Brainscape's Knowledge GenomeTM

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


See full index

semester 4 - CPT & Prescribing > 9. Diabetes mellitus > Flashcards

9. Diabetes mellitus Flashcards

You may prefer our related Brainscape-certified flashcards:
NASM ® CPT flashcards
1
Q

What increases secretion of insulin?

A
  • ↑glucose
  • incretins (GLP-1, GIP)
  • glucagon
  • parasympathetic activity (M3)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What decreases secretion of insulin?

A
  • ↓glucose
  • cortisol
  • sympathetic activity (α2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the role of insulin?

A
  • ↓hepatic glucose output via inhibition of gluconeogenesis
  • Inhibits glycogenolysis
  • Promotes uptake of fats
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe insulin regulation

A
  • Secreted into blood even during fasting – prevents receptor downregulation
  • Rate and extent of [glucose] change leads to biphasic pattern of insulin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the symptoms of diabetes?

A
  • polyuria – waking in the night is common
  • polydipsia
  • weight loss
  • fatigue/lethargy
  • generalised weakness
  • blurred vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is diagnosis of diabetes made?

A
  • Hyperglycaemia – fasting glucose ≥ 6.9 mmol/L or random plasma glucose ≥ 11 mmol/L
  • Plasma or urine ketones in presence of hyperglycaemia
  • HbA1c ≥ 48 mmol/mol (≥6.5%)
  • Single raised plasma glucose without symptoms not sufficient for diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Glucose vs HbA1c

A

• Glucose – immediate measure of glucose levels in blood mmol/L (mg/dL – USA)
• HbA1c – haemoglobin A1c – glycated haemoglobin - percentage of red blood cells with “sugar
coating” – reflects average blood sugar over last 10-12 weeks – mmol/mol or %

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

What are the risk factors for type 2 diabetes?

A
  • Obesity - 80-85% of risk
  • Family history
  • Ethnicity
  • Diet
  • Drugs - thiazides/thiazide-like, glucocorticoids and β-blocker
  • Low birth weight?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

WHat is the triad with DKA?

A

Hyperglycaemia, Acidosis, Ketonaemia

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

When might you suspect DKA?

A

*blood glucose >11 mmol/L AND…..
polydypsia, polyuria, abdominal pain, V+D, lethargy, confusion, visual disturbance, acetonic breadth, symptoms of shock

*Hyperglycaemia may not always be present

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

what are precipitating factors of DKA?

A

infection, trauma, non adherence to insulin treatment, DDIs

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

what should be tested for in DKA?

A

Test for ketones – urine and or blood

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

What is the priority when treating DKA?

A

i.v.i. fluids (with K+) and then i.v.i. soluble insulin

initial SBP and [K+] dictate precise treatment regimen

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

How must insulin be given and why?

A

Must be given parenterally to avoid digestion in the gut - as it is a protein

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

where is insulin usually obtained from?

A
  • Historically bovine and porcine

* now Human insulin - recombinant DNA (bacteria/yeast) or enzymatic modification of porcine

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

How is insulin usually formulated?

A

Usually formulated in 100 units/mL
obesity and insulin resistance
300 and 500 units/mL available to reduce volume

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

How is insulin usually administered?

A
  • Routine delivery by s.c. injection upper arms, thighs, buttocks, abdomen
  • i.v.i. for emergency treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the half life of insulin and where is it metabolised and eliminated?

A

t1/2 - ~ 5 minutes in plasma - renal and hepatic metabolism and elimination

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

what are ways in which insulin preparations can be made to slow absorption?

A
  • Protamine and/or zinc complex with natural (bovine/porcine) insulins – used less now
  • Soluble (neutral) insulin forms hexamers – delaying absorption from site of injection [plasma] greatest after 2-3 hr – dosing 15-30 min prior to meals often prescribed
  • Insulin analogues – recombinant modifications – a few amino acid changes – changes PK not PD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why is it important to rotate site of administration?

A

Avoid lipodystrophy

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

Give an example of rapid acting insulin.

A

Insulin aspart

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

Give examples of short acting insulin.

A

Soluble insulin - Humulin S, Actrapid

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

Give an example of intermediate acting insulin.

A

Isophane insulin (NPH)

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

Give an example of long acting insulin.

A

Insulin glargine

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

What is basal-bolus dosing?

A

Using rapid acting and long acting insulin to mimic normal levels of insulin
e.g. glargine BID (basal), aspart before meals (bolus)

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

what are ways in which insulin can be administered?

A

Syringes, pens, pumps, (inhalers?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are adverse effects of insulin?

A

hypoglycaemia, lipodystrophy – lipohypertrophy or lipoatrophy

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

what are warnings, contraindications of insulin?

A

Renal impairment - hypoglycaemia risk

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

what are important drug interactions of insulin?

A

dose needs increasing with systemic steroids caution with other hypoglycaemic agents

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

what are Emerging therapeutics for diabetes?

A
  • Immunotherapy – monoclonal antibodies for high risk groups – delay progression
  • Islet transplantation?
  • Islet cell regeneration?
  • Inhaled insulin – pharmaceutical challenge but for fast acting pre meal, doing challenges and problems for asthma and COPD patients
  • SGLT-2 inhibitors – TI and TII DM and other possibly cardiovascular diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what happens in type 2 diabetes?

A

• Insulin into cells reduced due to cellular resistance associated with obesity
• Insulin resistance initially overcome by increased pancreatic insulin secretion but…
↓insulin receptors – ↓GLP-1 secretion in response to oral glucose and response reduced at β- cells and eventually insulin production reduced

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

How is the blood sugar rise different in type 1 and 2 diabetes?

A

• Blood sugar rise typically slower than TIDM so variable symptoms – often diagnosed through midlife “MOT”

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

what are non pharmacological treatments for type 2 diabetes?

A 
• Lifestyle!!!, education
Weight loss (surgery in more and more instances)
34
Q

is insulin given to patients with type 2 diabetes?

A
  • Initially non-insulin therapies
  • Insulin may form part of treatment plan in poorly managed or later stage disease
  • Treat comorbidities – part of overall reduction in cardiovascular risk
35
Q

What are the different drugs used in treatment of type 2 diabetes? (6)

A
  • biguanides (e.g. metformin)
  • sulfonylureas (e.g. gliclazide)
  • thiazolidinedione(glitazones)
  • SGLT-2 inhibitors
  • DPP4 inhibitors
  • GLP1 agonists
36
Q

How do Biguanides work?

A
  • ↓hepatic glucose production by inhibiting gluconeogenesis

* Supress appetite so limit weight gain

37
Q

does biguanides have a risk of hypoglycaemia?

A

ome gluconegenic activity remains so hypoglycaemia risk reduced

38
Q

adverse effects of biguanides?

A

GI upset – nausea, vomiting, diarrhoea

39
Q

warnings, contraindications of biguanides?

A

excreted unchanged by kidneys – stop if eGFR < 30 mL/min, alcohol intoxication

40
Q

important drug reactions of biguanides?

A

ACEi, diuretics, NSAIDs – drugs that may impair renal function
loop and thiazide like diuretics ↑glucose so can reduce metformin action

41
Q

Give an example of Biguanides.

A

Metformin

42
Q

which drug is offered first to type 2 diabetic patients?

A

Metformin

can be taken concomitantly with other hypoglycaemic agents

43
Q

How do sulfonylureas work?

A
  • Stimulate β-cell pancreatic insulin secretion by blocking ATP-dependant K+ channels
  • Need residual pancreatic function
  • Weight gain through anabolic effects of insulin
44
Q

how are sulfonylureas typically prescribed?

A

Typically in combination with other agents or a first line option if metformin contraindicated

45
Q

adverse effects of sulfonylureas

A

mild GI upset – nausea, vomiting, diarrhoea, hypoglycaemia (works at low [glucose])

46
Q

warnings, contraindications of sulfonylureas

A

hepatic and renal disease – caution, those at risk of hypoglycaemia

47
Q

important drug reactions of sulfonylureas

A

Other hypoglycaemic agents,

loop and thiazide like diuretics ↑glucose so can reduce SU action

48
Q

Give an example of sulfonylureas?

A

gliclazide

49
Q

How do thiazolidinediones/glitazones work?

A

• Insulin sensitisation in muscle and adipose, ↓hepatic glucose output

  • activation of PPAR-γ nuclear receptor → gene transcription which leads to increased adipogenesis
  • t1/2 not related to duration of action - 6-8weeks
  • Weight gain - fat cell differentiation
50
Q

Are Thiazolidinediones/glitazones frequently prescribed?

A

Used much less frequently and other agents

51
Q

adverse effects of thiazolidinediones/glitazones

A

GI upset, fluid retention, fracture risk, bladder cancer

52
Q

warnings, contraindications of thiazolidinediones/glitazones

A

heart failure because of fluid retention

53
Q

important drug reactions of thiazolidinediones/glitazones

A

other hypoglycaemic agents

54
Q

Give 2 examples of thiazolidinediones.

A

pioglitazone, rosiglitazone

55
Q

how do Sodium-glucose co-transporter (SGLT-2) inhibitors (gliflozins) work?

A
  • ↓↓glucose absorption from tubular filtrate, ↑urinary glucose excretion
  • competitive reversible inhibition of SGLT-2 in PCT
  • Modest weight loss, hypoglycaemic risk is low
56
Q

Give 2 examples of Sodium-glucose co-transporter (SGLT-2) inhibitors (gliflozins).

A

dapagliflozin, canagliflozin

57
Q

how are glifozins prescribed?

A

Adjunct to insulin in TIDM (high BMI)

TIIDM as add on therapy

58
Q

adverse effects of gliflozins

A

UTI and genital infection, thirst and polyuria

59
Q

warnings, contraindications of gliflozins

A

risk of DKA in TIDM, possible hypotension

60
Q

important drug reactions of gliflozins

A

antihypertensive and other hypoglycaemic agents

61
Q

WHat are the physiological effects of GLP-1?

A
  • pancreas: ↑Insulin secretion ↓Glucagon secretion ↑Insulin biosynthesis
  • stomach: ↓Gastric emptying
  • brain: ↓Food intake through increased satiety
  • liver: ↓Glucose production
  • muscle: ↑Glucose uptake
62
Q

What is the function of Dipeptidyl peptidase-4 (DPP-4) in glucose metabolism?

A

Incretin (e.g. GLP1) degradation

63
Q

how do Dipeptidyl peptidase-4 (DPP-4) inhibitors

(gliptins) work?

A
  • Prevent incretin degradation - ↑[plasma] incretin levels Glucose dependant so postprandial action
  • Supress appetite ~ weight neutral
64
Q

is there risk of hypoglycaemia with gliptins?

A

do not stimulate insulin secretion at normal blood glucose – lower hypoglycaemic risk

65
Q

adverse effects of gliptins?

A

GI upset, small pancreatitis risk (up to 1%)

66
Q

warnings, contraindications of gliptins?

A

avoid in pregnancy, history of pancreatitis

67
Q

important drug reactions of gliptins?

A

other hypoglycaemic agents, drugs ↑glucose can oppose gliptin action – thiazide like and loop diuretics

68
Q

Give examples of DPP-4 inhibitors?

A

sitagliptin, saxagliptin

69
Q

how do Glucagon-like peptide-1 (GLP-1) receptor agonists (incretin mimetics) work?

A
  • ↑glucose dependant synthesis of insulin secretion from β-cells by activating GLP-1 receptor – resistant to degradation by DPP-4
  • Promote satiety – possible weight loss?
70
Q

How are GLP-1 agonists administered?

A

Subcutaneous injection

71
Q

how are GLP-1 agonists prescribed?

A

NICE suggest add-on if triple therapy ineffective

72
Q

adverse effects of GLP-1 agonists

A

GI upset, decreased appetite with weight loss

73
Q

warnings, contraindications of GLP-1 agonists

A

Renal impairment

74
Q

important drug reactions of GLP-1 agonists

A

other hypoglycaemic agents

75
Q

Give examples of GLP-1 agonists?

A

exenatide, liraglutide

76
Q

what is the advantage of Modified/extended release (metformin, incretin mimetics) ?

A

overcome GI upset, less frequent dosing, slower release changes PK properties

77
Q

Why swallow extended release tablet whole?

A

they are encapsulated to slow absorption, chewing or drinking with water will disrupt modified release so absorb too much

78
Q

what is the disadvantage of combined drugs?

A

fixed dose of drug 1 + fixed dose of drug 2 – presents a challenge if you want to change the dose of drug 2

79
Q

of the 6 diabetic drugs, which ones cause hypoglycaemia when prescribed alone and which do not?

A
  • biguanides - no
  • sulfonylureas - yes
  • thiazolidinedione - yes
  • SGLT-2 inhibitors - no
  • DPP4 inhibitors - no
  • GLP1 agonists -no
80
Q

of the 6 diabetic drugs, what are their effects of weight?

A
  • biguanides - suppress appetite
  • sulfonylureas - increased
  • thiazolidinedione - increased
  • SGLT-2 inhibitors - help to decrease
  • DPP4 inhibitors - reduce appetite
  • GLP1 agonists -increased satiety
81
Q

of the 6 diabetic drugs, what are their routes of administration?

A

all oral except GLP1 agonists which is subcutaneous

82
Q

what are the primary mechanisms of the 6 diabetic drugs?

A
  • biguanides - Reducing hepatic glucose output
  • sulfonylureas - Stimulating pancreatic insulin secretion
  • thiazolidinedione - Enhanced insulin sensitivity and glucose utilisation
  • SGLT-2 inhibitors - Reduce glucose reabsorption
  • DPP4 inhibitors - Incretins promote insulin secretion and supress glucagon release - Prevent incretin degradation
  • GLP1 agonists -Increased glucose- dependant synthesis of insulin

semester 4 - CPT & Prescribing (25 decks)

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