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411 > W14 Diabetes > Flashcards

W14 Diabetes Flashcards

1
Q

Symptoms of diabetes mellitus

A

Thirst
Hunger
Urination
Weight loss

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2
Q

Cause of Type 1 diabetes

A

Autoimmune destruction of B cells

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3
Q

Evidence that type E1 diabetes is an autoimmune disease

A

T lymphocyte infiltration of islet
Islet cell antibodies
Strong genetic association with certain HLA loci
Associated with other autoimmune diseases

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4
Q

What are some possible environmental triggers associated with type 1 diabetes?

A

Coxsackie B4, mumps, rubella

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5
Q

What treatments are Avaliable for prevention of and new onset diabetes?

A 
Immunosuppression 
Peptide therapy 
Lifestyle intervention 
Abatacept 
Ustekinemab 
Teplizumab 
Golimumab
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6
Q

What defects is type 2 diabetes associated with?

A 
Insulin action (increased insulin resistance) 
Insulin secretion
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7
Q

What is IGT ?

A

Increased glucose tolerance
- abnormal OGTT but normal fasting glucose
- treated with diet and exercise
Early progression of T2D

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8
Q

What is seen with overt but mild type 2 diabetes?

A

Moderate fasting hyperglycaemia (~7mM)
Insulin resistance present
Hyperinsulemia

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9
Q

How is overt but mild T2D treated?

A 
Diet and exercise 
Oral hypoglycaemic agents 
Insulin sensitizing agent 
DPP-IV inhibitors 
GLP-1 analogues
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10
Q

What is seen with advanced T2D?

A

Severe fasting hyperglycaemia (>9mM)
Insulin secretion greatly impaired or absent
Often require insulin

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11
Q

What is insulin resistance in T2D commonly associated with?

A

Obesity

Inflammation in adipose tissue

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12
Q

What are the characteristics of insulin resistance in type 2 diabetes?

A

Impaired glucose induced insulin secretion
Impaired pro insulin processing —> hyperproinsulinemia
Inability to adapt to increasing insulin resistance
Progressive decline in insulin secretion as the disease progresses

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13
Q

Causes of loss of insulin secretion in type 2 diabetes

A
  1. Glucose toxicity and lipotoxicity
  2. Pro inflammatory cytokines
    - increased # of islet macrophages —> proinflammatory cytokines
  3. Islet amyloid deposits
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14
Q

What are the monogenic forms of diabetes ?

A

MODY

Neonatal diabetes mellitus

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15
Q

What is Mature onset diabetes of the young (MODY)?

A
  • associated with genes that regulate beta cell mass or function
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16
Q

What is neonatal diabetes mellitus ?

A

Born with diabetes

Caused by mutations

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17
Q

What is gestational diabetes mellitus?

A

Diabetes that appears during pregnancy and disappears following birth
Insulin resistance —> increased insulin secretion
>50% with GDM go on to develop T2D and

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18
Q

What is the function of insulin and glucagon?

A

Insulin: promotes glucose uptake from the blood and storage in tissues
Glucagon: promotes glucose mobilization from tissues, increased blood glucose levels

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19
Q

Early manifestations of hypoglycaemia

A

Palpitations, tachycardia
Diaphoresis, anxiety
Weakness, hunger, nausea

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20
Q

What are the manifestations of prolonged/severe hypoglycaemia?

A

Hypothermia
Confusion, hallucinations, seizures
Coma

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21
Q

What are the early manifestations of hyperglycaemia?

A

Polydipsia, polyuria
Altered vision
Weight loss
Mild dehydration

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22
Q

What are the manifestations of severe/prolonged hyperglycaemia?

A

Cardiac arrhythmias

Coma

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23
Q

What is islet amyloid polypeptide (IAPP, amylin) and what is its function?

A

37 AA peptide
Co-secreted with insulin
Decreases gastric emptying, suppresses glucagon secretion, stimulates satiety centre in brain —> control glucose in insulin sparing fashion

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24
Q

What is the function of somatostatin ?

A

Inhibits the secretion of several other hormones such as insulin, glucagon and growth hormone

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25
Q

What do PP cells secrete and what is the function of the secretion?

A

Pancreatic polypeptide

Delays gastric emptying —> reduce food intake

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26
Q

What is the approximate composition of islets in terms of the 4 cell types?

A

65-80% B cells
15-20% a-cells
3-10% d cells
3-5% PP cells

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27
Q

What is the parasympathetic innervation of islets ?

A

Vagus nerve

Neurotransmitter is acetylcholine

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28
Q

What is sympathetic innervation of islets

A

Post ganglionic fibres originate in the celiac ganglion
Primary neurotransmitter is norepinephrine
Neural hormonal action of epinephrine from adrenal gland

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29
Q

What stimulates pro insulin synthesis ?

A

Glucose

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30
Q

What enzymes are involved in the cleavage of pro insulin

A

PC1/3, PC2, carboxypeptidase E,

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31
Q

What is insulin secretion always dependent on?

A

Glucose

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32
Q

What 3 ways is glucose regulated?

A

Neurally
Hormonally
Nutrient

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33
Q

How do the parasympathetic and sympathetic nervous system regulate insulin secretion?

A

Parasympathetic activation —> stimulation

Sympathetic activation —> inhibition

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34
Q

What hormones are involved in the regulation of insulin?

A

Incretins —> enhanced glucose stimulated insulin secretion
-GIP (gastric/GI inhibitory polypeptide)
- GLP1 —> suppress glucagon release
Somatostatin —> inhibition

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35
Q

Other than glucose what other nutrients help regulate the release of insulin?

A

Amino acids; arginine, lysine

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36
Q

How do B cells act as glucose sensors?

A

Glucose enters cell through GLUT2 —> G-6-P by glucokinase —> glycolysis producing ATP, ATP sensitive potassium channel closes —> B-cell depolarizes —> open voltage gated Ca2+ channels —> Ca2+ influx —> exocytosis of insulin secretory granules
Glucokinase phosphorylation is rate limiting step —> glucose sensor

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37
Q

What are the major target tissues of insulin?

A

Liver
Fat
Muscle

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38
Q

What is the fate of glucose in muscle cells?

A

Used for energy or stored as glycogen

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39
Q

What is the fate of glucose in adipocytes?

A

Stored as fat via glycerol 3-phosphate —> triglycerides

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40
Q

What enzymes can stimulate glycolysis in the liver?

A

Glucokinase
Phosphofructokinase
Pyruvate kinase

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41
Q

What inhibits glycogenolysis in the liver?

A

Inactivation of liver glycogen phosphorylase

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42
Q

What inhibits gluconeogenesis in the liver?

A

Inhibition of pyruvate carboxylase, phosphoenol pyruvate carboxykinase and fructose 1,6 diphosphatase

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43
Q

What causes increased fatty acid and triglyceride synthesis?

A

Stimulation of lipoprotein lipase
Stimulation of fatty acid synthesis from glucose via glycolysis
Inhibition of Lipolysis in adipocytes via inhibition of hormone sensitive lipase

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44
Q

How glucose intake cause increased protein synthesis?

A

Muscle: stimulation of AA uptake
Liver & muscle: increased rate of protein synthesis and inhibition of protein catabolism
Inhibition of gluconeogenesis

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45
Q

What is the significance of tyrosine kinase

A

It is the insulin receptor enzyme

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46
Q

What are the principle actions of glucagon?

A

Stimulate hepatic glycogenolysis and gluconeogenesis

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47
Q

How do parasympathetic and sympathetic activation impact glucagon release?

A

Both stimulate glucagon release

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48
Q

What hormones stimulate the release of glucagon?

A

GIP

CCK

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49
Q

What hormone inhibits the release of glucagon?

A

GLP-1
Somatostatin
Insulin

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50
Q

What is the effect of AAs on glucagon?

A

Stimulate secretion

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51
Q

What induces somatostatin release?

A 
Glucose
Sulfonylureas 
AAs
CCK
Cyclic AMP
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52
Q

What inhibits somatostatin release?

A

Cholinergic stimulation

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53
Q

What is the function of IAPP?

A

Retard gastric emptying and glucagon secretion

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54
Q

What is the function of pancreatic polypeptide?

A

Delay gastric emptying

Reduce food intake

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55
Q

What is the function of Ghrelin?

A

Stimulates release of growth hormone from the pituitary gland and has an important role in appetite regulation

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56
Q

What is the overall action of glucocorticoids?

A

Counter regulatory to the action of insulin

  • increased hepatic gluconeogenesis via stimulation of PEPCK
  • inhibit glucose uptake in muscle and adipose tissue
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57
Q

what are the 5 main classifications of diabetes mellitus?

A
  1. T1DM
  2. T2DM
  3. GDM
  4. MODY
  5. Secondary diabetes
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58
Q

What is the etiology of T1DM?

A

Autoimmune or non-autoimmune mediated destruction of B cells

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59
Q

What is the etiology of T2DM?

A

Insulin resistance due to obesity, abnormal insulin receptors, adipokines, inflammation, B cell defects and metabolic syndrome

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60
Q

What is the definition of GDM?

A

Glucose intolerance that develops or is first recognized during pregnancy.

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61
Q

What is the etiology of monogenic diabetes?

A

Single gene genetic variants causing defects in glucose induced insulin release. What

62
Q

How do cyclosporine, phenytoin and thiazides cause diabetes?

A

Interfere with insulin release from B cells

63
Q

How do glucocorticoidsi niacin, and anti-viral protease inhibitors cause diabetes?

A

Induce insulin resistance

64
Q

How do anti-psychotics cause diabetes?

A

Weight gain +/- B cell dysfunction

65
Q

How do PD-1 and CTLA-4 inhibitors cause diabetes?

A

Block inhibitory immune system

66
Q

What are some genetic causes of exocrine pancreas related diabetes?

A

Cystic fibrosis

Hemochromatosis

67
Q

What are some acquired causes of exocrine pancreas-related diabetes?

A 
Pancreatitis 
Trauma 
Infection 
Pancreatic cancer 
Pancreatectomy
68
Q

What are some disorders that cause endocrinpathy-related diabetes?

A 
Acromegaly 
Cushing’s syndrome 
Cushing’s disease
Ectopic Cushing’s syndrome 
Pheochromocytoma
69
Q

What is the disorder associated with Excess catecholamines?

A

Pheochromocytoma

70
Q

What is the disorder associated with excess growth hormone?

A

Acromegaly

71
Q

What are the screening guidelines for T2DM?

A

Use FPG and/or A1C every 3 years in individuals >40 or high risk individuals (33% chance of developing over 10 years)

72
Q

Risk factors for T2DM?

A 
>40 
1st degree relative with T2DM
High risk population 
History of pre-diabetes 
History of GDM 
History of delivery of macrosomic infant 
End organ damage 
Vascular risk factors 
Associated diseases
Use of meds
Secondary causes
73
Q

High risk populations for T2DM

A 
African 
Arab 
Asian 
Hispanic 
Indigenous 
South Asian 
Low SES
74
Q

Vascular risk factors for T2DM?

A 
HDL<1.0mmol/L (M) 
HDL<1.3 mmol/L (F) 
Triglycerides >1.7 mmol/L 
Hypertension 
Obesity 
Abdominal obesity 
Smoking
75
Q

Associated diseases with T2DM

A

PCOS
HIV
OSA
CF

76
Q

Medications that are risk factors for T2DM

A

Glucocorticoids
Atypical antipsychotics
HAART

77
Q

Screening guidelines for type 2 diabetes

A

FPG and/or A1C:

  • every 3 years when >40 or at high risk
  • very high risk, earlier and/or more frequent screening (6-12 months)
78
Q

FPG for diabetes diagnosis

A

> 7.0 mM

79
Q

A1C diabetic diagnosis cutoff

A

> 6.5%

80
Q

2hPG in 75 g OGTT amount for diabetes

A

> 11.1 mM

81
Q

Random PG for diabetes diagnosis

A

> 11.1 mM

82
Q

FPG and A1C amounts for normal, at risk, pre-diabetes and diabetes

A

Normal: <5.6mM, <5.5%
At risk: 5.6-6.0 mM, 5.5-5.9%
Pre-diabetes: 6.1-6.9 mM, 6.0-6.4%
Diabetes: >7mM, >6.5%

83
Q

What is prediabetes ?

A

IFG (FPG 6.2-6.9mM) (impaired fasting glucose)
Or
IGT (2hPG in a 75g OGTT 7.8-11.0 mM) (impaired glucose tolerance)
Or
A1C 6-6.4%

84
Q

What is the significance of patients with metabolic syndrome?

A

Significant risk of developing CVD and diabetes

85
Q

> /=3 of which criteria are required for the diagnosis of metabolic syndrome ?

A 
Elevated waist circumference: M >102 cm, W >88 cm 
Elevated TG >1.7 mM 
Reduced HDL-C <1.0 M, <1.3 W
Elevated BP 
Elevated FPG >5.6
86
Q

When should pregnant women be screened for GDM?

A

24-28 weeks

High risk: before 24 and if negative again from 24-28 weeks

87
Q

What is diabetic ketoacidosis?

A

Metabolic decompensation resulting from an absolute insulin deficiency

88
Q

What is diabetic ketoacidosis characterized by?

A

Hyperglycaemia
Ketonemia
Metabolic acidosis
Volume depletion

89
Q

Clinical features of DKA?

A 
Prodrome (1-2 days) 
Volume depletion 
Tachypnea
Acetone breath 
Myalgia 
Normal temp/hypothermia
90
Q

What is prodrome?

A

Polydipsia, polyuria, weakness (early)

Nausea, vomiting, abdominal pain (later)

91
Q

What is Kussmaul breathing and what is it a classic symptom for?

A

Rapid, deep inspirations

DKA

92
Q

Precipitating conditions for DKA

A 
Acute illness 
- infection 
- CVA/stroke 
- MI 
- acute pancreatitis 
New onset diabetes 
Insulin under dosing 
Drugs
93
Q

Triad of DKA

A

Hyperglycaemia, metabolic acidosis, ketones

94
Q

What is the mechanism behind DKA?

A
  • absolute insulin deficiency
  • loss of glucagon suppression
  • excess glucagon —> increased gluconeogenesis and ketogenesis
  • ketogenesis —> decreased malonyl coA —> mitochondrial oxidation of FFAs in the liver to acrylic-CoA then to acetoacetate
95
Q

Formula for anion gap

A

AG= [Na+] - ([Cl-]+[HCO3-])

96
Q

What is a wide anion gap

A

> 16 mEq/L

97
Q

Causes of wide anion gap acidosis

A

CAT MUDPILES

D= DKA

98
Q

Steps in DKA management

A
  1. Volume repletion: normal saline (5-10L)
  2. Stop ketogenesis- insulin infusion
  3. K+ repletion
  4. Normal glucose: insulin
  5. Treat precipitating condition
  6. Avoid complications
99
Q

What is a complication sometimes seen with paediatric DKA?

A

Cerebral edema

100
Q

Signs and symptoms of cerebral edema in paediatric DKA

A 
Mental status changes 
Focal neurological deficits 
Age-inappropriate incontinence 
Headache 
Cushing’s Triad 
Hypoxemia
101
Q

What is Cushing’s triad?

A

Hypertension, bradycardia, irregular resp

—> signs of increased intracranial pressure

102
Q

Management of suspected cerebral edema

A 
Elevation of the head of the bed 
Reduce IV fluids by 1/3 
Mannitol 
3% hypertonic saline 
Might require intubation and ventilation
103
Q

What is hyperglycaemic hyperosmolar state?

A

Metabolic decompensation (T2D) resulting from relative insulin deficiency, severe hyperglycaemia leading to hyper osmolality and volume depletion

104
Q

What is hyperglycaemic hyperosmolar state characterized by?

A

Hyperglycaemia
Hyperosmolality
Volume depletion

105
Q

Clinical features of hyperglycaemic hyperosmolor state

A 
Often >60 
Prodrome
Poor fluid intake 
Volume depletion 
Lethargy/stupor/coma
Hypothermia
106
Q

Plasma osmolality equation

A

2[Na]+[glucose]+[urea]

Normal 285-295 mosm/L

107
Q

Hyperglycaemic hyperosmolar state management

A
  1. Volume repletion: 1/2 N saline
  2. Normalize glucose: insulin
  3. K+ repletion
  4. Treat precipitating condition
  5. Monitor
108
Q

Checks in DKA and HHS before discharge

A
  1. Patient is eating and drinking well
  2. Glucose controlled with SC insulin
  3. Precipitating condition is treated
  4. Instructions
109
Q

Autonomic clinical features of hypoglycaemia

A 
Perspiration 
Tachycardia 
Tremor 
Hunger 
Anxiety 
Feeling warm 
Nausea
110
Q

CNS features of hypoglycaemia

A 
Dizziness 
Weakness
Blurred vision 
Drowsiness 
Confusion 
Seizure/coma
111
Q

What happens to hypoglycaemia symptoms over time?

A

<5 years: normal adrenergic symptoms
5-15 years: gradual loss of adrenergic sx
>15 years: increasing reliance on NGP sx

112
Q

Where does CGM measure glucose level in?

A

Interstitial fluid

113
Q

What steps are important in AGP graphic interpretation?

A
  1. Are there any patterns of hypoglycaemia
  2. Are the readings within the target range?
  3. What is the shape of the median curve
  4. What is the degree of variability?
114
Q

What is a glucose management indicator (GMI)?

A

An approximation of A1C, based on the average glucose from CGM readings for 14 or more days

115
Q

What is the difference between bolus and basal glucose?

A

Bolus:
- facilitates glucose uptake after meals
Basal:
- suppresses glucose production between meals and overnight

116
Q

How os bolus starting insulin dose determined?

A

Calculate average daily CHP intake and divide this by total bolus insulin dose
500/TD

117
Q

What is insulin sensitivity of correction factor?

A

Estimated decrease in blood glucose by 1 unit of rapid acting insulin
100/TD = insulin sensitivity factor

118
Q

Insulin pump basal rate adjustments at night

A 
Start at 5-8mM 
Measure at 3 am and before breakfast
Glucose should remain within 2mM 
Rises more—> increase basal 
Decreases more —> decrease basal
119
Q

Insulin pump basal rate adjustments, daytime

A 
Pre meal glucose 5-8mM 
Skip that meal and pre-meal bolus 
Glucose levels should remain within 2mM 
Rises more —> increase basal 
Decreases more —> decrease basal
120
Q

Bolus delivery options

A

Normal: insulin in small persistent increments until total quantity delivered
Square wave/extended: used in situations of slow steady need
Dual/combo: used meal has higher content of fat and/or protein with slower and later CHO rise

121
Q

What are some modifiable risk factors for diabetes?

A 
Overweight
Obesity 
Physical inactivity 
Unhealthy eating
 Smoking 
Literacy
122
Q

ABCDES of diabetes care

A 
A1C: <7% 
BP: <130/80
Cholesterol: LDL <2.0mM or >50% reduction 
Drugs to protect the heart 
Exercise / healthy eating
Screening for complications
Smoking cessation 
Self-management, stress and other barriers
123
Q

What are the benefits of aerobic exercise in regards to diabetes?

A

Inproved insulin sensitivity
150 min/week —> decrease A1C 0.5-0.9%
Enhanced cardiovascular health

124
Q

What are the benefits of resistance exercise in regards to diabetes?

A

60-90 min/week —> decrease A1C 0.5-1.0%
Increased lean body mass
Enhanced bone mineral density
Reduced risk of sarcopenia, osteoporosis

125
Q

Fuel metabolism in exercise

A

Liver: promotes glycolysis
Muscle: promotes glucose uptake

126
Q

What are the 2 glucose transporters?

A

GLUT1, GLUT4

127
Q

What is necessary for insulin stimulated glucose uptake?

A

Translocation of glucose transporter GLUT4 to plasma membrane

128
Q

What causes GLUT4 translocation independent of insulin?

A

Exercise

129
Q

Hormonal changes during exercise

A

Enhance fuel availability for muscles
Improve glucose transport to muscles
Increased sensitivity of insulin receptors
—> improved glucose uptake to support muscle activity

130
Q

How does intracellular hyperglycaemia lead to toxicity ?

A 
1.polyol pathway activation 
—> build up of ROS 
2. Advanced glycosylation end product formation 
—> influence transcription factors 
3. PKC activation 
4. Hexosamine pathway activation 
—> pro inflammatory state
131
Q

End results of protein kinase C activation

A
  • blood flow abnormalities
  • vascular permeability, angiogenesis
  • vascular and capillary occlusion
  • pro inflammatory gene expression
132
Q

What are the primary micro vascular complications of diabetes?

A

Diabetic nephropathy
Diabetic retinopathy
Diabetic neuropathy

133
Q

Pathophysiology of diabetic nephropathy

A 
Podocyte changes and dysfunction 
—> loss of glomerular basement membrane 
Mesangial cell alterations 
—> glomerular hypertension 
Inflammatory cell recruitment 
Renal tubule damage
134
Q

Risk factors for diabetic nephropathy

A 
Hyperglycaemia 
Hypertension 
Dyslipidemia 
Insulin resistance 
Obesity 
Smoking 
Age 
Genetics and epigenetics
135
Q

How is urinary albumin normally measured?

A

Estimated from spot urine ACR

136
Q

What are the stages of diabetic nephropathy ?

A 
Hyperfiltration 
Silent 
Microalbuminuria 
Macroalbuminuria 
Uraemia
137
Q

What are the screening tests for diabetic nephropathy and when should they be done?

A

Creatinine and EGFR
Spot urine ACR
Start at diagnosis in T2DM
Start after <5 years after diagnosis in T1DM

138
Q

What is important for management/prevention of diabetic nephropathy ?

A

Glucose control
BP control
Lipid control
Smoking cessation

139
Q

Pathophysiology of diabetic retinopathy

A

Retinal damage
Nonproliferative micro vascular changes
More advanced pre-proliferation changes
Proliferative diabetic retinopathy

140
Q

Risk factors for diabetic retinopathy

A 
Hyperglycemia 
Hypertension 
Genetics
Pregnancy 
Puberty 
Dyslipedemia
141
Q

Diagnosis of diabetic retinopathy

A

Dilated retinal exam

Optical coherence tomography

142
Q

Diagnosis of non proliferative DR

A 
Microaneurysms 
Cotton wool spots
Intraretinal microvascular abnormalities 
Hard exudates 
Venous abnormalities
143
Q

Loss of vision with DN

A

Vitreous hemorrhage
Traction retinal detachment
Diabetic macular edema
Neovascular glaucoma

144
Q

Treatments for diabetic retinopathy

A

Intravitreal injections of anti VEGF antibodies
Laser photo coagulation
Virectomy

145
Q

What are the different types of diabetic neuropathy ?

A

Distal symmetric polyneuropathy
Ridiculous/plexopathy
Mononeuropathy
Autonomic neuropathy

146
Q

Risk factors for diabetic neuropathy

A 
Hyperglycemia 
Metabolic syndrome
Obesity 
Smoking 
Alcohol
147
Q

Management for diabetic neuropathy

A

Gabapentinoids
SNRI antidepressants
Tricyclics antidepressants
Narcotics

148
Q

Macro vascular complications of diabetes

A

Cardiovascular disease
Cerebrovascular disease
Peripheral vascular disease

149
Q

Diabetic foot examination

A 
Inspection 
-overall 
-skin 
- nails
Palpation
- pulses, temp
Neurological 
- 10 gram monofilament testing 
-128 Hz tuning fork 
-strength, reflexes, proprioception
150
Q

Management of diabetic foot

A 
Regular foot examinations 
Proper footwear
Wound care as appropriate 
Treatment of infections 
Regular nail care
Involve podiatry
151
Q

Management for erectile dysfunction with diabetes

A

PDE5 inhibitors
Assess for other vascular disease
Check testosterone levels

411 (16 decks)

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