01122019 1 2 How this lecture will work Overview of topics prioritised and simplified Key important points are written on the slides Everything I say including some extra details that you almost defo dont need will be in the notes at the bottom no need to make your own notes ID: 920740
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Slide1
Adil Aliaa13816
LCRS 1: Endo 15-18
01/12/2019
1
Slide22
How this lecture will work
Overview
of topics (prioritised and simplified)
Key, important points are written on the slides
Everything I say, including some extra details (that you almost defo don’t need), will be in the notes at the bottom - no need to make your own notes!
Understand (basic) Endo conceptually to succeed – don’t deep what you don’t need
QUANTITY NOT QUALITY
Slide33
Learning Objectives
Endo 15: Type I Diabetes Mellitus
Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and explain the physiological basis of treatment
Hypoglycaemia: Define hypoglycaemia, explain its clinical presentation, risk factors for development, and management including prevention.
Endo 16: Type II Diabetes Mellitus
Type 2 Diabetes Mellitus: define type 2 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and explain the physiological basis of treatment
Endo 17: Microvascular complications of diabetes & diabetic foot
Endo 18: Macrovascular complications of diabetes
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
Slide44
Endo 15: Type I Diabetes Mellitus
Originally taught by Dr Harvinder Chahal on 21/11/19
Slide5LO: Type 1 Diabetes Mellitus:
define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and explain the physiological basis of treatment
5
Type 1 Diabetes: Definition
Definition:
Autoimmune insulin insufficiency
Slide6LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology,
explain the aetiology, pathophysiology, clinical presentations and explain the physiological basis of treatment
6
Type 1 Diabetes: Aetiology
T1DM is a mixture of environmental and genetic factors….
….leading to
autoimmune destruction
of islet cells….
….leading to
insulin deficiency
….leading to
hyperglycaemia.
Consider pancreatic damage or other endocrine conditions
Slide7LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology,
pathophysiology, clinical presentations and explain the physiological basis of treatment
7
Type 1 Diabetes: Pathophysiology
LIVER GLUCOSE
(FROM GLYCOGEN)
BLOOD GLUCOSE
MUSCLE
GLUCOSE
INSULIN
AMINO ACIDS
(FROM PROTEIN)
BLOOD AMINO ACIDS
PROMOTES
INHIBITS
INSULIN
ADIPOSE GLYCEROL
(FROM TRIGLYCERIDES)
BLOOD GLYCEROL
INSULIN
ADIPOSE FATTY ACIDS
(FROM TRIGLYCERIDES)
INSULIN
BLOOD FATTY ACIDS
LIVER FATTY ACYL CoA
BLOOD KETONE BODIES
Slide8LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology,
pathophysiology, clinical presentations and explain the physiological basis of treatment
8
Type 1 Diabetes: Pathophysiology
Notice the steep drop off
C-peptide drop
Auto-antibody rise
‘Relapsing-remitting’ theory
Slide9LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology,
clinical presentations and explain the physiological basis of treatment
9
Type 1 Diabetes: Clinical Presentation
Symptoms
Polydipsia
Polyuria
Nocturia
Blurred vision
Thrush
Weight loss
Fatigue
Signs
Dehydration
Cachexia
Glycosuria
Diabetic Ketoacidosis (DKA signs):
Hyperventilation
Vomiting
Abdominal pain
Ketone breath
Ketonuria
Slide10LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology,
clinical presentations and explain the physiological basis of treatment
10
Type 1 Diabetes: Clinical Presentation
COMMONLY patients are young and lean due to weight loss……
….but not always e.g. LADA and childhood T2DM
Can present with diabetic ketoacidosis (DKA) symptoms:
…..but this can be a feature of T2DM
Monogenic diabetes can present as Type 1 or 2 – careful with children
Slide11LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
11
Type 1 Diabetes: Treatments
Short term:
Aim to reduce early mortality and avoid acute metabolic decompensation
Long term:
Aim to prevent long term complications (e.g. retinopathy, neuropathy – will cover in detail later)
Slide12LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
12
Type 1 Diabetes: Treatments
Medical treatment:
Exogenous (external) insulin – needs to mimic bodily release, can do so via manual injections or insulin pump
Islet cell transplants – requires immunosuppression
Overmedication results in hypoglycaemia
Dietary treatment:
Reduce fat and refined carbohydrate consumption
Increase complex carbohydrate consumption
Spread out meals and snacks
Slide13LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
13
Type 1 Diabetes: Treatments
Short term: measure blood glucose with capillary glucose (finger prick) or CGM
Long term: measure blood glucose with HbA1c
Slide14LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
14
SBA 1
Q: Which of the following statements regarding diabetes is correct?
A) Insulin promotes the movement of glucose from muscles into the blood
B) Protein is broken down into amino acids and released into the blood to enter the liver for glycogenesis
C)
B-peptide is a protein bound to insulin – it’s levels can be measured to assess the extent of insulin deficiency
D) DKA occurs when an excess of ketone bodies causes the blood to turn alkaline
E) Islet cell autoantibodies can be used to differentiate between Type 1 and Type 2
Slide15LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
15
SBA 1
Q: Which of the following statements regarding diabetes is correct?
A) Insulin promotes the movement of glucose from muscles into the blood
B) Protein is broken down into amino acids and released into the blood to enter the liver for glycogenesis
C)
B-peptide is a protein bound to insulin – it’s levels can be measured to assess the extent of insulin deficiency
D) DKA occurs when an excess of ketone bodies causes the blood to turn alkaline
E) Islet cell autoantibodies can be used to differentiate between Type 1 and Type 2
Slide16LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
16
Type 1 Diabetes: Summary
Autoimmune destruction of beta cells leads to insulin insufficiency
This causes hyperglycaemia
Body tries to compensate by breaking down fat and protein and excreting excess glucose
This leads to polydipsia, polyuria, nocturia, weight loss etc
DKA is a serious complication
T1DM patients need an insulin replacement and a way of monitoring blood glucose
Dietary interventions also important
Slide1717
Endo 16: Type II Diabetes Mellitus
Originally taught by Dr Harvinder Chahal on 21/11/19
Slide18LO: Type 2 Diabetes Mellitus:
define type 2 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and explain the physiological basis of treatment
18
Type 2 Diabetes: Definition & Epidemiology
Definition:
chronic hyperglycaemia sufficient to cause long term damage to specific tissues, notably the retina, kidney, nerves and arteries.
Epidemiology:
Increasing prevalence across all populations
Increasingly in younger people
Seen most in those who move from rural to urban lifestyle
Slide1919
Type 2 Diabetes: Aetiology
LO: Type 2 Diabetes Mellitus: define type 2 diabetes mellitus, recall the epidemiology,
explain the aetiology
, pathophysiology, clinical presentations and explain the physiological basis of treatment
Exact mechanism unknown – look at MODY
T2DM is a mixture of environmental (obesity) and genetic factors….
….leading to
over secretion of insulin AND (some) lack of insulin
....leading to
insulin resistance
of tissues AND eventual B cell failure….
….leading to
hyperglycaemia
.
Insulin resistance cause progression of atheroma…..
….leading to
macrovascular complications
.
Hyperglycaemia leads to
microvascular complications
.
Slide2020
Type 2 Diabetes: Aetiology
LO: Type 2 Diabetes Mellitus: define type 2 diabetes mellitus, recall the epidemiology,
explain the aetiology
, pathophysiology, clinical presentations and explain the physiological basis of treatment
Resistance makes the secretion worse
A lot more genetic than people think
Speculated contributing factors:
IUGR
Fatty acids
Pancreatic damage or other endocrine conditions
T2DM is about supply and demand
Slide2121
Type 2 Diabetes: Aetiology
LO: Type 2 Diabetes Mellitus: define type 2 diabetes mellitus, recall the epidemiology,
explain the aetiology
, pathophysiology, clinical presentations and explain the physiological basis of treatment
Microbiota may influence T2DM
Adipocytes, and therefore obesity, is very important in T2DM:
Multiple adipocytokines are linked to T2DM
Central adipocytes are more important
70-80% of T2DM patients are obese
Slide22LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology,
pathophysiology, clinical presentations and explain the physiological basis of treatment
22
Type 2 Diabetes: Pathophysiology
LIVER GLUCOSE
(FROM GLYCOGEN)
BLOOD GLUCOSE
MUSCLE
GLUCOSE
INSULIN
AMINO ACIDS
(FROM PROTEIN)
BLOOD AMINO ACIDS
PROMOTES
INHIBITS
INSULIN
ADIPOSE GLYCEROL
(FROM TRIGLYCERIDES)
BLOOD GLYCEROL
INSULIN
ADIPOSE FATTY ACIDS
(FROM TRIGLYCERIDES)
INSULIN
BLOOD FATTY ACIDS
VLDL TG
Small dense VLDL
Slide2323
Type 2 Diabetes: Clinical Presentation
Symptoms:
Polydipsia
Polyuria
Nocturia
Blurred vision
Thrush
Fatigue
LO: Type 2 Diabetes Mellitus: define type 2 diabetes mellitus,
recall the epidemiology, explain the aetiology, pathophysiology,
clinical presentations
and explain the physiological basis of treatment
Signs
Obesity
Glycosuria
May present with complications:
Micro: Retinopathy
Macro: Ischaemic Heart Disease
Metabolic: Lactic acidosis
Slide2424
Type 2 Diabetes: Treatments
LO: Type 2 Diabetes Mellitus: define type 2 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
Short term aim
: treat symptoms, reduce (unlikely) chance of acute metabolic complications
Long term aim
: reduce chance of chronic complications
Education
Dietary treatment:
Reduce saturated fat and refined carbohydrate consumption
Increase unsaturated fat and complex carbohydrate consumption
Increase fibre consumption
Lower salt intake
Lifestyle treatment is expensive but more effective than medication
Slide2525
Type 2 Diabetes: Treatments
LO: Type 2 Diabetes Mellitus: define type 2 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
Metformin
- first line
AKA biguanide
Overweight patients where diet hasn’t worked
Reduced insulin resistance
Has GI side effects
Contraindicated for sever cardiac/renal/liver failures
Sulphonylureas
and
metaglinides
e.g.
Glibenclamide
Act on remaining beta cells to bypass faulty glucose metabolism and make more insulin
Causes weight gain
Slide2626
Type 2 Diabetes: Treatments
LO: Type 2 Diabetes Mellitus: define type 2 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
a-Glucosidase inhibitor
e.g. Acarbose – slows glucose absorption, causes flatus
Thiazolidinediones
e.g. Pioglitazone – reduce insulin resistance, weight gain is peripheral not central
GLP-1 agonist
e.g. liraglutide / DPP4 inhibitor (gliptins) :
Incretin effect – stimulates insulin & suppresses glucagon
Increases fullness and stimulate weight loss
Restore beta cell sensitivity
DPP4 inhibitor (oral) can prolong half life of GLP-1 agonist
Slide2727
Type 2 Diabetes: Treatments
LO: Type 2 Diabetes Mellitus: define type 2 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
Other medical treatments:
Orlistat
- weight loss
Gastric bypass – reduce intake and absorption
SGLT2 inhibitor e.g.
empaglifozin
– increase glycosuria
Insulin – when eventual pancreatic failure kicks in
Treatments for blood pressure and dyslipidaemia
Complication screening
Slide28LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
28
SBA 2
Q: What is the main action of sulfonylureas?
A) Increase peripheral sensitivity to insulin
B) Bypass faulty glucose metabolism in beta cells to make more insulin
C)
Exert an incretin effect to
stimulate insulin & suppress glucagon
D) Slow down the absorption of glucose
E) Act as a GI lipase inhibitor to promote weight loss
Slide29LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
29
SBA 2
Q: What is the main action of sulfonylureas?
A) Increase peripheral sensitivity to insulin
B) Bypass faulty glucose metabolism in beta cells to make more insulin
C)
Exert an incretin effect to
stimulate insulin & suppress glucagon
D) Slow down the absorption of glucose
E) Act as a GI lipase inhibitor to promote weight loss
Slide30LO: Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and
explain the physiological basis of treatment
30
Type 2 Diabetes: Summary
Slide3131
Endo 18: Macrovascular complications of diabetes
Slide32LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
32
Atheroma
Artery wall starts normal
Inside wall, foam cells and intracellular lipid collection begins
This turns into fatty streaks (around age 20)
Small extracellular pools develop
Ends up as fibroatheroma with multiple lipid cores and fibrotic / calcified layers
This can lead to a lesion e.g. haemorrhage
Slide33LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
33
Atheroma
Risk factors for atheroma / cardiovascular risk:
High blood glucose
Low HDL
High BP
Waist circumference
Insulin resistance
Adipocytokines
……so all very similar to diabetes
Insulin resistance is associated with atheroma development
Slide34LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
34
Macrovascular disease
Diabetes
increases risk
of cardiovascular disease
Higher glucose levels increase risk of macrovascular disease
Microvascular disease = morbidity
Macrovascular disease = morbidity AND mortality
Macrovascular diseases
(e.g. cerebrovascular disease, ischaemic heart disease, peripheral vascular disease) are
systemic and widespread
Treatments ONLY targeting glucose are not effective at reducing cardiovascular risk –
target other risk factors e.g. blood pressure, dyslipidaemia, smoking
Slide3535
Endo 17: Microvascular complications of diabetes & diabetic foot
Slide36LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
36
Microvascular complications
Poor diabetes control increases risk for microvascular complications:
Retinal artery disease –
retinopathy
Glomerular arteriole disease –
nephropathy
Vasa nervorum (nerve blood vessel) disease –
neuropathy
Risk factors for complications
Severity of hyperglycaemia (& hyperglycaemic background)
Hypertension
Genetic background
Slide37LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
37
Background Diabetic Retinopathy
Presentation
Hard exudates – yellow looking
Microaneurysms – vessels sprouting out
Blot haemorrhages – bleeds
Management
Improve glucose control
Warn patients that warning signs are present
Slide38LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
38
Pre Proliferative Retinopathy
Presentation
Cotton wool spots / soft exudates – sign of retinal ischaemia, faded yellow
Suggests general ischaemia
Management
Pan retinal photocoagulation
Slide39LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
39
Proliferative Retinopathy
Presentation
New vessels being made – not straight, growing in multiple directions
Management
Pan retinal photocoagulation
Slide40LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
40
Maculopathy
Presentation
Same as background retinopathy but the hard exudates are near the macula – can damage vision badly
Management
A grid of photocoagulation around the macula
Slide41LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
41
Nephropathy
Presentation
Hypertension
Proteinuria – urine dipstick
Decreasing kidney function
Risk factors
Age at diagnosis of diabetes (younger is worse)
Cardiovascular co-morbidities
Slide42LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
42
Nephropathy
Management
Diabetes control
Blood pressure control
ACE inhibitors
Stopping smoking
Slide43LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
43
Neuropathy
Aetiology
Neuropathy is blockage of vasa nervorum blood vessels which supply nerves
Peripheral neuropathy
is most common in diabetes patients
Mononeuropathy
– sudden motor loss,
eg
wrist drop or 3rd nerve palsy
Mononeuritis multiplex
– random combo of peripheral nerve lesions
Slide44LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
44
Neuropathy
Aetiology
Radiculopathy
– pain over spinal nerves affecting a dermatome
Autonomic neuropathy
– loss of (para)sympathetic nerves to GI tract, CVS etc
Slide45LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
45
Peripheral Neuropathy
Pathophysiology
Affects nerves in the feet – loss of sensation
More common in tall people
Can injure foot without realising
Presentation
Loss of ankle jerks
Loss of tuning fork vibration sense
Multi fractured foot (Charcot foot)
Slide46LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
46
The Diabetic Foot
Pathophysiology
Sensory neuropathy
– loss of sensation
Motor neuropathy
– imbalance of nerves and resulting anatomy
Limited joint mobility
– due to glucose sticking to proteins
Autonomic neuropathy
– loss of sweat and moisture
Peripheral vascular disease
– artery blockage
Trauma, weakened immunity, diabetic co morbidities
Slide47LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
47
The Diabetic Foot
Presentation
Neuropathic foot:
numb, warm, dry, pulses present, ulcers at pressure points
Ischaemic foot:
cold, pulseless, ulcers at foot margins
Neuro-ischaemic foot:
both, rip
Slide48LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
48
The Diabetic Foot
Management
Preventative:
control diabetes, inspect feet daily, get well fitting shoes, cut nails straight across, don’t walk barefoot
Surgery
– revascularisation, amputation
Pressure relief
– bed rest
Antibiotics
Slide49LO:
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
49
SAQ
Q: A man walks into clinic with a history of smoking, high blood pressure and a diabetic foot. What would be your initial treatment?
(3 marks)
A: Relieve pressure to foot, antibiotics, surgery e.g. revascularisation
Q: State 3 causes of foot ulcers
(3 marks)
A: Sensory / motor / autonomic neuropathy, limited joint mobility, trauma, PVD
Q: Name the tissue in the pancreas associated with endocrine function
(1 mark)
A: Islets of Langerhans
Q: How could you differentiate between Type 1 and Type 2 diabetes?
(4 marks)
A: Early vs late onset, ketone vs no ketone, insulin deficiency vs presence in blood, islet cell antibodies present vs absent
Slide5050
Learning Objectives
Endo 15: Type I Diabetes Mellitus
Type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and explain the physiological basis of treatment
Hypoglycaemia: Define hypoglycaemia, explain its clinical presentation, risk factors for development, and management including prevention.
Endo 16: Type II Diabetes Mellitus
Type 2 Diabetes Mellitus: define type 2 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and explain the physiological basis of treatment
Endo 17: Microvascular complications of diabetes & diabetic foot
Endo 18: Macrovascular complications of diabetes
Complications of Diabetes; explain the development and presentations of microvascular and macrovascular disease, recall risk factors for developing these complications and explain their management including prevention.
Slide5151
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