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0Finals Revision > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What type of drug is Metformin?

A

Biguanide

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2
Q

What actions does Metformin have?

A
  • reduce hepatic gluconeogenesis
  • increase glucose uptake and utilisation in skeletal muscle (reduce insulin resistance)
  • reduce carbohydrate absorption from the intestine
  • increase fatty acid oxidation
  • reduce circulating LDL and VLDL
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3
Q

What potential unwanted effects does Metformin have?

A
  • dose-related GI disturbances (so should not be taken on a full stomach)
  • lactic acidosis (rare but potentially fatal so should not be given routinely in patients with renal or hepatic disease, hypoxic pulmonary disease or shock)
  • longterm use may affect B12 absorption
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4
Q

What are the clinical uses of Metformin?

A
  • generally used as first-line drug treatment in T2DM
  • can be combined with SUs
  • occasionally used in T1DM alongside insulin
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5
Q

What is the target of SUs?

A

Potassium ATP channels on pancreatic beta cells

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6
Q

Name the commonly prescribed SUs

A
  • gliclazide

- glimepiride

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7
Q

What is the action of SUs?

A

Reduce plasma glucose by stimulating insulin secretion (blocking of the channels causes depolarisation of the cell, Ca2+ entry and insulin secretion)

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8
Q

What are the potential unwanted effects of SUs?

A
  • hypoglycaemia
  • cardiovascular risk (greater than metformin)
  • weight gain
  • multiple drug interactions can result in severe hypoglycaemia (e.g. NSAID, warfarin, alcohol, MAOi)
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9
Q

What is the clinical use of SUs?

A
  • commonly used in early T2DM
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10
Q

What is the only Thiazolidinedione licensed for use in the UK?

A

Pioglitazone

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11
Q

What is the target of Pioglitazone?

A

PPARy (mainly in adipocytes)

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12
Q

What is the action of Pioglitazone?

A
  • enhances the effects of endogenous insulin so reduces the amount that is required to maintain a given level of blood glucose
  • promotes transcription of genes that are important in insulin signalling
  • causes differentiation of adipocytes
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13
Q

What unwanted effects can Pioglitazone cause?

A
  • weight gain (due to fat cell differentiation)
  • fluid retention (can precipitate or worsen HF: contraindicated)
  • increased risk of fractures with chronic use (especially in women)
  • increased risk of bladder cancer (monitor for haematuria)
  • non-specific adverse effects e.g. headache, fatigue, and GI upset
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14
Q

Why were older Thiazolidinediones withdrawn?

A

Cardiovascular and hepatic risk

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15
Q

What is the clinical use of Pioglitazone?

A

For use in addition to other oral hypoglycaemic agents in T2DM

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16
Q

What type of drug is Acarbose?

A

Intestinal alpha-glucosidase inhibitor

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17
Q

What is the action of alpha-glucosidase inhibitors?

A
  • delays carbohydrate absorption

- reduces post-meal blood glucose spike

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18
Q

What unwanted effects may be caused by alpha-glucosidase inhibitors?

A
  • flatulence
  • loose stools
  • abdominal pain
  • bloating
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19
Q

What is the clinical use of alpha-glucosidase inhibitors?

A
  • Used in T2DM, particularly in obesity

- Can be co-administered with Metformin

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20
Q

What is the target of gliptin-type diabetes drugs?

A

DPP-4

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21
Q

What is DPP-4?

A

An enzyme which inactivates GLP-1

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22
Q

What is the action of gliptin-type diabetes drugs?

A

Reduces inactivation of GLP-1, so potentiates its effects:

  • stimulate insulin secretion
  • promote satiety
  • regulates gastric emptying
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23
Q

What unwanted effects may come from gliptin-type diabetes medications?

A 
Commonly: a range of GI symptoms
Rarely:
- liver disease
- worsening of heart failure
- pancreatitis
ALSO: concerns over potential action as tumour promoters
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24
Q

What is the clinical use of gliptin-type medications?

A

T2DM in addition to other oral hypoglycaemic agents

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25
Q

What is the target of the Gliflozins?

A

Sodium Glucose Cotransporter type 2 (SGLT-2)

26
Q

What are the three SGLT-2 inhibitors which are licensed in the UK?

A
  • Empagliflozin
  • Dapagliflozin
  • Canagliflozin
27
Q

What actions do SGLT-2 inhibitors have?

A
  • reversibly block glucose reuptake in the proximal convoluted tubule to induce glucosuria and lower plasma glucose levels
  • promotes weight loss
28
Q

What unwanted effects can be brought on by SGLT-2i use?

A
  • constipation
  • increased risk of UTIs and thrush
  • thirst
  • polyuria
  • increased risk of DKA
29
Q

What is the clinical use of SGLT-2 inhibitors?

A

Additional therapy in T2DM

30
Q

What are “incretin mimetics”?

A

GLP-1 analogues

31
Q

How are GLP-1 analogues administered?

A

Subcutaneous injection

32
Q

Give examples of GLP-1 analogues

A
  • Exenatide
  • Semaglutide
  • Liragultide
33
Q

What actions to GLP-1 analogues have?

A
  • lower blood glucose post-meal by increasing insulin secretion, suppressing glucagon secretion and slowing gastric emptying
  • promote satiety and so has modest weight loss effects
  • reduce hepatic fat accumulation
  • reduce mortality when used in combination with Metformin
34
Q

What unwanted effects can GLP-1 analogues have?

A
  • hypoglycaemia
  • GI disturbances
  • pancreatitis
  • injection site reactions
35
Q

What is the clinical indication for GLP-1 use?

A
  • T2DM
  • obese
  • dual therapy has failed
  • should be trialled for 6 months and continued only if shown to reduce weight and HbA1c
36
Q

Define T1DM

A

Lack of glycaemic control due to autoimmune destruction of pancreatic beta cells and the resulting deficit in insulin secretion

37
Q

What is the aetiology of T1DM?

A

Thought to be a combination of genetic predisposition and an environmental trigger

38
Q

How is T1DM managed?

A
  • exogenous insulin administration
  • healthy diet and exercise can aid good glycemic control and minimise the risk of long-term complications but cannot reverse the disease or eliminate the need for insulin
39
Q

Define T2DM

A

Lack of glycaemic control due to insulin resistance or insulin deficiency

40
Q

What is the aetiology of T2DM?

A

Combination of environmental and genetic factors

41
Q

What are the risk factors for T2DM?

A
  • being overweight or obese
  • central obesity
  • eating an unhealthy diet
  • physical inactivity
  • having a first degree relative with T2DM
  • hypertension
  • hypercholesterolaemia
  • being of south asian or afro-caribbean descent
  • smoking
42
Q

How is T2DM managed?

A

Depends on severity, progresses through the following:

  • lifestyle modification (high fibre, low GI diet, regular exercise)
  • oral glycaemic agents
  • injected glycaemic agents
  • insulin
43
Q

Why is insulin administered by injection?

A

It is destroyed in the GI tract

44
Q

How is insulin usually administered? How can it be administered?

A
  • usually subcutaneous injection
  • can be given IM or IV in emergencies
  • can be given with peritoneal dialysis in patients with end stage real failure
45
Q

What are the indications for insulin?

A
  • T1DM
  • T2DM with inadequate glycaemic control on oral hypoglycaemic agents (OHAs)
  • T2DM when OHAs are contraindicated
  • Impaired glucose tolerance in pregnancy (gestational diabetes)
46
Q

What is diabetic ketoacidosis?

A
  • excessive glucose
  • lack of insulin
  • glucose cannot be taken up into cells to be metabolised
  • cells enter starvation-like state and use ketoacidosis to produce energy
47
Q

How does DKA present?

A
  • gradual drowsiness
  • vomiting
  • dehydration
48
Q

What might trigger a DKA?

A
  • infection
  • surgery
  • MI
  • pancreatitis
  • chemotherapy
  • antipsychotics
  • wrong insulin dose or non-compliance
49
Q

Diagnostics for DKA?

A

1) acidosis (venous pH <7.3 or bicarb <15mmol/L)
2) hyperglycaemia (BM >11mmol/L) OR known diabetic
3) ketonaemia (>3mmol/L) or significant ketonuria (++ or more on dipstick)

50
Q

What investigations should you order for a patient with suspected DKA?

A
  • ECG
  • CXR
  • urine dip
  • MSU
  • capillary and lab glucose
  • venous bloods: ketones, pH, U+E, bicarb, osmolality, FBC, cultures
  • use ABG only if declining GCS or hypoxic *
51
Q

What presentations might indicate a severe DKA and should prompt consideration of HDU/ICU?

A
  • blood ketones >6mmol/L
  • venous bicarb <5mmol/L
  • blood pH <7
  • K <3.5mmol/L
  • GCS <12
  • O2 sats <92% on air
  • sysBP <90mmHg
  • pulse >100 or <60
  • anion gap above 16
52
Q

What are the potential complications of DKA?

A
  • cerebral oedema
  • aspiration pneumonia
  • hypokalaemia
  • hypomagnesaemia
  • hypophosphataemia
  • thromboembolism
53
Q

How does hypoglycaemia present?

A
  • rapid onset
  • sweating
  • rapid pulse
  • seizures
  • may be accompanied by odd behaviour e.g. aggression
54
Q

How do you manage hypoglycaemia?

A

CONSCIOUS, ORIENTATED, ABLE TO SWALLOW:
- 15-20g of quick acting carb snack (e.g. 200ml orange juice) and recheck BM after 10-15min
- repeat up to 3 times
CONSCIOUS BUT UNCOOPERATIVE:
- squirt glucose gel between teeth and gums
UNCONSCIOUS OR NOT RESPONDING TO TREATMENT:
- start glucose IVI or give glucagon 1mg IV or IM

  • Expect a rapid recovery
  • When glucose >4mmol/L and patient has recovered, give long acting carb (e.g. toast)
55
Q

What does HHS stand for?

A

Hyperglycaemic hyperosmolar state

56
Q

When might lactic acidosis occur in diabetics?

A
  • septicaemia

- Metformin use

57
Q

Blood lactate >5mmol/L

1) What is it?
2) What do you need to do?

A

1) Lactic acidosis
2) Management:
- get expert help
- stop metformin
- treat sepsis vigorously
- maintain BP to maintain tissue perfusion

58
Q

Who tends to get HHS?

A

Unwell type 2 diabetics

59
Q

How does HHS present?

A
  • not a rapid onset: usually around ~1/52 history
  • marked dehydration
  • glucose >30mol/L
  • ketones normal so pH normal
  • osmolality typically >320mosmol/kg
60
Q

What are the principles of HHS management?

A
  • prevent occlusive events: give LMWH prophylaxis unless contraindicated
  • rehydrate slowly
  • replace K+ when urine output resumes
  • only use insulin if not responding to treatment or if ketonaemic
  • maintain glucose >10mmol/L for first 24h to avoid cerebral oedema
  • look for the cause
61
Q

What might precipitate HHS?

A
  • MI
  • drugs
  • sepsis
  • bowel infarct

0Finals Revision (21 decks)

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