Brainscape's Knowledge GenomeTM

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


See full index

Endocrine System > Complications of Diabetes > Flashcards

Complications of Diabetes Flashcards

1
Q

What is the prevalence of DKA in diabetic patients?

A

4.6-8 cases of DKA per 1,000 patients

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

How is DKA defined?

A

pH below 7.3
bicarbonate <15mmol/l
glucose >13.9 mol/l
ketosis present

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

DKA can present as a result of T1DM but also as a result of…?

A

Poor compliance to treatment

Intercurrent infection

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

Describe osmotic diuresis in DKA?

A

Glucose and ketones are freely filtered at the glomerulus but in hyperglycaemia the maximal reabsorption threshold of glucose is exceeded and the resultant increased glucose concentration in the tubular lumen causes an osmotic gradient which leads to increased water loss in the urine

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

What affect does DKA have on total body potassium?

A

Decreased total body potassium

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

When there is insulin deficiency in DKA, this allows unopposed action of counter-regulatory hormones such as…?

A

Adrenaline
Cortisol
Growth hormone

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

Describe the role of adrenaline as a counter-regulatory hormone to insulin

A

Adrenaline increases glycogenolysis, gluconeogenesis and lipolysis

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

Describe the role of cortisol and growth hormone as a counter-regulatory hormone to insulin

A

Cortisol and growth hormone increase gluconeogenesis and lipolysis and inhibit peripheral glucose uptake

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

Describe how insulin deficiency (possibly alongside increase counter-regulatory hormone action) leads to profound dehydration, potassium depletion and ketoacidosis?

A

This decreases peripheral glucose uptake, leading to hyperglycaemia which causes osmotic diuresis
Insulin deficiency also causes increased lipolysis, increased glycogenolysis and increased glycogenesis which promotes the production of ketones leading to acidaemia.
Hyperglycaemia and academia lead to vomiting
The combined effects of osmotic diuresis, vomiting, academia, hyperglycaemia and ketone production leads to profound dehydration, ketoacidosis and potassium depletion

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

How is DKA treated?

A

IV fluid, IV insulin, IV potassium and NH tube, antiemetics and treatment of precipitating causes

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

How is hyperosmolar hyperglycaemic state different from DKA?

A

HHS is more of a relative insulin deficiency rather than an absolute insulin deficiency. It presents in older patients typically in those with T2DM rather than T1DM. There is no ketogenesis due to residual insulin but more profound hyperglycaemia

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

DKA is treated more aggressively than HHS. Why is this?

A

In HHS there is no ketoacidosis and so there is not such an immediate requirement for IV insulin
Also treatment of HHS tends to be more conservative and the patients who get HHS tend to be older and have more co-morbidities than those who get DKA
There are also less profound potassium shifts in HHS than DKA

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

In the treatment of HHS, fluid resuscitation is used to dilute plasma glucose before insulin is administered. T/F?

A

True

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

Treatment of HHS can carry serious risks to the brain due to large fluid shifts. What are these potential risks?

A

Central,pontine mylinolysis

Cerebral oedema

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

Patients with HHS are usually alert whereas those with DKA are often drowsy. T/F?

A

False - the opposite is true

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

What are the symptoms of hypoglycaemia?

A 
Sweating
Tremor
Palpitations
Hunger
Anxiety
Confusion
Impaired consciousness level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In long term aggressive treatment of T1DM there is reduced action go counter-regulatory hormones which give a an increased risk of hypoglycaemia. T/F?

A

True

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

What is hypoglycaemia unawareness?

A

An autonomic dysfunction where there is altered sensing of hypoglycaemia in the CNS

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

Patients with true hypoglycaemia unawareness are banned from driving. T/F?

A

True

20
Q

How is mild hypoglycaemia treated?

A

Ingestion of 15-20g of fast acting carbohydrate

21
Q

What is the most common metabolic complication of type 1 diabetes?

A

Hypoglycaemia

22
Q

Intensive glycemic control is particularly important in reducing the risk of developing what kind of complications of diabetes?

A

Microvascular

23
Q

Most tissues need insulin in order to take up glucose. What are the exceptions to this?

A

Retina
Kidneys
Nerve

24
Q

Which enzyme converts glucose to sorbitol?

A

Aldose reducatse

25
Q

How does the accumulation of sorbitol lead to diabetes complications?

A

This leaves less NADPH for cell metabolism leading to a build up of reactive oxidative species which cause oxidative stress and cell damage

26
Q

Microvascular disease can be cured. t/f?

A

False

27
Q

Diabetic retinopathy occurs in all diabetic patients to some extent. T/F?

A

True

28
Q

Describe the early non proliferative stage of diabetic retinopathy

A

Hyperglycaemia results in damage to the small vessels in the retina and micro aneurysms occurs. Dot haemorrhages occur when the vessel wall is breached. Additionally fluid can leak from the vessels and protein and fluid left behind in the retina forms hard exudates
Micro-infarcts cause cotton wool spots

29
Q

Ischaemia in the later stages of diabetic retinopathy leads to neovascularisation by the action of which growth factor?

A

VEGF

30
Q

What are the signs of proliferative diabetic retinopathy?

A

Vitreous haemorrhages

Macular oedema

31
Q

How can retinopathy be treated?

A 
Good glycemic control
smoking cessation
good blood pressure control
VEGF inhibitors
Vitrectomy
Laser treatment
32
Q

Retinal screening is offered annually to diabetic patients from what age?

A

12 years

33
Q

Describe the pathophysiology of diabetic nephropathy

A

Renal hypertrophy occurs in response in GFR increase and the afferent arteriole vasodilator - this damages the glomerular basement membrane.
This, alongside capillary damage and shear stress results in leakage of proteins into the urine

34
Q

What are the progressive stages of diabetic nephropathy?

A

Renal enlargement and hyperfiltration
Microalbuminuria
Macroalbuminuria
Renal failure

35
Q

If microalbuminuria is found in a diabetic patient they are treated to prevent progression to macroalbuminuria and renal failure. What is involved in this treatment?

A

ACE inhibitors

Angiotensin II receptor blockers

36
Q

What is the pathophysiology of diabetic neuropathy>

A

Capillary damage due to hyperglycaemia occludes the vessels of the vasa nervorum. reduced blood supply to the neural tissue results in impairments in nerve signalling which affects both sensory and motor function

37
Q

What are the signs and symptoms of diabetic neuropathy?

A

Numbness
Prickling/tingling
Aching pain
Burning pain
Unusual sensitivity or tenderness with feet are touched
Diminished vibratory perception
Decreased knee and ankle reflexes
Reduced protective sensation such as pressure, hot, cold and pain
Diminished ability to sense position of toes and feet

38
Q

What drugs are used to treat diabetic neuropathy?

A

Duloxtine
Amiltriptyline
Pregabalin

39
Q

Diabetic Patients with neuropathy or absent pulses in the feet are at medium risk of diabetic foot and should be reviewed by the podiatrist how often?

A

3-6 months

40
Q

Diabetic Patients with deformities or ulcerations are at medium risk of diabetic foot and should be reviewed by the podiatrist how often?

A

every 1-3 months

41
Q

What is the 5 year mortality of patients with diabetic foot?

A

80%

42
Q

How can autonomic neuropathy as a result of diabetes manifest?

A

Postural hypotension
Erectile dysfunction
Gustatory sweating
Gastroparesis

43
Q

What is mono neuritis multiples?

A

A painful, asymmetric motor and sensory neuropathy which affects two or more nerves

44
Q

When diabetic patients undergo their annual review, what factors are assessed?

A 
HbA1c
cholesterol, HDL and TAG
Creatinine
Microalbuminuria
Vascular acuity
Retinal screening
Pedal pulses
Foot sensation
BMI
Blood pressure
Erectile function
Contraception
Lifestyle
Drug therapy
Mental well-being
45
Q

Poor glycemic control during pregnancy can lead to macrosomia. T/F?

A

True

Endocrine System (12 decks)

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