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Endocrinology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

define type 1 diabetes

A

Pancreatic islet β-cells destroyed - autoimmune

Absolute insulin insufficiency

-> lipolysis and ketogenesis

Associated with HLA DR3/4

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2
Q

Define type 2 diabetes?

A

Associated with obesity, HTN, inactivity, disturbed lipids

Reduced peripheral sensitivity to insulin

Reduced insulin production (over time)

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3
Q

what is the typical presentation of type 1 diabetes

A

5-15 y/o peak age

Polyuria and polydipsia (osmotic diuresis)

Weight loss (muscle and fat breakdown)

DKA: Abdo pain, N&V, tachypnoea (Kussmaul), coma

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4
Q

what is the typical presentation of type 2 diabetes?

A

Asymptomatic- picked up routine Ix

RFs present- (truncal) obesity; FHx,

South Asian, black), age

Fatigue

Polydipsia/polyuria

Infections (fungal, cellulitis)

Acanthosis nigricans

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5
Q

what are the causes of type 1 diabetes?

A

destruction of pancreatic beta-cells -> absolute insulin deficiency

Autoimmune disease with environmental trigger

  • HLA-DQ, -DR3/4

Associated autoimmune conditions

  • Vitiligo
  • Addison’s disease
  • Hashimoto’s thyroiditis
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6
Q

what are the causes of type 2 diabetes

A
  • MODY (maturity onset diabetes of the young) – autosomal dominant
  • Pancreatic disease e.g.chronic pancreatitis, pancreatic ca.
  • Endocrinopathies e.g. Cushing’s syndrome, acromegaly, PCOS
  • Drugs e.g. corticosteroids
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7
Q

what are the risk factors of type 2 diabetes?

A
  • Genetic predisposition: 90% concordance amongst monozygotic twins
  • Older age
  • Physical inactivity
  • Obesity - ↑FFAs, hyperglycaemia
  • Hypertension
  • Dysplipidaemia
  • Cardiovascular disease
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8
Q

what are the symptoms and signs of diabetes?

A
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9
Q

what is HHS and how is it worked out?

A

hyperglycaemia hyperosomolar state- people with type 2 diabetes

blood glucose levels over 40mmol/L

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10
Q

how is diabetes diagnosed and interpret the results?

A
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11
Q

when should HbA1c not be used?

A
  • ALL children and young people
  • patients of any age suspected of having Type 1 diabetes
  • patients with symptoms of diabetes for less than 2 months
  • patients at high risk who are acutely ill (e.g.those requiring hospital admission)
  • patients taking medication that may cause rapid glucose rise e.g.steroids, antipsychotics
  • patients with acute pancreatic damage, including pancreatic surgery
  • in pregnancy
  • presence of genetic, haematologicand illness-related factors that influence HbA1c and its measurement
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12
Q

interpret the bloodand urine results for a suspected DKA?

A

Bloods

  • FBC – elevated WCC
  • U&Es – high urea and Cr
  • Glucose >11mmol/l
  • Ketones >3mmol/l
  • Culture
  • ABG – metabolic acidosis with high anion gap (VBG pH <7.3)

Urine

  • Glycosuria
  • Ketonuria ++
  • MC&S
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13
Q

what is the management of type 1 diabetes?

A
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14
Q

what is the management for DKA?

A

• IV fluid replacement with 0.9% saline

• Start IV dextrose when glucose reaches 15mmol/l

• Insulin infusion

• Potassium (in fluids)

• Monitor blood glucose, ketones, urine output and venous blood gases

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15
Q

outline the management for type 2 diabetets?

A
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16
Q

which blood pressure medication should all type 2 diabetics be started with?

A

BP management in all type II diabetics begins with ACEi/ARB rather than CCB (even if the patient is black or over the age of 55)

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17
Q

outline the step approach for glycaemic control in type 2 diabetics?

A

If HbA1c >48 on lifestyle interventions, add metformin

If HbA1c >58, try:

  • Metformin +DPP-4i e.g., sitagliptin (-gliptin) or
  • Metformin +Pioglitazone or
  • Metformin +A sulfonylurea e.g., gliclazide or
  • Metformin +An SGLT-2i e.g.,dapaglifozin(-gliflozin)

If HbA1c still >58, try:

  • Metformin + DPP-4i + sulfonylurea
  • Metformin + pioglitazone + sulfonylurea
  • metformin, pioglitazoneaor an SU, and an SGLT-2i
  • Insulin based treatment
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18
Q

outline the action of metformin?

A

Inhibits hepatic gluconeogenesis

Also promotes weight loss

Advice is to offer standard release metformin and to increase the dose gradually to avoid adverse effects. If side effects are experienced and intolerable, you can switch to modified release metformin. The patient’s renal function has to be monitored before initiating metformin and during its use.

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19
Q

what are the SE of metformin?

A

GI upset, MALA

Given Metformin MR if gastro symp don’t go in a month

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20
Q

Why does metformin cause lactic acidosis in liver/renal/heart failure?

A

Metformin inhibits hepatic gluconeogenesis (ie. the regular way in which excess lactate is converted back into sugars). More lactic acid is produced in heart failure. With increased lactate production (in heart failure), a decreased lactate clearance (with metformin use on top of liver failure) and decreased metformin clearance by kidneys (in kidney failure) - lactic acidosis may occur. Metformin is very safe, and you only see lactic acidosis when the drug is taken in large doses in people who shouldn’t be on it (eg severe renal failure, heart failure and liver failure)

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21
Q

outline the action of sulphonylureas and in which group of people they are used in?

A

not overweight who need rapid hyperglycaemia control due to symp

e.g. gliclazide, glibenclamide

Blocks K+ sensitive channels in beta cells -> insulin release

22
Q

what are the SEs of sulphonylureas?

A

hypoglycaemia(which is why you need to make sure patients take before), weight gain

23
Q

outline the action of thiazelidione?

who is it contraindicated in?

A

insulin sensitiser

e.g. pioglitazone

Activates PPARγ and ↓ insulin resistance

Contraindicated in Heart Conditions

24
Q

outline the action of acarbose?

A

(alpha-glucosidase inhibitor)

Reduces carbohydrate digestion

25
Q

what are the SEs of acarbose?

A

bloating, flatulence

26
Q

outline the action of incretin?

A

GLP-1 analogue

e.g. exenatide, liraglutide

↑ insulin secretion, ↓ glucagon release, gastric emptying and so increases hypothalmic satiety

27
Q

what are the side effects of GLP analogues?

A

GI upset

28
Q

outline the action of DPP4- inhibitors

A

-gliptin e.g. sitagliptin, vildagliptin

Increases GLP-1 half life as DPP4 breaks down GLP-1

29
Q

outline the action of SGLT-2 inhibitors?

A

glifozin

e.g. canagliflozin

↓ renal threshold for glucose -> ↓ glucose reabsorption

30
Q

what are the side effects of SGLT-2 inhibitors?

A

thirst, N, constipation, more UTIs, poluria

31
Q

outline the use of insulin in T2DM and state what should be monitored carefully?

A

Very good treatment for T2DM but they ARE NOT dependent on it, unlike with T1DM

T2DM can go on insulin and come off it!!!

Watch potassium and phosphate carefully as insulin causes activation of glut4 which pumps in glucose, potassium and phosph into cells

32
Q

what are the side effects of insulin?

A

weight gain, lipid hypertrophy at injection sites

33
Q

what are the 3 acute metabolic disturbances in diabetes?

A

Hypoglycaemia (result of treatment)

Diabetic ketoacidosis (mainly T1DM)

Hyperosmolar hyperglycaemic state

34
Q

what are the long term microvascular complications of diabetes?

A
  • Retinopathy
  • Neuropathy
  • Nephropathy
35
Q

what are the long term macrovascular complications of diabetes?

A
  • Ischaemic heart disease
  • Cerebrovascular disease
  • Peripheral artery disease
36
Q

what is hypoglycaemia in diabetics?

A

Low sugar (<3.6 mmol/L)

37
Q

what are the causes of hypoglycaemia in diabetics?

A

Missed meals/inadequate snacks

Alcohol

Unaccustomed exercise

Inappropriate insulin regime

Some drugs (sulfonylureas, SGLT-2i

38
Q

what are the signs of hypoglycaemia in diabetics?

A

Palpitations (tachycardia), tremor, sweating, pallor, anxiety

Drowsiness, confusion, altered behaviour(aggression), coma

39
Q

outline the treatment of hypoglycaemia in diabetics?

A

GIVE SUGAR!

Conscious:

ORAL Glucose (solution/tablet) AND complex CHO

Impaired consciousness:

PARENTERAL: 1mg glucagon IM. If fails, IV dextrose e.g., 10%glucose infusion

40
Q

compare the DKA and HHS?

A
41
Q

what is seen in diabetics retinopathy on fundoscopy and outline the management?

A
42
Q

outline diabetic nephropathy?

A

One of commonest cause of CKD

commonest secondary cause of nephrotic syndrome

Albuminuria, reduction of eGFR, associated with retinopathy

43
Q

what are the investigations for diabetic nephropathy?

A

1st- Urinalysis (proteinuria/raised ACR)

eGFR (see chronic kidney disease)

Biopsy is gold standard but rarely needed- Kimmelstiel-Wilson nodules (mesangial expansion)

44
Q

outline the management of diabetic nephropathy?

A

Improve glycaemic control

ACEi/ARB

45
Q

what is diabetic neuropathy?

A

Commonest cause of neuropathy

Caused by blockage of vasa nervorum

46
Q

what is the cause of peripheral neuropathy?

A

Loss of sensation (particularly feet-glove and stocking)

May not sense injury to foot

INSPECT FEET!

Monofilament examination

Loss of ankle jerk/vibration sense/fractures (Charcot’s joint)

47
Q

what is mononeuropathy?

A

Sudden motor loss usually

E.g., wrist drop, foot drop, 3rdnerve palsy (eye down and out, pupil responds to light

48
Q

what is autonomic neuropathy?

A

GI tract: difficulty swallowing, delayed gastric emptying, bladder dysfunction

Postural hypotension (collapse on standing)

Cardiac autonomic supply

49
Q

outline the management of diabetic neuroathy?

A

Glycaemic control

If painful, use neuropathic pain agent

e.g., duloxetine, pregabalin or gabapentin

50
Q

what is charcot’s arthropathy?

A

Charcot arthropathy is a progressive degeneration of a weight bearing joint, a process marked by bony destruction, bone resorption, and eventual deformity.

onset is usually insidious

More commonly seen in the lower extremities and caused by a combo of diabetic neuropathy and vasculopathy

Endocrinology (26 decks)

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