaporin 2 channels in cells of the proximal tubule.

Oxytocin;
- Released upon stimulation of mammary glands, stimulating release of milk.
- Stimulates contraction of uterine smooth muscle during child birth (important for contractions)

275
Q

Name and describe 3 histological types of pituitary tumours

A

Chromophobe (70%) - Non secretory but 50% produce prolactin.

Acidophil - Secrete Growth Hormone or Prolactin. Responsible for majority of Acromegaly cases.

Basophil - Secrete ACTH

276
Q

Give 5 clinical features of pituitary tumours

A

Headaches
Visual field defects - Bitemporal hemianopia
Palsy of cranial nerves 3,4,5 and 6 (pressure on cavernous sinus)
Diabetes insipidus (cranial)
CSF Rhinorrhoea (CSF leaking into nose and sinuses)

277
Q

A pituitary tumour secreting prolactin can cause what? (3)

A

Galactorrhoea

Decreased Libido

Amenorrhoea

278
Q

A pituitary tumour secreting Growth Hormone can cause what? (1)

A

Acromegaly

279
Q

A pituitary Tumour secreting ACTH can cause what? (1)

A

Cushing’s Disease

280
Q

What investigations are required for ? pituitary adenoma? (3)

A

Pituitary blood profile (inc GH, prolactin, ACTH, FSH, LSH and TFTs)

Visual Field Testing

MRI brain with Contract

281
Q

What suppression tests may be useful in distinguishing pituitary adenomas? (3)

A

Water deprivation test = Diabetes Insipidus

Dexamethasone Suppression Test = Cushing’s Disease

Glucose tolerance test = Acromegaly

282
Q

What is pituitary apoplexy?

A

Describes haemorrhage into the pituitary, resulting in pituitary enlargement.

283
Q

How may pituitary apoplexy present? (4)

A

Headache
Meningism (triad = headache, neck stiffness and photophobia)
Low GCS
Bitemporal hemianopia

284
Q

How is pituitary apoplexy treated? (2)

A

Urgent IV hydrocortisone and meticulous fluid balance.

285
Q

Define a craniopharyngioma and describe where it originates.

A

Describes a benign pituitary tumour located at the top of the pituitary gland (suprasellar)

50% present in children (5-14yrs) with growth failure.

Originates from squamous epithelial remnants of Rathke’s pouch (originates between pituitary and 3rd ventricle floor)

286
Q

What is the most common hormonal disturbance of the pituitary?

A

Hyperprolactinaemia (overproduction of prolactin)

287
Q

Give 3 causes of hyperprolactinaemia

A

Drugs (most common) - Dopamine antagonists (metoclopromide, anti-psychotics, MDMA/Ectasy)

Physiological changes (pregnancy, breastfeeding, stress)

Disease (prolactinoma, pituitary stalk damage, hypothyroidism)

288
Q

Give 3 drugs that can cause hyperprolactinaemia

A

Dopamine antagonists;

Metoclopromide (anti-emetic)

Risperidone (anti-psychotic)

MDMA/Ectasy

289
Q

Give 5 symptoms of hyperprolacinaemia

A

Lactation (galactorrhoea)

Amenorrhoea (absent periods)

Decreased libido

Erectile dysfunction (men)

Increased weight

290
Q

What physiologically causes the symptoms of hyperprolactinaemia?

A

Prolactin suppresses GnRH from the hypothalamus > Decreases FSH + LH secretion from the anterior pituitary > reduced levels of testosterone and oestrogen.

291
Q

How is hyperprolactinaemia treated?

A

1st line - Dopamine agonists - Capergoline or Bromocroptine

2nd line - Trans-sphenoidal resection (surgery)

292
Q

Describe the function of side effects of dopamine agonists. What are they used to treat? (3)

A

Used to treat Hyperprolactinaemia (capergoline and bromocroptine)

Function to inhibit prolactin secretion

Side effects; nausea, postural hypotension, fibrosis (lung/heart)

293
Q

Define acromegaly

A

Acromegaly is characterised by excessive production of growth hormone from the anterior pituitary.

This results in excessive growth of body tissues.

294
Q

What is the main cause of acromegaly?

A

Pituitary acidophil adenomas

295
Q

What hormone stimulates growth hormone secretion?

A

Growth Hormone Releasing Hormone (GHRH)

296
Q

What hormone inhibits growth hormone secretion?

A

Somatostatin

297
Q

What hormone produced by the stomach stimulates growth hormone secretion?

A

Ghrelin

298
Q

Describe the Growth Hormone/IGF-1 axis

A

Growth hormone stimulates IGF-1 production from the Liver > This exerts growth effects on the body > IGF-1 feeds back negatively to suppress GH and GHRH release

299
Q

Give 6 symptoms of acromegaly

A

Acroparasthesia (numbness/tingling in extremities (hands and feet))

Amenorrhoea and decreased libido

Headache

Bitemporal Hemianopia

Snoring

Sweating

300
Q

What hand pathology is linked to acromegaly?

A

Carpal Tunnel Syndrome

301
Q

Give 4 clinical signs of acromegaly

A

Acral enlargement (enlargement of hands and feet)

Coarsening (harsh/rough) face (wide nose, big ears, prominent supraorbital ridges - frontal bossing)

Prognathism (protruding mandible)

Macroglossia (large tongue)

302
Q

Give 3 complications of acromegaly

A

Glucose intolerance (IGF-1 competes with insulin for it’s binding site)

Diabetes mellitus

CVS ossies (Hypertension, Left ventricular Hypertrophy, Stroke)

303
Q

What investigations are used to diagnose acromegaly?

A

1st - Serum IGF-1 (screening)
2nd - Oral Glucose Tolerance Test (confirms diagnosis)

Additional - Blood tests (Elevated glucose, calcium and phosphate - indicates skeletal growth)

304
Q

What are the expected results of an oral glucose tolerance test for a patient with acromegaly?

A

No suppression of Growth Hormone

305
Q

How is acromegaly managed? (4)

A

1st - Trans-sphenoidal resection of pituitary adenoma

2nd - Somatostatin Analogies - Octerotide or Lanreotide

3rd - GH antagonist - Pregvisomat

4th - Radiotherapy

306
Q

Name 2 somatostatin analogues used in the treatment of acromegaly

A

Octerotide and Lanreotide

307
Q

Name one Growth Hormone antagonist used in the treatment of acromegaly

A

Pregvisomat

308
Q

Describe SIADH

A

Syndrome of Inappropriate Anti-Diuretic Hormone Secretion (SIADH)

Characterised by a euvolemic state, concentrated urine, hypotonic hyponatraemia secondary to impaired free water excretion, arising from excessive vasopressin release (ADH)

309
Q

What does diagnosis of SIADH require?

A

Concentrated urine (osmolality >100mOsmol/Kg or Na >20mmol/L)

Hyponatraemia

Low plasma osmolality

310
Q

Give 5 causes of SIADH

A

Malignancy (lung small cell, pancreatic, prostate, thymus)

CNS disorders (meningoencephalitis, SAH, trauma)

Respiratory disease (Carcinoma, TB, pneumonia)

Endocrine (hypothyroidism)

Drugs (Cyclophosphamide, SSRIs, Opiates, Psychotropics)

311
Q

Give 4 drug classes that can cause SIADH

A

Cyclophosphamide

SSRIs

Opiates

Psychotropics (carbamazepine)

312
Q

What investigations are performed to diagnose SIADH? (2)

A

Urine osmolality (High - >100mOsm/kg)

Urine sodium concentration (High - >40mmol/L)

313
Q

How is SIADH managed? (3)

A

Fluid restriction

Demeclocycline (reduces responsiveness of collecting tubule cells to ADH)

Vaptans (ADH receptor antagonists)

314
Q

Why is it important to that fluid correction is done slowly in SIADH?

A

To avoid precipitating central pontine myelinolysis.

315
Q

Give 3 features of Growth Hormone deficiency and what is the Rx

A

Short stature

Abnormal body composition

Reduced muscle mass

Rx - Growth Hormone

316
Q

What is the function of the parathyroid glands?

A

Regulate calcium levels in the body by producing parathyroid hormone

317
Q

What stimulates secretion of parathyroid hormone?

A

Low ionized calcium levels.

As Extracellular calcium levels decrease, PTH levels increase (and vice versa)

318
Q

Give 4 actions of Parathyroid Hormone

A

Increases osteoclast activity (releasing calcium and phosphate from bone)

Enhances the distal tubular resorption of calcium

Decreases renal tubular resorption of phosphate

Increases production of 1,25 dihydroxy-vitamin D3

319
Q

What is the net effect of PTH on calcium and phosphate?

A

Increase in calcium and a decrease in phosphate

320
Q

Describe primary hyperparathyroidism

A

Characterised by overstimulation of the parathyroid glands, resulting in excessive release of parathyroid hormone.

Leading to symptoms of hypercalcaemia

321
Q

In relation to calcium and PTH levels, how is hyperparathyroidism characterised?

A

Characterised by hypercalcaemia in the presence of elevated PTH levels.

(Usually this relationship is the inverse)

322
Q

Give 3 causes of hyperparathyroidism

A

80% - Solitary Adenoma

20% - Hyperplasia

<5% - Parathyroid cancer

323
Q

Give 6 clinical features of hyperparathyroidism

A

Associated with symptoms of hypercalcaemia;

Weak/tired
Depressed
Polydipsia/Polyuria
Bone pain
Abdomoinal pain
Pancreatitis

(Bones, Moans and Abdominal Groans)

324
Q

What may blood tests show in a patient with primary hyperparathyroidism?

A

PTH - High
Ca - High
Alkaline Phosphatase - High
Phosphate - Low

325
Q

How is primary hyperparathyroidism treated?

A

General;
- Increased fluid intake to prevent stones
-Avoid thiazides and high calcium intake

Surgical
- Excision of adenoma

326
Q

What should be avoided in patients with primary hyperparathyroidism? (2)

A

Thiazides

High calcium intake

327
Q

Give 2 surgical complications in the management of primary hyperparathyroidism

A

Hypoparathyroidism

Damage to recurrent laryngeal nerve

328
Q

Describe secondary hyperparathyroidism. Give 2 common causes.

A

Any disorder that results in hypocalcaemia will elevate parathyroid hormone levels, resulting in secondary hyperparathyroidism.

Chronic Kidney Disease
Vitamin D deficiency

329
Q

What will blood tests show in a patient with secondary hyperparathyroidism? (5)

A

PTH - High
Calcium - Low
Alkaline phosphatase - High
Phosphate - Low
Vitamin D - Low

330
Q

Define hypoparathyroidism

A

Characterised by a relative or absolute deficiency of plasma PH synthesis and secretion. Usually occurs due to gland failure.

331
Q

Give 9 symptoms of hypoparathyroidism (SPASMODIC)

A

S - Spasms
P - Perioral paraesthesia
A - Anxious
S - Seizures
M - Muscle tone increase
O - Orientation impaired (confusion)
D - Dermatitis
I - Impetigo
C - Chovsteks, cardiomyopathy

332
Q

Define pseudohypoparathyroidism

A

Characterised by a failure of the target organ to respond to PTH

333
Q

Describe pseudopseudohypoparathyroidism

A

Patient expresses normal (maternal) receptors in the kidney but also has abnormal (paternal) receptors in the body.

334
Q

Describe blood test results for primary hyperparathyroidism (PTH, Ca, Phosphate)

A

PTH - High
Ca - High
Phosphate - Low

335
Q

Describe blood test results for secondary hyperparathyroidism (PTH, Ca, Phosphate, Vitamin D)

A

PTH - High
Calcium - Low
Phosphate - High
Vitamin D - Low

336
Q

Describe blood test results for tertiary hyperparathyroidism (PTH, Ca, Phosphate, Vitamin D, Alkaline Phosphatase)

A

PTH - High
Ca - Normal/High
Phosphate - Low/Normal
Vitamin D - Low/Normal
Alkaline Phosphatase - High

337
Q

What is the most common cause of primary hyperparathyroidism?

A

Solitary adenoma

338
Q

What is the most common cause of secondary hyperparathyroidism

A

Vitamin D deficiency

Chronic kidney disease

(Lead to parathyroid gland hyperplasia)

339
Q

What is the most common cause of tertiary hyperparathyroidism

A

Occurs due to ongoing hyperplasia of the parathyroid gland AFTER correction of underlying renal disorder.

Hyperplasia of all 4 glands is usually the cause.

340
Q

What drug is known to cause gynecomasita? And how?

A

Spironolactone (potassium-sparing diuretic and aldosterone antagonist)

Competitively inhibits binding of dihydrotestosterone (DHT) to androgen receptors, leading to decrease in testosterone levels and an increase in oestrogen levels.

Hormonal imbalance leads to development of breast tissue in men.

341
Q

Describe the water deprivation test and describe when it is used.

A

Used to help evaluate patients who have polydipsia

Method;

Prevent patient from drinking water.
Ask the patient to empty their bladder.
Measure hourly urine and plasma osmolalities.

342
Q

Describe the results of a water deprivation test in a patient with cranial Diabetes Insipidus

A

Starting Plasma Osmolality - High

Final Urine Osmolality - Low

Urine Osmolality after Desmopressin - High

(Occurs due to insufficient ADH secretion, but kidneys still respond to ADH, hence osmolality increase after Desmopressin is given)

343
Q

Describe the results of a water deprivation test in a patient with nephrogenic Diabetes Insipidus

A

Starting Plasma Osmolality - High

Final Urine Osmolality - Low

Urine Osmolality after Desmopressin - Low

(Kidneys are unable to respond to ADH, hence why urine osmolality remains low after Desmopressin is given)

344
Q

What are the 2 predominant causes of hypercalcaemia?

A

Malignancy (PTHrP secreting tumour)

Primary hyperparathyroidism

345
Q

What part of the adrenal gland secretes aldosterone?

A

Zona Glomerulosa

Phase 4 Medicine (15 decks)

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