diabetes Flashcards
1
Q
what do alpha cells produce
A
glucagon
2
Q
what do beta cells produce
A
insulin
3
Q
what do delta cells produce
A
somatostain
4
Q
what time frame does HbA1c measure from
A
2-3 months
5
Q
normal HbA1c level
A
< 4.1
6
Q
prediabetes HbA1c level
A
4.2-4.7
7
Q
diabetes HbA1c level
A
> 4.8
8
Q
normal fasting glucose level
A
< 6
9
Q
prediabetes fasting glucose level
A
6.1-6.9
10
Q
diabetic fasting glucose level
A
> 7
11
Q
normal 2 hour GTT level
A
< 7.7
12
Q
prediabetes 2 hour GTT level
A
7.8-11
13
Q
diabetic 2 hour GTT level
A
> 11.1
14
Q
diabetic random glucose level
A
> 11.1
15
Q
what is LADA
A
- latent onset diabetes of adulthood
- slow onset vesion of type 1 diabetes
- normally presents 25-40
16
Q
what is type 1 diabetes
A
state of absolute insulin deficiency due to autoimmune destruction of the beta cells in the islets of Langerhans
17
Q
type 1 diabetes auto-immune antibodies
A
- anti-GAD
- anti-IA2
- anti-ZnT8
18
Q
type 1 diabetes presentation
A
- fatigue
- weight loss
- polyuria and polydipsia
- diabetic ketoacidosis
19
Q
diabetic ketoacidosis
A
presents with abdominal pain, vomiting and signs of systemic shock)
20
Q
type 1 diabetes diagnosis
A
- glucose testing
- urine (ketones to rule out diabetic ketoacidosis)
- bloods (auto-antibodies)
21
Q
type 1 diabetes management
A
- insulin therapy
- target HbA1c 48-59
- need to check blood sugar at least twice a day
- diet advice (control sugar intake)
- even if sick, don’t stop insulin as illness can cause hyperglycaemia
- try to eat/drink as much as possible when sick
- increase blood sugar monitoring to minimum of four times a day when sick
- seek medical advice if ketones found on urine dip
22
Q
give 3 examples of short acting insulins
A
- Humulin
- Humalog
- Novarapid
23
Q
give 2 examples of long acting insulins
A
- Lantus
- Lenevinir
24
Q
type 1 diabetes complications
A
- hypoglycaemia
- lipohypertrophy
- diabetic ketoacidosis
25
what is lipohypertrophy
fatty lumps that develop due to continual use of the same injection site
26
type 2 diabetes pathophysiology
- associated with varying levels of insulin resistance and insulin deficiency
- obesity and high sugar intake is thought to contribute to insulin resistance
- insulin deficiency occurs due to the genetic susceptibility of individuals resulting in them failing to produce more insulin to overcome degree of resistance
- progression is associated with a static level of resistance but a progressive failure of insulin secretion, eventually resulting in production becoming non-existent
27
what is metabolic syndrome
type 2 diabetes with at least two of
* hypertension
* central obesity
* dyslipidaemia
* micro-albuminuria
28
type 2 diabetes presentation
- often asymptomatic
- fatigue, thirst, polyuria, weight loss
- symptoms of complications (blurred vision, peripheral neuropathy, ulcers, genital thrush, claudication, acute coronary syndrome)
29
type 2 diabetes symptomatic diagnosis
one raised fasting or OGTT result
30
type 2 diabetes asymptomatic diagnosis
two raised fasting or OGTT results
31
type 2 diabetes HbA1c aim
48-53
32
type 2 diabetes first line management
* diet
* exercise
* smoking cessation
33
type 2 diabetes second line management
medication
- 1st line medication is always metformin
- next drug chosen is tailored to individual
- when all other drug therapy is exhausted, insulin is commenced
- GLP-analogues and gliptins can be used as insulin delaying drugs
34
blood pressure target for uncomplicated type 1 diabetics
< 135/80
35
blood pressure target for uncomplicated diabetics
< 140/80
36
blood pressure target for coomplicated diabetics
< 130/75
37
first line blood pressure management for type 2 diabetics
ACE inhibitor with possible calcium channel blocker or diuretic if African American
38
what is type 3 diabetes
any form of diabetes that has an underlying cause
39
type 3 diabetes causes
- genetics: MODY
- drug side effects: steroids, anti-psychotics
- endocrine disorders: cushing’s acromegaly, pheochromocytoma
40
what is MODY
- maturity onset diabetes of the young
- monogenic, autosomal dominant form of diabetes that can present in neonates, teenagers and young adults
41
MODY presentation
- young onset
- strong family history
- normal body weight
- no auto-antibodies
- mild onset of symptoms over several months
- associated with renal cysts
- increased sensitivity and response to sulphonylureas
42
what is type 4 diabetes
gestational diabetes
43
insulin mechanism of action
direct replacement for endogenous insulin
44
metformin mechanism of action
increases insulin sensitivity and decreases hepatic gluconeogensis
45
sulphonylureas mechanism of action
stimulate pancreatic beta cells to secrete insulin
46
thiazolidinediones mechanism of action
activate PPAR gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake
47
DPP4 inhibitors (gliptins) mechanism of action
increases incretin levels which inhibit glucagon secretion
48
SGLT-2 inhibitors (gliflozins) mechanism of action
inhibitrs reabsorption of glucose in the proximal renal tubule
49
GLP-1 agonists (tides) mechanism of action
incretin mimetic which inhibits glucagon secretion
50
which diabetic drugs cause weight loss
* SGLT-2
* GLP-1
51
what is hypoglycaemia
blood sugar < 4 mmol
52
hypoglycaemia causes
- alcohol excess
- excess institution or oral hypoglycaemic
- acute illness (sepsis, liver failure)
- endocrine (adrenal failure, pituitary insufficiency, insulinoma)
- dumping syndrome (complication of bypass surgery)
53
hypoglycaemia sympathetic symptoms
- sweating
- anxiety
- hunger
- tremor
- nausea
- palpitations
- dizziness
54
hypoglycaemia neurological symptoms
- sweating
- anxiety
- hunger
- tremor
- nausea
- palpitations
- dizziness
55
hypoglycaemia diagnosis
- ABCDE
- finger prick glucose
- bloods (FBC, UE, LFT, glucose)
56
hypoglycaemia management if conscious, orientated and able to swallow
- 15-20g rapid acting glucose (4-5 glucose tablets, 90-120 ml Lucozade)
- recheck blood sugar after 10-15 minutes
- repeat up to 3 times
- if blood sugar is still under 4 call for help and consider IV glucose and 1 mg IM glucagon
57
hypoglycaemia management if conscious and able to swallow, but confused, disoriented or aggressive
- if capable and co-operative treat as per mild
if not capable/co-operative, then:
- 1.5-2 tubes glucogel
- recheck blood sugar after 10-15 minutes
- repeat up to 3 times
- if ineffective: 1 mg IM glucagon
- if deteriorating or blood sugar still under 4, consider IV therapy
58
hypoglycaemia management if unconscious, fitting or nil by mouth
- ABCDE
- stop any IV insulin
- start IV glucose over 10 minutes
- 75 ml 20% glucose
- - 150 ml 10% glucose
- recheck blood sugar after 10 minutes
- check for ketones if insulin stopped
- once blood sugar > 4, give 10% glucose infusion at 100 ml/hour and restart infusion
59
what is diabetic ketoacidosis
- state of insulin deficiency resulting in hyperglycaemia and dehydration
- associated with hyperglycaemia due to insulin deficiency and release of stress hormones such as adrenaline and cortisol trapping glucose within the blood
60
diabetic ketoacidosis biochemical markers
- hyperglycaemia
- ketonemia
- high anion gap acidosis
61
diabetic ketoacidosis causes
- drugs and alcohol
- undiagnosed type 1 diabetes
- non-compliance with insulin therapy
- acute illness (sepsis, MI, trauma, surgery)
62
diabetic ketoacidosis presentation
- symptoms take hours to develop
- increasing lethargy
- confusion
- abdominal pain and vomiting
- polyuria and polydipsia
- reduced GCS
- deep, sighing breathing
- sweet smelling breath
- dehydration (due to polydipsia and vomiting)
63
diabetic ketoacidosis diagnostic criteria
- glucose > 11 or bicarb < 15
- ketones > 3
- pH: acidosis (under 7.35)
- anion gap > 12
64
diabetic ketoacidosis management
- fluid resuscitation
- IV insulin (monitor potassium and replace as necessary if infusion rate of potassium > 20 mmol/hour)
- cardiac monitoring may be required
- monitor bicarbonate and pH
- continue infusion until stable (add in 10% dextrose once blood sugar under 14)
- assess for ICU based on severity of metabolic disturbance and shock
- long-acting insulin should be continued. short acting insulin should be stopped
65
what is lactic acidosis
reduction in pH due to build up of lactate in blood
66
lactic acidosis causes
- sepsis
- complication of diabetic ketoacidosis
- use of metformin in acute kidney injury
67
lactic acidosis presentation
* hyperventilation
* confusion
* stupor
* coma
68
lactic acidosis diagnosis
* bloods (lactate > 5, reduced phosphate)
* pH < 7.35
* reduced bicarb
* high anion gap
69
what is hyperglycaemia hyperosmolar syndrome (HONK)
- hyperglycaemia emergency seen in those with type 2 diabetes caused by a severe uncorrected hyperglycaemia that results in dehydration
- not associated with ketoacidosis due to there being some residual production of insulin, which prevents ketosis
70
HONK causes
- undiagnosed type 2 diabetes or poor compliance with medications
- acute illness (sepsis, pancreatitis, MI)
- drugs (steroids)
71
HONK presentation
- symptoms take days to weeks to develop
- increasing lethargy
- confusion
- abdominal pain and vomiting
- polyuria and polydipsia
- reduced GCS
- deep, sighing breathing
- sweet smelling breath
- dehydration (due to polydipsia and vomiting)
- more elderly patients
72
HONK diagnosis
- finger prick glucose
- bloods (FBC, UE, glucose, osmolality)
- blood sugar is usually sky high (> 35)
- osmolality > 340
73
HONK management
- start on insulin sliding scale
- monitor UE, glucose
- monitor for occlusive events such as stroke
74
lactic acidosis management
- fluid resuscitation
- bicarbonate infusion
- treat underlying cause
