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METABOLIC > ENDOCRINOLOGY - DIABETES > Flashcards

ENDOCRINOLOGY - DIABETES Flashcards

1
Q

What’s the structure of insulin?

A

A 51 amino acid peptide hormone comprising 2 polypeptide chains

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2
Q

Where is insulin synthesised?

A

Beta cells of the pancreatic islets of Langerhans

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3
Q

What is insulins prime target organ?

A

The liver - 50% of secreted insulin is extracted and degraded in the liver with the remainder being broken down by the kidneys

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4
Q

Why does C-peptide provide a useful index of the rate of insulin secretion?

A

It is produced in equimolar amounts to endogenous insulin
C-peptide can assess a person’s own insulin secretion even if they receive insulin injections, and because the liver metabolizes a large and variable amount of insulin secreted into the portal vein but does not metabolise C-peptide, meaning blood C-peptide may be a better measure of portal insulin secretion than insulin itself

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5
Q

Where are most peptide hormones synthesised?

A

Pituitary gland
Pancreas
Parathyroid gland

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6
Q

What are insulins effects on muscle and adipose tissue?

A
  • it increases the rate of glucose transport across the cell membrane
  • it increases glycolysis by increasing hexokinase and 6-phosphofructokinase activity
  • it increases glycogenesis
  • decreases lipolysis and hence lowers the plasma fatty acid level
  • it stimulates lipogenesis
  • it increases the rate of transport of some amino acids into tissues
  • it increases the rate of protein synthesis
  • it decreases the rate of protein degradation in muscle
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7
Q

Why do glucose levels rise overnight aka the sundowner effect?

A

Low blood sugars from intake mean the body reacts by increases glycogenolysis, gluconeogenesis and decreases glycogenesis

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8
Q

Why is the pancreas known as a heterocrine gland?

A

Because its got exocrine and endocrine cells

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9
Q

What cells are present in endocrine pancreas? What are their functions?

A

Alpha cells - glucagon
Beta cells - insulin

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10
Q

What cells are present in exocrine pancreas? What are their functions?

A

Acinar cells - secrete digestive enzymes

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11
Q

What are islets of langerhans?

A

Areas of endocrine pancreas consisting of alpha and beta cells

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12
Q

What proportion of the pancreas is endocrine?

A

5%

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13
Q

Outline what happens in beta cells in a hyperglycaemic situation?

A

Glucose enters beta cell through GLUT-2 receptor -> glucose undergoes glycolysis -> ATP production -> ATP binds to a channel on the cell membrane, inhibiting it -> K+ now cannot leave the cell and so builds up inside the cell -> this increased membrane potential opens a voltage gated Ca2+ Channel so calcium floods in to the cell -> calcium links the cell membrane and vesicles of insulin and C-peptide and amylin -> fuse and move into the blood

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14
Q

Outline what happens when insulin reaches the liver?

A

Insulin binds to a tyrosine kinase receptor on the surface of the liver -> glucose enters the cell, independent of insulin, through the GLUT-2 receptor -> insulin can convert glucose into glycogen (glycogenesis) or convert it into pyruvate (glycolysis)

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15
Q

What happens when insulin reaches the muscles?

A

Glucose uptake : Insulin activates the tyrosine kinase receptor which stimulates GLUT-4 increasing glucose uptake into the muscle cell -> glucose can now undergo glycolysis
Insulin also stimulates the amino acid channels which increases amino acid uptake. This increases protein synthesis.
Insulin can also stimulate glycogenesis in the muscles

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16
Q

What happens when insulin reaches the adipose tissue?

A

Insulin binds to receptor which stimulates GLUT-4 and moves glucose into the cell. Glucose can now undergo glycolysis or be converted to glycerol or convert acetyl coA to fatty acids.
Glycerol and fatty acids combine to form triglycerides.

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17
Q

What are the susceptibility genes for T1 diabetes?

A

HLA DR3 and HLA DR4

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18
Q

What other autoimmune disease are the diabetes susceptibilit genes associated with?

A

RA
SLE
Coeliacs disease
Vitiligo

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19
Q

What do autoantibodies attack in diabetes? What are they called?

A

Beta cells in pancreas
Anti-islet cell antibodies
Anti-glutamic acid antibodies
Anti-insulin antibodies

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20
Q

Outline the pathophysiology of diabetes?

A

Antibodies damage beta cells in the pancreas which decreases insulin production which can lead to hyperglycaemia - this is because GLUT transporters expression is diminished

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21
Q

What is metabolic syndrome?

A

You need 3 of the following…
Fasting glucose >100mg/dL
Triglycerides >150mg/dL
HDL <50 if female or 40 if male
Blood pressure >130/85
BMI >35 in females or 40 in males

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22
Q

What’s the pathology behind the insulin resistance in type 2 diabetes?

A

A defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin

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23
Q

What’s the pathology behind type 2 diabetes?

A

defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin relative to increased demand leads to insulin hypersecretion by a depleted β-cell mass and progression towards absolute insulin deficiency

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24
Q

What symptoms does diabetes cause?

A

Polyuria
Glucosuria
Thirst
Weight loss
Increased hunger

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25
Q

Why does diabetes cause polyuria?

A

Glucose is osmotically active so glucosuria causes water to follow

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26
Q

Why does diabetes cause polydypsia?

A

Polyuria means blood volume starts to drop but glucose levels are still high (low fluid levels and high glucose = hyperosmolar blood)
This stimulates osmoreceptors in hypothalamus which triggers an increase in thirst

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27
Q

Why does diabetes cause unexplained weight loss?

A

When glucose is not being utilised in cells we get decreased ATP production. In response, other pathways must be used for sources of fuels
Increased lipolysis and proteolysis means breaking down fat and protein stores

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28
Q

Why does diabetes cause polyphagia?

A

Tissues aren’t getting the energy they need from glucose because of the insulin resistance. The body responds increasing hunger

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29
Q

How do you diagnose diabetes?

A

Diabetes symptoms plus…
Fasting glucose >7 mmol/L
Random glucose >11 mmol/L
Haemoglobin A1C >48mmol/mol

If asymptomatic then 2 abnormal glucose of HbA1c tests are required

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30
Q

What is haemoglobin A1C

A

Glycated haemoglobin (RBCs lifespan 3 months so this is a 3 month test)

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31
Q

When is the oral glucose tolerance test required?

A

Where there is diagnostic uncertainty
As well as for diagnosis of cystic fibrosis-related diabetes and gestational diabetes

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32
Q

What is pre-clinical diabetes?

A

a condition characterized by slightly elevated blood glucose levels, regarded as indicative that a person is at risk of progressing to Type 2 diabetes
This is when a person has impaired fasting glycemic and impaired glucose tolerance

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33
Q

What is non-enzymatic glycation?

A

excessive chemical attachment of glucose to proteins/lipids without the involvement of enzymes

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34
Q

Why can diabetes cause accelerate atherosclerosis?

A

Non-enzymatic glycation with proteins and lipids causes the synthesis of very inflammatory molecules which can cause inflammation to occur in blood vessels and LDL deposition.

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35
Q

Why can diabetes cause hyaline arteriolosclerosis?

A

Non enzymatic glycation results in protein deposits occurring in vessels and around the basemenebt membrane (hyaline arteriolosclerosis)

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36
Q

Whats the effect of atherosclerosis and hyaline arteriolosclerosis?

A

Decreased blood flow distal and decreases gas exchange across tissue because BM is thickened

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37
Q

What disease are associated with non-enzymatic glycation?

A

Coronary artery disease
Peripheral artery disease
Stroke
Retinopathy
Nephropathy

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38
Q

What are the 3 things classified with diabetic retinopathy?

A

Microaneurysms
Cotton wool spots
Flame haemorrhages
(All affect vision)

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39
Q

Why can diabetes lead to progression of cataracts?

A

the denaturation of the protein and other components of the lens of the eye, which renders it opaque

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40
Q

What proportion of those with diabetes does diabetic retinopathy affect?

A

One third

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41
Q

What are the earliest changes seen in the retina?

A

Background retinopathy
Microaneurysms which may leak small amounts of bloods but sights is not affected
Cotton wool spots are also seen where occluded vessels cause micro infarcts

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42
Q

What is stage 2 diabetic retinopathy?

A

Pre-proliferative retinopathy
Damage to walls of veins causes venous beading and elongation to occur, causing venous loops
At this stage you’re at high risk of vision being affected
You will be advised to have more frequent screening appointments

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43
Q

What is stage 3 diabetic retinopathy?

A

Proliferative retinopathy
Blockage of blood vessels leads to ischaemia = release of VEGF which promotes neovascularization
Haemorrhage and retinal detachment can occur as a result and now you’re at very high risk of losing vision
Treatment will now be offered to stabilise your vision but it cannot restore it

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44
Q

What is maculopathy?

A

Fluid from leaking vessels is cleared poorly in the macular area because the anatomy is different. If clearance fails then macular oedema can occur which can distort and thicken the retina at the macula, causing a loss of central vision

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45
Q

What are some treatment options for diabetic retinopathy?

A

Laser photocoagulation
Eye injections - anti-VEGF drugs
Vitreoretinal surgery

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46
Q

Outline the eye screening for diabetics in the UK?

A

All people with diabetes over the age of 12 years are offered annual measurement of their acuity and retinal photographs.

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47
Q

What is diabetic nephropathy?

A

gradually increasing urinary albumin excretion and blood pressure as the glomerular filtration rate falls insidiously towards end-stage renal disease

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48
Q

What’s the pathophysiology of diabetic nephropathy?

A

As the kidney becomes damaged by diabetes, the afferent arteriole becomes vasodilated to a greater extent than the efferent glomerular arteriole. This increases the intraglomerular filtration pressure, further damaging the glomerular capillaries. This contributes to mesangial cell hypertrophy and increased secretion of extracellular mesangial matrix material, eventually leading to glomerular sclerosis. These changes result in disruption of the protein cross-linkages that normally make the membrane an effective filter. In consequence, there is a progressive leak of proteins into the urine.

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49
Q

How do we screen for diabetic nephropathy?

A

The urine of all people with diabetes should be checked at least annually for the presence of microalbuminuria

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50
Q

How do we manage diabetic nephropathy?

A

Similar to CKD:
- antihypertensives to reach bp <130/80
ACEi and ARBs
- meticulous glycemic control

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51
Q

Whats the main cause of diabetic neuropathy?

A

occlusion of the vasa nervorum leading to ischaemia of nerves

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52
Q

What are early signs of diabetic peripheral neuropathy?

A

Loss of vibration, pain and temperature sensation in the feet

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53
Q

What do diabetic feet look like?

A

High arch, clawing of toes which causes abnormal distribution of pressure on walking resulting in callus formation under first metatarsal head or tips of toes

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54
Q

What are the effects of autonomic neuropathy?

A

Sweating
Cardiac denervation
Postural hypotension
Gastroparesis
Diarrhoea
Atonic bladder
Erectile dysfunction

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55
Q

What are the effects of somatic neuropathy?

A

Ocular palsies
Carpal tunnel syndrome
Small muscle wasting
Amyotrophy
Painful neuropathy
Neuropathic foot

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56
Q

What is Charcot neuroarthropathy?

A

a chronic, devastating, and destructive disease of the bone structure and joints in patients with neuropathy

it is characterized by painful or painless bone and joint destruction in limbs that have lost sensory innervation

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57
Q

How is diabetic foot screened for?

A

Healthcare professionals should screen for foot problems at least once a year; this process should include questions about past or present ulceration, an examination of the foot to detect structural abnormalities or callus formation and an assessment of neuropathy and peripheral vascular disease

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58
Q

How can you distinguish between ischaemia and neuropathy in the diabetic foot?

A

Ischaemia - claudation, rest pain, trophic changes on inspection, cold, pulseless, painful ulceration on heels and toes

Neuropathy - painless, high arch, clawing of toes, no trophic changes, warm, bounding pulses, painless ulcers on plantar region

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59
Q

What are some macrovascular complications of diabetes?

A

Heart failure
Stroke
MI
PVD

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60
Q

How do you manage atherosclerotic cardiovascular risk?

A

Tight glycemic control - SGLT2 inhibitors and GLP-1 receptor agonists have protective effect
Anti-hypertensive treatment - ACEi and ARBs
Statins for those over 40 or after 10 year history of diabetes with micro vascular complications
Smoking cessation
Low dose aspirin but is associated with morbidity from bleeding

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61
Q

What cancers are more common in type 2 diabetes?

A

Cancer of uterus and pancreas is doubled in risk
20-50% increase in risk of colorectal and breast cancer

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62
Q

Why is fracture risk increased in both type 1 and type 2 diabetes?

A

Type 1 have lower bone mineral density due to deficiency in insulin and insulin-like growth factors

Type 2 - unknown reason

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63
Q

How is type 1 diabetes treated?

A

Insulin

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64
Q

How is type 2 diabetes treated?

A

Exercise
Diet
Anti diabetic meds
Insulin

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65
Q

How do you treat diabetic neuropathy?

A

Gabapentin and pregabalin

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66
Q

How do you treat diabetic nephropathy?

A

ACEi and ARBs
Monitor kidney function
Check microalbuminuria

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67
Q

What are symptoms of hypoglycaemia?

A

Sweating
Confusion
Drowsiness
Coma
Palpitations
Weakness
Blurred vision
Seizures or fits
Collapsing or passing out

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68
Q

What are possible causes of hypoglycaemia?

A

Taking too much anti-diabetic drugs e.g. insulin, sulfonylureas, glinides
Skipping or delaying a meal
Not eating enough carbs
Unplanned or intense exercise
Drinking alcohol

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69
Q

How do you treat hypoglycaemia?

A

If conscious and able to swallow then have 15-20g fast-acting carbohydrate by mouth e.g. pure fruit juice or dextrosol tablets, glucojuice, 3-4 heaped tsps sugar dissolved in water

If unconscious or seizing and IV access available then give 100ml of 20% glucose over 15 mins or 200ml of 10% glucose over 15 mins

If the patient doesnt have IV access then give IM glucagon or glucose

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70
Q

What are the physiologic mechanisms to prevent hypoglycaemia?

A

Insulin decreases and counter regulatory hormones increase
Glucagon increases through glycogenolysis
Autonomic nervous system gets activated - causes symptoms
Neuroglycopenia

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71
Q

What are some counter regulatory hormones against insulin?

A

Cortisol
Growth hormone
Catecholamines

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72
Q

How much glucose is usually required to correct hypoglycaemia?

A

15 rule: have 15g carbs, wait 15 mins and measure blood sugar again
(Or 300ml of 5% dextrose)

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73
Q

What are the DVLA rules for driving with diabetes?

A

You have to let DVLA know when you have a diagnosis of diabetes but you can continue to drive unless you become hypglycaemia unawareness

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74
Q

What is hypoglycaemia unawareness

A

when someone doesn’t experience or perceive the symptoms of hypoglycemia

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75
Q

What are the major classes of antidiabetic drugs?

A

Biguanides
Sulfonylureas
Meglitinide
Thiazolidinedione
DPP-4 inhibitors
SGLT2 inhibitors

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76
Q

Whats the moa of Biguanides?

A

Increase insulin sensitivity and decreases hepatic gluconeogenesis

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77
Q

What are the side efefcts of metformin?

A

GI upset
Lactic acidosis
Vitamin B12 deficiency

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78
Q

Why isn’t metformin used in type 1 diabetes?

A

it acts only in the presence of endogenous insulin it is effective only if there are some residual functioning pancreatic islet cells.

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79
Q

What are contraindications for metformin?

A

Acute metabolic acidosis (DKA and lactic acidosis)
EGFR <30ml/min

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80
Q

Whats the moa of sulfonylureas?

A

They inhibit potassium rectifier channels in B cells which prevents K+ efflux and causes depolarisation of the cells = insulin vesicle release

81
Q

What are the contraindications of sulfonylureas?

A

Ketoacidosis

82
Q

What are side efefcts of sulfonylureas?

A

Hypoglycaemia
Weight gain
GI side effects

83
Q

Whats the moa of SGLT2 inhibitors?

A

Reversibly inhibits sodium-glucose co-transporter 2 (SGLT2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.

84
Q

What are the side efefcts of SGLT2 inhibitors?

A

Urinary infections and candidiasis
Hypovolemia - uncommon
DKA - rare
Weight loss

85
Q

What are the contraindications of SGLT2 inhibitors?

A

ketoacidosis

86
Q

Whats the moa of GLP-1 receptor agonists?

A

Analogues of GLP-1but are DPP-4 resistant so enhance insulin secretion and inhibit glucagon secretion from pancreatic islet cells
Increase the incretin effect

87
Q

Whats the side effects of GLP-1 receptor agonists?

A

Nausea and vomiting
Pancreatitis
Weight loss

88
Q

Whats the contraindications of GLP-1 receptor agonists?

A

Ketoacidosis and severe GI disease

89
Q

Whats the moa of DPP4 inhibitors?

A

inhibit DPP4 which prevents the rapid inactivation of GLP-1, which in turn increases insulin secretion and reduces glucagon secretion

90
Q

What are side effects of DPP4 inhibitors?

A

Generally well tolerated but increases risk of pancreatitis

91
Q

What are contraindications for DPP4 inhibitors?

A

Ketoacidosis

92
Q

Whats the moa of thiazolidinediones?

A

Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake

93
Q

What are the side effects of glitazones?

A

weight gain 5-6kg. Pioglitazone can cause fluid retention precipitating heart failure. Small bone fractures, oedema and a small increased risk of bladder cancer

94
Q

What are the contraindications of glitazones?

A

history of heart failure, bladder cancer, uninvestigated macroscopic haematuria

95
Q

What is Monogenic diabetes?

A

Maturity onset diabetes if the young

96
Q

What are some secondary causes of diabetes?

A

Chronic pancreatitis
Endocrinopathies e.g. Cushing syndrome
Drugs e.g. steroids, thiazide diuretics and olanzapine

97
Q

What is the dawn phenomenon?

A

a natural rise in blood sugar that occurs in the early morning hours.

98
Q

Whats the difference between the GLUT 1,2,3,4 receptors?

A

GLUT 1,2,3 are all insulin independant
GLUT 4 is insulin dependant

99
Q

What are sick day rules for diabetes?

A

Keep taking your diabetes medication and checking your blood glucose
Try and drink sugar free fluids to prevent dehydration

100
Q

What makes insulin short acting, intermediate and long acting?

A

When you inject insulin under the skin, 6 insulins bind together to form a hexameric unit. This is too big to be absorbed into the circulation and so waits to be broken down into dimers and monomers and then can be absorbed into the circulation and have its actions.
The stability of the hexameter ad the slowing down of its dissociation into dimers and monomers determine the rate and duration of its action once injected. So, if the hexameter is unstable and breaks down fast the action is quick. Several substances have been added to insulin to make the hexameter more stable and delay its action.

101
Q

What is Lipohypertrophy?

A

fatty lumps may occur following overuse of a single injection site

102
Q

What is lipoatrophy?

A

As modern insulin is highly purified, allergy is rare however immunoglobulin G immune complexes against insulin can be formed and produce local atrophy of fat tissue.

103
Q

Outline the peak action time and duration of action of short acting insulin?

A

usually injected subcutaneously 30 minutes before a main meal so that the peak of blood insulin corresponds to the blood glucose rise after the meal. The time of peak action is about 1-3 hours and the duration of action is 4-8 hours

104
Q

Outline the peak action time and duration of action of long acting insulin?

A

The onset of action is 1-2 hours, the time of peak action is 4-12 hours and duration of action is up to 24 hours thereby providing background insulin cover.

105
Q

What is biphasic insulin?

A

30% short acting and 70% long acting insulin that’s injected twice daily before breakfast and dinner

106
Q

How can you monitor diabetic control?

A

Self monitoring of capillary BG
Continuous glucose monitoring of interstitial glucose
HbA1C

107
Q

Outline how intrauterine life can affect aetiology of diabetes type 2?

A

decreased birth weight and thrifty phenotype. there is a J-shaped relationship between low weight at birth and glucose intolerance later in life, particularly in those who gain excessive weight in adulthood (the concept is that poor nutrition early in life impairs beta cell development and function, predisposing to diabetes later on)

108
Q

When are most type 2 diabetics diagnosed?

A

Over 40

109
Q

How can you prevent or delay the onset of type 2 diabetes?

A

Reduce body weight
Reduce dietary fat
Increase dietary fibre
Moderate physical activity 30 mins a day
Metformin and orlistat can reduce the incidence also but the effects are not as great as lifestyle changes and should only be reserved for those who cannot change their lifestyle or whose glucose concentration rises despite lifestyle changes

110
Q

What anti diabetic drug should you give for patients with established atherosclerotic CVD or CHF?

A

Metformin or SGLT2 inhibitor

111
Q

Outline the medication treatment regime for type 2 diabetes?

A

Start in metformin unless contraindicated and support the person to aim for an HbA1c level of 48mmol/mol.
If HbA1c rises to 58 then consider dual therapy of metformin and DPP-4i/glitazone/Sulphonylurea/SGLT2i and support the person to aim for HbA1c level of 53.
If not then consider triple therapy of… metformin, DPP-i and SU… or metformin, pioglitazone and SU… or metformin, SGLT2 and piogltazone/SU.
Otherwise, consider insulin based treatment.

112
Q

Whats the different between Monogenic and type 1 diabetes?

A

type 1 diabetes does not present in children before 6 months of age and so infant who develop diabetes at this age are more likely to have Monogenic defect (maturity onset diabetes of the young)
People with MODY are more likely to have an affected parent.
The pancreas continues to produce insulin in people with MODY. In type 1 diabetes insulin production is very low or stops entirely three to five years after diagnosis

113
Q

What blood glucose is hypoglycaemia?

A

<4 mmol/L

114
Q

Why do patients with adrenal insufficiency get hypoglycaemic much faster than those who are not?

A

Depleted cortisol increases insulin sensitivity (no counter regulation)

115
Q

What are the major risk factors for macrovascular disease?

A

Hypertension, smoking, dyslipidaemia

116
Q

What are the causes of DKA?

A

Decreased insulin supply/ insulin deficiency - undiagnosed diabetes or a diabetic not complying with insulin, pump failure
Increased insulin demand - infections, inflammation, intoxication, infarction, pregnancy, ischaemic and iatrogenic

117
Q

What infections can trigger DKA?

A

Pneumonia, UTIs or cellulitis

118
Q

What inflammatory conditions can trigger DKA?

A

Pancreatitis and cholecystitis

119
Q

What toxins can cause DKA?

A

Alcohol
Cocaine
Metamphetamines

120
Q

What infarctions can trigger DKA?

A

Acute MI
Cerebrovascular stroke

121
Q

What are iatrogenic causes of DKA?

A

Corticosteroids and surgery

122
Q

Why can corticosteroid use trigger DKA?

A

Steroids can induce hyperglycaemia by inducing insulin resistance by effects on insulin receptors in liver, muscle and adipose tissue

123
Q

Why can surgery trigger DKA?

A

Surgery and anaesthesia cause the release of cortisol which make the body less sensitive to insulin = hyperglycaemia

124
Q

Outline the pathology behind diabetic ketoacidosis when you have an insulin deficiency?

A

Not enough insulin to meet demands leads to a drop in ATP
The body starts using triglycerides for energy; glycolysis to FFA and glycerol, the FFA get converted into acetyl coA through beta oxidation. Acetyl CoA is converted to ketone bodies (ketogenesis)
Ketone bodies get into the blood stream and can release protons causing ketoacidosis.

125
Q

Outline the pathology behind diabetic ketoacidosis when you have an increase in insulin demand?

A

Increased stress triggers sympathetic NS which causes release of catecholamines which stimulates glucagon production by pancreatic alpha cells. These can promote gluconeogenesis and glycogenolysis at the liver. It can also generate lipolysis leading to ketoacidosis.
The increase in glucose means glucosuria and osmotic diuresis = polyuria and dehydration
Little water and lots of glucose in the blood = hyperosmolar state

126
Q

Whats the difference between DKA and hyperglycaemic hyperosmolar syndrome?

A

DKA is mostly caused by dehydration and ketoacidosis and onset is <1 day. Most common in T1 diabetics because of insulin deficiency

HHS is mostly caused by dehydration and hyperosmolarity. Onset is usually >1 day. Seen more commonly in T2 diabetes. (Think: common in T2 diabetics who fall and can’t access insulin. They can produce a little bit so wont fall into ketosis or acidosis but not enough to control glucose. Glucose will rise and cause glucosuria = osmotic diuresis = dehydration = hypovolemic)

127
Q

Why does ketoacidosis cause nausea and vomiting?

A

Ketone bodies trigger CTZ in the medulla oblong at a - stimulates emetic centre - N+V

128
Q

Why does ketoacidosis cause palpitations?

A

Ketone bodies release H+ into the blood stream. For every H+ that goes into the cell, K+ is pumped out so K+ accumulates in extracellular fluid.
The Na+/K+ ATPase is driven by insulin so K+ cannot be pushed into the cell if no insulin
This means there’s a net movement of K+ out of the cell into the blood
This may cause hyperkalaemia which can cause arrhythmias

129
Q

Why does ketoacidosis case Kussnauls respiration?

A

Ketone bodies create acidic environments in the blood which stimulates the peripheral chemoreceptors which creates a reflex that tries to increase respiratory rate - trying to breathe out more CO2

As you breathe off acetone it causes a fruit breath

130
Q

What is HAGMA?

A

High anion gap metabolic acidosis

131
Q

What symptoms are caused by dehydration in DKA?

A

Reduced skin turgor, dru mucous membranes, hypotension, decreased renal perfusion/urine output, diaphoresis and reflex tachycardia

132
Q

Why does DKA cause reflex tachycardia and diaphoresis?

A

Dehydration and decreased blood volume triggers baroreceptors which increase sympathetic nervous system activity

133
Q

Why does DKA cause seizures and comas?

A

Water inside cells of neurones in brains and muscles moves into blood which is hyperosmolar due to DKA. This shrinks the cells of the nervous system which can cause altered mental state and can progress to seizures and coma
Shrunk muscle cells causes muscle weakness

134
Q

What investigations do you need for DKA?

A

FBC
CMP
ABG
UA
Ketones
Serum osmolality
12 lead ECG +/-

135
Q

Outline how you can work out if its DKA or hyper osmolality hypoglycaemia syndrome?

A

Serum glucose is higher in HHS
PH in DKA will be lower
HCO3- will be lower in DKA
Ketones positive in DKA but not in HHS
Increased anion gap in DKA >12 but in HHS it will be <12
Variable serum osmolality in DKA but super high in HHS

136
Q

In which diabetics is hyper osmolality hypoglycaemia syndrome most likely?

A

Type 2 as still have some insulin

137
Q

How shouldyou manage DKA?

A

Admit and treat with 500ml 0.9% NaCl over 15 minutes and another 500ml bolus over 15 mins if SBP still <100mmHg

Commence a fixed rate insulin infusion at 0.1unit/kg/hour
Potassium chloride replacement

Assess patient
Further investigations
Establish monitoring regime - hourly capillary blood glucose, ketones, venous bicarbonate and potassium etc

138
Q

Why should you wait until hypokalaemia is restored before starting insulin?

A

Insulin lowers serum K+ by moving it into cells

139
Q

Which electrolytes will be high in urine in DKA?

A

K+ and phosphate as they do not enter cells with glucose

140
Q

What conditions cause preserved appetite but decreased weight?

A

Hyperthyroidism
T1 diabetes
Malabsorption
Phaeochromocytoma

141
Q

Whats the diagnostic criteria for DKA?

A

Blood glucose >11mmol/L
Ketones >3mmol/L
PH <7.35
HCO3- <15

142
Q

What investigations should you do on a diabetic check?

A

FBC
HbA1c
Albumin:creatinine ratio and kidney checks
Thyroid
LFTs
Lipid panel
Vitamin B12 and folate
Feet - sensation, pulses, skin changes, calluses and ulcers
Eyes - fundocscopy
Erectile dysfunction

143
Q

What the link between thyroid disease and diabetes?

A

Insulin levels can affect thyroid hormone production and activity - high thyroid = high metabolism = insulin eliminated too soon
- low thyroid = insulin lingers = hypoglycaemia
Thyroid disease also increases your risk of metabolic syndrome and therefore T2 diabetes

144
Q

Why should you check LFTs in diabetic patients?

A

Insulin metabolises a lot of anti diabetic drugs
Screen for steatohepatitis

145
Q

Why should you check B12 and folate levels in diabetics?

A

Metformin causes deficiency
Also checks for pernicious anaemia (an associated autoimmune condition)

146
Q

What can make HbA1C reading inaccurate?

A

Haemolysis
Alcoholism
Chronic liver disease
Pregnancy second trimester
Sine drugs e.g. sulfonamide, antiretrovirals, hydroxyurea
Some genetic haemoglobin disorders such as sickle cell and thalassaemia

147
Q

What is the relationship between obesity and type 2 diabetes?

A

There is a seven times greater risk of diabetes in obese people compared to those of healthy weight, with a threefold increase in risk for overweight people

High BMI and large weight circumference are both associated with increased likelihood of developing diabetes

148
Q

What are the likely mechanisms for the link between type 2 diabetes and obesity?

A

Abdominal obesity may cause fat cells to release pro-inflammatory chemicals which make the body less sensitive to insulin
When insulin resistance is accompanied by dysfunction of pancreatic islet beta-cells it leads to failure to control blood glucose

149
Q

Outline the pharmacokinetics of rapid -acting insulin?

A

Onset 5-15 mins
Peak 1 hour
Duration 3-4 hours

150
Q

Outline the pharmacokinetics of short -acting insulin?

A

Onset 30 mins
Peak 2-3 hrs
Duration 4-6 hours

151
Q

Outline the pharmacokinetics of intermediate -acting insulin?

A

Onset 1-2 hours
Peak 6-10 hours
Duration 10-16 hrs

152
Q

Outline the pharmacokinetics of long -acting insulin?

A

Onset 1-4 hrs
Peak not defined
Duration 24 hours

153
Q

What are examples of rapid-acting insulin?

A

Insulin lispro
Insulin aspart
Insulin glulisine

154
Q

What are examples of short-acting insulin?

A

Regular insulin

155
Q

What are examples of intermediate-acting insulin?

A

NPH insulin

156
Q

What are examples of long-acting insulin?

A

Insulin glargine
Insulin detemir
Insulin degludec

157
Q

What is diabetes insipidus?

A

When the kidneys reabsorbed too little water causing polyuria which is very dilute
associated with polyuria, dilute urine and polydypsia and symptoms of hypernatraemia
Can be central, primary, nephrogenic and gestational

158
Q

What is central diabetes insipidus?

A

Abnormal secretion and synthesis of ADH

159
Q

What are the causes of central diabetes insipidus?

A
  • familial hypothalamic diabetes insipidus (autosomal dominant mutation of ADH gene)
  • tumours (craniopharyngioma and pinealoma)
  • Trauma and surgery
160
Q

What is primary polydypsia?

A

A type of diabetes insipidus
Ingestion of large quantities of water, excess IV fluids
which reduces ADh release
Can be psychological e.g. schizophrenia and compulsive drinking

161
Q

What is nephrogenic diabetes insipidus?

A

Problems in kidneys response to ADH
May be a problem a mutation of ADH receptor (congenital)
It can also be acquired: Polycystic renal disease, renal ischaemia, hypercalcaemia, hypokalaemia, lithium and demeclocyclin

162
Q

What is gestational diabetes insipidus?

A

Placenta releases vasopressinase which breaks down vasopressin
It can’t exert its full effects
Usually starts week 8 and peaks in trimester 3

163
Q

How can you test if its complete central or nephrogenic diabetes insipidus?

A

Do a dehydration test and at hour 10 give desmopressin (synthetic vasopressin/ADH). In central DI the urine osmolality will increase but it will not in nephrogenic because the kidneys are damaged so that even at sufficient ADH levels they cannot exert their effect

164
Q

How much urine does someone with diabetes insipidus excrete a day?

A

3L

165
Q

How do you treat diabetes insipidus?

A

Desmopressin in central and gestational diabetes
Thiazide diuretics in nephrogenic diabetes as it increases urine excretion of Na+ which reduces blood osmolality and stops polydypsia
For dipsogenic diabetes, behavioural therapy may be needed

166
Q

What are the risk factors for gestational diabetes?

A

BMI >30
Previous macrosomic baby
Previous gestational diabetes
First degree relative with diabetes

167
Q

Do we screen for gestational diabetes?

A

For women who’ve previously had gestational diabetes, an oral glucose tolerance test should be performed as soon as possible after booking as well as at 24-48 weeks if the first test is normal

168
Q

When do you offer insulin in gestational diabetes?

A

Fasting glucose >=7
Plasma glucose is 6-6.9mmol/L and there is evidence of complications such as macrosomia or hydramnios

169
Q

What are the complications of gestational diabetes?

A

Macrosomia
Shoulder dystocia
Polyhydramnios

170
Q

What are 2 examples of incretins?

A

gastric inhibitory peptide (GIP) which is glucose dependent and released from the duodenum, and glucagon-like peptide (GLP-1) produced from the distal ileum.

171
Q

Which anti-diabetic drugs are most likely to cause weight gain?

A

Insulin and thiazolidinediones

172
Q

How can alcohol cause hypoglycaemia?

A

the carbohydrates in alcoholic drinks can cause blood glucose to rise. This is then followed by the alcohol inhibiting glycogenolysis and so causing a late hypoglycaemia, in this case, through the night.

173
Q

What is neuroglycopenia?

A

The shortage of glucose in the brain resulting in alteration of neuronal function

174
Q

Why can GH abuse cause diabetes?

A

growth hormone mobilises glucose from fat stores to build muscle, thus increasing its concentration in the blood. Subsequently, the pancreas has to secrete greater amounts of insulin to combat the increased levels of glucose.

175
Q

Which drugs can impair glucose tolerance?

A

thiazides - furosemide (less common)
steroids
tacrolimus, ciclosporin
interferon-alpha
nicotinic acid
antipsychotics

176
Q

How can maternal diabetes affect foetal development?

A

It can cause…
Macrosomia
Neural tube defects
Polyhydramnios
Preterm labour
Caudal regression syndrome

177
Q

What are the 4 autoantibodies that are markers of beta cell autoimmunity in type 1 diabetes?

A

islet cell antibodies, antibodies to glutamic acid decarboxylase (GAD-65), insulin autoantibodies (IAA), and autoantibodies to protein tyrosine phosphatase.

178
Q

Outline the questions you should ask to find out if type 1 or type 2 diabetes?

A

Age of onset
Phenotype - weight, ethnicity
Treatment they’re on and how soon it was started after diagnosis
Symptoms - polyuria, polydypsia and weight loss - how soon and suddenly did they start
Other autoimmune conditions e.g. coeliacs, RA
Smoker? Hypertension? High cholesterol? (A way of asking this could be by asking of on cholesterol medications like statins)
Ask about complications: heart problems, cerebro-vascular problems, PVD, retinopathy, nephropathy, peiperhal neuropathy, feet changes

179
Q

What are the first line drugs for type 2 diabetes?

A

Metformin
SGLT2 inhibitors

180
Q

How do you manage HHS?

A

Iv fluids 0.9% NaCl
No IV insulin until glucose stops falling by 5mmol/hr using fluids (fluids dilute so glucose drops)
IV insulin if needed - low dose 0.5 units/kg/hour
Thromboprophylacis
Look for infections and treat

181
Q

What is the HbA1c target for diabetes managed by lifestyle and metformin?

A

<= 48mmol/mol

182
Q

What is the HbA1c target for diabetes managed by drugs which may cause hypoglycaemia?

A

<=53

183
Q

What are blood pressure targets for type 2 diabetics

A

Same as non diabetics
<80 years old - 140/90
>80 years old - 150/90

184
Q

In which diabetes will C peptide levels be low?

A

Type 1 diabetes - reflects lack of insulin production

185
Q

Whats the target blood glucose on waking and before meals at other times of day in type 1 diabetes?

A

Before meals 3-4mmol/l
On waking 5-7mmol/l

186
Q

Which type of diabetes is associated with Acanthosis nigricans and why?

A

Type 2 as its. Sign of insulin resistance

187
Q

Whats the fasting plasma glucose or HbA1c of pre-diabetes?

A

Fasting plasma glucose of 6.1-6.9
HbA1c level of 42-27mmol/mol

188
Q

Whats the pathology of micro vascular complications?

A

Basement membrane thickening of capillaries and arterioles causes small vessels to become progressively narrower and eventually become blocked = ischaemia and tissue dysfunction

189
Q

Outline the earliest changes seen in diabetic retinopathy?

A

Microaneurysms caused by outpouchings of the weakened capillary walls attempting to re-vascularise the ischaemic retina

190
Q

What are the grades of retinopathy?

A

Non-proliferative
Pre-proliferative
Proliferative
Advanced retinopathy

191
Q

Whats the pathogenesis of diabetic retinopathy?

A

Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls = precipitates damage to endothelial cells and pericytes
Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy. Pericyte dysfunction predisposes to the formation of microaneurysms. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia

192
Q

What are the 2 stages of diabetic retinopathy?

A

Non-proliferative DR
Proliferative DR

193
Q

What is background diabetic retinopathy?

A

Microaneurysms and haemorrhages
Hard exudates

194
Q

What is pre-proliferative diabetic retinopathy?

A

Cotton wool spots
Venous beading
Intra-retinal micro vascular abnormalities

195
Q

What is seen in proliferative diabetic retinopathy?

A

Neovascularization
Fractional retinal detachment

196
Q

What is maculopathy?

A

Clinically significant macular oedema
Occurs when there is increased vascular permeability and resultant deposition of hard exudates in central retina. There is associated oedema

197
Q

At what point in diabetic retinopathy will visual acuity be loss?

A

Macular oedema can cause it
Vitreous haemorrhage
Retinal detachment

198
Q

What are cotton wool spots?

A

Aka soft exudates
Represent areas of retinal infarction

METABOLIC (43 decks)

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