Diabetes & Pituitary - MedEd lecture

Question 1

Symptoms of Type 1 diabetes + pathophysiology

Answer 1

Polyuria (osmotic diuresis due to hyperglycemia)
Polydipsia
Weight loss (no insulin, therefore no feedback mechanism to tell the body to stop breaking down fat and muscle)

Question 2

DKA symptoms

Answer 2

Abdo pain
Nausea and vomiting
Tachypnoea - Kussmaul’s breathing
Coma

Question 3

Signs/presentation of type 2 DM

Answer 3

Picked up on routine investigation/RF being south asian/black/age

Acanthosis nigrans
Infections due to glucose - fungal, cellulits
Fatigue
Polydipsia/polyuria

Question 4

Normal level for fasting glucose

Answer 4

<5.5

Question 5

Normal level for random glucose

Answer 5

<11.1

Question 6

Normal level for glucose after food

Answer 6

<7/.8

Question 7

Normal HbA1c

Answer 7

<42

Question 8

Random glucose levels in diabetics

Answer 8

> or equal to 11.1

Question 9

Fasting glucose levels in diabetics

Answer 9

> or equal to 7

Question 10

Post prandial glucose levels in unmanaged diabetics

Answer 10

> or equal to 11.1

Question 11

Mx of type 1 diabetes

Answer 11

Basal bolus

Question 12

What does basal bolus mean?

Answer 12

Long acting + short acting before meals

Question 13

Long acting example

Answer 13

Glargine SC

Question 14

Example of short acting

Answer 14

Lispro / Aspart SC pre meal

Question 15

Type 2 DM Mx - step 1 (glycemic control)

Answer 15

Diet, exercise, education
Metformin

If HbA1c above 48, give metformin

Question 16

Type 2 DM Mx - step 2 (glycemic control)

Answer 16

If HbA1c still above 48 with metformin, give another drug e.g. DPP4i,

Or also: piogliatazone, SU, SGLT-2i

Question 17

Type 2 DM Mx - step 3 (glycemic control)

Answer 17

Add another drug or try insulin

Question 18

T2DM BP Mx

Answer 18

Depending on age (below or above 55yrs)

ACEi/ARB
+ CCB/Thiazide Diuretics
ACEi/ARB + CCB + Diuretics

or if afrocarribean, CCB then +ACEi/ARB/Diuretics then all three

Question 19

Step 4 of BP Mx in T2DM

Answer 19

If potassium is less than 4.5, add spiro

If more than 4.5, BB

Question 20

Lipid management in T2DM if low risk vs high risk

Answer 20

Atorvastatin 20mg if 10 year cardiovascular risk is >10% on QRD

80mg if IHD/Cerebrovascular D/peripheral artery disease

Question 21

If high Qrisk score/evidence of CVD what else do you need to give besides atorvastatin?

Answer 21

Antiplatelet - aspirin 75mg

Question 22

Acute complications of DM

Answer 22

Hypoglycemia
Diabetic ketoacidosis (DKA)
Hyperosmolar hyperglycemic state (HHS)

Question 23

Long term complications of DM

Answer 23

Microvascular

• Diabetic retinopathy
• Diabetic nephropathy
• Diabetic neuropathy

Macrovascular

• IHD
• Cerebrovascular disease
• Peripheral vascular disease

Question 24

Causes of hypoglycemia in diabetics

Answer 24

Missed meals 
Alcohol
SU (sulphonylureas)/SGLT-2i
Unaccustomed exercise 
Inappropriate insulin

Question 25

Hypoglycemia symptoms + BM level

Answer 25

``` Palpitations Tremor Sweating Pallor Anxiety Drowsiness Confusion Altered behaviour Seizures Coma AND Low sugar <3.6 ```

Question 26

Treatment for hypos + why it works

Answer 26

If conscious - oral glucose and complex carbs If unconscious, 1mg GLUCAGON IM AKA PARENTERAL (tells liver to convert glycogen into glucose) If that fails, IV dextrose (10-20% glucose) Note: if you give any more glucose, it would damage the tissues.

Question 27

DKA triad

Answer 27

Hyperglycemia Ketonaemia Metabolic acidosis (due to acidity of ketones)

Question 28

Explain the pathophysiology of DKA - what causes it? What metabolic changes happen?

Answer 28

Stress hormones and insulin deficiency cause hyperglcemia. This in turn causes osmotic diuresis, leading to dehydration. Reduced flow to kidneys means that hydrogen ions aren't excreted out well, therefore you get metabolic acidosis. The pt ends up vomiting in order to deal with the metabolic acidosis, which leads to even more dehydration. Note: ketonemia also massively contributes towards the metabolic acidosis, causing KUSSMAUL's BREATHING and VOMITING. ALSO, as there is no insulin, there is nothing to tell the body to take in potassium, therefore TOTAL BODY POTASSIUM remains LOW, though in the blood it varies.

Question 29

Compare HHS and DKA

Answer 29

HHS - caused by hyperglycemia but not ketonemia as pt has some insulin therefore suppressing ketone production HHS - no abdo pain but other symptoms of DKA like collapse, confusion, vomiting, nausea, kussmaul breathing HHS - normal ketones <3mmol/L and normal pH, but plasma glucose above 30 DKA - ketones above 3mmol/L, pH below 7.3, plasma glucose above 11

Question 30

Causes of DKA/HHS

Answer 30

Infection Illness Non-adherence to diabetes meds May be initial presentation of diabetes

Question 31

Mx of DKA/HHS

Answer 31

IV fluids + potassium chloride if below 5.5 THEN IV insulin, only if potassium is above 3.5 If sugar below 14, give dextrose Treat underlying cause

Question 32

Stages and features of diabetic retinopathy / maculopathy

Answer 32

Background: blot and dot haemorrhages/hard exudates (paint first) Pre-proliferative: background + cotton wool spots (add cotton) Proliferative: non-proliferative + new vessels on disk (neovascularisation) (add strawberry laces) Maculopathy: hard exudates (i.e., background retinopathy) happens to be near macula

Question 33

Management of diabetic retinopathy

Answer 33

Background - improve sugar control Pre-proliferative and proliferative - pan-retinal photocoagulation Maculopathy - grid photocoagulation