Brainscape's Knowledge GenomeTM

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


See full index

Med 2 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is the relevant epidemiology of diabetes?

A

4.4 million in the UK
Estimated 1.2million undiagnosed type 2
People of Asian and Black Caribbean descent are 2-4x more likely to have diabetes compared to white populations
90% type 2
8% type 1
2% other forms

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

What is the epidemiology/genetics of type 1 DM?

A

Usually diagnosed in childhood
Peak around puberty
Worldwide incidence increasing
10-15% affected 1st degree relative
36% concordance in MZ twins
Lower genetic link than type 2 DM

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

What is the relevant epidemiology and genetics of Type 2 diabets?

A

Risk: Age, obesity, FH, ethnicity, sedentary lifestyle, low socio-economic status
Increasing prevalence in under 40s in the UK
40% lifetime risk with 1st degree relative
60-100% concordance in MZ twins
Stronger genetic link than T1

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

What is the ideal blood glucose range?

A

4.4 to 6.1 mmol/L

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

Where is insulin produced?

A

Beta cells
Islets of langerhans in the pancreas

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

What is the role of insulin?

A

Anabolic hormone - reduce blood glucose
Cells in the body absorb glucose from blood
Muscles and liver absorb glucose from the blood and store it as glycogen (glycogenesis)

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

Where is glucagon produced?

A

By alpha cells in the islets of Langerhans in the pancreas

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

What is the role of glucagon?

A

Catabolic -> increase blood glucose
Liver -> glycogenolysis
Liver -> gluconeogenesis -> protein and fats into glucose

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

What is the key pathophysiology of T1DM?

A

Autoimmune destruction of beta cells in the islets of Langerhans in the pancreas
No longer able to produce adequate insulin
T cell-mediated response

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

What is the key presentation of T1DM?

A

4Ts
Toilet - frequent urination
Thirsty -
Tired
Thinner - weight loss

May also present with diabetic ketoacidosis

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

At what blood glucose levels can type 1 DM be diagnosed?

A

Must also have clinical suspicion
Random >=11.1mmol/L
Fasting >=7.0mmol/L
OGTT >=11.1mmol/L

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

What autoantibodies may be tested for in DM type 1?

A

Anti-GAD
Anti-islet cell
Anti-insulin

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

How does serum C peptide relate to insulin?

A

Connects alpha and beta chains of pro-insulin
Reflects levels of insulin
Not routinely measured
Longer half life than insulin

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

What are the different aspects of managing T1DM?

A

Blood glucose monitoring
Subcutaneous insulin
Monitoring dietary carbohydrate intake and ‘carb counting’
Monitoring for complications, both short term and long term.
Patient/carer education
Support and individualised care
Physical activity
Hypoglycemia awareness and management
DKA awareness and ketone monitoring
Optimisation of cardiovascular risk
DVLA /occupational implications

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

What are the main methods that diabetics monitor their blood glucose?

A

BM machines - capillary blood glucose
Continuous glucose monitors - conc in interstitial fluid

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

Who manages the insulin prescription in a MDT for diabetics?

A

A diabetic specialist nurse

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

What are the different types of insulin available?

A

Rapid-acting - ActRapid
Short acting - NovoRapid
Intermediate acting - Humulin 1
Long-acting - Levemir and Lantus

Can be given as combination with rapid and intermediate insulin
Humalog 25
Humalog 50
Novomix 30

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

Why might diabetics need to contact the DVLA?

A

When on insulin therapy - risk of Hypos
Needs assessment and medical risk evaluation

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

What are the three characteristics of insulin?

A

Onset - lenght of time before reaches bloodstream and stars to lower blood glucose
Peak time - insulin at maximum activity
Duration - how long continues to lower blood glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Compare the peak and duration of different types of insulin

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

What is the once daily regime of insulin?

A

Long or intermediate acting insulin given at bedtime
Suitable in T2 - combined with oral hypoglycemic drugs
Used if dependent on others for injection

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

What is the twice daily insulin regime?

A

Biphasic insulin - before breakfast/evening meals
Assumes three meals a day
Peak action varies with solubility of insulin
Difficult to get glycemic control - risk of hypos

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

What is the basal bolus insulin regmie?

A

Long acting insulin at bed for overnight requirements
Combined with rapid/short acting for meals
Most common regime
May suffer hypos between meals and at nigh

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

Why must the insulin injection site be rotated?

A

Lipodystrophy - subcuntaneous fat hardens if repeated injected
Prevents insulin absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Breifly describe how continuous sub-cut insulin infusions work?

A

Canula - subcut injection (must be rotated 2-3days)
Pump of rapid acting insulin - continuous low dose (mimic long acting insulin), larger doses bolused for mealtimes and hyperglycemia
Must have back up prescription of insulin pens just in case

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the pros/cons of a continuous sub-cut insulin infusion?

A

+ better glycaemic control
+ inc flexibility
+ fewer injections

  • technical difficulties (must have back up prescription of insulin pens)
  • wearing a device
  • blockages in the line
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is a closed loop system for insulin control for diabetics?

A

Continous blood glucose monitoring measures glucose and sends signal to glucose pump (Bluetooth)
Glucose control algorithm automatically determines insulin dose
Insulin pump delivers dose
This reduced hypos however may still need to carb count for meals/snacks and adjust for exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How can a pancreas transplant be used to treat T1DM?

A

Donor pancreas produce insulin
Host pancreas remain insitu to produce digestive enzymes
Risky and requires life long immunosuppression
Reserved for patients with severe hypos and having kidney transplants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How is an islet transplant used to treat T1DM?

A

Inserting donor islet cells into liver to produce insulin
Patients still often require insulin therapy after this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the relevant pathophysiology of T2DM?

A

Combination of peripheral insulin resistance and relative secretory failure
Hyperglycemia has secondary affect on liver -> glycogenolysis -> further raises levels
Progressive decline in B cell function - B cell apoptosis - often have 50% function remaining at diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is metabolic syndrome?

A

A group of condition that often occur together and increase your risk of heart disease, T2DM and stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What conditions are included within metabolic syndrome?

A

Increase BP (130/85)
High triglycerides
Large waistline (central obesity)
Low HDL cholesterol
Elevated fasting blood sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the sub-acute presentation of T2DM?

A

Excessive tiredness
Polyuria
Excessive thirst
Unintended weight loss
Many are asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the late established complications of T2DM?

A

Diabetic retinopathy
Polyneuropathy
Erectile dysfunction
Arterial disease
Susceptible to infections e.g thrush
Slow healing skin wounds
Acanthosis nigricans (signs of insulin resistance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the reliance on blood glucose for diagnosis of T2DM?

A

Symptomatic and single abnormal blood glucose - can diagnose but should repeat the test
Asymptomatic - do not diagnose based on a single result, repeat the test in one month

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What can cause transient hyperglycemia?

A

Acute infection
Trauma
Circulatory stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the different diagnostic ranges for HbA1c?

A

In mmol/mol
>=48 is T2DM
42-47 pre-diabetes
<42 is normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the diagnostic range for fasting plasma glucose?

A

mmol/L
>7.o is T2DM
6.1-6.9 is Pre-diabetes
<= 6.o is normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the diagnostic range of random plasma glucose?

A

mmol/L
>=11.1 T2DM
7.8 to 11.0 is pre-diabetes
<7.8 is normal

40
Q

What is the HbA1c?

A

Glycated haemoglobin - made when glucose sticks to red blood cells
Average blood glucose levels for the last 2-3 months

41
Q

When should HbA1c not be used as a test?

A

Children <18yrs
Pregnant or <2months post partum
People with symptoms for <2months or acutely unwell
Taking medications that cause hypers e.g steroids
Acute pancreatic damage or end stage renal disease
People with HIV infection or rbc turnover/Hb type

42
Q

How often is HbA1c measured in adults with T2DM?

A

A. 3-6months until stable on unchanging therapy
B. 6 months once stable

43
Q

What is the target HbA1c for diabetics?

A

48mmol/mol if manafed by lifestyle/diet/single drug not associated with hypos

53mmol/mol is drug associated with hypos

44
Q

What HbA1c level is concerning in Diabetics and what changes are made?

A

> 58mmol/mol
reinforce lifestyle advice
Discuss drug compliance
Intensify drug treatment

45
Q

What management plan for T2DM include?

A

Structured education program
Low glycaemic index, high fibre diet
Exercise and weight loss (if overweight)
Anti-hyperglycaemic drugs
Monitoring and managing complications

46
Q

What is the first line medical management for T2DM?

A

Metformin

47
Q

How does metformin benefit diabetics?

A

A biguanide medication
increases insulin sensitivity and decrease glucose production by the liver
Note acts only in the presence of endogenous insulin so some functioning beta cells must remain

48
Q

What is the relevant side effect profile of metformin?

A

Gastrointestinal upset (can reduce by trying modified release metformin)
Lactic acidosis (secondary to AKI)

DOES NOT cause weight gain or hypos

49
Q

What is the second line treatment for T2DM?

A

Already on metformin
Add a sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor

50
Q

Example SGLT2 inhibitors

A

(gliflozin)
Dapagliflozin, empagliflozin

51
Q

What is the basic mechanism of action of SGLT2 inhibitors in diabetics?

A

Block SGLT-2 in proximal tubule of the kidney = more glucose excreted in urine
Causes weight loss and reduce BP to lower cardiovascular risk

Also used in HF and CKD
Used alongside metformin as first line if high risk CVD

52
Q

What are the side effects of SGLT2 inhibitors for treating T2DM?

A

Glycosuria
Increased urine output
Gential/UTI
Fourniers gangrene
Weight loss
Euglycaemic ketoacidosis

53
Q

What is an example of a thiazolidinediones?
How do they treat T2DM?

A

(glitazone) Pioglitazone
Increase insulin sensitivity and decrease liver production of glucose

54
Q

What is the side effect profile of thiazolidenodiones?

A

Weight gain
Heart failure
Increased risk of bone fracture
Small increased risk of bladder cancer

55
Q

What is sulfonylureas example?
How does it treat T2DM?

A

Gliclazide
Stimulate insulin release from the pancreas

56
Q

What is the side effect profile of sulfonylureas/gliclazide?

A

Weight gain
Hypoglycaemia

57
Q

How do DPP-4 inhibitors (gliptin) treat T2DM?

A

DPP-4 inhibits incretins (produced after large meal)
Incretins - increase insulin, inhibit glucagon and slow absorption from GI -> this would decreased blood glucose
DPP-4 inhibitors -> lead to unopposed incretins action

Examples = sitagliptin, algoliptin

58
Q

What is the side effect profile of DPP_4 inhibitors? (sitagliptin, alogliptin)

A

Headaches
Acute pancreatitis

59
Q

How do GLP-1 mimetics treat T2DM?

A

GLP-1 is a type of incretin
Released after a large meal
Decreases blood glucose by stimulating insulin secretion, inhibiting glucagon production and slowing absorption by the GI tract
Mimetics also cause this effect
Given as a subcut injection

Examples = semaglutide, liraglutide

60
Q

What is the side effect profile for GLP-1 mimetics?

A

Reduced appetite
Weight loss
Gastro-intestinal upset

61
Q

What is the third line treatment for T2DM?

A

Triple therapy - metformin + two others
If triple therapy fails and BMI >35kg/m2 add a GLP-1 mimetic
Insulin therapy

62
Q

What other medications (not directly for blood glucose) might a T2DM receive?

A

ACEi - for HTN control
Statins - lipid-lowering drugs
Treatment of specific complications - retinopathy, neuropathy

63
Q

What influences the chance of complications from diabetes?

A

Duration and degree of hyperglycaemia
Compliance with extensive screening programmes - eye screening, podiatry, annual diabetes reviews, routine bloods.

64
Q

What are the macrovascular complications of diabetes?

A

Coronary artery disease
Peripheral ischaemia
Diabetic foot ulcers
Stroke
HTN

65
Q

What are the microvascular complications of DM?

A

Peripheral neuropathy
Diabetic retinopathy
Kidney disease (glomerulosclerosis)

66
Q

What are some other complications of DM?

A

Depression
Infection risk
Lipohypertrophy

67
Q

In a healthy person how is glucose handled by the kidneys?

A

Produce 20-25% of total endogenous glucose
All filtered glucose is re-absorbed into the blood by SGLT2/1

68
Q

How is glucose reabsorbed in the kidenys?

A

SGLT2 - proximal tubules - 90% - high capacity low sensitivity
SGLT1 - further along proximal tubule - 10% - low capacity - high sensitivity

69
Q

What enzyme is important for endogenous glucose production?
Where is it found?

A

Glucose-6-phosphatase enzyme
Liver, cortex of kidney, intestinal epithelium

70
Q

What is the relationship between the kidney and insulin?

A

25% daily insulin from pancrease is cleared by kidneys
Increased insulin - suppress gluconeogenesis in the kidney and enhance glucose re-uptake

71
Q

How does hyperglycaemia drive diabetic nephropathy?

A
  1. activates protein Kinase C and growth factors leading to tubulointerstitial injury
  2. Accelerates RAAS -> HTN -> Glomerular damage
  3. AGEs form -> overproduction of mesnagial cell matrix -> glomerular damage
    All lead to nephron loss and proteinuria.
72
Q

How does HTN cause diabetic nephropathy?

A
  1. intraglomerular HTN
  2. Glomerulosclerosis
  3. Reduce funcationing glomeruli = decline in renal function
  4. Increased blood flow to remaining neprhons
    Process repeats
73
Q

How does obesity drive diabetic nephropathy?

A

A. Inc risk of HTN = CKD
B. Increased insulin resistance/visceral adiposity -> (point c) and altered adipokines -> CKD
C. glomerular hyperfiltration and hypoperfusion -> glomerular hypertrophy and proteinuria -> CKD D. CDK = glomerulosclerosis and end stage kidney disease

74
Q

How is chronic kideny disease diagnosed in adults?

A
  1. Estimate GFR using CKD-EPI creatine equation, urine dip for proteinuria and measure ACR is risk factor present
  2. eGFR annually is taking medication that affect kidney
  3. If below 60 repeat eGFR within two weeks - treat as AKI and test for haematuria
  4. If still <60 repeat after 3months diagnose CKD is ACR >3mg/mmol or eGFR<60
75
Q

What blood glucose is considered hypoglycaemia?
What is meant by severe hypoglycaemia?

A

4.0
Severe - when requires help from another person

76
Q

What are the signs of hypoglycaemia?

A

Asymptomatic
Sweating
Trembling
Feeling of hunger
Anxiety
Poor concentration
Palpitations
Tingling of lips
Pale
Vague/confusion
Convulsions
Coma

77
Q

How should hypolgycaemia be treated?

A

IV insulin should be stopped
Mild - fast acting carbs (dextrose tables or glucojuice)
Moderate - disorientated or aggressive -glucose gel
Both - retest in 10mins - repeat above up to 3 times
If BM above 4 give long acting carb

Severe = NBM or less than 2.6mmols/L
Check ABCDE, secure IV access - 100ml 20% glucose over 10-15mins, recheck after 10mins

78
Q

How do most children with unknown T1DM tend to present?

A

In diabetic ketoacidosis

79
Q

What is the process of ketogenesis?

A

Insufficient glucose and glycogen e.g prolonged fasting, low carb diets
Liver converts fatty acids to ketones
Ketons are soluble fatty acids than can be used as fuel and cross the BBB
Not harmful in healthy individuals

80
Q

How can ketone levels be measured?

A

Urine dipstick
Blood ketone meter

81
Q

What is the mechanism behind DKA?

A
  1. Cells in body have no fuel as unable to process glucose due to insulin resistance (despite hyperglycaemia).
  2. Ketogenesis initiated for fool
  3. Bicarb is produced by kidenys to buffer ketone acids in blood.
  4. Bicarb runs out - blood becomes acidic - ketoacidosis
82
Q

What is the mechanism behdin dehydration in DM?

A
  1. Hyperglycemia - not all glucose reabsorbed in kidney -. glucosuria
  2. Osmotic diuresis
    3 Polyuria, severe dehydration and polydispsia
83
Q

How does DM lead to potassium imbalance?

A
  1. Insulin drives potassium into cells - does not happen as insulin resistance
  2. Some potassium excreted in urine
  3. Total body potassium is low because not potassium is stored in cells
  4. Insulin can trigger severe hypokalemia, leading to data arrhythmias.
84
Q

How does DKA present?

A

Signs of dehydration, potassium imbalance and acidosis

Polyuria and polydipsia
Nausea and vomiting
Weight loss
Pear drop breath
Dehydration and subsequent hypotension
Symptoms underlying trigger e.g infection

85
Q

What is the triad for DKA diagnosis?

A

Ketonaemia - blood >3.0mmol/L, ketonuria 2+
Acidosis pH<7.3 or bicard <15mmol/L
Hyperglycaemia - BM >11.0mmol/L

86
Q

How is DKA managed?

A

Fluid resuscitation
Followed by IV insulin infusion - take up potassium, glucose and stop producing ketones
Long acting insulin if taken should be continued
Treat underlying trigger for infections

87
Q

What is the link between DKA and cerebral oedema?

A

High risk in children
Hyperglycaemia and dehydration cause water to move from intra to extracellular space -> brain cells shrink due to dehydration
Rapid correction causes rapid shift back into intracellular space
Brain becomes oedematous -> brain cell destruction/death

88
Q

What are the signs of cerebral oedema in DKA?

A

GCS decline
Headache
Altered behaviour
Bradycardia

89
Q

How should cerebral oedema due to childhood DKA be managed?

A

Senior paediatrician
Slowing rate of IV fluids and administering IV mannitol and IV hypertonic saline

90
Q

What is hyperglycaemic hyperosmolar state (HHS)?

A

Rare but potentially fatal complication of T2DM.
Characterised by hyperosmolarity, hyperglycaemia and absence of ketones

91
Q

How does hyperglycaemic hyperosmlar state present?

A

Polyuria and dehydration
Polydyspia
Weight loss
Tachycardia and hypotension
Confusion

92
Q

What is the treatment for hyperglycaemic hyperosmolar state?

A

IV fluids and careful monitoring

93
Q

What is gestational diabetes?

A

Diabetes triggered by pregnancy - resolves after birth
Caused by reduced insulin sensitivity
Anyone with risk factors should be screened with an OGTT

94
Q

What are the complications of gestational diabetes?

A

Large foetus
Macrosomia (higher risk of should dystocia)
Women remain at higher risk of T2DM in the long term

95
Q

What is the treatment regarding pre-existing diabetes in pregnant women?

A

Pre-conception - optimise glycaemic control - folic acid 5mg until 12w gestation
Oral medications should be stopped
Retinopathy screening after booking and at 28w
NICE planned delivery 37-38+6 weeks
Sliding scale insulin and dextrose infusion is considered during labour

96
Q

What is the post-natal care for diabetes during pregnancy?

A

If gestational - stop all medication immediately after birth
Pre-existing - lower insulin doses and be wary of hypoglycaemia
Babies need close monitoring for neonatal hypoglycaemia

97
Q
A

Med 2 (4 decks)

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