Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 4- Paediatrics > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is type 1 diabetes?

A

This is a disease where the pancreas stops being able to produce insulin. What causes the pancreas to stop producing insulin is unclear, there may be a genetic component and it may be triggered by certain viruses- coxsackie B virus and enterovirus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does the body ideally want to keep the blood glucose concentration at?

A

4.4 and 6.1mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does insulin reduce blood sugar?

A

It reduces blood sugar in two ways…
Causes cells to take up glucose and use it as fuel
Secondly, it causes liver and muscle to take up glucose and store it as glycogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the role of glucagon?

A

It is a hormone that increases blood sugar levels. It is produced by the alpha cells in the islets of langerhans in the pancreas.
It tells the liver to break down glycogen to glucose (glycogenolysis). It also tells the liver to convert protein and fats into glucose (gluconeogenesis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is ketogenesis and when does it occur?

A

Ketogenesis occurs when there is an insufficient supply of glucose and glycogen stores are exhausted
It is where the liver takes fatty acids and converts them to ketones (water soluble fatty acids) that can be used as fuel. Ketones can cross the blood brain barrier and be used by the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do type 1 diabetics present?

A

About 25-50% of new type 1 diabetic children present in DKA. This is the result of a situation where the pancreas can no longer produce enough insulin to maintain basic blood glucose regulation.

Remaining present with:
Polyuria
Polydypsia
Weight loss

Less typical presentations= secondary enuresis (bed wetting in a previously dry child) and recurrent infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When a new diagnosis of diabetes is established, what bloods should be taken to exclude other pathology.

A

You need to get a baseline idea of the child’s overall health
Baseline bloods-FBC, U and Es, formal laboratory glucose
Blood cultures in patients with suspected infection (fever)
HbA1C allows doctors to get a picture of how long they had diabetes before presenting
Thyroid function tests and thyroid peroxidase antibodies to test for associated autoimmune thyroid disease
Tissue transglutaminase (anti TTG) antibodies for associated coeliac disease.
Insulin antibodies, anti GAD antibodies, islet cell antibodies to test for antibodies associated with destruction of the pancreas and the development of type 1 diabetes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the basis for the management?p of type 1 diabetes?

A

Monitor daily carbohydrate intake
Subcutaneous insulin regimes
Monitor blood sugar levels on waking, at each meal and before bed
Monitor for and management of complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What should you suspect if a patient is not responding to their insulin?

A

Suspect lipodystrophy- this is when a patient is injecting insulin into the same spot, causing subcutaneous fat to harden and the absorption of insulin to decrease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the usual insulin regime for patients?

A

Basal bolus- give a long acting insulin (lantus) which acts as a constant background insulin throughout the day.

Bolus is the short acting (actrapid) typically given 3 times a day 30 mins before carbohydrates, it is also injected according to the number of carbohydrates the patient has as a snack.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is an insulin pump and when would one be used?

A

Small devices that continuously infuse insulin at different rates to control blood sugar levels. They are an alternative to basal bolus regimes. The pump pushes insulin through a cannula that is inserted under the skin. The cannula is replaced every 2-3 days and the insertion sites are rotated to prevent lipodystrophy and absorption issues.

To qualify you have to be over 12 and have difficulty controlling HbA1C.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the benefits/disadvantages of using insulin pumps?

A

Benefits= better blood glucose control, less injections, more flexibility with eating

Disadvantages= risk of infection, difficulties using the pump and having it attached at all times

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the short term complications of T1DM?

A

Hypoglycaemia

Hyperglycaemia (and DKA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is hypoglycaemia in T1D caused by?

A

Too much insulin
Not enough carbohydrates
Not processing carbs properly (this would happen in diarrhoea/vomiting/sepsis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the symptoms of hypoglycaemia?

A 
Hunger 
Tremor 
Sweating 
Irritability 
Dizziness 
Pallor

More severe= reduced consciousness, coma, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is hypoglycaemia treated?

A

Needs to be treated with a combination of rapid acting glucose- lucozade and slower acting (biscuits or toast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the options for treating severe hypoglycaemia?

A

IV dextrose and intramuscular glucagon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

If a cannula is sited, what dextrose solution is given?

A

2mg/kg/hour bolus followed by a 5mg/kg/hour infusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the other causes of hypoglycaemia, other than diabetes?

A 
. hypothyroidism 
. Glycogen storage disease 
. Growth hormone deficiency 
. Liver cirrhosis 
. Alcohol and fatty acid oxidation defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What damage does chronic exposure to hyperglycaemia cause?

A

Damages endothelial cells of blood vessels. This leads to leaky malfunctioning vessels which are unable to regenerate.
As well as this it leads immune suppression and therefore an optimal environment for the infectious organisms to thrive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the macrovascular complications of chronic exposure to hyperglycaemia?

A

Coronary artery disease
Peripheral ISCHAEMIA
Stroke
Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the microvascular complications of exposure to high blood glucose?

A

Peripheral neuropathy
Retinopathy
Kidney disease- glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the infection related complications of hyperglycaemia?

A

UTI
Pneumonia
Skin and soft tissue infections (particularly in feet)
Fungal infections- oral and vaginalis candidiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What monitoring is in place for tpT1DM?

A

HbA1C
Capillary blood glucose (finger prick)
Flash glucose monitoring (not available everywhere)

25
Q

What are the reasons a T1 diabetic would suffer from DKA?

A

When the person is not producing adequate insulin and not injecting insulin to compensate for this.

26
Q

What are the main problems in DKA?

A

. Potassium imbalance
. Dehydration
. Ketoacidosis

27
Q

What is ketoacidosis?

A

Initially kidneys produce bicarbonate to buffer the ketone acids in the blood and maintain a normal pH, however over time the ketones use up the bicarbonate and the blood becomes acidic.v

28
Q

What is the reason for dehydration in DKA?

A

Hyperglycaemia overwhelms the kidney and therefore glucose starts to be filtered into the urine, this causes water to be drawn out with it in a process of osmotic DIURESIS, this causes the patient to urinate a lot (polyuria), resulting in severe dehydration.

29
Q

What happens in terms of potassium balance in DKA?

A

Insulin normally drives potassium into cells. Without insulin, potassium is not added to and stored in cells. Serum K+ can be can be high or normal but the overall is low (due to little K+ in cells) patients can develop severe hypokalaemia and arrhythmias.

30
Q

What is a risk of treating DKA?

A

In DKA the hyperglycaemia and the Dehydration causes Water to move from the intracellular space to the extracellular space, when you treat too rapidly it will then cause the water from the extracellular
Space to the intracellular space in the brain cells, causing the brain cells to become oedematous, leading to brain cell destruction and death.

31
Q

How would you manage cerebral oedema that is caused by treating the DKA?

A

Slowing IV fluids
IV mannitol
IV hypertonic saline

32
Q

How would a patient with DKA present?

A

They will present with symptoms of the underlying hyperglycaemia, dehydration and acidosis….

. Hypotension 
. Polyuria
. Polydypsia
. N+V 
. Weight loss 
. Acetone smell to their breath
33
Q

What are the 3 key things needed to diagnose DKA?

A

Blood glucose >11mmol/l
Ketones >3mmol/l
Acidosis pH<7.3

34
Q

How would you manage DKA?

A
  1. Correct dehydration evenly over 48 hours (correcting it faster increases the risk of cerebral oedema)
  2. Give a fixed rate insulin infusion

Other measures;
. Prevent hypoglycaemia with IV dextrose once the blood glucose falls below 14mmol/l
. ADD potassium to IV fluids and monitor serum K+ closely
. Monitor for signs of cerebral oedema
. Monitor glucose, ketones and pH to assess when to switch to subcut insulin.

35
Q

What is adrenal insufficiency?

A

This is where the adrenal glands to not produce enough steroid hormones (cortisol and aldosterone), steroids are essential for life and therefore this condition is life threatening unless the steroids are replaced.

36
Q

What is Addison’s disease?

A

This is also known as primary adrenal insufficiency
It is where the adrenal gland is damaged resulting in reduced cortisol and aldosterone. The most common cause is autoimmune.

37
Q

What is secondary adrenal insufficiency?

A

This is caused by inadequate ACTH stimulating the adrenal glands, resulting in low levels of cortisol being released. It is a result of loss or damage to the pituitary gland.

38
Q

Secondary adrenal insufficiency is caused by a loss of adrenal gland or damage to the adrenal gland, what causes this?

A 
Congenital underdevelopment (hypoplasia) 
Surgery 
Infection 
Loss of blood flow 
Radiotherapy
39
Q

What is tertiary adrenal insufficiency?

A

This is where the hypothalamus doesn’t produce enough CRH, and it is usually caused by the fast withdrawal of steroids, the hypothalamus does not ‘wake up’ fast enough which leads to endogenous steroids not being adequately produced, this is why it is important to taper steroids to allow the adrenal axis to regain normal function!

40
Q

What are the features of adrenal insufficiency in babies?

A 
Lethargy 
Vomiting 
Poor feeding 
Hypoglycaemia 
Jaundice 
Failure to thrive
41
Q

What are the features of adrenal insufficiency in older children?

A 
Failure to thrive 
N+V 
Weight loss 
Abdo pain 
Reduced appetite (anorexia) 
Muscle weakness or cramps 
Developmental Delay 
Bronze hyperpigmentation in ADDISONS (due to ACTH stimulating melanocytes)
42
Q

What are the investigations for adrenal insufficiency?

A

U+Es (would expect hyponatraemia and hyperkalaemia due to the low aldosterone levels)
Glucose (Hypoglycaemia)
Check cortisol, ACTH, aldosterone, renin
Short synacthen test

43
Q

What is the short synacthen test?

A

This involves giving synacthen (synthetic ACTH) and then measuring blood cortisol at baseline, 30 mins and 60 mins after administration. The synthetic ACTH would stimulate healthy adrenal glands to produce cortisol, the cortisol levels should at least double in response to synacthen. A failure of cortisol to rise indicates primary adrenal insufficiency (Addison’s)

44
Q

How do you manage patients with adrenal insufficiency?

A

Replacement steroids titrated to signs,symptoms and electrolytes.
Hydrocortisone replaces cortisol
Fludrocortisone replaces aldosterone

Patients are given a steroid card and emergency ID tag

No doses should be missed

Doses should be increased in acute illness to reflect the normal steroid response to illness

Individual care plan

Growth and development 
Blood pressure
U and Es
Glucose 
Bone profile
Vit D
45
Q

What are the ‘sick day rules’ for people with adrenal insufficiency?

A

Minor coughs or colds do not require a change in medications
If they are more unwell, have a temperature, have nausea and vomiting etc then the body needs more steroids to deal with the illness.
Patient should take a higher dose of steroids and more regularly
If they are vomiting or have diarrhoea then they will need an IM steroid at home and likely admission for IV steroids
They are also at risk of hypoglycaemia and therefore need frequent blood glucose monitoring.

46
Q

What is addisonian crisis/ adrenal crisis?

A

This is a term used to describe an acute presentation of very severe Addison’s. The absence of steroid hormones results in a life threatening presentation! Patients present with…

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia

47
Q

What is an adrenal crisis caused by?

A

First presentation of Addison’s
Infections/trauma
Stopping taking steroids abruptly

48
Q

What is the management of addisonian crisis?

A

Intensive monitoring if they are acutely unwell
Parenteral steroids (IV hydrocortisone)
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance

49
Q

What is congenital adrenal hyperplasia?

A

Caused by a congenital deficiency of the 21- hydroxylase enzyme which causes an underproduction of cortisol and aldosterone and an overproduction of androgens from birth. Genetic condition which has an autosomal recessive pattern. Occasionally it is caused by a deficiency of 11- beta hydroxylase rather than 21- hydroxylase.

50
Q

What is the role of testosterone?

A

Androgen hormone which is found in high levels in men and low levels in women. It acts to promote male sexual characteristics.

51
Q

What is the role of glucocorticoid hormones?

A

Helps the body deal with stress
Raises blood glucose
Reduce inflammation
Suppress the immune system

Main one= cortisol

52
Q

What are the action of mineralcorticoid hormones?

A

They act on the kidneys to control the balance of salt and water in the blood. Aldosterone acts on the kidneys to increase sodium reabsorption and increase potassium excretion into the urine.

53
Q

What is the pathophysiology of congenital adrenal hyperplasia?

A

So there is a defect in the 21- hydroxylase enzyme. This is an enzyme which is responsible for converting progesterone to aldosterone and cortisol. Progesterone is also used to create testosterone, however the conversion of progesterone to testosterone does not involve the 21- hydroxylase enzyme and therefore because there is free progesterone floating about which can’t be converted to aldosterone or cortisol it gets converted to testosterone; resulting in high testosterone and low aldosterone/cortisol.

54
Q

What is the presentation of congenital adrenal hyperplasia?

A

Female patients usually present at birth with virilised genitalia (ambiguous) and enlarged clitoris due to high testosterone levels

Patients with more severe CAH will have hyponatraemia, hyperkalaemia and hypoglycaemia, leading to: poor feeding, vomiting, dehydration and arrhythmias.

55
Q

How do people with congenital ad4nal hyperplasia present in mild cases?

A

Patients who are less severely affected present during childhood or after puberty, the symptoms relate to the high androgen levels.

Female: tall for age, facial hair, amenorrhoea, deep voice, early puberty
Male: tall for age, deep voice, large penis, small testicles, early puberty

Also will have hyperpigmentation of skin due to lots of ACTH being produced in response to the low cortisol levels.

56
Q

What is the management of CAH?

A

Cortisol replacement
Aldosterone replacement
Female patients with virilised genitalia can have corrective surgery

57
Q

Where is growth hormone produced from, and what is it responsible for?

A

Produced by the anterior pituitary gland
Responsible for stimulating cell reproduction and the growth of organs, muscles, bones and height. It also stimulates the release of insulin like growth factor 1 which is important in promoting growth in children and adolescents.

58
Q

What does congenital growth hormone deficiency result from?

A

A disruption to the growth hormone axis at the hypothalamus or the pituitary gland. It can be due to a known genetic mutation such as GH1 (growth hormone 1) or GHRHR (growth hormone releasing hormone receptor) genes or due to another condition- empty sella syndrome where the pituitary gland is under developed/damaged.

59
Q

What causes secondary growth hormone deficiency?

A

Secondary to infection, trauma, interventions like surgery.

Year 4- Paediatrics (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions