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Phase 2a Sam > ENDOCRINE > Flashcards

ENDOCRINE Flashcards

1
Q

Outline what type 1 diabetes is

A

Type 1 diabetes mellitus is a metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency.

  • Can’t move glucose from blood into cells.
    Leads to low glucose in cells which ‘starve’ of energy.
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2
Q

What is the difference between Signs and Symptoms?

A

sign is the effect of a health problem that can be observed by someone else.
A symptom is an effect noticed and experienced only by the person who has the condition.

The key difference between signs and symptoms is who observes the effect.

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3
Q

What is the definition of diabetes?

A

Symptoms of Diabetes (3Ps) + Fasting plasma glucose > 7 mmol/l

OR
No symptoms - GTT (75g glucose) fasting > 7 or 2h value > 11 mmol/l (repeated on 2 occasions)
HbA1c of > 48mmol/mol (6.5%)

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4
Q

What is the epidemiology for type 1 diabetes?

A

10% of all patients with diabetes.

  • More common amongst Northern Europeans.
  • Causes more than 85% of diabetes in under 20s.

-Highest incidents amongst 10–14-year-olds.

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5
Q

What is the genetic aetiology of type 1 diabetes?

A

Some human leukocyte polymorphisms can increase susceptibility to the disease - seen in
HLA-DR and HLA-DQ (Human Leucocyte antigen system) Genes

Coeliac disease may have link

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6
Q

What is the environmental aetiology of type 1 diabetes?

A

Much higher rates in Europe may indicate environmental factors no known specific ones.

Vitamin D can be protective
• Cleaner environment may increase type 1 susceptibility

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7
Q

What virus is believed to have a link to type 1 diabetes?

A

Coxsackie B virus and
Human enterovirus

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8
Q

What does insulin do at muscle and fat cells?

A

Insulin binds to muscle and fat cells via receptors

Which leads to intracellular glut4 vesicles to go to bind to the plasma membrane, which means that glucose will go and enter the cell via these GLUT4 membranes

Glucose enters the cells

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9
Q

What are the risk factors for type 1 diabetes?

A

Family history, having other autoimmune dieases

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10
Q

Outline the pathophysiology that typically causes Type 1 diabetes.

A
  • Autoimmune destruction of pancreatic β-cells leading to an insulin deficiency

- β cells express HLA antigens on MHC in response to an environmental event (potentially a virus)
- Activates a chronic cell mediated immune response leading to chronic insulitis

Up to 90% of people have autoantibodies

80-90% of beta cells need to be destroyed before symptoms usually appear for type 1 diabetes

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11
Q

How long does beta cells destruction occur for before symptoms usually start to present for type 1 diabetes?

A

Months to years

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12
Q

What % of beta cells need to be destroyed before symptoms usually appear for type 1 diabetes?

A

80-90%

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13
Q

What happens as a result of low insulin levels?

A

Due to insulin deficiency glucose can’t be utilised from muscle and adipose.

So increased Lipolysis, = weight loss

Stimulates secretion of glucagon (adrenaline, cortisol, and growth hormone)

More glucose in urine - Polyuria and Polydipsia

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14
Q

What does the secretion of glucagon, adrenaline, cortisol, result in? (Type 1 diabetes)

How do they present?

A

Gluconeogenesis, Glycogenolysis and ketogenesis.

Patients as a result present with ketoacidosis and hyperglycaemia.

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15
Q

What are the most common key presentations of type 1 diabetes?

A
  • Hyperglycaemia (above 11.1).
  • Polyuria (passing urine frequently).
  • Polydipsia (drinking water frequently)
  • Weight loss
  • Tiredness
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16
Q

What are some other common key presentations of type 1 diabetes?

A

young age, weight loss, blurred vision, nausea, and vomiting, Abdo pain,

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17
Q

What are the first line investigations for children in type 1 diabetes?

A
  • Random plasma glucose (above 11)
  • Fasting plasma glucose (above 7)
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18
Q

What are the first line investigations for adults in type 1 diabetes?

A

Random glucose tolerance test if at GP - blood sugar of >11.1mmol/L
a glucose tolerance test.

In this test, a fasting blood glucose is taken after which a 75g glucose load is taken. After 2 hours a second blood glucose reading is then taken

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

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

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19
Q

What is the gold standard test for diagnosing type 1 diabetes? What is it a measurement of?

A

Glycohemoglobin test (HbA1c)

It measures Glycated haemoglobin, a form of haemoglobin that is measured to identify the three month average plasma glucose concentration

Reflects the degree of hyperglycaemia over the preceding 3 months greater than 6.5% (48 mmol/mol) indicates diabetes

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20
Q

What are other diagnostic tests you do to confirm a diagnosis of type 1 diabetes?

A
  • Plasma or urine ketones,
  • C-peptide,
  • Autoimmune markers
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21
Q

What are some differential diagnoses of type 1 diabetes?

A

Monogenic diabetes: maturity onset diabetes of the young
Neonatal diabetes
Type 2 diabetes

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22
Q

What is the management of type 1 diabetes?

A

o Basal-bolus insulin (insulin glargine s/c)
o Pre-meal insulin correction dose

2nd line: Metformin and fixed insulin dose

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23
Q

What is the difference between Basal and Bolus insulin dosing for Diabetes?

A

The two main ways to take insulin are bolus and basal.

Bolus insulin is the quick-acting delivery that you often take before mealtimes.

Basal insulin is longer-acting and helps keep your glucose levels steady day and night

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24
Q

What is the main medical drug given to treat T1DM?

A

Using a combination of long-acting insulin (insulin detemir, degludec, or glargine) for basal dosing,

and rapid-acting insulin (insulin lispro, aspart, or glulisine) for bolus dosing

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25
Q

What are the side effects of insulin?

A

hypoglycaemia, weight gain, lipodystrophy

Lipodystrophy - where you loose fat in some regions, but gain it in others, like on Organs like the Liver

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26
Q

What would you monitor for patients with diabetes?

A

Measure HbA1c levels every 3 months in children and every 3-6 months in adults
Make sure level is under 6.5% (48 mmol/mol)

Also monitor;
Blood Pressure
Kidney function

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27
Q

What are the short-term complications associated with type 1 diabetes?

A

Death due to ketoacidosis

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28
Q

What are the long-term complications associated with type 1 diabetes?

A
  • Microvascular: retinopathy, peripheral or autonomic neuropathy
  • Cardiovascular disease, diabetic kidney disease.
  • Potential for depression and eating disorder#
  • Foot amputations
  • Blindness
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29
Q

Define type 2 diabetes

A

A progressive disorder defined by deficits in insulin secretion and insulin resistance that lead to abnormal metabolism and related metabolic derangements

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30
Q

What percentage of diabetes cases are type 2?

A

90%

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31
Q

What BMI is overweight?

A

25-29.9

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32
Q

What BMI is considered obese?

A

> 30

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33
Q

What is a basal bolus that is given in type 1 DM and sometimes in bad T2DM

A

Basal - One long acting dose in the morning

Bolus:
Givng a dose before each meal in order to miminc the effect of insulin released

So three times a day

eg. Insulin Inspiro, or Insulin Aspart

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34
Q

What insulin medication pattern do you see in T2DM

A

Just once a day, (Basal) sometimes twice (BD)

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35
Q

What is the epidemiology of type 2 diabetes

A

OLDER! >30 years of age. Often overweight around the abdomen
- More prevalent in South Asian, African and Caribbean ancestry

Common is all populations enjoying an affluent lifestyle
More common in males

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36
Q

What is the Aetiology of Type 2 diabetes

A

Decreased insulin secretion and/or increased insulin resistance
Associated with obesity, lack of exercise, calorie and alcohol excess

No immune disturbance
Also a genetic link

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37
Q

Regarding Glucose, what do you see in Type 2 diabetes?
What do you see regarding glucose levels in a type 2 diabetic patient after they eat a meal?

A

Glucose levels, in general, are far higher than normal. When you eat a meal with T2DM, it takes alot longer for your blood sugar levels to come down again like in normal physiology.

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38
Q

What are the risk factors of Type 2 diabetes?

A

Family History of it - genetics
Obesity and poor exercise - Ageing and being overweight (body mass index [BMI] 25.0 to 29.9 kg/m²), and obesity (BMI >30 kg/m²)
Age
Low birth weight has been shown to predisposose

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39
Q

Outline the pathophysiology of Type 2 diabetes

A

Repeated exposure to high levels of Glucose and insulin makes the cells in the body come resistant to insulin.
Over time, the pancreas (specifically the beta cells) becomes fatigued and damaged by producing so much insulin and they start to produce less.

Fasting glucose levels increases

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40
Q

What are the key presentations of someone coming in with suspected type 2 diabetes?

A

Having the risk factors eg
Older age
Overweight/obese
Being of a certain ethnic groups inc Black, south asiain,

And coming in with:
Fatigue
Polydipsia and polyuria (thirsty and urinating a lot)
Unintentional weight loss
Opportunistic infections
Slow healing

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41
Q

What are some symptoms that a patient with Type 2 diabetes may complain of?

A

Polyphasia - Eating lots, Polydipsia, Drink, Polyuria - wee lots, unexplained weight loss

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42
Q

What are some first line investigations to order for suspected Type 2 diabetes?

A

Fasting plasma glucose - Order after a minimum 8-hour fast. Positive result is ≥7.0 mmol/L (≥126 mg/dL)

2 hour post load glucose test after 75g oral glucose - Plasma glucose is measured 2 hours after 75 g oral glucose load Positive result is ≥11.1 mmol/L (≥200 mg/dL)

Random Plasma glucose - positive test is >11mmol/L

Bear in mind that a repeat confirmatory test is required for diagnosis in most cases.

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43
Q

What is the gold standard test for type 2 diabetes, and what does it measure?

What is a positive result for this?

A

HbA1c
glycated haemoglobin how much glucose is attached to the haemoglobin molecule, shows blood glucose levels over the past 3 months

  • HbA1c > 6.5% normal (48mmol/mol) = DIABETES DIAGNOSIS
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44
Q

What other tests could be performed for suspected type 2 diabetes

A

Urine ketones, fasting lipid profile (high LDL), Albumin to creatine ratio*

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45
Q

Outline some of the other differential diagnosises for type 2 diabetes

A

Non-diabetic hyperglycaemia (pre-diabetes)
Diabetes mellitus, type 1
Latent autoimmune diabetes in adults (LADA)
Diabetes, gestational

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46
Q

Outline some non medicinal management for someone with type 2 diabetes **(This is the first line treatment for T2DM)

A

Patient education about their condition and the lifestyle changes, advise that there is a possible cure.
Exercise and weight loss, stop smoking

Regarding food:
- Include high-fibre, low-glycaemic-index sources of carbohydrate in their diet, such as fruit, vegetables, wholegrains, and pulses
- Eat low-fat dairy products and oily fish
- Limit their intake of foods containing saturated and trans fatty acids.

Needs annual reinforcement and review
Optimise treatment for other illnesses, eg hypertension

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47
Q

What is the second line treatment for someone with type 2 diabetes?

A

Medical management: First line: metformin titrated from initially 500mg once daily as tolerated.
Metformin is a “biguanide”. It increases insulin sensitivity and decreases liver production of glucose. It is considered to be “weight neutral” and does not increase or decrease body weight.

Management cardiovascular risks:
An ACE inhibitor or an angiotensin-II receptor antagonist
If an ACE inhibitor is not tolerated, use an angiotensin-II receptor antagonist instead

because metformin only increases insulin sensitivity instead of stimulating more insulin, it’ll rarely cause hypoglycaemia

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48
Q

What is the 3rd line of medication for T2DM?

When do you give a 3rd line treatment??

A

If HbA1c rises to 58mmol/mol, consider dual therapy or metformin and one of

either a sulfonylurea, - (Gliclazide)

DPP-4 inhibitor (Sitagliptin)
or
SGLT-2 inhibitor (Dapagliflozin), or Glitazone. (Pioglitazone) The decision should be based on individual factors and drug tolerance.

Most commonly metformin and an SU

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49
Q

Give an example of
a Sulfonylurea
DPP4 inhibitors
SGLT-2 inhibitor
Glitazone

A

Gliclazide
Sitagliptin
Dapagliflozin
Pioglitazone

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50
Q

3rd line treatment for T2DM: What do Sulphonlureas
do? Give an example What are its side effects? 3rd line of treatment

A

Eg - Gliclazide

stimulate insulin release by binding to Beta-cell receptors
Improve glycaemic control (1-2% in HbA1c)
give beta cells an extra kick to promote insulin

Increase weight
Increase the risk of heart failure
Increase the risk of fractures
CI: Pregnancy & breastfeeding (can cross placenta & enter breast milk)
(May cause hypoglycaemia in newborns)

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51
Q

3rd line treatment for T2DM: What can SGLT2 inhibitors do, and what can they lead to, as side effects?

eg empagliflozin, canagliflozin, dapagliflozin

A

They block the reabsorption of glucose in the kidney, increase glucose excretion, and lower blood glucose levels
Make you pee lots of glucose out =UTI and Thrush

Peeing out glucose can make your body think you’re in a fasting state - leading lipid break down - KETOACIDOSIS euglycaemic ketoacidosis

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52
Q

Medications for Type 2 diabetes
How do DPP4 inhibitors work?
Give an example

Side effects?

A

Inhibit DPP4 (so increase effect of incretins (GLP-1 and GIP) which stimulates insulin secretion
Incretin = A group of hormones released after eating & augment secretion on insulin (inhibited by DPP4)

DOES NOT CAUSE weight gain or weight loss

Sitagliptin

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53
Q

When would you start 4th line treatment for T2DM? What does it involve?

A

If HbA1c still 58mml/mol, consider triple therapy with:
Metformin + SU + DPP4 inhibitor
Metformin + SU + pioglitazone
Metformin + SU/pioglitazone + SGLT-2i
Insulin-based therapy

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54
Q

What is the fifth line treatment for someone with T2DM?

A

Insulin. Start with Basal Dose

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55
Q

What monitoring do you need to continue to do for someone with type 2 diabetes?

A

Take HbA1c every 3 to 6 months. Measure blood pressure once a year, to look out for hypertension. Monitor for complications

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56
Q

Other types of diabetes - what is MODY?

A

“Maturity-onset diabetes of the young” Commonest type of monogenic diabetes (~1% diabetes)
Diagnosed <25y
Autosomal dominant
Non-insulin dependent
Single gene defect altering beta cell function
Tend to be non-obese

Monogenic - caused a mutation of one gene only

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57
Q

patients with MODY tend to be missed diagnosed as type 1 or early onset type 2. What are some features of MODY that make it different to type one and two?

A

Parent affected with diabetes

Absence of islet autoantibodies

Measurable C - Peptide - NOT SEEN ON SYNTHETIC INSULIN

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58
Q

Drug induce diabetes - what drugs can lead to diabetes?

A

Glucocorticoids increase insulin resistance
Thiazides / protease inhibitors (HIV) / antipsychotics – mechanisms not clearly understood

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59
Q

What are some signs of permanent Neonatal diabetes?

A

Diagnosed <6 months (usually de novo):
Signs:
Small babies, epilepsy, muscle weakness

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60
Q

What complications can someone get from type 2 diabetes?

A
  • Diabetic retinopathy
  • Kidney disease
    Diabetic foot - due to neuropathy

Cardiovascular disease - atherosclerosis, stroke TIA, CHD

Glucose sticks in the vessels everywhere - eyes, brains, Kidney,

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61
Q

Brief description of what ketoacidosis is.

A

Ketoacidosis is High levels of ketones in the blood due to cells in the body initiating the process of ketogenesis for fuel.

The ketone acids use up the bicarbonate buffer and the blood starts to become acidic.

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62
Q

What are the main risk factors for Ketoacidosis?

A

Inadequate supply of insulin
New onset of diabetes/ Uncontrolled diabetes

Infection

Myocardial Infarction

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63
Q

Which diabetes would you see Ketoacidosis?

A

Seen in TYPE 1 DM
Won’t get it in early TYPE 2 DM, but is possible later on 10 years

In Type 2, you do have some insulin, so some glucose can go in the cell

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64
Q

Why can infection and MIs cause ketoacidosis?

A

Infection (pneumonia, UTI) ==> due to the systemic response that it causes in the body (eg adrenaline release leads to increased lipolysis, ketogenesis)

Myocardial Infarction (provoke the release of counter-regulatory hormones likely to result in DKA in patients with diabetes.)

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65
Q

What is the basic pathophysiology of ketoacidosis?

A

nsulin deficiency leads to release of free fatty acids from adipose tissue (lipolysis), hepatic fatty acid oxidation, and formation of ketone bodies), which result in ketonaemia and acidosis, as the bicarbonate buffer from the kidneys is used up

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66
Q

What is the predominant ketone body seen in DKA?

A

he primary ketone body involved in diabetic ketoacidosis is acetoacetate

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67
Q

What are the key presentations seen in a patient with Ketoacidosis?

A

Known to have diabetes, and are unwell

Hyperkalaemia
Polydipsia
polyuria, recent unexplained weight loss, or excessive tiredness,
Acetone smell on breath

Secondary:
Nausea
Abdominal pain[4][49]
Hyperventilation
Reduced consciousness.

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68
Q

What are the first investigations you would do for suspected Ketoacidosis?

What is the key one?

A

Venous blood gas (key)
Blood Glucose
Blood ketones

Urea and Electrolyte count
Urine stick for ketones

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69
Q

What other tests could you do in ketoacidosis?

A

Full blood count
ECGs
Pregnancy test

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70
Q

What things would be seen on examination/investigation for someone with Ketoacidosis?

A

Venous blood gas of:
pH ≥7.0 indicates mild or moderate DKA.
pH <7.0 indicates severe DKA

Diabetes - blood glucose is >11.0 mmol/L

blood ketones are >3.0 mmol/L - Ketonemia
ketonuria (2+ or more on standard urine sticks)

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71
Q

Why can serum potassium high in Ketoacidosis?

A

(Insulin makes you hypokalaemic), as it move postassium into your cells
Serum potassium can be high or normal in diabetic ketoacidosis, as the kidneys continue to balance blood potassium with the potassium excreted in the urine, however total body potassium is low because no potassium is stored in the cells.

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72
Q

What would be in a differential diagnosis for Diabetic Ketoacidosis?

A

Hyperosmolar hyperglycaemic state (HHS)
Lactic acidosis
Starvation ketosis
Alcoholic ketoacidosis

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73
Q

DKA management - what do you give first?

A

IV fluids.

  1. Give a fluid bolus of 500 mL of normal saline (0.9% sodium chloride) over 10 to 15 minutes if the initial systolic blood pressure (SBP) is <90 mmHg.

If BP is >90mmHg, give 1L of normal saline over 60 minutes.

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74
Q

DKA management - after the first round of IV fluids, what do you also give?

A

Potassium and Insulin!!

  1. Add potassium to the second litre of intravenous fluid if serum potassium is ≤5.5 mmol/L **(Insulin makes you hypokalaemic), as it move postassium into your cells **
  2. Start a fixed-rate intravenous insulin infusion (FRIII) according to local protocols; continue FRIII until DKA has resolved

Ensure intravenous fluids have already been started before giving a FRIII.

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75
Q

How do you monitor a patient with Ketoacidosis? (5 things)

A

Order hourly blood glucose and hourly blood ketones.

Perform a venous blood gas
(for pH, bicarb, K+) 60 minutes, 2 hours, and 2 hourly thereafter.

  • Maintain the potassium level between 4.0 and 5.0 mmol/L.
  • Maintain an accurate fluid balance chart.
  • Keep an eye on GCS
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76
Q

What are some complications of Ketoacidosis?

A

Hypokalaemia

hypoglycaemia

arterial or venous thromboembolic events
cerebral oedema/brain injury

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77
Q

What will worsen the prognosis of Ketoacidosis?

A

Prognosis is worsened at the extremes of age and in the presence of coma and hypotension

Death is rarely caused by the metabolic complications of hyperglycaemia or ketoacidosis but * rather relates to the underlying illness.*

Mortality rates have fallen significantly in the last 20 years from 7.96% to 0.67%.

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78
Q

What are the classifications of Hypoglycaemia

A

Level 1 - Alert value Plasma glucose <3.9 mmol/l and no symptoms

Level 2 - Serious biochemical
Plasma glucose <3.0 mmol, patient has symptoms but can self treat, cognitive function is mildly impaired.

Level 3 - Patient has impaired cognitive function sufficient to require external help to recover (Level 3)

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79
Q

What are the autonomic symptoms of Hypoglycaemia?

(palms are sweaty)

A

Trembling
Palpitations
Sweating
Anxiety
Hunger

Nausea and Headache are non specific

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80
Q

What are the neuroglycopenic symptoms of hypoglycaemia?

A

Difficulty concentrating
Confusion
Weakness
Drowsiness, dizziness
Vision changes
Difficulty speaking

Nausea and Headache are non specific

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81
Q

What does your body do at
a) 4.6
b)3.8
c) 3.5
d) 2.4-3
e)<1.5
mmol/L
of Glucose?

A

a) Stop secreting insulin
b) starts secreting glucagon
c) Adrenaline release - Causes neuroglypenic symptoms
d) Cognitive dysfunction
e) Reduced conscious level, convulsions, coma

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82
Q

What are some risk factors of hypoglycaemia?

A

Long duration of diabetes
Use of drugs (prescribed or alcohol)
Sleeping (not gonna notice)
Increased physical activity
Increasing age

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83
Q

What are some risk factors for getting episodes of severe hypoglycamia?

A

§ Long duration of diabetes
§ previous hypoglycaemia
§ Impaired awareness of hypoglycaemia (IAH)*
§ Recent episodes of severe hypoglycaemia
§ Daily insulin dosage >0.85 U/kg/day
§ Physically active (e.g. athlete)
Impaired renal and/or liver function

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84
Q

How do you simply treat hypoglycaemia?

A

Recognise symptoms
Confirm need for treatment
Treat with 15g of fast acting carbohydrate
RETEST in 15 mins to ensure blood glucose >4mmol/L
Eat a long - acting carbohydrate to prevent the recurrence of symptoms - because after you’ve used up the fast acting carb, but the insulin will still be in the body

If unconscious, IV Glucose or IM Glucagon

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85
Q

What is the main factor preventing patients achieving tight glucose targets during treatment

A

Hypoglycaemia.

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86
Q

How many types of Hyperparathyroidism are there?
How many types of Hypoparathyroidism??

What are the two main causes of Hypercalcaemia?

A

3 types of HYPERparathyroidism - Primary, Secondary, Tertiary
Just one Hypoparathyroidism - due to parathyroid damage) (No prim,sec,tert etc)

Primary Hyperparathyroidism and Hypercalcaemia of malignancy are the two main causes of Hypercalcaemia

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87
Q

What does Parathyroid Hormone do?

What cells in the parathyroid gland release it?

A

Increasaes Bone resorption
Increased Ca2+ in kidney
Increased Ca2+ absorption in gut, through increased vit D
Decreases phosphate reabsorption in kidney

All to increase serum calcium

RELEASED FROM CHIEF CELLS IN THE PARATHYROID

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88
Q

Name the main causes of Hypocalcaemia.

A

Hypoparathyroidism - due to surgery/autoimmune/radiation @ parathyroid gland

Vit D deficiency
Alcohlism
Hyperphosphatemia or Lots of Bisphosphate meds

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89
Q

What are the main causes of hypercalcaemia?

A

c CHIMPANZEES- Calcium supplements,
Hydrochlorothiazide, Iatrogenic/Immobilisation, Multiple myeloma/Medication (lithium), Parathyroid
hyperplasia, Alcohol, Neoplasm, Zollinger ellison syndrome, Excessive Vit D, Excess Vit A, Sarcoidosis

Also Thyrotoxicosis

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90
Q

How can hypoparathyroidism be caused by alcoholism

A

Excessive can lead to a magnesium deficiency, as it promotes the excretion of it.

Magnesium is needed for parathyroid hormone synthesis, so low magnesium can lead to low parathyroid hormone, which will in turn lead to hypocalcaemia.

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91
Q

What can influence the levels of calcium in the blood?

A

Levels of albumin, what calcium binds to. If this is low, it might make calcium low. Adjust by looking at
corrected calcium

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92
Q

What are the signs of Hypocalcaemia?

A

CATS go numb:
● C - convulsions
● A - Arrhythmias
● T - Tetany (intermittent involuntary muscle contractions)
● S - spasms
● Numb - numbness

Hypocalcemia causes prolonged QT

Chvostek’s Sign
_ Cause spasms of facial nerve
Trousseau’s Sign
Fill up blood pressure cough more than systolic pressure for 5 mins- aggravated Italian hands

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93
Q

How can hypocalcaemia influence ECGs?

A

Hypocalcaemia
Prolonged ST Segment
Prolonged QT interval

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94
Q

Signs of Hypocalcaemia - what is
a)Chvostek’s Sign
b)Trousseau’s Sign

A

a) Tap over the facial nerve
Look for spasm of facial muscles
b)Inflate the blood pressure cuff
to 20 mm Hg above systolic
for 5 minutes - makes hand spasm upwards, like aggrivated italian sign with hands

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95
Q

Outline Vitamin D synthesis

A
  • 7-dehydroxycholesterol is made directly from ingested chloresterol
    Which is converted into Vitamin D3, by UV radiation
  • Vitamin D3 is converted into Calcidiol in the Liver via the cytochrome P450 system)
  • Calcidiol is converted to Calcitriol (Vit D) in the presence of PTH in the Kidneys
    CALCITRIOL (VIT D) CAN GO ON AND PROMOTE GUT CALCIUM ION ABSORPTION
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96
Q

What are the main causes of Hypoparathyroidism? What is Di George Syndrome?

A

DAMAGE TO PARATHRYOID GLAND!! - WHAT WOULD CAUSE THIS:
Surgery/Chemotherapy on the neck to target cancer, that damages the Parathyroid gland

Genetic
Autoimmune disesases
Magnesium Deficiency

Syndromes, like Di George - Developmental abnormality of third and fourth branchial pouches

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97
Q

What is Pseudoparathyroidism? What would a patient with it look like?

How would you treat it?

A

Resistance to parathyroid hormone. It is a rare, hereditary condition

  • Short stature
  • Obesity
  • Round facies
  • Mild learning difficulties
  • Subcutaneous ossification
  • Short fourth metacarpal

A FORM OF HYPOCALCAEMIA , Treat as such

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98
Q

What things can appear like hypercalcaemia?

A

Tourniquet on too long, which damages vessels
IF sample has been left around for too long - calcium comes out of cells in blood sample

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99
Q

What are the symptoms of Hypercalcaemia?

A

Thirst, polyuria
* Nausea
* Constipation (gut isnt working properly)

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100
Q

What are some of the causes of Hypercalcaemia

A

Malignancy (Lymphoma, bone mets)
Primary Hyperparathyroidism
^^^^Cause 90% of all hypercalcaemia

Thiazides Diuretics (make you retain calcium)

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101
Q

What does Hypercalcaemia of malignancy
lead to?

A

Low PTH
so
Decreased Bone Resorption
Decreased Ca2+ reabsorption
Decreased Ca2+ absorption

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102
Q

What do you give to treat Hypercalcaemia of malignancy?

A

Intravenous normal saline ==> Reverses dehydration (do first

IV bisphosphonates (most effective,) block osteoclastic bone resorption ===> (slower acting though)

Calcitonin interferes with renal tubular reabsorption of calcium, ==> more immediate.

All to stop more calcium entering the blood, and to loose it in the Kidney!

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103
Q

What are the Symptoms of Hyperparathyroidism? (Bones and Stones)

A

Symptoms
Painful bones
Painful bone condition – typically osteitis fibrosa cystica

Renal stones
Calcium deposition in renal tubules causes polyuria and nocturia
Can lead to kidney stones and kidney failure

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104
Q

What are the Symptoms of Hyperparathyroidism? (Moans and Groans)

A

Psychiatric moans – effects on nervous system
- Fatigue
- Depression

Abdominal groans – GI symptoms
- Nausea
- Constipation
- Indigestion
- Polyuria
- Polydipsia (thirst)

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105
Q

What is the Epidemiology of hypercalcaemia?

A

~1 in 1000 have mild asymptomatic hypercalcaemia
Typically affects older women

Eradication of underlying malignancy is crucial for continued maintenance of normocalcaemia.

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106
Q

What do you see on ECGs when there are disturbed calcium levels ?

A

If calcium is TOO HIGH, the QT interval gets SHORTER
If calcium is TOO LOW, the QT interval gets LONGER

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107
Q

What is secondary Hyperparathyroidism?

A

It’s elevation of parathyroid hormone (PTH) due to hypocalcaemia.

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108
Q

Outline the aetiology and then pathophysiology of Secondary hyperparathyroidism.

A

Caused by Insufficient vitamin D or chronic renal failure
==> low absorption of calcium from the intestines, kidneys and bones,
==> Causes hypocalcaemia:

==> So parathyroid secretes More PTH, so Parathyroid glands become more bulky.

Serum Calcium and Phosphate will remain low but PTH will be high

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109
Q

What investigations would you order if you suspect hyperparathyroidism?

A

Serum Calcium
Serum PTH

25-hydroxyvitamin D level

Eradication of underlying malignancy is crucial for continued maintenance of normocalcaemia.

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110
Q

What is the cause of Primary Hyperparathyroidism?

A
  • Primary – excessive PTH secretion
    ○ Usually caused by single parathyroid adenoma
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111
Q

What is tertiary hyperparathyroidism? How would you treat it?

A

Development of parathyroid hyperplasia (more cells) after long-standing secondary hyperparathyroidism

most commonly in renal disease

So PTH will remain high even with calcium is high
(phosphate is also high)

Plasma calcium and PTH are both raised
Treated by parathyroidectomy

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112
Q

Hyperosmolar Hyperglycaemic state: what characterises it?

A

by marked hyperglycaemia, hyperosmolality and mild/no ketosis

Basically just mental dehydration

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113
Q

Hyperosmolar Hyperglycaemic state: Define Hyperosmolarity - what can it do?

A

Hyperosmolarity = the loss of water making the blood more concentrated than usual.

==>blood has a high concentration of salt (sodium), glucose, etc

draws the water out of the body’s other organs, including the brain.

In the case of Hyperglycaemia, high blood glucose makes you wee loads, dehydrating you, and drawing water out of bodies organs

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114
Q

Where is HHS most commonly seen? What can it be the initial presentation of.

A

HHS is seen most commonly in older people and, in the US, those of African-American ethnicity with diabetes.

However, HHS is now being seen in younger adults and even in children/teenagers, often as the initial presentation of type 2 diabetes

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115
Q

What are the common Causes of HHS?

A

Infection is the most common cause, mainly UTIs/pneumonia
Diabetes that is uncontrolled

Or any trauma that provokes the release of counter-regulatory hormones (catecholamines, glucagon, cortisol, and growth hormone) and/or compromises water intake - eg MI/ Stroke/Sepsis

In elderly patients, being bed-ridden and having an altered thirst response compromise access to water and water intake, leading to severe dehydration and HHS.

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116
Q

What are some risk factors for HHS?

A

Illness, bed ridden, diabetes, older age. Little access to water

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117
Q

Outline the pathophysiology of HHS.

Why does it often present in T2DM?

A

HHS is extreme elevations in serum glucose concentrations and hyperosmolality , but no ketosis.

Seen in T2DM, where insulin produced is sufficient to suppress lipolysis and ketogenesis but not enough to promote glucose regulation

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118
Q

What are the key presentations/signs of someone with HHS?

A

Consider a diagnosis of hyperosmolar hyperglycaemic state (HHS) in any patient who is unwell and has a raised blood glucose.

Look for
- Hypovolaemia

  • Marked hyperglycaemia (≥30 mmol/L [≥540 mg/dL]) without significant hyperketonaemia (ketones ≤3 mmol/L) or significant acidosis
  • High serum osmolality (usually ≥320 mOsm/kg [≥320 mmol/kg]).
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119
Q

What are the main symptoms someone with HHS might have?

A

Polyuria
Polydipsia
Hypothermia
Weakness
Dehydration
Acute cognitive impairment measure GCS

Signs of the underlying cause.
- Common causes include myocardial infarction, sepsis, and stroke

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120
Q

What test would you run first if someone presented with the symptoms
of HHS?

A

Blood glucose – v high >30mmol/L
Blood ketones - To make sure DKA is not involved
Venous Blood gas

Calculate Serum osmolality
ECG
Full blood count
U and Es

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121
Q

What Serum osmolality would be positive for HHS?

A

Positive for HHS is >320 mOsm/L

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122
Q

What would you look for on a venous blood gas for someone with suspected HHS?

A

A mild acidosis (pH >7.3, bicarbonate >15 mmol/L due to renal impairment secondary to dehydration.
=====>Lactic acidosis may be present due to sepsis.

Use a venous blood gas to monitor the patient’s biochemical progress (urea, electrolytes, glucose, serum osmolality, bicarbonate)

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123
Q

What other investigations could you do for suspected HHS?

A

Urinalysis - looks for symptoms for UTI, and look for ketones to rule out DKA

Cardiac enzyme test - Look for Troponin T or I if positive MI

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124
Q

What could be a differential diagnosis for someone with suspected HHS?

A

Diabetic Ketoacidosis
Latic Acidosis
Alcohol Ketoacidosis

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125
Q

What is the first line of management for HHS?

A

Start IV fluids as soon as you suspect hyperosmolar hyperglycaemic state (HHS) Requested Critical care support if you cant get IV access

Give 1 L of 0.9% sodium chloride (normal saline) over 1 hour. Can give more rapidly if SBP is <90 mmHg

Think about treating underlying cause!!! MI, Stroke/Sepsis

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126
Q

After fluids, what next do you give for HHS?

A

Start intravenous fluids before giving insulin. If not, could cause CV collapse
* Give 0.05 units/kg/hour if blood ketones >1 mmol/L and ≤3.0 mmol/L and the patient is not acidotic (venous pH ≥7.3 and bicarbonate >15.0 mmol/L),*

* Give 0.1 units/kg/hour if blood ketones  >3.0 mmol/L or ketonuria (2+ or more) with a pH <7.3 and bicarbonate <15 mmol/L (i.e. mixed diabetic ketoacidosis and HHS),*

Think about treating underlying cause!!! - eg MI, Stroke/Sepsis

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127
Q

What do you monitor in patients with HHS?

A

Hourly blood glucose for the first 24 hours

hourly sodium, potassium, urea, and calculated serum osmolality for the first 6 hours,
which can be reduced to every 2 hours after 6 hours if serum osmolality is decreasing by 3 to 8 mOsm/kg/hour (3-8 mmol/kg/hour)

Continuous cardiac monitoring if necessary
Vital signs including early warning score (EWS).

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128
Q

What are some complications of HHS? aka Side effects of management, what you’re looking out for

A

Insulin related Hypoglycaemia -
Treatment related Hypokalaemia - due to all the insulin you’re giving

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129
Q

Name some causes of Hyperthyroidism.

A

Graves’ disease

Other causes are:
- multinodular goiter, toxic adenoma
- inflammation of the thyroid, - –eating too much iodine,
-too much synthetic thyroid hormone.

A less common cause is a pituitary adenoma.[

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130
Q

What is the most common cause of Hyperthyroidism? What percentages of cases of Hyperthyroidism does it account for?

A

Graves Disease, makes up for 50-80% of cases

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131
Q

How prevalent is Graves disease in Iodine sufficient parts of the world? More common in men or women and by how much?

A

In iodine-sufficient parts of the world, the prevalence of overt hyperthyroidism around 1%

6 times more common in women than men

Any age can be affected

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132
Q

What causes Graves Disease?

A

Stimulation of the thyroid by TSH receptor antibodies

Combination of genetic and environmental risk factors.

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133
Q

What genetic causes have been linked to Grave’s Disease?

A

No specific genes but HLA linked.

Complex pattern of inheritance. Defect in certain gene regions such as human leukocyte antigen (HLA)-DRB1*16:02 allele

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134
Q

What type of antibodies bind to what specific receptors, as seen in Grave’s Disease?

A

Formation of IgG antibodies to the TSH receptors on the Thyroid Gland

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135
Q

Normal Physiology: Outline the relationship between Hypothalamus, Anterior Pituitary and Thyroid gland, and how what they release influences each other.

A

HYPOTHALAMUS: Releases THYROTROPIN RELEASING HOROMONE
====> causes ANTERIOR PITUITARY GLAND TO RELEASE THYROID STIMULATING HOROMONE (THYOTROPIN)

The binding of TSH to thyroid gland promotes every aspect of T3 and T4 production - Iodine pumping, Thyroglobulin synthesis, releasing of thyroid hormone in the blood

T3 - NEGATVIE FEEDBAKC ON THE ANTERIOR PITIUARY TO STOP REALSING TSH

Thyroxine = T4 (4 iodine)
Triiodothronine = T3 (3 iodine)

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136
Q

Normal Physiology - What is T3 and T4? What is more active?

A

Thyroxine = T4 (4 iodine)
Triiodothronine = T3 (3 iodine)

T3 is more active than T4 (half life of 1-2 days vs 6-8 days)

T4 is generally converted into T3 by enzymes known as deiodinases in target cells

Thus its often said that T3 is the major thyroid hormone, despite the fact that the concentration of T4 in the blood is much higher than that of T3

T4 can be thought of as a RESERVOIR for additional T3

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137
Q

What do T3 and T4 actually do?

A

More Na/KATPases - seen in temperature homeostasis –> More heat produced
- MORE Moving Cholesterol from Plasma to cells (so in Hypothyroidism there is high plasma cholesterol)
-MORE Gluconeogenesis
-MORE Bone resorption
-MORE Fat Oxidation

-Increase Heart Rate
-Negative Feedback on TSH

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138
Q

What are some risk factors for Graves Disease?

A
  • Female
    • Family History/Genetic – association with HLA-B8, DR3 and DR4
    • Stress
    • Smoking
      Amiodarone
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139
Q

What is the pathophysiology behind Graves Disease?

A

Serum IgG antibodies called TSH receptor stimulating antibodies (TRAb) bind to TSH receptors on the thyroid and stimulate T3/4 production
This results in excess secretion, hyperplasia of the thyroid follicular cells, hyperthyroidism and goitre

TSH receptor autoantibodies cause thyroid hormone hyperproduction as well as thyroid hypertrophy and hyperplasia of thyroid follicular cells. ===> Leads to clinical manifestations of hyperthyroidism

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140
Q

What are some signs of Grave’s Disease?

A
  • Tremor
  • Tachycardia/AF
  • Goitre
  • Hair loss/thin hair
  • Lid lag/retraction
  • Hyperkinesia - increased muscle activity
  • Exophthalmos – bulging of the eye out of the orbit
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141
Q

What are some symptoms a Patient might experience if they have Grave’s Disease?

A

** Weight loss
* Irritability
* Heat intolerance*
* Insomnia
* Diarrhoea
* Sweats
* Palpitations
Anxiety

Pretibial myxedema specific to Grave’s

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142
Q

What is the first line investigation you would do for expected Grave’s Disease?

What would it show?

A

TSH levels test - it would be low, as lots of T3 and T4 being produced that is leading to the symptoms - so negative feedback.

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143
Q

If TSH levels are normal/high but there are symptoms of Hyperthyroidism + Elevated free T4 levels, what may you suspect?

A

If serum TSH is normal or even (slightly) elevated in the presence of hyperthyroid symptoms and elevated free T4 level, consider other causes of hyperthyroidism such as a TSH-producing pituitary tumour and partial resistance to thyroid hormone

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144
Q

What is post partum thyroiditis? What symptoms would a patient with this disease experience? What is the prognosis?

A

Where the immune system attacks the thyroid within 6 months after giving birth.

So rise in T3 and T4 (hyperthyroidism),
Followed by a decrease in T3 and T4, (hypothyroidism)
^^similar to De Quaverain

Will normally correct over 12 months, but may need treatment

145
Q

Name some drugs that can cause Drug induced Thyroiditis

A

Lithium (used to treat Bipolar)
Amiodarone (used to treat arrhythmias - can cause either Hyper or Hypo)
Interferons (used to treat cancer)

146
Q

What is another Key test you would do for suspected Grave’s disease/Hyperthyroidism?

A

Measure TSH receptor antibodies (TRAb) not available in all places

147
Q

What are some other alternative tests you can do for Hyperthyroidism/Grave’s Disease?

A

Serum T4 or T3, thyroid isotope scan to see size, ultrasound of thyroid

148
Q

What does hormone hCG have on TSH, and what can this lead to?

A

Stimulates the release of it as it stimulates TSH receptors, which can lead to Gestational hyperthyroidism - resolves in second trimester

149
Q

Name some of the Differential Diagnosis for Graves Disease.

(aka What else could cause hyperthyroid symptoms??)

A

Toxic multinodular goitre (benign tumour on thyroid gland,)
Gestational hyperthyroidism
Iodine induced hyperthyroidism
TSH producing pituitary adenoma

150
Q

What are the 4 main types of treatment you can give someone with Hyperthyroidism/Graves disease?

A

Beta blockers for rapid system control in attacks
Decreases SNS activation

Carbimazole – anti-thyroid drug decreases the synthesis new thyroid hormone

Potassium iodide – to acutely block release of thyroid hormone from gland - Damage follicular cells (ionisation)

Thyroidectomy – removal of the thyroid gland leaving a small remnant in order to maintain thyroid function

151
Q

What should you bear in mind when you prescribe Carbimazole? (Anti thyroid drug)

A

It should not be prescribed to pregnant women, as it can be toxic. Prescribe Propylthiouracil (a different Anti thyroid drug, also inhibits T4==> T3

152
Q

Hyperthyroidism/ Grave’s disease: What does Carbimazole do? What must you tell a patient before you perscribe it to them?

A
  • Carbimazole – anti-thyroid drug
    ○ Blocks thyroid hormone synthesis and also have immunosuppressive effects which affect Graves’ disease
153
Q

Hyperthyroidism/ Grave’s disease: What is a severe side effect of key anti thyroid drug, Carbimazole?

A

Severe side effect is agranulocytosis — a deficiency of granulocytes in the blood, causing increased vulnerability to infection.
Due to the fact is depresses the activity of the bone marrow

YOU MUST TELL THE PATIENTS THIS, AND THAT THEY MUST STOP THIS IF THEY GET SIGNS OF INFECTIONS EG SORE THROAT

154
Q

What is a “Thyroid Crisis”?

A

Thyroid crisis (Thyroid storm)
Rare life threatening condition
- Hyperpyrexia
- Tachycardia
- Extreme restlessness
Delirium, Coma, death

155
Q

How do you monitor patients when you are treating them for Grave’s Disease/Hyperthyroidism?

A

monitor replacement thyroxine therapy with serum TSH at 6-week intervals until stable, then with serum TSH at least annually.

156
Q

What are some complications of Hyperthyroidism/Grave’s Disease?

A

Bone mineral loss - if left untreated - in extreme cases, osteoporosis
Atrial fibrillation - can lead to thromboembolic complications and stroke
Congestive heart failure.

157
Q

What is the Epidemiology of Hypothyroidism? What are the two types?

A

Primary - Problem with Thyroid Gland
Central/Secondary - Problem with Pituitary Gland

Primary has prevalence range between 0.2-5.3%.
More common in women and white people. Incidence increases with age

Central accounts for less than 1% of hypothyroidism. Affects population equally. 1 in 100,000

158
Q

What are some causes for Hypothyroidism (Both Primary and Central)

A

Primary:
- Hashimoto’s disease - most common cause of primary.
- Iodine deficiency - common in developing world and mountainous areas
- Sub-acute granulomatous (De Quervain’s
- Other infections
- Drug induced

Central:

Pituitary adenomas (most common)
Other infections
Radiation

159
Q

Outline what De Quervain’s Thyroiditis is, and what can cause it

How was a Patient present with it?

A

Subacute Granulomatous disease - caused by a virus eg mumps
1. First, T3 and T4 will lead out of colloid - Symptoms of Hyperthyroidism
2. Then, it will be used up and Thyroid Gland can’t make more T3 and T4 - Symptoms of HYPOthyroidism

eg Caused by viruses like Mumps, Coxsaccie virus, Adenovirus

160
Q

What are some risk factor for hypothyroidism

A

Iodine deficiency,
female, middle age, family history, treatment,
- turners and down syndrome.

-
radiation therapy to head and neck,

amiodarone and lithium use (both interfere with Thyroid hormone synthesis)

161
Q

How can amiodarone lead to hyper/hypothyroidism?

A

Amiodarone is structurally similar to thyroxine and also contains iodine,

Amiodarone is an antiarrhythmic medication used to treat and prevent a number of types of irregular heartbeats (including atrial fibrillation which this lady has). It is known to cause thyroid problems, including both hyperthyroidism and hypothyroidism.

162
Q

Outline the Pathophysiology of Hasimoto’s Thyroiditis. What 2 things are specifically attacked?

A

It is caused by autoimmune inflammation of the thyroid gland.
It is associated with antithyroid peroxidase (anti-TPO) antibodies and antithyroglobulin antibodies

Initially it causes a goitre after which there is atrophy of the thyroid gland.

163
Q

Normal Physiology, Hypothyroidism - What do Thyroid peroxidase enzyme and Thyroglobulin normally do?

A

Thyroid peroxidase stimulates MIT (Monoiodotyrosine) and DIT (Diiodotyrosine) binding forming T3 and T4.

Thyroglobulin basically acts a storage peptide in the colloid, storing until T3 and T4 they are ready to be used

164
Q

What are some key signs of Hypothyroidism/Hasimoto’s Thyroiditis?

A

Bradycardia
Unexplained weight gain
Slow reflexes, Ataxia
Round Puffy face
Immobile Ileus - temporary arrest of Intestinal peristalsis
ASCITES - fluid in abdomen

165
Q

What are some symptoms a patient might experience if they have any form Hypothyroidism?

A

Hoarse voice
Goitre - lump or swelling on neck from thyroid gland
Weight gain
Constipation
Cold intolerance
Menorrhagia – heavy periods
Tiredness
Lethargy
Poor memory
Puffy eyes
Arthralgia/myalgia
Symptoms of anaemia

166
Q

What are the first line key investigations you would do for Hypothyroidism?
How would results for Primary and Secondary differ?

What would you tests for specifically in Hashimoto’s, and what’s more common here?

A

Thyroid function test
Measure Free T4 and TSH levels

○ Primary - High TSH, low free T4

○ Secondary – inappropriately low TSH, low T3/T4 (since issue is in pituitary)

In Hashimoto’s Thyroid antibodies
○ Thyroid antibodies (TPO) - Look for Thyroperoxidases and Thyroglobulin antibodies

(TPO antibody more common than antithyroglobulin)

167
Q

What other tests would you do in testing for Hypothyroidism?

(What is the relationship of T3 with Chloresterol)

A

Look for serum chloresterol and Blood glucose

Serum Cholesterol would be high, as T3 moves it from the blood

Fasting blood glucose may also be elevated (Hypothyroidism can be assosiated with T1DM)

168
Q

What are some differentials for Hypothyroidism?

A

Central hypothyroidism/Primary hypothyroidism, vice versa depending on what you are looking for
Depression
Anaemia

169
Q

What is the key drug you can give in Hypothyroidism? What do you aim for with it?

A

Thyroid hormone replacement agents such as levothyroxine Life long, oral, Start 25mcg (microgram)

LEVOTHYROXINE IS SYNTHETIC T4

With primary,
Primary – titrate dose until TSH normalises
Aim is to get TSH to >0.5

IN secondary, treat underlying pituitary issue!

170
Q

What things do you monitor for in Hypothyroidism?

A

Check TSH every 8 weeks after adjusting a dose - it takes that long for synthetic T4 to have an effect.

Primary - Stable patients need TSH measured every 12 months

Secondary – TSH will always be low, monitor T4

171
Q

What are some complications of Hypothyroidism??

A

Angina
Complications in pregnancy

172
Q

Thyroid Cancer: What are the 3 main types? What one is most common? What is most deadly

A

Papillary Carcinoma 62%
Follicular Carcinoma 17%
Medullary Carcinoma

Anaplastic is most deadly

PFM

173
Q

Where is thyroid cancer most common? What age?

A

More common in women than in men.
Most likely age to be diagnosed is 45-54.

174
Q

What is thought to cause thyroid cancer?

A

Genetic alterations are thought to underlie thyroid cancers

175
Q

Name some risk factors for thyroid Cancer.

A

Head and neck irradiation, female sex, Family history of thyroid cancer,

176
Q

What are some key signs/presentations of Thyroid cancer?

A

THINK SIGNS OF TUMOUR ON THYROID GLAND

  • Lymph node metastases
  • Thyroid nodule with history of progressive increase in size
    Enlarged lymph nodes
    Tracheal Deviation
    Hoarse voice
    Dysphagia     Difficulty swallowing

Weight loss

177
Q

What are some symptoms of Thyroid Cancer?

A
  • Thyroid nodules – increased size, hardness and irregularity
  • Dysphagia
  • Hoarseness of voice – tumour pressing on recurrent laryngeal nerve

Symptoms of Hyper/Hypothyroidism

178
Q

What are some key investigations you would do if you suspected Thyroid Cancer?

A

THINK -NEED TO LOOK AT THYROID GLAND, AND TREAT SYMPTOMS

  • Fine needle aspiration cytology biopsy best for distinguishing between benign and malignant thyroid nodules
  • Thyroid ultrasound
  • Thyroid Function tests – hyper/hypothyroidism needs to be treated before surgery - Look for TSH
179
Q

What other investigations could you do when testing for thyroid cancer?

A

Free T3 and T4

180
Q

How do you treat Papillary and Follicular thyroid cancer tumours?

A

Total thyroidectomy with neck dissection for local nodal spread

Ablative radioiodine subsequently given – taken up by remaining thyroid tissue or metastatic lesions

181
Q

how do you treat Anaplastic and lymphoma thyroid cancer tumours?

A

Anaplastic and lymphoma:
○ External radiotherapy may produce brief respite
○ Otherwise treatment is largely palliative

182
Q

How do you monitor thyroid cancer?

A

Check to see if tumour has metastised

183
Q

What is the main differential diagnosis for thyroid cancer?

A

A Benign thyroid nodule

184
Q

What are complications of thyroid cancers and treatment?

A

Airway obstruction, surgery related hypoparathyroidism, surgery related recurrent laryngeal nerve damage , secondary tumours

185
Q

Adrenal Physiology: What are the two parts of the adrenal glands? What can the outer part be divided into, and what is made in the adrenal glands and where?

A

Adrenal glands consist of:
Outer cortex – steroids(aldosterone, cortisol and androgens)
Zona glomerulosa (G) – Mineralocorticoids e.g. aldosterone
Zona fasciculata (F) – Glucocorticoids e.g. cortisol
Zona reticularis (R) – Androgens (sex hormones)
GFR – Makes Good Sex

Inner medulla – catecholamines
Under sympathetic control and secretes catecholamines e.g. adrenaline and noradrenaline

186
Q

What are the 6 hormones secreted by the anterior pituitary?

A

Follicle-stimulating hormone (FSH)
Luteinising hormone (LH)
Adrenocorticotrophic hormone (ACTH)
Thyroid-stimulating hormone (TSH)

Prolactin (PRL)
Growth hormone (GH)

FLAT PIG

187
Q

What should you bear in mind when you perscribed Carbimazole? (Anti thyroid drug)

A

It should not be prescribed to pregnant women, as it can be toxic. Prescribe Propylthiouracil (a different Anti thyroid drug, also inhibits T4==> T3

Also can cause Agranulocytosis, more on that later

188
Q

What is Cushing Syndrome?

A

Cushing’s Syndrome is used to refer to the signs and symptoms that develop after prolonged abnormal elevation of cortisol.

Cushing’s Disease causes a Cushing’s syndrome, but Cushing’s Syndrome is not always caused by Cushing’s Disease.

189
Q

What is Cushing’s Disease? How much Cushing syndrome is it responsible for?

A

Cushing’s Disease is used to refer to the specific condition where a pituitary adenoma (tumour) secretes excessive ACTH. (Adrenocorticotropic hormone)

Responsible for 70-80% ENDOGENOUS of Cushing syndrome

Cushing’s Disease causes a Cushing’s syndrome, but Cushing’s Syndrome is not always caused by Cushing’s Disease.

190
Q

Cushing’s - is it more common in men or women? What age is diagnosis most likely?

A

More Common in Women
Age 20-50 is most likely diagnosis

191
Q

Although 70-80% of endogenous Cushing’s syndrome is caused by ACTH secreting pituitary adenomas, what percentage of all pituitary tumours secrete excessive ACTH?

A

10%

192
Q

What are the 4 main causes of Cushing’s Syndrome?

A

Either ACTH (Adrenocorticotropic hormone) Dependant

  1. adrenocorticotrophic hormone (ACTH)-secreting pituitary adenoma - Cushing’s Disease
  2. Ectopic Cushing’s Syndrome – coming from elsewhere Due to paraneoplastic syndrome e.g. small cell lung cancer producing ACTH

or Non ACTH Dependant:

  1. Exogenous - Oral Steroid Use (Iatrogenic)
  2. An Adrenal adenoma or carcinoma, a tumour on the adrenal gland that releases Cortisol

Think Tumours of various locations, and exogenous steroid use

193
Q

What is the main cause of Cushing’s syndrome? What is the 2nd most common?

A

Most common cause of Cushing’s Syndrome is is exogenous therapeutic steroid use

Then the second most common cause of Cushing’s syndrome is Cushing’s disease

194
Q

What are some risk factors of Cushing’s Syndrome?

A

exogenous corticosteroid use, pituitary or adrenal adenoma, or adrenal carcinoma.

195
Q

What are some signs of Cushing’s Syndrome?

A

○ Cataracts
○ Ulcers
○ Striae – purple strokes on skin
○ Hypertension and hyperglycaemia (due to impaired glucose tolerance)
○ Increased risk of infection – dampening of inflammatory response
○ Glucosuria - due to the hyperglycaemia

196
Q

What are some symptoms of Cushings?

A

Truncal/central obesity
Moon face - FACIAL PLETHORA
Buffalo hump – fatty hump on upper back
Acne
Hirsutism – unwanted male pattern hair growth in women
Thin skin/bruising - EASY BRUSING
Osteoporosis

197
Q

What are the first line investigations you would do for suspected Cushing’s syndrome?

A

Late night salivary cortisol (would be elevated)
Blood glucose (would be elevated)
Urine pregnancy test (need to confirm not pregnant)
1 mg overnight dexamethasone suppression test morning cortisol Positive result : >50 nanomol/L

198
Q

What extra imaging tests can you do in Cushings?

A

pituitary MRI
CT scan of adrenals

199
Q

Cushing’s: In a healthy human, what would you expect to see in the 1mg overnight Dexamethasone test and why?

A

Decreased Cortisol levels in blood, due to negative feedback that Dexamethasone would exert on the hypothalamus and the pituitary gland (so less ACTH and CRH as well)

It would suppress the morning spike of cortisol that you see when you retest in the morning.

200
Q

In a patient with Cushing’s, what would you expect to see in the 1mg overnight Dexamethasone test and why?

A

If they have Cushing’s Disease, (Adenoma on Pituitary Gland), Then ACTH will still be high due to the tumour, so cortisol will not be suppressed. (Dexamethasone won’t have made a difference)

morning cortisol >50 nanomol/L

201
Q

Cushing’s Investigations - if 1mg is abnormal, what would you expect to see if you give 8mg of Dexamethasone overnight in a patient that actually had:
a) Adrenal Adenoma/Carcinoma
b) Ectopic ACTH Tumour
c) Cushing’s Disease

A

a) Low levels of ACTH, but high levels of Cortisol in the blood

b) High levels of both ACTH and cortisol in the blood

c) Low levels of Cortisol and low levels of ACTH -as In Cushing’s Disease (pituitary adenoma) the pituitary still shows some response to negative feedback and 8mg of dexamethasone is enough to suppress cortisol.

202
Q

What are some differential diagnosis for Cushing’s Syndrome?

A
  • Pseudo-Cushing’s syndrome
    ○ Caused by alcohol excess
    ○ Resolves after 1-3 weeks of alcohol abstinence

Obesity

Poorly controlled T2DM
Metabolic Syndrome

203
Q

How do we treat Cushing’s Syndrome?

A

Depends on the cause!

If Exogenous, stop the steroids

or surgery to remove relevant tumour on either Pituitary gland/ or Ectopic. trans sphenoid removal

Remove adrenal glands (adrenalectomy)

Give drugs

204
Q

What drugs can we give to treat Cushing’s Syndrome?

A

Steroidogenesis inhibitor (osilodrostat, ketoconazole, metyrapone, mitotane, etomidate),

Glucocorticoid receptor antagonist (mifepristone) is occasionally used for mild hypercortisolism, or short term for severe hypercortisolism, before other therapies are undertaken

205
Q

What can result as a complication of the an adrenalectomy?

A

Nelson’s Syndrome:
removed Adrenal glands means No Cortisol so nothing to negatively feedback on ACTH from Pituitary, so too much ACTH

ACTH can lead to:
§ causing a bronze pigmentation of the skin, visual disturbances and headache

206
Q

After surgery, what we measure to monitor patients with Cushings?

A

Measure Cortisol -
Patients with a postoperative morning cortisol of <55 nanomol/L (<2 micrograms/dL) are considered to be in remission and can transition into long-term follow-up

Patients with Cortisol >138nanomol need further evaluation/therapy

Recheck patients with Cortisol 55-138 nanomol the next morning.

207
Q

What are some complications of Cushing’s Syndrome?

A

Adrenal Insufficiency secondary to adrenal suppression
Cardiovascular disease
Hypertension
Diabetes Mellitus
imunosuppression - as high levels of cortisol lead to immunosuppression

208
Q

Outline what acromegaly is.

A

Acromegaly is a rare, chronic disease caused by excessive secretion of growth hormone (GH), usually due to a pituitary somatotroph adenoma.

209
Q

What is the difference between acromegaly and Gigantism?

A

Acromegaly = excessive production of growth hormone occurring in adults after fusion of the epiphyseal plates

Gigantism = excessive production of growth hormone occurring in children before fusion of the epiphyses of long bones - gonna grow lots

210
Q

What is the epidemiology of acromegaly?

A

Acromegaly is often recognised in middle-aged men or women but can occur at any age.

The disease is equally distributed between both sexes.

Global prevelance is 5.9 cases per 100,000 people

211
Q

What is the main cause of acromegaly?

What % is prolactin secreted?
What gene mutation is sometimes seen in acromegaly?

A

Due to a pituitary somatotroph adenoma in 95-99% of cases.
Prolactin co-secreted in 25% of cases .

Activating mutation in the GNAS1 gene is shown in 30% to 40% of somatotroph adenomas

212
Q

Pathophysiology of Acromegaly - what can promote pituitary tumour development?

What does Excessive GH secretion lead to, directly that is seen in acromegaly?

A

Dysregulation of
hormones
transcription factors
growth factors
that all act on the pituitary can promote tumour development.

Pituitary somatotroph adenomas chronically secrete excessive GH, which stimulates insulin-like growth factor 1 production

Function of GH:
* Direct – acts on tissues such as liver, muscles, bones and fat to induce metabolic changes

213
Q

What are some indirect results of excessive Growth hormone secretion, as seen in Acromegaly? (Via IGF-1)

A
  • Indirect – IFG-1
    ○ Stimulate growth by protein synthesis and cell division
    ○ Increases lipolysis and calcium retention
    ○ Decrease blood glucose
    ○ Stimulate hypertrophy and hyperplasia of bone, skeletal muscle etc.
214
Q

What are some signs of Acromegaly you may see on examination?

A
  • Morphological facial changes: frontal bossing, enlarged nose, prognathism (protuding jaw) and separation of teeth, macroglossia (massive tongue), large ears and nose
  • Thick skin, + Skin tags
  • Obstructive sleep apnoea
  • Deep voice
  • Hypertension
  • HF

Visual field defect (“bitemporal hemianopia”)
Elevated IGF-1, elevated GH

215
Q

What are some symptoms someone with acromegaly may experience?

A

Sweating
Headaches, due to pressure locally
Increase in hands and feet (Show and ring size)
Oligo/amenorrhea
Joint pain
Development of Skin Tags
Fatigue

More GH ==> Body works harder, so increase in Temperature/Sweat. Also, increased GH leads to more oil and sweat glands

216
Q

What are the first line investigation tests for acromegaly?

A

Serum GH and Serum IGF-1

217
Q

What is the gold standard test of acromegaly?

A
  • Oral glucose tolerance test
    ○ Normally a rise in blood glucose will suppress GH levels
    ○ Give glucose and then test GH levels – if they remain high this is diagnostic for acromegaly
218
Q

What is the 1st line management for treatment of acromegaly?

What are some complications of this?

A
  • 1st line - Transphenoidal surgical resection to remove the adenoma and correct compression of surrounding structures e.g. optic chiasm○ Complications
    § Hypopituitary
    § Infection
    § Diabetes Insipidus
219
Q

What medication can also be given to help treat acromegaly?

A
  • Somatostatin analogues e.g. IM octreotide/lanreotide – inhibit GH secretion
    § Given by s/c or IM injection
220
Q

What monitoring do you do in acromegaly?

A

Monitor GH and IGF-1 levels.
Monitor for complications of acromegaly, ie cardiac complications

221
Q

What are some complications of acromegaly, if not treated?

A

Cardiac complications
Hypertension
Sleep apnoea
Osterartiucalr complications ie arthritis
Impaired glucose tolerance and diabetes mellitus

222
Q

What are the most common type of pituitary tumours?

A

Prolactin-secreting pituitary adenomas

(Prolactinomas)

Prolactinomas are the most common type of pituitary adenoma, constituting about 50% of these tumours

223
Q

What are three vital points when assessing a Pituitary tumour?

A

There are three vital points when assessing a tumour:
Pressure on local structures: e.g. optic nerves
Pressure on the normal pituitary (🡪 hypopituitary)
Functioning tumour (🡪 Prolactinoma, acromegaly or cushings)

224
Q

What can be the consequences of a pituitary tumour that is putting pressure on local structures?

A

Headaches (due to stretching of the Dura)
Visual field defects
Cranial Nerve palsy
Hydrocephalus - accumulation of cerebrospinal fluid (CSF) within the brain
Pressure on Hypothalamic centres - so increased thirst, obesity, early puberty in children (precocious)
Cerebrospinal fluid rhinorrhoea (downward extension through the pituitary fossa) 🡪 CSF dripping out of the nose

225
Q

What substance has an inhibitory effect on prolactin? What are the implications of this?

A

dopamine, so tumours inhibiting dopamine can cause hyperprolactinaemia.

226
Q

What can be an effect of primary hypothyroidism, in relation to prolcatin?

A

In patients with hypothyroidism, an increase in prolactin is due to compensatory increase in the discharge of central hypothalamic TRH as a result of low thyroxine

==> Can lead to Hyperprolactinaemia

227
Q

What is the epidemiology of prolactinoma?

A

Prolactin-secreting adenomas are more frequent in women between 20 and 50 years old, mainly during the child-bearing years, with an estimated ratio of frequency between women and men of 10:1.

SO WOMEN ARE 10 X MORE LIKELY TO GET IT THAN MEN

30-60 years is when men are most likely to get it

228
Q

What non tumour cause can lead to hyperlactaemia?

A

oestrogen therapy

(Also, Primary Hypothyroidism due to high levels of TRH)

229
Q

What are some key symptoms some would experience with hyperprolactinaemia or a prolactinoma?

A

Increased prolactin ==> increased milk production in the breast (also galactorrhoea)
Menstruation stops (amenorrhoea)
Infertility/ reduced fertility
Visual deterioration - temporal hemianopia

230
Q

Why can hyperprolactinaemia cause infertility?

A

as prolactin inhibits GnRH (Gonadotrophic releasing Hormone)

231
Q

What are some symptoms of Hyperprolactinoma you would see in men?

A
  • Decreased libido, erectile dysfunction*
    Visual deterioration - temporal hemianopia
232
Q

What key diagnostic tests would you do in suspected prolactinomas/hyperprolactinaemia?

A

Serum prolactin - would be elevated
Pituitary MRI
Computerised visual field examination

233
Q

What is the main treatment you give for a prolactinoma?

A

Dopamine agonist (inhibits Prolactin)– CABERGOLINE or BROMOCRIPTINE

234
Q

What are some complications of prolactimonas?

A

Visual field impairment,
Anterior pituitary failure/diabetes insipidus
Hypopituitarism

235
Q

Name 4 conditions associated with pituitary adenomas.

A

Cushing’s Disease - PA = too much ACTH = too much cortisol
Acromegaly - PA - Too much growth hormone = too much IGF-1
Prolactinoma - PA - Too much prolactin produced
Secondary Hyperthyroidism - Too much TSH - Too much Thyroxine

236
Q

What does Aldersterone action lead to?

A

Aldosterone acts on the kidneys

Extracellular volume goes up
Renal blood pressure goes up
More Na+ and water retention
K+ excretion
Decreased Extracellular fluid of K+

237
Q

What is Conn’s Syndrome?

A

Conn’s syndrome refers ONLY to PRIMARY Aldosterone producing adenoma

A tumour in the adrenal gland!!

238
Q

What % of hypertension cases were Conns?

A

2.6%
Incidence is rising

239
Q

What are the different types of adrenal adenomas seen in Conns?

A

30% Unilateral forms - Treat with Laparoscopic adrenalectomy
70% Bilateral forms - treat with aldosterone antagonistic medicines

240
Q

What are some Risk factors for Conns

A

family history of Primary aldersosteronism and family history of early onset (e.g., <40 years) hypertension and/or stroke

241
Q

What does Conn’s do, and what does this lead to?

A
  • Excess production of aldosterone, independent of RAAS causes○ Increases K+ loss, Na+ and water retention 🡪 raised BP○ Decreased renin release
    ○ Hypokalaemia
242
Q

What are some signs and symptoms of Conn’s?

A

Hypertension
Increased risk of cardiac arrhythmias, particularly in patients with cardiac disease

Symptoms

Polyuria, Nocturia
Lethargy/tiredness
Muscle weakness
Paraesthesia
Headaches
Mood disturbance

243
Q

What is a the first line basic investigation for suspected Conn’s

A

Plasma potassium - Low in approx. 20% of patients with PA

244
Q

What is the gold standard investigation for someone with Conns?

A

Aldosterone : Renin ratio

Positive result would be >70 for aldosterone in picomol/L

(High aldosterone, low renin, as primary)

245
Q

What are some differential diagnosis for Conn’s disease

A

Essential hypertension
Thiazide induced hypokalaemia in a patient with essential hypertension
Renal artery stenosis
Secondary hyperaldosteronism (too much renin and aldosterone)

246
Q

What are the two main things you can do to treat Conn’s?

A
  • Laparoscopic adrenalectomy

Prescribe
* Oral spironolactone – aldosterone antagonist (K+ sparing diuretic)

247
Q

What should you monitor in a patient with Conn’s /Primary aldosteronism

A
  • BP, plasma electrolytes, and aldosterone and renin levels should be monitored every 6 to 12 (after adrenalectomy)

Look for any delveloping hyperkalaemia

248
Q

Normal physiology -
When is renin released, and what inhibits it?

A

Renin is produced by Juxtaglomerular cells in Kidney, in response to Decreased renaal perfusion at the Juxtaglomerular apparatus (aka Low Blood pressure
Renin is inhibited by Atrial natriuretic peptide (ANP), released by stretched atria in response to increases in blood pressure.

249
Q

Normal Physiology - Outline the the relationship between Renin, Angiotensin 1 and Angiotensin 2.

Where is ACE made?

A

Renin cleaves angiotensinogen into angiotensin 1,

Angiotensin 1 becomes Angiotensin 2 by Angiotensin converting enzyme ACE,

This reaction happens in the lungs, where ACE is made.

250
Q

Normal physiology - Name some of the actions of Angiotensin 2

A
  • ALDOSTERONE SECRETION FROM THE ADRENAL CORTEX (zona Glomerulosa)
  • ADH (vasopressin) from the Posterior Pituitary Gland
  • More sympathetic activity,
    ○ Increased release from noradrenaline
    Arteriolar vasoconstriction
251
Q

Normal Physiology - what does Aldosterone do?
Where does it act?

A

Acts on the Principle cells of the collecting duct

Causes vasoconstriction (greater in the efferent arteriole)
Increased Na+ and Cl- reabsorption AND INCREASED K+ SECRETION INTO URINE , and H2O retention

Increases Na+ reabsorption in exchange for K+

252
Q

What is secondary hyperaldosteronism?

A

Occurs when there is excessive Renin (and hence angiotensin II) which stimulates the adrenal glands to produce more aldosterone

253
Q

What are some conditions that lead to secondary hyperaldosteronism - and why do they lead to it?

A

Renal artery Stenosis
Renal artery obstruction
Heart Failure

Which leads to Blood pressure in the kidneys being disproportionately lower than the blood pressure in the rest of the body, from decreased renal perfusion ===> Too Much Renin Released, leading to too much aldosterone release (hyperaldosteronism)

254
Q

In primary aldosteronism, what would the renin/aldosterone ratio be?

A

High aldosterone and low renin

255
Q

In secondary aldosteronism, what would the renin/aldosterone ratio be?

A

High aldosterone and high renin indicates secondary hyperaldosteronism

256
Q

What are some complications of Conn’s?

A

Stroke, MI, heart failure, AF, impaired renal function,

aldosterone antagonist induced hyperkalaemia - if you give too much treatment
or Hypokalaemia, if it is left untreated.

Monitor for these!

257
Q

What is Addison’s disease?

A

Adrenal glands have been damaged, resulting in reduced secretion of cortisol and aldosterone.

Also called primary adrenal insufficiency.

258
Q

What is the most common cause of Addison’s disease in a) the world
b) The UK

A

Worldwide = TB
In UK = Autoimmune adrenalitis

259
Q

Name some causes of Secondary adrenal insufficiency?

A

Problem with the pituitary gland means not enough ATCH is secreted, so not enough Cortisol is secreted from the adrenal glands.

Either due to
Surgery, Congenital deformation, infection

Or long term steroid use being suddenly stopped, HPA axis hasn’t “woken up” and started making its own steroids again. ( End of Use) ABCDE Drug reaction

260
Q

What is the pathophysiology of tertiary adrenal insufficiency?

A

Due to inadequate CRH Being released from the Hypothalamus Corticotropin-releasing hormone

261
Q

What is the main cause of tertiary adrenal insufficiency?

A

Normally because people get taken off steroids too quickly, and not enough time for Hypothalamus to wake up again and start releasing CRH

262
Q

What is the main causes of Addison’s Disease?

A

○ Addison’s - autoimmune adrenalitis (90% of cases) most common in the UK
○ Adrenal TB - most common worldwide
○ Surgical removal of adrenal glands

263
Q

Name some risk factors for addisons disease

A
  1. Female sex,
  2. adrenocortical autoantibodies *ie 21 Hydroxylase antibody enzyme

adrenal haemorrhage, autoimmune diseases, coeliac disease
Adrenalectomy??

264
Q

What is the Pathophysiology behind Addison’s?
More importantly, what does it lead to?

What antibodies may be seen?

A

Destruction of Entire adrenal cortex resulting in reduced glucocorticoid (cortisol), mineralocorticoid (aldosterone) and androgen production

Adrenal antibodies – 21-hydroxylase - involved in biosynthesis of aldosterone and cortisol.

Leads to symptoms, and Increased CRH and ATCH levels

265
Q

What does Increased ATCH levels lead to?

A

Hyperpigmentation of the skin

266
Q

What are some signs of Addison’s disease (Primary Adrenal Insufficiency) that you would detect from examination?

For each sign, what hormone abnormality is causing this?

A
  • Postural hypotension caused by salt and water loss Lacking aldosterone
  • Bronzed Hyperpigmentation caused by excess ACTH in primary hypoadrenalism
  • Vitiligo and loss of body hair in females due to dependence on adrenal androgens
  • Hypoglycaemia - Steroids can increase blood sugar

REMEMBER – Tanned, Tired, Toned and Tearful

267
Q

What are some symptoms a patient with Addisons/Adrenal insuffiency experience?
Think why they are feeling these things!)

A

Lethargy Lack of steroids
Feeling faint - LOW BP due to low Aldosterone
Dehydration - Due poor water retention due to Poor aldosterone
Weight Loss - due to lack of steroids
Abdominal Pain
Depression/tearfullness

  • Impotence
    Amenorrhoea - stopped period - due to lack of Androgens
268
Q

An Addison Crisis is a presentation of severe Addison’s disease. How would a patient in Addison Crisis present??

A

Presentation of Severe Addison’s, where the absence of steroid hormones result in a life threatening presentation. Very unwell!!
They present with:

Reduced consciousness/confusion
Hypotension
Hypoglycaemia, hyponatraemia and hyperkalaemia
Muscle cramps
Hypovolemic Shock

269
Q

How do you treat an Addisonian Crisis?

A

Urgently!

Give IV Fluids, and IV Hydrocortisone

Correct any hypoglycaemia

270
Q

What are some first line investigations for Addisons?

What are the ATCH and cortisol levels seen in Primary and Secondary/Tertiary Hypoadrenalism

A

Morning Serum cortisol - less than <140 nanomols/L

Look at ATCH levels -

○ HIGH ACTH with low or normal cortisol confirms primary hypoadrenalism

○ LOW ACTH and cortisol indicate secondary or tertiary hypoadrenalism

271
Q

What is the gold standard test for Addison’s disease?

What antibodies are seen in Addisons?

A
  • Short ACTH stimulation test (Synacthen test)
    ○ Take baselines cortisol

○ Give ACTH (synACTHen) then measure cortisol level –
§ In Addison’s – cortisol remains low after giving ACTH

  • Adrenal antibodies – 21-hydroxylase - *involved in biosynthesis of aldosterone and cortisol.
272
Q

What would be the plasma levels of
a) Renin
b) Sodium
c) Potassium

In Addisons disease, and why?

A

In addisons, would have high plasma renin , low sodium, high potassium) due to low aldosterone

273
Q

What are some differential diagnosis for Primary adrenal insufficiency (Addisons)

A

Hyperthyroidism
Adrenal suppression due to drugs
Central (secondary or tertiary) adrenal insufficiency (pituitary or hypothalamic lesions)

274
Q

What two main drugs can you give to treat Primary Adrenal insuffiecincy?

A
  • Glucocorticoids - oral Hydrocortisone/prednisolone to replace cortisol

Mineralocorticoids - fludrocortisone to replace aldosterone

275
Q

What do you monitor in Addison’s disease

A

Evaluate annually to judge adequacy of glucocorticoid and mineralocorticoid replacement.

Look at serum electrolytes measurement to monitor mineralocorticoid replacement.

Sick day rules are really important in anyone taking long term steroids -
patients must double the dose when they are sick!

276
Q

How can hypocalcaemia influence ECGs?

A

Long QT interval

277
Q

How can we think of serum/plasma osmolarity?

A

As a Concentration so high serum or urine osmolarity means high concentration of Solutes in the serum or urine

A Low Urine osmolarity would be low concentration of solutes in urine, as seen in Diabetes Insipidus

278
Q

Other types of diabetes - what is MODY?

A

Commonest type of monogenic diabetes (~1% diabetes)
Diagnosed <25y
Autosomal dominant
Non-insulin dependent
Single gene defect altering beta cell function
Tend to be non-obese

Monogenic - caused a mutation of one gene only

279
Q

What Serum osmolality would be positive for HHS?

A

Positive for HHS is >320 mOsm/kg

280
Q

Outline what SIADH is (Syndrome of Inapproptiate ADH secretion)

A

Continued secretion of ADH despite plasma being very dilute 🡪 water retention, excess blood volume and hyponatraemia

Too much ADH

281
Q

Name some things that can cause SIADH.

A

Malignancy eg Cancer tumours that secrete Ectopic ADH

Drugs

Head Injury, Meningitis

282
Q

What Types of cancer has been known to secrete ectopic ADH? (3 locations)

A

lead to ectopic secretion of ADH. Seen in *Small cell carcinomas of the lungs, Prostate and Pancreatic

283
Q

What kind of drugs have been known to cause SIADH?

A

Opiates,
Carbamazepine (anti epileptic) .
Chlorpropamide (to treat diabetes) SSRIs
Thiazide diuretic

284
Q

What are some risk factors for SIADH?

A

The listed causes (Malignancy, Drugs, Head Injury)
Also
Recovering from major surgery
Including age >50 years, nursing home residence,
Presence of a postoperative state,
Pulmonary conditions (e.g., pneumonia),
CNS (eg MS) disease
Trauma

285
Q

Outline the pathophysiology of SIADH that leads to Water retention.
Where on the Nephron does ADH act?

A

a) Excess ADH ==> insertion of aquaporin 2 increases ==> water retention ==> Dilution of Blood plasma .
This in itself can lead to hyponatraemia

ADH acts on the collecting ducts and distal convoluted tubules of the Nephron

286
Q

Outline the pathophysiology of SIADH that leads to hyponatraemia

A

But more water means less RAAS so les Aldosterone released, so more Na+ secretion and loss into urine
(body is removing sodium from blood that already has a low concentration of sodium) ==> NORMOVOLAEMIC yet HYPONATRAEMIC

The excessive water reabsorption is not usually significant enough to cause a fluid overload, therefore you end up with a “euvolaemic hyponatraemia”

287
Q

In SIADH, will you get marked hypervolemia due to the water retention?

A

Not usually. The excessive water reabsorption is not usually significant enough to cause a fluid overload, therefore you end up with a “euvolaemic hyponatraemia”

You See low serum osmolarlty and
High urine osmolartity - concentrated sodium

288
Q

What things must there be an absence of in order to diagnose a patient with SIADH?

A

Need to have an absence of hypovolaemia and hypervolemia
No signs of adrenal insufficiency or hypothyroidism

You also need to rule out Hyponatraemia in order to diagnose SIADH

289
Q

What are some signs of SIADH?

A
  • Concentrated urine
  • Mild dilutional hyponatraemia – could lead to fits and coma
290
Q

What are some symptoms of SIADH?

A
  • Reduction in GCS and confusion with drowsiness
  • Irritability
  • Headaches
  • Anorexia
  • Nausea/Vomiting
291
Q

How do you go about differentiating SIADH from Hyponatraemia?

A

Test by giving with 1-2L of 0.9% saline – sodium depletion WILL respond, SIADH will NOT

292
Q

What is the diagnostic criteria for SIADH?

A

Diagnostic Criteria for SIADH:
- Hyperosmolar Urine
- Hypo osmolar Serum
- No hyper or hypovolaemia
- Hyponatraemia
Adrenal, Thyroid and renal function all normal

293
Q

What tests would you want to order to investigate suspected SIADH?

A

Serum Sodium - will be low
Serum Osmolality - Will be low
Serum urea
Urine osmolality will be high
Urine sodium will be high

294
Q

What 2 non pharmaceutical things do you do first when treating SIADH?

A
  • Treat underlying cause
  • Restrict fluid – to increase Na+ concentration
295
Q

What 3 types of medications can you give to treat SIADH?

A

Demeclocycline – inhibits action of vasopressin on kidney

  • Vasopressin receptor antagonists (vaptans) – V2 blocker
    ○ Tolvaptan – used for treatment of hyponatraemia secondary to SIADH as promotes water excretion with no loss of electrolytes

Oral furosemide – salt and loop diuretics if severe and to prevent circulatory overload

296
Q

What is Potassium essential for in the body?

A

Maintaining the resting potentials in all muscles in the body, involving the heart

297
Q

What does Hypokalaemia result in for
a) Smooth Muscle
b) Skeletal Muscle
c) Cardiac Muscle

Remember the rule!

A

Hypo - Everything Slows
a) Constipation
b) Weakness/Cramps
c) Arrhythmias and Palpitations

298
Q

What does Hyperkalaemia result in for
a) Smooth Muscle
b) Skeletal Muscle
c) Cardiac Muscle

Remember the rule!

A

a) Smooth - Cramping
b) Skeletal - Weakness/Flaccid Paralysis *(Due to over contraction of muslces, become totally drained of energy)

c) Cardiac- Arrhythmias and arrest.

299
Q

How does the body control Potassium’s Intracellular and serum levels?
3 ways

A

Uptake of K+ into cells
Renal excretion – mainly controlled by aldosterone
Extrarenal losses e.g. GI

300
Q

Hyperkalaemia - how can it cause arrhythmias and a Cardiac Arrest?

A

The amount in the blood determines the excitability of nerve and muscle cells including the heart muscle (myocardium)

When K+ levels in blood rise, this reduced the difference in electrical potential between cardiac myocytes and outside of the cells 🡪 threshold for action potential significant decreased 🡪 abnormal action potential 🡪 arrhythmias 🡪 cardiac arrest

301
Q

What are some causes of Hyperkalaemia?

A

Low levels of aldosterone in kidneys – adrenal insufficiency - as it gets rid of K+ in the urine

Certain Drugs

AKI - decreased filtration rate so more K+ is maintained in the blood

302
Q

What drugs can cause Hyperkalaemia?

A

ACE inhibitors – block the binding of aldosterone to receptor
Diuretics that spare K+
NSAIDs
Heparin

303
Q

What are some symptoms of Hyperkalaemia?

A

Typically, asymptomatic until high enough to cause cardiac arrest

Muscle weakness
Flaccid paralysis
Chest pain
Light-headedness

304
Q

What are some symptoms of Hypokalaemia?

A

Metabolic acidosis causing Kussmaul’s respiration – low, deep, sighing inspiration and expiration
Tachycardia
ECG abnormalities

305
Q

What investigations would you order for suspected Hyperkalaemia

A

U and Es
ECG

306
Q

What are features of an ECG in a hyperkalaemic patient?

(Draw it!)

A

Tall tented T waves (Normally smaller secondary wave)

Wide, flat P waves (Tiny initial wave)

Wide QRS complex (Big main wave)

Look up a picture

307
Q

What are the ranges of U and Es that are indictive of
a) Hyperkalaemia
b) Medical emergency grade Hyperkalaemia

A

Over 5.5mmol/L = hyperkalaemic
Over 6.5mmol/l = MEDICAL EMERGENCY

308
Q

How would you treat Mild Hyperkalaemia?

A

Treat underlying cause
Restrict Dietary potassium
Restriction of drugs causing hyperkalaemia

Loop diuretics e.g. furosemide – increase urinary K+ excretion

309
Q

How would you treat severe Hyperkalaemia?

A

Calcium gluconate – decreases VF risk in the heart and protects myocardium by reducing excitability of cardiac myocytes
Insulin and dextrose – drives K+ into the cells
Polystyrene sulphonate resin – binds K+ in the gut decreasing uptake

310
Q

What is the pathophysiology behind Hypokalaemia? (Low serum K+)

A

Less K+ in the blood means that there a greater will be a greater-than-normal stimulus required for depolarization of the membrane to initiate an action potential.

(The membrane is said to be Hyperpolarised)

In heart, therefore the excitability of the myocyte decreases

311
Q

What are some of the causes of Hypokalaemia?

A

Fasting, Anorexia

High levels of ALDOSTERONE

Increased renal excretion, bu
Thiazides diuretics e.g. Bendroflumethiazide
Loop diuretics e.g. furosemide

GI losses – vomiting, severe diarrhoea and laxative abuse

312
Q

Why would high levels of Aldosterone cause Hypokalaemia? In What disease would you see this?

A

Because the Majority of K+ excretion is through the kidneys

Aldosterone stimulates secretion of K+

Seen in Cushing’s and Conn’s

313
Q

What are some symptoms of Hypokalaemia?
What could you say its kind of similar to

A

Usually asymptomatic
Muscle weakness
Cramps
Tetany – intermittent muscle spasms
Palpitations
Constipation

Some of those are also seen with Hypocalcaemia?

314
Q

What investigations would you order in suspected Hypokalaemia?

A

U&Es
ECGs

315
Q

What values would you seen for Serum K+ in hypokalaemia?

A

Serum K+ < 3.5mmol/L = hypokalaemia
Serum K+ < 2.5mmol/L = MEDICAL EMERGENCY

316
Q

Would you see on an ECG for someone with Hypokalaemia? Rhyme?

A

U waves
Small or inverted T waves
Depressed ST segments
Prominent U Wave
Long PR
Long QT
Rhyme – You have no Pot (K+) and no Tea (T Wave) but a Long PR and a Long QT, FOR YOU (Prominent U wave)

317
Q

What treatment do you give for
a) Mild Hypokalaemia
b) Severe Hypokalaemia

A

Mild – Oral K+ e.g. oral Sando-K and spironolactone (K+ sparing)
Severe- IV K+

318
Q

What is a Carcinoid Tumour and what is Carcinoid Syndrome

A

A Carcinoid tumour is a slow-growing type of neuroendocrine tumour originating in the cells of the neuroendocrine system.

Carcinoid syndrome is a paraneoplastic syndrome comprising the signs and symptoms that occur secondary to carcinoid tumours.

319
Q

Where do most Carcinoid tumours occur?

A

GI tract
Can also be in lung, and can metastisise elsewhere eg Liver

Carcinoid syndrome generally does not occur until the disease is so advanced that it overwhelms the liver’s ability to metabolize the released serotonin

320
Q

What two things do Carcinoid tumours secrete? What do they both do?

A

serotonin and kallikrein

Serotonin is involved with initiating peristalsis, and plays a role in bronchoconstriction
In Carcinoid Syndrome, Serotonin can cause fibrous of heart valves, especially on the the right hand side.

Kallikrein - leads to formation of bradykinin, one of the most potent vasodilators known. Therefore has great effect on Blood flow (can cause flushing)

321
Q

What are some symptoms of Carcinoid syndrome?

A

Flushing: The most important clinical finding is flushing of the skin, usually of the head and the upper part of thorax. - Due to vasodilation
- Abdominal pain, due to Hepatomegaly , or bowel obstruction or bowel ischaemia,
- Diarrhoea - due to abdominal cramping, and abnromal peristalsis
- Carcinoid Heart disease - Serotonin leads to fibrous of right hand side heart valves

Bronchoconstriction, due to serotonin/histmaine, leads to Flushing, sneezing, and SOB

322
Q

What are some investigations you would do for a carcinoid syndrome?

A
  • 24 hr urine 5-hydroxyindoleacetic acid: show increased levels - (its a major metabolite of 5-HT/serotnin) GOLD STANDARD
  • Chest X-ray/ chest or pelvis MRI/ CT: to identify location
  • Ostreoscan: injected radiolabelled somatostatin analogue, octreotide, to bind to the increased number of somatostatin receptors on tumour cells.
323
Q

What are 2 treatments for Carcinoid Syndrome?

A

Somatostatin analogues, which decreases the secretion of serotonin by the tumour

Will also decrease the breakdown product of serotonin

Surgery to remove the tumour

324
Q

Outline what Diabetes Insipidus is

A

a lack of antidiuretic hormone (ADH) or a lack of response to ADH

325
Q

What are the two types of diabetes insipidus?

A

Cranial Diabetes Insipidus - Too little ADH from Posterior Pituitary Gland

Nephrogenic Diabetes Insipidus - Kidney not responding to ADH.

326
Q

Normal physiology - Where is
a) ADH/Vasopressin Made?
b) ADH/Vasopressin stored?

A

a) made in the Hypothalamus
b) Stored in the posterior pituitary gland, ready for secretion.

327
Q

What can cause Nephrogenic Diabetes insipidus?

A

Drugs, particularly lithium used in bipolar affective disorder, and Demeclocycline

Mutations in gene that codes for the ADH receptor - so Familial

Kidney disease
Electrolyte disturbance (hypokalaemia and hypercalcaemia)

Renal Tubular Acidosis

328
Q

Can damage to the Hypothalamo - neurohyophysical tract or damage to the posterior pituitary with an intact hypothalamus cause ADH deficiency?

A

No, as ADH can still “leak” from the damaged end of the intact neurone

329
Q

What are some causes of Cranial Diabetes Insipidus?

A

Brain tumours
Head injury
Brain infections (meningitis, encephalitis and tuberculosis)
Brain surgery or radiotherapy
Pituitary Tumour

330
Q

What are some symptoms of Diabetes Insipidus?

A

Polyuria/Nocturia
Polydipsia
Dehydration

331
Q

What is the main test of choice for diagnosing Diabetes Insipidus?

What are other investigations you can use to test for Diabetes Insipidus?

A

The water deprivation test - main one

Also
Look at Serum and Urine Osmolarity
MRI of Hypothalamus
Plasma biochemistry

332
Q

What does the water deprivation test look for? How does it work (Two Parts)? (Main investigation in Diabetes Insipidus)

A

It aims to determine whether kidneys continue to produce dilute urine despite dehydration.

You restrict fluid for 8 hours, and measure Urine osmolarity, which can check for Diabetes insipidus.

Then, give Synthetic ADH (Desmopressin) and recheck the urine osmolarity to distinguish between Cranial DI and Nephrogenic DI

333
Q

What would urine osmolarity after Water deprivation in
a) A normal person
b) Someone with Diabetes Insipidus

A

a) Concentrated/high, but in normal ranges
b) Still low, (lots of urine produced) despite dehydration

334
Q

After giving Synthetic ADH (Desmopressin) after water deprivation to test for DI, what would urine osmolarity be in
a) Cranial Diabetes Insipidus
b) Nephrogenic Diabetes Insipidus

A

a) Cranial - High urine osmolarity (as kidneys are still capable of responding to ADH)

b) Nephrogenic - Still low Urine osmolarity, as problem is not with the lack of ADH but the lack of response in the kidneys to it.

335
Q

How do you treat
a) Cranial Diabetes Insipidus?
b) Nephrogenic Diabetes Insipidus?

A

a) Desmopressin - Synthetic ADH
b) Bendroflumethiazide Diuretic - (Causes more Na+ secretion), so more water lost so body responds by reducing GFR)

Treat underlying cause!

336
Q

Normal physiology - where is adrenaline produced? By what cells?

A

Adrenaline is produced by the “chromaffin cells” in the adrenal medulla of the adrenal glands.

337
Q

What is a phaeochromocytoma?

A

A phaeochromocytoma is a tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline.

338
Q

What is a familial cause of pheochromocytoma?

A

MEN 2a (or 2B)

MEN = Multiple Endocrine Neoplasia, autosomal dominant

339
Q

In Phaeochromocytoma, how is the adrenaline secreted?

A

The Adrenaline tends to be secreted in bursts, giving periods of worse symptoms followed by more settled periods

340
Q

What tests would you use to diagnose Phaechromocytoma?

A

24 hour urine catecholamines
Plasma free metanephrines

Measure over 24 hours to get a better picture of how much adrenaline is secreted.

Metanephrines are a breakdown product of adrenaline and have a longer half life -so more reliable to diagnose with

341
Q

Adrenergic Pharmacology: what
a) Alpha 1
b) Alpha 2
receptor do
Both G coupled

A

a1- Vasoconstriction, increased BP, Increased closure of internal sphincter of the bladder, pupil dilation

a2 - Inhibits NA release, and inhibits Ach release. Also inhibits Insulin release

342
Q

Adrenergic Pharamcology: what
a) Beta 1
b) Beta 2
c) Beta 3
receptor do?
All G coupled, sympathetic (obvs)

A

a) Chronotropic and inotropic effects on heart (tachycardia and increased contractility)

b) Relaxes smooth muscle (seen in labour/asthma) bronchodilation, inhibits labour, causes insulin and glucagon to be secreted)

c) Enhances lipolysis relaxes bladder detrusor (urine retention)

343
Q

What are the signs/symptoms of Phaeochromocytoma?

A

Symptoms of Adrenaline release!
Anxiety
Sweating
Headache
Hypertension
Palpitations, tachycardia and paroxysmal atrial fibrillation

Signs and symptoms tend to fluctuate with peaks and troughs relating to periods when the tumour is secreting adrenaline.

344
Q

What is the management of Phaechromocytoma?

A

Alpha blockers (i.e. phenoxybenzamine)
Beta blockers once established on alpha blockers
^^To control the symptoms

Adrenalectomy to remove tumour

Patients should have symptoms controlled medically prior to surgery to reduce the risk of the anaesthetic and surgery.

345
Q

In primary aldosteronism, what would the renin/aldosterone ratio be?

A

High aldosterone and low renin

346
Q

Endocrine Fundamentals - In what disease would you see too much blood glucose/not enough insulin?

A

Diabetes.

347
Q

Endocrine Fundamentals - In what disease would you see too much ADH?

A

SIADH.

348
Q

Endocrine Fundamentals - In what disease would you see Too much Aldosterone?

A

Conns, primary aldosteronism

349
Q

Endocrine Fundamentals - In what disease would you see too little cortisol and too little aldosterone?

A

Addison’s

350
Q

Endocrine Fundamentals - In what disease would you see not enough ADH?

A

Diabetes insipidus

351
Q

Endocrine Fundamentals - In what disease would you see too much Cortisol?

A

Cushing’s disease

352
Q

Endocrine Fundamentals - In what disease would you see too much Thyroid hormone?

A

Graves disease, iodine induced hyperthyroidism

353
Q

How can amiodarone lead to hyper/hypothyroidism?

A

Amiodarone is structurally similar to thyroxine and also contains iodine,

Amiodarone is an antiarrhythmic medication used to treat and prevent a number of types of irregular heartbeats (including atrial fibrillation which this lady has). It is known to cause thyroid problems, including both hyperthyroidism and hypothyroidism.

354
Q

What hormones can be secreted in order to raise blood glucose? What is the first to be secreted?

A

Glucagon - First ot be secreted

Cortisol and Glucagon can also raise blood sugar

355
Q

Give an example of
a Sulfonylurea
DPP4 inhibitors
SGLT-2 inhibitor

A

Gliclazide
Sitagliptin
Dapagliflozin

356
Q

What extra imaging tests can you do in Cushings?

A

pituitary MRI
CT scan of adrenals

357
Q

What would Hyperkalaemia look like on an ECG?

A

Flat P wave
Prolonged PR interval
Tall, Peaked T wave
Wide QRS

Go, Go long, Go tall, Go wide

358
Q

What would Hypokalaemia look like on an ECG?

A

ST Depression,
Flat, inverted T wave
presence of a U Wave

U Wave

Comes after T wave, - ‘U’ waves are thought to represent repolarization of the Purkinje fibres.

359
Q

What is a U wave?

A

The U wave is a small (0.5 mm) deflection immediately following the T wave, its polarity is the same as the T wave, meaning that they will both be in the same direction

may be a sign of hypokalemia or drug effect or toxicity

Phase 2a Sam (18 decks)

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