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Aneesha Flashcards BRS 2 > Type 1&2 Diabetes Mellitus > Flashcards

Type 1&2 Diabetes Mellitus Flashcards

(102 cards)

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1
Q

what is type 1 diabetes?

A

autoimmune disease in which insulin producing beta cells in pancreas are attacked and destroyed by the immune system resulting in partial/complete deficiency of insulin and hyperglycemia
This resultant hyperglycemia requires lifelong insulin treatment

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2
Q

WHO 2019 Diabetes classifiction

A

Type 1 Diabetes
Type 2 Diabetes
Hybrid forms
Other
Unclassified
During pregnancy

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3
Q

Dichotonomy of type nd type 2 diabetes

A
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4
Q

what is the onset of type 1 diabetes?

A

thought to be childhood but adulthood becoming more common
Autoimmune diabetes leading to insulin deficiency can present later in life = latent autoimmune diabetes in adults

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5
Q

Stages of development of type 1 diabetes in relation to beta cell mass

A
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6
Q

what are the stages of development for type 1 diabetes?

A
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7
Q

what can constitute a precipitating event?

A

viral illness

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8
Q

what is immune infiltration in T1DM

A

immune cells infiltrate islet cells in T1DM

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9
Q

what is the importance of understanding T1DMs immune basis?

A

Increased prevalence of other autoimmune disease
Risk of autoimmunity in relatives
More complete destruction of B-cells
Auto antibodies can be useful clinically
Immune modulation offers the possibility of novel treatments
Not there yet

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10
Q

Brief overview of immunology of T1DM

A

Primary step is the presentation of auto-antigen to autoreactive CD4+ T lymphocytes
CD4+ cells activate CD8+ T lymphocytes
CD8+ cells travel to islets and lyse beta-cells expressing auto-antigen
Exacerbated by release of pro-inflammatory cytokines
Underpinned also, by defects in regulatory T-cells that fail to supress autoimmunity

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11
Q

Are all beta cells destroyed in T1DM?

A

NO
Some people with type 1 diabetes continue to produce small amounts of insulin ((some B cells evade immune system))
Not enough to negate the need for insulin therapy

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12
Q

Genetic susceptibility for T1DM

A

HLA is the biggest
risk modulater

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13
Q

what are some environmental risk factors of T1DM?

A

Multiple factors implicated, but causality has not been established

enteroviral infections
cows milk protein exposure
seasonal variation
changes in microbiota

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14
Q

what are some detectable pancreatic autoantibodies?
Are these needed for diagnosis?

A

Insulin antibodies (IAA)
Glutamic acid decarboxylase (GADA) – widespread neurotransmitter
Insulinoma-associated-2 autoantibodies (IA-2A)-Zinc-transporter 8 (ZnT8)
Not generally needed for diagnosis in most cases

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15
Q

what are the symptoms of T1DM?

A

polyuria
nocturia
polydypsia
blurring of vision
recurrent infections
weight loss
fatigue

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16
Q

what are the signs of T1DM?

A

dehydration
cachexia
hyperventilation
smell of ketones
glycosuria
ketonuria

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17
Q

what are the physiological effects of insulin deficiency? T1DM

A

proteinolysis (amino acids)
increased hepatic glucose output
lipolysis- ketogenesis, NEFA and glycerol

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18
Q

Involvement of insulin and glucagon in generation of ketone

A
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19
Q

what are the ketone bodies?

A

3-beta-hydroxybutyrate
acetoacetate
acetone

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20
Q

what are the treatment aims for T1DM?

A

maintain glucose levels
restore close to physiological profile of insulin
prevent acute metabolic decompensation
prevent microvascular and macrovascular complications

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21
Q

what are the complications of hyperglycaemia?
Complication of treatment

A

diabetic ketoacidosis (mostly T1DM)
microvascular - retinopathy, neuropathy, nephropathy
macrovascular - ischaemic heart disease, cerebrovascular disease, peripheral vascular disease

of treatment- hypoglycemia

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22
Q

what is the management of T1DM?

A

Insulin Treatment
Dietary support / structured educations
Technology
Transplantation

Type 1 diabetes is a condition that is ‘self-managed’

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23
Q

Physiological insulin profile

A
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24
Q

what are the types of insulin treatments?

A

short insulin (with meals)
background/basal insulin

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25
what are examples of short acting insulin?
human insulin - actrapid insulin analogues - lispro, aspart, glulisine
26
what are the types of basal insulin?
bound to zinc/protamine - neutral protamine hagedorn (NPH) insulin analogues - glargine, determir, degludec
27
what are the typical bolus regimes for insulin?
once daily long acting three times daily short acting OR twice daily intermediate acting insulin three times daily actrapid
28
what is insulin pump therapy?
Continuous delivery of short-acting insulin analogue e.g. novorapid via pump Delivery of insulin into subcutaneous space Programme the device to deliver fixed units / hour throughout the day (basal) ((useful if you do something like run a marathon- can adjust based on daily requirement)) Actively bolus for meals
29
what is the dietary advice for T1DM?
Dose adjustment for carbohydrate content of food. All people with type 1 diabetes should receive training for carbohydrate counting Where possible, substitute refined carbohydrate containing foods (sugary / high glycaemic index) with complex carbohydrates (starchy / low glycaemic index)
30
What is DAFNE
Structured Education Programme (all people with T1DM should be offered one) 5 day course on skills and training in self-management
31
what is a closed loop/artificial pancreas?
real time continuous glucose sensor detecting glucose with algorithm to calculate insulin requirement for that glucose level and delivers dose however lags around 15mins
32
what types of transplantation are available for T1DM?
islet cell transplants simultaneous pancreas and kidney transplants
33
What happens during islet cell transplants? Disadvantage of this?
Isolate human islets from pancreas of deceased donor Transplant into hepatic portal vein Requires life-long immunosuppression
34
Advantage and disadvantage of simultneous pancreas and kidney transplant
Better survival of pancreas graft when transplanted with kidneys Requires life-long immunosuppression
35
Aim of transplantation in treating T1DM Limitations
Aim: try to restore physiological insulin production to the extent that insulin can be stopped Even if incomplete, often results in better control Limitations: availability of donors, complications of life-long immunosuppression
36
how can glucose be monitored?
capillary finger prick blood glucose monitoring continuous glucose monitoring
37
what is HbA1c?
reflects last 3 months of glycaemia Biased to the 30 days preceding measurement Glycated NOT glycosylated -enzymatic so linear relationship irreversible
38
What are the limitations of HbA1c?
Affected by red cell turnover, only can be done by 3 months
39
What is used to guide insulin doses?
Using self-monitoring of blood glucose results at home and HbA1c results every 3-4 months Based on results, increase or decrease insulin doses
40
Acute complications of T1DM
Diabetic ketoacidosis Uncontrolled hyperglycemia Hypoglycemia
41
Diabetic ketoacidosis is often a presenting feature of new-onset type 1 diabetes but can occur in those with established T1DM- in what situation would this occur?
Acute illness Missed insulin doses Inadequate insulin doses
42
Does diabetic ketoacidosis only occur in T1DM?
Can occur in any type of diabetes ((TYPE 2 ALSO SOMETIMES)) Commonly in T1 though
43
What is diabetic ketoacidosis?
Acute life threatening complication of t1DM pH less than 7.3, ketones increased (urine or capillary blood), HCO3- less than15 mmol/L and glucose >11 mmol/L
44
Numerical definition of hypoglycemia What is severe hypoglycemia?
below 3.6 mmol/L Severe hypoglycaemia: any event requiring 3rd party assistance
45
when does hypoglycaemia on insulin therapy become problematic?
excessive frequency impaired awareness (unable to detect low glucose) nocturnal hypoglycaemia recurrent severe hypoglycaemia
46
what are the risks of hypoglycaemia?
seizure/coma/death impacts on: emotional wellbeing driving day to day function cognition
47
what are the risk factors for hypoglycaemia with t1dm?
exercise missed meals inappropriate insulin regime alcohol intake lower HbA1c lack of training dose-adjustment around meals
48
how can problematic hypoglycaemia be supported?
insulin pump therapy different insulin analogues revisit carb counting/education behavioural psychology support transplantation
49
what are the treatments for hypoglycaemia but alert and oriented?
oral carbohydrates juice/sweets - fast acting sandwich - slow acting
50
what are the treatments for hypoglycaemia but drowsy/confused but swallowing intact?
buccal glucose e.g glucogel/hypostop complex carbohydrate
51
what are the treatments for hypoglycaemia when unconscious/concerned about swallowing?
IV access 20% glucose IV
52
what should you consider for a deteriorating / refractory /insulin induced /difficult IV access patient with hypoglycemia?
IM/SC 1mg glucagon
53
what is type 2 diabetes?
a condition in which beta cell failure and insulin resistance result in hyperglycaemia Associated with obesity but not always The resultant chronic hyperglycaemia may initially be managed by changes to diet / weight loss and may even be reversible With time glucose lowering therapy including insulin, is needed
54
How can monogenic diabetes (MODY, mitochondrial diabetes) present?
As T1 or T2DM
55
Can diabetes present following pancreatic damage or other endocrine disease
Yes
56
what is the epidemiology and trend of T2DM?
increasing prevalance increasing in younger adults greatest in ethnic groups moving from rural to urban lifestyles
57
what are normal fasting glucose levels?
less than/ equal to 6mmol/L
58
what are normal 2hr glucose levels? (OGTT)
less than 7.7mmol/L
59
what is normal HbA1c?
less than 42mmol/L
60
how can random glucose readings confirm T2DM diagnosis?
above 11.1mmol/L WHEN SHOWING SYMPTOMS
61
what fasting glucose levels indicate T2DM?
above/equal to 7mmol/L
62
what 2hr glucose levels (OGTT) indicate T2DM?
above/ equal to 11mmol/L
63
what HbA1c indicates T2DM?
over/equal to 48mmol/mol
64
what does a fasting glucose of between 6-7mmol/L indicate?
impaired fasting glycaemia
65
what does a 2hr glucose OGTT reading between 7.7-11mmol/L indicate?
impaired glucose tolerance
66
what does an HbA1c of between 42-48mmol/L indicate?
prediabetes or non diabetic hyperglycaemia
67
how do insulin levels change over the course of developning T2DM?
normal for normal people intermediate stage - production increases to compensate as resistance is increasing full blown T2DM - insulin production much reduced and body is maximally insulin resistant
68
how does insulin production differ in T1 and T2DM?
T1 - no/little production of insulin due to cell death T2- insulin still produced by beta cells but tissues are resistant, therefore a relative insulin deficiency (not enough produced to overcome resistance)
69
Beta-cell function at diagnosis of T2DM
70
what is known about the pathophysiology of T2DM?
Genes and intrauterine environment and adult environment. Insulin resistance and insulin secretion defects Fatty acids important in pathogenesis and complications HETEROGENOUS People develop T2D at variable BMI, ages and progress differently
71
Why does hyperglycemia in T2DM not usually lead to ketosis?
Insulin is produced by pancreatic beta-cells but not enough to overcome insulin resistance There is therefore a relative deficiency of insulin However it is enough to suppress ketone body formation
72
What happens to insulin production in long duration type 2 diabetes What should we do then
In long-duration type 2 diabetes, beta-cell failure may progress to complete insulin deficiency Usually on insulin at this point in any case, but important not to stop as at risk of ketoacidosis
73
how do glucose clamp tests differ between impaired glucose tolerance and T2DM in terms of insulin release?
IGT - blunted response to glucose T2DM- no response to glucose, first phase of insulin response lost (first phase insulin release is lost)
74
Doesglucose just come from diet in T2DM?
No In type 2 diabetes, reduced insulin action causes less uptake of glucose into skeletal muscle Hepatic glucose production is also increased due to both a reduction in insulin action and increase in glucagon action
75
what are the physiological consequences of insulin resistance?
increased hepatic glucose output Excess of inflammatory adipocytokines increased fatty acid uptake from gut by adipocytes, increased triglycerides and unhealthy lipids in muscle less glucose uptake
76
Relationship between insulin resistance and insulin secretion in people with T2DM
77
Genetics of diabetes- monogenic vs polygenic
Monogenic- Single gene mutation ==> Diabetes (MODY) ‘Born with it, always going to develop diabetes’ Polygenic- Polymorphisms increasing risk of diabetes ‘Not born with it but high risk and may develop later depending on other factors’
78
what have GWAS shown for T2DM?
each individual SNP has only mild effect on risk cumulative SNPs have greater effect
79
what is the role of obesity in T2DM?
Major risk factor for T2DM Fatty acids and adipocytokines important Central vs visceral obesity- visceral higher risk 80% T2DM are obese Weight reduction useful treatment
80
T2DM associations other than obesity
Perturbations in gut microbiota Intra-uterine growth retrdation
81
what is the presentation of T2DM like?
Hyperglycaemia Overweight Dyslipidaemia Fewer osmotic symptoms With complications Insulin resistance Later insulin deficiency
82
what are the main risk factors for T2DM?
age high BMI PCOS ethnicity family history inactivity
83
what is first line diagnostic test for T2DM?
HbA1c - above 48mmol/L either with symptoms or twice above 48 with no symptoms
84
Diagnosis of type 2 diabetes- how does this occur
Osmotic symptoms Infections Screening test: incidental finding at presentation of complication Acute; hyperosmolar hyperglycaemic state, Chronic; ischaemic heart disease, retinopathy
85
what is hyperosmolar hyperglycaemic state?
Presents commonly with renal failure. Insufficient insulin (NOT ABSENT) for prevention of hyperglycemia but sufficient insulin for suppression of lipolysis and ketogenesis. Absence of significant acidosis. Often identifiable precipitating event (infection, MI). unchecked gluconeogenesis leads to hyperglycemia and osmotic diuresis to dehydration
86
what is the management for T2DM?
Diet Oral medication Structured education May need insulin later Remission / reversal
87
what makes up a typical T2DM consultation?
Glycaemia: HbA1c, glucose monitoring if on insulin, medication review Weight assessment Blood pressure Dyslipidaemia: cholesterol profile Screening for complications: foot check, retinal screening
88
what are the dietary recommendations for someone with T2DM?
Healthy eating or diet Total calories control Reduce calories as fat Reduce calories as refined carbohydrate Increase calories as complex carbohydrate Increase soluble fibre Decrease sodium
89
Drug treatments for type 2 diabetes
90
what is metformin?
biguanide - insulin sensitiser first line treatment if lifestyle hasnt made diff reduces insulin resistance, reduces hepatic glucose output, increased peripheral glucose disposal has GI side effects contraindicated in severe liver, severe cardiac or moderate renal failure
91
what are sulphonylureas?
glicazide bind to ATP K+ channel on pancreatic b cells and close it, independent of glucose - causes insulin production helps insulin release, increase insulin production
92
what is pioglitazone?
Peroxisome proliferator-actived receptor agonists PPAR-γ Pioglitazone Insulin sensitizer, mainly peripheral Adipocyte differentiation modified, weight gain but peripheral not central Improvement in glycaemia and lipids Evidence base on vascular outcomes Side effects of older types hepatitis, heart failure
93
which diabetes drug increases weight gain the most?
thiozolidinediones - TZDs
94
what is the role of GLP-1 in T2DM?
Gut hormone Secreted in response to nutrients in gut Transcription product of pro-glucagon gene, mostly from L-cell Stimulates insulin, suppresses glucagon ↑ satiety (feeling of ‘fullness’)
95
Why does GLP-1 have a short half life
Due to rapid degradation from enzyme dipeptidyl peptidase-4 (DPP4 inhibitor)
96
What is the gastrointestinal incretin effect
97
what are GLP-1 agonists? How are they administered? Effects?
Liraglutide, Semaglutide Injectable –daily, weekly Decrease [glucagon] Decrease [glucose] Weight loss
98
what are DPPG-4 inhibitors? Example
Increase half life of exogenous GLP-1 Increase [GLP-1] Decrease [glucagon] Decrease [glucose] Neutral on weight Gliptins
99
what are SGLT-2 inhibitors?
Empagliflozin, dapagliflozin, canagliflozin inhibits Na-glu transporter in kidney increases excretion of glucose in urine lowers HbA1c Lowers all cause mortality, risk of hear failure and improves CKD
100
What does the DIRECTstudy/ DROPLET study show?
very low-calorie diet (800 kcal/day) for 3-6 months has the potential to induce remission in T2DM, which appears to be sustained at 2 years
101
Other than glucose lowering, what aspects of T2DM management are important
Blood Pressure management Hypertension very common in T2DM Clear benefits for reduction esp with use of ACE-inhibitors Lipid management Total cholesterol raised Triglycerides raised HDL cholesterol reduced!!!!!!!!!!! Clear benefit to lipid-lowering therapy
102
how can remission of T2DM be encouraged non medically?
surgery - gastric bypass (roux en y)

Aneesha Flashcards BRS 2 (47 decks)

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