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Endocrinology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What are the fasting glucose ranges?

A

<=6: Normal
6.1 - 6.9: Impaired
>=7: Diabetic

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2
Q

What are the OGTT 2hr glucose ranges?

A

<=7.7: Normal
7.7-11: Impaired
>=11: Diabetic

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3
Q

What is the diagnostic criteria for DM?

A

2 abnormal tests or 1 abnormal test + symptoms

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4
Q

What is HbA1c?

A

A form of haemoglobin that is measured primarily to identify the 3 month average of glucose plasma concentrations

Test is limited to 3month lifespan of RBCs

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5
Q

How is HbA1c formed?

A

Non-enzymatic glycation pathway by Gb exposed to glucose forming glyco-haemoglobin

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6
Q

What are the ranges of HbA1c?

A

42-47: Pre-diabetes
>46: Diabetic

Not yet in use in Glasgow

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7
Q

List 5 types of diabetes

A
  1. T1D
  2. T2D
  3. Maturity onset diabetes of the young (MODY) - autosomal dominant
  4. Gestational D - 20% prevalence; 3rd trimester; increased BMI
  5. Secondary D: due to pancreatitis, CF, HHC (iron overload), steriod induced, acromegaly (increase GH from pituitary)
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8
Q

What type of diabetes in insulin deficient?

A

T1DM
MODY

Also secondary:
Pancreatitis
CF
HHC

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9
Q

What type of diabetes is insulin resistant?

A

T2DM
Gestational

Also secondary:
Steroid-induced
Acromegaly (GH)

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10
Q

List the common antibodies in T1DM

A

ICA - Islet Cell Antibody
I-A2 - Insulinoma-Associated Antigen-2
GAD65 - Glutamic Acid Decarboxylase-65

Others:
IAA - Insulin Auto-Antibody
ZnT8 - Zinc Transporter

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11
Q

List common symptoms of T1DM

A 
Weight loss
Polydipsia (thirst)
Polyuria (excess urination)
Nocturia (urinating at night)
Cachexia
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12
Q

What are common acute complications of T1DM?

A

Hypoglycaemia
- Iatrogenic (from medication)

Diabetic Ketoacidosis

  • Suffers from biological stress e.g. infection, MI, trauma
  • Fails to administer insulin = Hyperglycaemic ketoacidosis

High levels of ketone bodies in the blood lowers blood pH and triggers kidneys to excrete acidic urine

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13
Q

What are the common T1DM susceptibility genes?

A

Polygenic

HLA DR3/4 and DR2/8 and DQ-A1

Located on chromosome 6 in the major histocompatibility complex (MHC)

Region is also associated with susceptibility genes associated with other autoimmune diseases; meaning that patients with T1DM are more susceptible to other autoimmune diseases such as Graves’ Disease, Addison’s Disease, and Coeliac Disease

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14
Q

What is pernicious anaemia?

A

Body cannot make enought RBCs because of Vit. B12 deficiency

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15
Q

What is the most common monogenic form of diabetes?

A

HNF alpha 1 MODY
Hepatic nuclear factor alpha-1

Changes in HNFa1 genes causes T1D by lowering the amount of insulin that is produced by the pancreas. It allows insulin to be normally produced in childhood but the amount of insulin reduces with age

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16
Q

Define T1DM

A

T1DM is an autoimmune disease resulting in ABSOLUTE deficit of insulin and requires replacement therapy

Autoimmune destruction of pancreatic B-cells due to an abnormal T-cell response

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17
Q

What age groups are most commonly effected by T1DM?

A

<35

Peak at 12

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18
Q

List potential participating factors of T1DM

A

Viral infection
Environmental toxins
Autoimmune (hypersensitivity type 4) could be initiated by cytokine response to infection

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19
Q

What is the pathophysiology of T1DM?

A
  1. Insulin deficit (due to lymphocytic infiltration and destruction of insulin-secreting b-cells in the pancreas)
  2. B-cell mass declines, insulin secretion decreases until the available insulin is no longer adequate to maintain normal blood glucose
  3. Hyperglycaemia
  4. Glucosuria
  5. Polyuria (osmotic diuresis)
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20
Q

How does dehydration result in T1DM?

A

Fluid loss through the urine and high blood glucose concentrations (solution) in the blood (high osmolality) draws water from the cells, resulting in dehydration

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21
Q

Why do T1DM have a strong appetite to eat?

A

Polyphagia
Lack of nutrients entering the cells stimulates appetite
No insulin to translocate GLUT4 onto membranes

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22
Q

How does DKA result?

A
  1. Lack of glucose in cells results in catabolism of fats and proteins
  2. Excess amounts of FAs and their metabolites (ketones) in the blood
  3. Amount of lipids, FAs, and ketones in the blood exceeds capacity and rate at which the liver can process within a given time
  4. Excessive amounts of ketones decreases blood pH
  5. Ketoacids bind with HCO3- buffer in the blood, leading to reduced [HCO3-]serum
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23
Q

What are the main themes of T1DM Tx?

A
  1. Diet and exercise
  2. Oral medication to increase insulin secretion or reduce insulin resistance
  3. Insulin replacement
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24
Q

What dietary advice would you give to a T1DM patient?

A
  • Maintain optimum body weight
  • Eat more complex CHOs with a LOW glycaemic index
  • Maintain a LOW cholesterol and LOW lipid profile
  • Food intake must match available insulin and metabolic needs including activity level
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25
Q

What exercise advice would you give to a T1DM patient?

A
  • Exercise can promote uptake of glucose by skeletal cells
  • Weight control; reduce stress; improve CV fitness

RISK of hypoglycaemia with strenous and prolonged exercise - increased absorption of glucose by muscle and action of insulin

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26
Q

What insulin replacement therapy is available for T1DM patients?

A

Recombinant human insulin (Humulin)
3 forms:

1) Rapid-onset, short acting insulin
2) Intermediate-acting insulin
3) Slow-onset, long-acting insulin

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27
Q

Define hypoglycaemia and how might it occur in T1DM? And what it can lead to

A

<4mmol/L glucose

  • Insulin shock
  • Occur suddenly following exercise, insulin dosage error, vomiting, or skipping a meal

Lack of glucose quickly affects the nervous system because neurons cannot use AA/FAs as energy source

<2.5mmol/L = impaired neurological function (poor concentration, slurred speech, lack of coordination, staggering gait) and over stimulation of SNS (increase PP, moist skin, anxiety)

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28
Q

What could happen if hypoglycaemia is left untreated in T1DM?

A

Neuroglycopenia

  • Loss of consciousness
  • Seizures
  • Death
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29
Q

How would you Tx hypoglycaemia in T1DM?

A

IV: 50% dextrose
Gel: 40% dextrose
Oral: High glycaemic index CHO

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30
Q

What processes are activated by insulin in the fed state?

A
  1. Glucose uptake in muscle and adipose tissue
  2. Glycolysis –> Energy
  3. Glycogen synthesis –> Storage
  4. Protein Synthesis
  5. Uptake of ions (especially K+ and PO43-)
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31
Q

What processes are inhibited by insulin in the fed state?

A
  1. Gluconeogenesis
  2. Glycogenolysis
  3. Lipolysis
  4. Ketogenesis
  5. Proteolysis
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32
Q

What are the insulin counter-regulatory hormones?

A
  1. Glucagon - a-cells pancreas
  2. Adrenaline - medulla of adrenal gland
  3. glycocorticoids (cortisol) - adrenal cortex
  4. Growth hormone - Anterior pituitary
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33
Q

List clinical symptoms of gyperglycaemia

A
  1. Polyuria
  2. Polydipsia (excessive thirst)
  3. Lassitude (state of mental/physical weariness and lack of energy)
  4. Pruritus Vulvae (itchy valva)
  5. Balanitis - inflammation of the glans penis
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34
Q

Define DKA

A

DKA is characterised by uncontrolled catabolism

  1. Metabolic acidosis
    - pH <7.3
    - HCO3- <15mmol/L (due to buffering)
  2. Hyperglycaemia
    - >13.9mmol/L (leads to osmotic diuresis, dehydration, and loss of electrolytes)
  3. Ketosis
    - increased ketone bodies
  4. Ketouria and glucosuria
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35
Q

Characterise metabolic acidosis

A

Increased: H+
Decreased: HCO3- and CO2

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36
Q

List the counter-regulatory hormones

A

GH
Adrenaline
Cortisol
Glucagon

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37
Q

What hormones are increased during DKA?

A

Counter-regulatory hormones

GH, adrenaline, glucagon, cortisol

38
Q

DKA Tx

A
  1. Hypovolaemia: IV fluids
    - electrolyte + water loss = 0.9% saline
    - only water loss = 5% dextrose
  2. Insulin deficiency: IV insulin
    - turns off ketogenesis and uncontrolled catabolism
    - can cause hypokalaemic, as insulin causes K+ to move into cells
    * resolution of acidosis requires insulin
  3. Hypokalaemia
    - IV insulin
    - Total body K+ will require supplementation
39
Q

What is a common patient with DKA?

A

T1DM
<65
Hyperglycaemia
Dehydrated

40
Q

What does HONK stand for and what is it characterised by?

A

Hyperosmolar, hyperglycaemic, non-ketotic State

Characterised by:

  • Hyperglycaemia,
  • Hyperosmolality
  • Dehydration
  • ABSENCE of ketoacidosis
41
Q

How does HONK occur?

A

A partial/relative insulin deficiency may initiate HONK by reducing glucose utilisation while inducing a glucagon-stimulated increase in hepatic glucose output

42
Q

What are the cerebral risks of HONK

A
  1. Central Pontine Myelinolysis
    - due to hyponaturaemia (low Na+) causing water to move out of the cells (hyperosmolality)
  2. Cerebral oedema
    - due to rapid Tx for hyponaturaemia
    - infusing rapidly with IV saline will cause a abrupt shift in fluids from extracellular compartment to intracellular compartment, which will cause oedema - treat slowly!!!
43
Q

HONK Tx

A
  1. Hypovolaemia
    - IV fluids
    - SLOWLY to return to normal osmolality
  2. Insulin deficiency
    - IV insulin
  3. Hypokalaemia
    - IV K+
44
Q

Which patients typically get HONK?

A

T2DM

Incidious onset

45
Q

What are the symptoms of hypoglycaemia?

A
  1. Over activation of SNS
    - Increased pulse rate
    - Pale, moist skin
    - Anxiety
    - Tremors
    If untreated: loss of consciousness, seizures, and death.
  2. Neuroglycopaenic symptoms - Impaired neurological function
    - Poor concentration
    - Slurred Speech
    - Lack of coordination
    - Staggering gait
    - Look DRUNK
46
Q

Define hypoglycaemia

A

<4mmol/L

47
Q

Tx of hypoglycaemia

A

Mild
- 15-20g of fast acting CHO (high-GI)

Severe

  • 15-20g of fast acting CHO (high-GI)
  • IM glucagon
  • IV dextrose
  • Longer acting CHO to prevent further episode
48
Q

What is the most common metabolic complication of diabetes?

A

Hypoglycaemia

49
Q

In T2DM what is the most common cause of insulin resistance?

A

Adipokines

50
Q

List the adipokines involved in insulin resistance in T2DM

And their functions

A

Leptin - Tells hypothalamus how much fat is stored
Adiponectin - reduces levels of FFAs
TNFa - inhibited by adiponectin; inflammatory cytokine
Resistin - enhances hypothalamic stimulation of glucose production

51
Q

How do the adipokines change in T2DM

A

Increased:

  • Letpin = increases resistance
  • TNFa = increases inflammation
  • Resistin = causes hyperglycaemia

Decreased:
- Adiponetin = Increased FFAs levels

52
Q

Where are adipokines produce?

A

Adipocytes

53
Q

What adipokine inhibits TNFa?

A

Adiponectin

54
Q

How is insulin resistance caused?

A

Insulin receptor mutation

Results in:
- Severe hyperinsulinaemia 
Associated with:
- Acanthosis Nigricans (darkened, thickened, patches of skin that usually develop in the armpit, and around the groin and neck)
- Hyperandrogenism
55
Q

Define acanthosis nigricans

A

Acanthosis nigricans is a brown to black, poorly defined, velvety HYPERPIGMENTATION of the skin.

It is usually found in body folds, such as the posterior and lateral folds of the neck, the armpits, groin, navel, forehead, and other areas

56
Q

What common symptoms would you find with insulin receptor mutation

A

Hyperinsulinaemia

  • Acanthosis nigricans
  • Hyperandrogenism
57
Q

In normal renal glucose handling what happens?

A

90% SGLT2 in PCT

10% SGLT1 in descending loop of Henle

58
Q

What are the effects of GLP1?

A
  1. b-cells - release more insulin
  2. a-cells - inhibit glucagon release
  3. Stomach - slows gastric emptying
  4. Liver- reduces hepatic glucose output
  5. brain - promotes satiety (feeling full) and reduces appetite
59
Q

What is the main factor in the development of T2DM?

A

Obesity

Family history

60
Q

Define T2DM

A

Impairment of pancreatic B-cell function (consequently insulin secretion) or peripheral insulin resistance

61
Q

What does adiponectin do?

A

Decrease FFAs

62
Q

What is the first presentation of insulin resistance?

A

Hyperinsulinaemia

63
Q

What is the % of inheritability of T2DM from 1st degree relatives

A

40-50%

64
Q

Tx for T2DM?

A

Hypoglycaemic drugs and insulin

65
Q

List the main chronic microvascular complications of diabetes

A

Neuropathy
Nephropathy
Retinopathy

66
Q

What are the acute complications of T1DM?

A

DKA

Hypoglycaemia

67
Q

What are the main landmark trials that changed diabetic glycaemic control? And what where their outcomes

A

DCCT (Diabetes Control and Complications Trial)

  • T1DM
  • 1993
  • Conventional vs intensive treatment regimes

UKPDS (UK Prospective Diabetes Study)

  • T2DM
  • 1998
  • Conventional vs intensive regimens

= both: clear evidence that intensive glycaemia control can help PREVENT micovascular disease

68
Q

What’s involved in the conventional vs intensive regimen

A

Conventional

  • Mix
  • 2 injections/day

Intensive (basal bolus)
- 4 injections/day

69
Q

What is the pathophysiology of microvascular disease?

A
  1. Capillary Damage
    - Increased blood flow
    - Increase capillary pressure
    - Thickened and damaged blood vessels
    - Endothelial damage - leakage of albumin and other proteins
  2. Metabolic Damage
    - Increase in glucose concentration, excess glucose enters the POLYOL PATHWAY (glucose –> Sorbitol –> Fructose)
    - Glucose metabolises to sorbitol by aldose reductase
    - Sorbitol accumulates
    - Less NADPH available for cell metabolism
    - Buildup of ROS and oxidative stress

= Oxidative stress activation
= Increased glycation = Advanced Glycation End-Products (AGEs)

70
Q

What are the glucotoxic effects the lead to endothelial/metabolic dysfunction?

A
  • Sorbitol accumulation via aldose reductase
  • Formation of advanced glycation end-products (AGEs)
  • PKC activation
  • Oxidative stress
  • Angiogenic factors
71
Q

What is the hallmark of diabetic complications? T1DM

A

Diabetic retinopathy

72
Q

What is the leading case of impaired vision in ages 20-74?

A

Diabetic retinopathy

73
Q

What did the DCCT show in respect to Diabetic retinopathy?

A

Reduction in Diabetic retinopathy complications in the intensive group compared to the conventional group

74
Q

Pathophysiology of diabetic retinopathy

A
  • High retinal blood flow called by hyperglycaemia causes capillary pericyte damage
    1. Capillary endothelial damage
    2. Vascular leak
    3. Microaneurysms
    4. Capillary occlusion - cotton wool stops (infarcts) +- dot haemorrhages
    5. Local Ischaemia + ischaemia
    6. Neovascularisation (VEGF) - proliferate, bleed, fibrose
\_\_\_\_
1. Early stages (non-proliferative)
• Hyperglycaemia
– Damage to small vessel wall
– Microaneurysms (swelling blood vessels)
• When vessel wall is breached
– Dot haemorrhages
• Protein and fluid left behind
– Hard exudates
• Micro-infarcts
– Cotton wool spots
2. Later stages (proliferative)
• Damage to veins
– Venous budding
– Blockage of blood supply
• Ischaemia→ VEGF and other growth factors
– Neovascularisation
– Proliferative retinopathy
– Vitreous haemorrhage
• Fluid not cleared from macular area
– Macular oedema
75
Q

What is the difference between transudate and exudate?

A
  • Transudate is fluid pushed through the capillary due to high pressure within the capillary.
  • Exudate is fluid that leaks around the cells of the capillaries caused by inflammation.
76
Q

How could you prevent diabetic retinopathy?

A
  • Good glycaemic control
  • Stop smoking
  • BP control
  • Retinal Screening: annual from 12yo.
77
Q

Tx diabetic retinopathy

A
  • Address risk factors
  • Ophthalmic review

Laser
VEGF inhibitors
Virectomy

78
Q

What is the pathogenesis of nephropathy

A
  • Increased sorbitol (polyol pathway)
  • PKC activation
  • Oxidative stress
  • Advanced glycation End-Products (AGEs)

All result in: endothelial and metabolic dysfunction

79
Q

What are the stages of nephropathy?

A
  1. Renal enlargement and hyperfiltration
  2. Microalbuminuria
  3. Macroalbuminuria
  4. End-stage renal failure
80
Q

What is the physiology of nephropathy?

A
  1. First steps
    - renal hypertrophy
    - increased GFR
    - afferent arteriole dilates: increased glomerular pressure, thickened GBM capillary damage, and shear-stress on endothelial cells
    - end result: leakages of protein into urine
  2. Later steps
    - progressive glomerularsclerosis: hardening of glomerulus/scarring
    - glomeruli destroyed
    - progressive proteinuria
    - RENAL FAILURE
81
Q

Diabetic nephropathy management

A
  • Screening for micoalbuminuria - every year from Dx
  • Improve glycaemic control
  • Refer to renal clinic once developed CKD (GFR<30)
82
Q

Tx diabetic nephropathy

A
  • ACEi/AngII blocker (ARB) - if micoalbuminuria present
  • Lower BP
  • Statins
  • STOP SMOKING
83
Q

List the different types of diabetic neuropathy

A
  • Peripherial (sensory) neuropathy
  • Autonomic neuropathy
  • Mononeuritis multiplex = damage to >=2 different nerve areas
  • Diabetic amyotrophy = weakness followed by wasting of pelvifemoral muscles; uni/bilateral
84
Q

Tx diabetic neuropathy

A
  • Sertonin/nor-adrenaline reuptake inhibitors (Duloxetine)

- Pain management clinic

85
Q

What pathologies cause diabetic foot?

A

Neuopathy and peripheral vascular disease

86
Q

What is charcot foot?

A

Diabetic foot
Numb foot - repetitive microtrauma/stress fractures
Dysregulated blood flow - increased bone turn over/fragile foot

87
Q

What are the features of autonomic neuropathy?

A
  • CV: postural hypotension
  • GU: erectile dysfunction
  • GI: gastatory sweating and gastroparesis (vagus nerve damage; delayed gastric emptying)
88
Q

What is included on the annual review for screening for diabetic microvascular complications

A 
• HbA1c
• Chol, HDL, TG
• Creatinine
• Microalbuminuria
• Visual acuity
• Retinal screening
• Pedal pulses
• Foot sensation
• Lifestyle
– Exercise, diet
– smoking
• Drug therapy
• Mental well-being
• Foot sensation
• BMI
• BP
• Erectile function
• Contraception
89
Q

How are ROS made?

A

increased glucose + transition metal (e.g. copper) = ROS

90
Q

How are advanced glycated end products (AGEs) made

A

glucose + protein (lysine or valine) = Schiff base = ketoamine (amadori product) = (oxidation etc,,,) AGEs

Endocrinology (11 decks)

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