Brainscape's Knowledge GenomeTM

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


See full index

Inflammation > Diabetes mellitus > Flashcards

Diabetes mellitus Flashcards

1
Q

Microvascular complications of diabetes mellitus? (specific to diabetes)

A

Retinopathy, nephropathy, neuropathy (foot)

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

Macrovascular complications of diabetes mellitus?

A

Cerebrovascular, ischaemic heart disease, peripheral vascular disease (foot)

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

Difference between type 1 a and b?

A

1a is destruction of beta cells due to an AI response

1b is idiopathic

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

Hallmark of type 1?

A

Absence of C-peptide

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

MODY 1-7 =

A

Monogenic diabetes

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

Genetic defects in insulin action:

A

Type a insulin resistance
Leprechaunism
Rabson-Meldenhall syndrome

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

Diabetes can develop secondary to which conditions?

A

Other endocrine conditions e.g. Cushing’s or acromegaly

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

Endocrine causes of diabetes?

A

Glucocorticoids and thyroxine

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

Infectious causes of diabetes?

A

Congenital rubella

CMV

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

Stiff man =

A

Antibodies to the insulin receptor

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

Osmotic symptoms of diabetes?

A

Thirst, polyuria and polydipsia

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

Associated genetic syndromes:

A

Down’s

Huntington’s

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

Proteolysis and lipolysis in marked/complete insulin insufficiency leads to…

A

Weight loss

Ketogenesis and ketosis leading to acidosis resulting in vasodilation and causing (along with dehydration) hypotension

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

Mononeuritis in diabetes?

A

Diplopia

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

Neuropathies:

A

Peripheral - numbness/pain/tingling in hands and feet
Autonomic - sweating, gastroparesis, postural dizziness, erectile dysfunction, diarrhoea and incontinence
Radiculopathy - pain and wasting
Mononeuritis - diplopia
Compression - carpal tunnel, ulnar nerve, lateral popliteal nerve

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

Diagnosis of diabetes mellitus (symptomatic):

A

Diabetes symptoms (e.g. polyuria or weight loss in type 1) and any one of:

1) Random venous plasma glucose > 11.1mmol/L
2) Fasting plasma glucose concentration > 7mmol/L, whole blood > 6.1mmol/L
3) Two hour plasma glucose > 11.1mmol/L after 75g glucose in an oral glucose tolerance test

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

Diagnosis of diabetes mellitus (asymptomatic):

A

Absence of any symptoms with raised venous plasma glucose with a raised fasting plasma glucose or OGTT on a seperate day

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

Diagnosis with HbA1c:

A

Pre-diabetes = 6.1-6.4% (43-47 mmol/L)
Diabetes = 6.5% (48 mmol/L)
A value of less than 6.5% does not exclude diagnosis of diabetes with glucose tests

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

When is HbA1c not an appropriate diagnostic tool?

A 
All children and young people
Suspected type 1
Diabetes symptoms < 2 months
High risk acutely ill patients
Patients taking any medications that can cause rapid glucose rise e.g. antipsychotics or steroids
Acute pancreatic damage
Pregnancy
Other influencing factors on HbA1c
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Features of the oral glucose tolerance test (OGTT):

A 
180gm CHO for 3 days before
Overnight fast
Sedentary during test
Fasting venous plasma glucose
75g anhydrous glucose over 5 minutes
2 hour venous plasma glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Clinical features of type 1:

A 
Insulin deficient
Ketosis prone
HLA markers
Autoimmune (other AI conditions)
Peak of onset in adolescence
Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clinical features type 2:

A 
Insulin resistant and deficient
Not ketosis prone
Polygenic
South Asians > Africans and Carribeans > Europeans
Increases with ageing
Associated with central obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Genetic markers of type 1 diabetes:

A 
HLA-DR3
HLA-DR4
DQalpha and beta
IDDM2
IDDM12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Can a patient with a HbA1c under 6.5% be diagnosed with diabetes?

A

Yes

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

What are the hyperglycaemic diabetic emergencies?

A

Diabetic ketoacidosis

Hyperosmolar hyperglycaemic state

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

Triad of DKA:

A

Hyperglycaemia, hyperketonaemia, metabolic acidosis

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

Diagnosis of DKA:

A

Blood glucose > 11mmol/L or known diabetes
Blood ketones > 3mmol/L or ketonuria > 2+
Bicarbonate < 15mmol/L and/or venous pH < 7.3

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

Which hormones can cause DKA?

A

Stress hormones - catecholamines, cortisol

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

Why can DKA cause disordered potassium?

A

Insulin causes K to move into cells
Insulin deficiency means that K moves into the blood (hyperkalaemia) and is lost in the urine - whole body loss
Acidosis causes similar effect as H and K compete

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

Problem with treating DKA?

A

K moves from the blood to the intracellular compartment too quickly and can cause arrhythmias

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

What can cause DKA?

A

Infection
Poor compliance
Newly diagnosed/failure of care

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

Complications of DKA:

A 
Cerebral oedema (fluid shift)
Adult respiratory distress syndrome/acute lung injury
PE (dehydration)
Arrhythmias
Multi-organ failure (acidosis)
Co-morbid state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Symptoms of DKA:

A

Blurred vision not due to retinopathy but due to fluid-shifts
Leg cramps
Weakness
Osmotic symptoms

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

Signs of DKA:

A 
Kussmaul respiration (laboured and deep, hyperpnoea)
Ketotic fetor (sweet smell on breath)
Dehydration
Tachycardia
Hypotension
Mild hypothermia
Confusion, drowsiness, coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Step 1 of treating DKA:

A

Fluid replacement
IV 0.9% saline
Perfuse the kidneys to normalise the acid-base balance

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

Step 2 of treating DKA:

A

Insulin replacement

Fixed rate IV 0.1 units/kg/hour

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

Step 3 of treating DKA:

A

Potassium replacement

Replace the K as soon as in normal range as serum K falls very rapidly post fluid and insulin correction

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

Step 4 of treating DKA:

A

Address cause of the DKA

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

Step 5 of treating DKA:

A

VTE prophylaxis - LMWH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Step 6 of treating DKA:

A

Monitor - HDU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Type 2 diabetic emergency?

A

Hyperosmolar hyperglycaemic state (HHS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

HHS osmolality and glucose =

A

Hyperosmolality > 320 mosmol/kg

Hyperglycaemia > 30 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

HHS pathology:

A

Severe dehydration and hypovolaemia
Without ketonaemia
Without acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

HHS complications:

A 
Cerebral oedema
Osmotic demyelination syndrome
Seizures
Arterial thrombosis - MI, CVA, strokes
VTE, PE
Multiorgan failure
Foot ulceration
Co-morbid condition
45
Q

Clinical features of HHS:

A 
Osmotic symptoms
Blurred vision
Weakness
Dehydration
Tachycardia
Hypotension
Confusion, drowsiness and coma
46
Q

What is the potentially life-threatening complication of not gradually normalising HHS?

A

Cerebral oedema

47
Q

How is HHS treated?

A

The exact same protocol as for DKA except a lower fixed rate of insulin at 0.05 units/kg/hour
(Still have to give LMWH for VTE risk)

48
Q

When do you give an extra short-acting insulin bolus?

sick day rules

A

If CBG > 13mmol/L

If blood ketones >1.5mmol/L

49
Q

Why are sick day rules necessary?

A

When ill, glucose levels and insulin requirements go up causing ketones to rise as well

50
Q

Sick day rules:

A

Never stop background long-acting insulin
Check cap BG every 2-4 hours
100ml/hour fluid
Bolus for carbohydrate
Med help if start vomiting, CBG/ketones not improving, hypos

51
Q

Definition of a hypo:

A

<3.5mmol/L (<4 in hospital)

52
Q

Main effect of sever hypo:

A

Confusion, seizure, coma and death (neuro)

53
Q

Drug induced hypo:

A

Side effect of insulin or sulphonylureas

54
Q

Symptoms of hypos:

A

Autonomic: sweaty and palpitations
Neuro: confusion, visual disturbances, circumoral paraesthesia
Hunger

55
Q

Treatment for hypo with conscious patient who can walk?

A

Fast-acting carbohydrate oral 15-20g

Check in 10 mins, if still hypo then repeat and then check again in 5 minutes

56
Q

Treatment for severe hypo with unconscious patient?

A

IV glucose 20% 75-100ml or 1mg SC/IM
Re-check and repeat if need be
If they can swallow and it is severe but two glycogen tablets in the inner cheek

57
Q

Treatment after initial management of the hypo?

A

Eat 15-20g long acting carbohydrate like one slice of bread or two biscuits, do not omit insulin injection and address the cause

58
Q

Effect of somatostatin?

A

Blocks both insulin and glucagon release

59
Q

Example of a biguanide:

A

Metformin

60
Q

Effect of Metformin?

A

Decreases hepatic gluconeogenesis (+gene expression)
Also activates AMPK which increases GLUT4 expression in muscle cells
Stimulates glycolysis in tissues
Decreases carbohydrate reabsorption in the gut
Stimulates lactate production
Lowers LDL and VLDL
Reduces microvascular complications

61
Q

Benefits of Metformin?

A

Does not stimulate appetite
Does not cause hypos
Does not cause weight gain

62
Q

Side-effects of Metformin?

A

Metallic taste
Diarrhoea, nausea
Decreased B12 and folate absorption
Rare: lactate acidosis

63
Q

Features of Metformin:

A

Not bound to plasma protein
t(1/2) = 3hours
Absorbed in the small intestine

64
Q

Sulphonylureas:

A

-mide/-zide
e.g. Glibendamide, Glipizide
(Old: carbutamide, tolbutamide, chlorpropramide)

65
Q

Effect of Sulphonylureas?

A

Bind to KATP channels causing depolarisation of Beta cells and release of insulin
Decrease hepatic clearance of insulin

66
Q

Features of Sulphonylureas?

A

Plasma protein bound so displace other plasma bound drugs and increase their plasma concentration e.g. NSAIDs, MAO inhibitors and Abx
Excreted in urine with enhanced effect in elderly/renal impairment

67
Q

Main side-effect of sulphonylureas?

A

Hypos

May need IV glucose, glucagon or adrenaline

68
Q

Meglitinides:

A

Rapaglinide and Nateglinide

t(1/2) = 1 hour

69
Q

Effect on meglitinides?

A

Close KATP channels selective in beta cells

70
Q

Guidelines for meglitinides:

A

Can be used as monotherapy

Take just before meal

71
Q

Comparison between sulphonylureas and meglitinides?

A

Meglinitides are less potent but more rapid and are less prone to causing hypos

72
Q

Glutaziones:

A

Pioglitazone (risk of bladder cancer)

73
Q

Effect of glutaziones:

A

Nuclear receptor (PPARgamma and RXR) agonists
Decrease insulin resistance in peripheral tissues
Reduces hepatic gluconeogenesis
Increases uptake and potentiates action of insulin

74
Q

Side-effects of glutaziones:

A

Increased food intake in the brain
Decrease in bone density
Increase in sodium and water retention in the kidney
Increased growth and lipid storage in the heart
Increases adipocyte no. and lipogenesis so weight

75
Q

Directions for glutaziones:

A

The t(1/2) = 7 hours, 24 hours for the active metabolite
Give with metformin or other hypo drugs
6-12 weeks of therapy for the maximum effect

76
Q

Incretins:

A

Glucagon-like peptide-1 (GLP-1) agonists and dipeptidylpeptidase-4 (DPP-4) inhibitors

77
Q

Effect of incretins?

A

Incretins are gut derived peptides that stimulate insulin release, decrease glucagon release
In the brain they reduce appetite so help lose weight
They slow glucose absorption in the gut by slowing gastric emptying
Stimulate an increase in beta cells

78
Q

Guidance for incretins:

A

Must be given IV as an injection
No effect on weight or hypos however Loraglutide has been given at a high dose as a weight loss drug (daily injections)
Possible increase in cancer
DPP-4 breaks down GLP-1 so glistens inhibit this
Reduce risk of microvascular and renal outcomes

79
Q

alpha-glucosidase inhibitors:

A

Acarbose - inhibits alpha-glucosidase at the intestinal brush border

80
Q

Effect of alpha-glucosidase inhibitors?

A

Decrease in carbohydrate breakdown and postprandial absorption

81
Q

Features of alpha-glucosidase inhibitors:

A

Does not cause hypos
Used in both T1DM and T2DM
May cause flatulence and diarrhoea

82
Q

SGLT2 inhibitors:

A

Dapagliflozin + empagliflozin are both SGLT2 inhibitors
Cangliflozin is an SGLT1 and an SGLT2 inhibitor
Xigduo = metformin + dapagliflozin
Vokanamet = metformin + canagliflozin

83
Q

Effect of SGLT2 inhibitors?

A

SGLT2 is responsible for 80-95% of the glucose reabsorption in the proximal tubule
Inhibits glucose re-uptake in the kidney
Causes around 10% excretion of calorie intake
Decreases CVD secondary to diabetes

84
Q

Effect of amylin analogues:

A

Inhibits glucagon release
Decreases gastric emptying
Promotes satiety

85
Q

Features of amylin analogues:

A

Can cause amyloid aggregates - Alzheimer’s
Pramlintide is an analogue that doesn’t cause aggregates
Adjunct for both T1DM and T2DM

86
Q

Which drugs increase insulin secretion?

A

Sulphonylureas
Meglitinides
Incretins

87
Q

Which drugs decrease glucagon secretion?

A

Incretins

Amylin analogues

88
Q

Which drugs decrease appetite?

A

Incretins

Amylin analogues

89
Q

Which drugs decrease glucose reabsorption?

A

SGLT2 inhibitors

90
Q

Which drugs increase cellular glucose uptake and utilisation?

A

Glutaziones (thiazolidinediones)

Metformin

91
Q

Which drugs decrease hepatic gluconeogenesis?

A

Glutaziones (thiazolidinediones)

Metformin

92
Q

Obesity treatment:

A

Serotonin uptake agonists help appetite control

93
Q

What does U100 mean?

A

100 units of insulin per ml

94
Q

Basal dose of insulin?

A

Long acting for whole day
One per day = glargine (acid solution in vial that precipitates at body pH)
Twice per day = detemir (attached to fatty acid as bigger molecules = longer action)

95
Q

Prandial dose of insulin?

A

Fast acting dose before meal (e.g. monomers Lispro and Aspart)

96
Q

What does insulin pump therapy provide (CSII)?

A

Basal and prandial spikes

97
Q

Insulin for type 2 diabetes?

A

Long dose e.g. glargine once a day or mixed before breakfast and before dinner

98
Q

CKD in diabetes type 2:

A

GFR can drop by 1ml a year (if 10 or over in a year then biopsy)
GFR can drop without proteinuria
SGLT2 inhibitor empagliflozin and incretin loraglutide improves renal outcomes

99
Q

Side-effects of insulin?

A

Hypos increase risk of cardiac arrhythmias
Neuroglycopaenia
Higher risk of hypo if patient taking insulin has poor renal function

100
Q

Weight reduction therapies:

A

Orlistat = weight reduction 5%, improves HbA1c

Bariatric surgery = weight reduction 15-25%, diabetes remission

101
Q

Reducing cholesterol:

A

Statins

PSK9 inhibitors - Evolcumab

102
Q

BP targets?

A

< 140/80

< 130/80 if there are complications

103
Q

Step 1 of drug BP control:

A

ACE inhibitor

+ CCB/diuretic if African/Carribean

104
Q

Step 2 of drug BP control:

A

+ CCB/diuretic

105
Q

Step 3 of drug BP control:

A

+ diuretic/CCB

106
Q

Step 4 of drug BP control:

A

+ alpha-blocker/beta-blocker/K-sparing diuretic

107
Q

Step 5 of drug BP control:

A

+ alpha-blocker/beta-blocker/K-sparing diuretic/refer to a specialist

108
Q

When can reducing BP too much increase mortality risk?

A

Elderly patients >65 y/o

Patients with reduced kidney function

109
Q

Contraindication of glutaziones?

A

Heart failure (they caused oedema and heart failure)

Inflammation (9 decks)

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