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W14 Diabetes Flashcards

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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
What do PP cells secrete and what is the function of the secretion?
Pancreatic polypeptide | Delays gastric emptying —> reduce food intake
26
What is the approximate composition of islets in terms of the 4 cell types?
65-80% B cells 15-20% a-cells 3-10% d cells 3-5% PP cells
27
What is the parasympathetic innervation of islets ?
Vagus nerve | Neurotransmitter is acetylcholine
28
What is sympathetic innervation of islets
Post ganglionic fibres originate in the celiac ganglion Primary neurotransmitter is norepinephrine Neural hormonal action of epinephrine from adrenal gland
29
What stimulates pro insulin synthesis ?
Glucose
30
What enzymes are involved in the cleavage of pro insulin
PC1/3, PC2, carboxypeptidase E,
31
What is insulin secretion always dependent on?
Glucose
32
What 3 ways is glucose regulated?
Neurally Hormonally Nutrient
33
How do the parasympathetic and sympathetic nervous system regulate insulin secretion?
Parasympathetic activation —> stimulation | Sympathetic activation —> inhibition
34
What hormones are involved in the regulation of insulin?
Incretins —> enhanced glucose stimulated insulin secretion -GIP (gastric/GI inhibitory polypeptide) - GLP1 —> suppress glucagon release Somatostatin —> inhibition
35
Other than glucose what other nutrients help regulate the release of insulin?
Amino acids; arginine, lysine
36
How do B cells act as glucose sensors?
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
37
What are the major target tissues of insulin?
Liver Fat Muscle
38
What is the fate of glucose in muscle cells?
Used for energy or stored as glycogen
39
What is the fate of glucose in adipocytes?
Stored as fat via glycerol 3-phosphate —> triglycerides
40
What enzymes can stimulate glycolysis in the liver?
Glucokinase Phosphofructokinase Pyruvate kinase
41
What inhibits glycogenolysis in the liver?
Inactivation of liver glycogen phosphorylase
42
What inhibits gluconeogenesis in the liver?
Inhibition of pyruvate carboxylase, phosphoenol pyruvate carboxykinase and fructose 1,6 diphosphatase
43
What causes increased fatty acid and triglyceride synthesis?
Stimulation of lipoprotein lipase Stimulation of fatty acid synthesis from glucose via glycolysis Inhibition of Lipolysis in adipocytes via inhibition of hormone sensitive lipase
44
How glucose intake cause increased protein synthesis?
Muscle: stimulation of AA uptake Liver & muscle: increased rate of protein synthesis and inhibition of protein catabolism Inhibition of gluconeogenesis
45
What is the significance of tyrosine kinase
It is the insulin receptor enzyme
46
What are the principle actions of glucagon?
Stimulate hepatic glycogenolysis and gluconeogenesis
47
How do parasympathetic and sympathetic activation impact glucagon release?
Both stimulate glucagon release
48
What hormones stimulate the release of glucagon?
GIP | CCK
49
What hormone inhibits the release of glucagon?
GLP-1 Somatostatin Insulin
50
What is the effect of AAs on glucagon?
Stimulate secretion
51
What induces somatostatin release?
``` Glucose Sulfonylureas AAs CCK Cyclic AMP ```
52
What inhibits somatostatin release?
Cholinergic stimulation
53
What is the function of IAPP?
Retard gastric emptying and glucagon secretion
54
What is the function of pancreatic polypeptide?
Delay gastric emptying | Reduce food intake
55
What is the function of Ghrelin?
Stimulates release of growth hormone from the pituitary gland and has an important role in appetite regulation
56
What is the overall action of glucocorticoids?
Counter regulatory to the action of insulin - increased hepatic gluconeogenesis via stimulation of PEPCK - inhibit glucose uptake in muscle and adipose tissue
57
what are the 5 main classifications of diabetes mellitus?
1. T1DM 2. T2DM 3. GDM 4. MODY 5. Secondary diabetes
58
What is the etiology of T1DM?
Autoimmune or non-autoimmune mediated destruction of B cells
59
What is the etiology of T2DM?
Insulin resistance due to obesity, abnormal insulin receptors, adipokines, inflammation, B cell defects and metabolic syndrome
60
What is the definition of GDM?
Glucose intolerance that develops or is first recognized during pregnancy.
61
What is the etiology of monogenic diabetes?
Single gene genetic variants causing defects in glucose induced insulin release. What
62
How do cyclosporine, phenytoin and thiazides cause diabetes?
Interfere with insulin release from B cells
63
How do glucocorticoidsi niacin, and anti-viral protease inhibitors cause diabetes?
Induce insulin resistance
64
How do anti-psychotics cause diabetes?
Weight gain +/- B cell dysfunction
65
How do PD-1 and CTLA-4 inhibitors cause diabetes?
Block inhibitory immune system
66
What are some genetic causes of exocrine pancreas related diabetes?
Cystic fibrosis | Hemochromatosis
67
What are some acquired causes of exocrine pancreas-related diabetes?
``` Pancreatitis Trauma Infection Pancreatic cancer Pancreatectomy ```
68
What are some disorders that cause endocrinpathy-related diabetes?
``` Acromegaly Cushing’s syndrome Cushing’s disease Ectopic Cushing’s syndrome Pheochromocytoma ```
69
What is the disorder associated with Excess catecholamines?
Pheochromocytoma
70
What is the disorder associated with excess growth hormone?
Acromegaly
71
What are the screening guidelines for T2DM?
Use FPG and/or A1C every 3 years in individuals >40 or high risk individuals (33% chance of developing over 10 years)
72
Risk factors for T2DM?
``` >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
High risk populations for T2DM
``` African Arab Asian Hispanic Indigenous South Asian Low SES ```
74
Vascular risk factors for T2DM?
``` HDL<1.0mmol/L (M) HDL<1.3 mmol/L (F) Triglycerides >1.7 mmol/L Hypertension Obesity Abdominal obesity Smoking ```
75
Associated diseases with T2DM
PCOS HIV OSA CF
76
Medications that are risk factors for T2DM
Glucocorticoids Atypical antipsychotics HAART
77
Screening guidelines for type 2 diabetes
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
FPG for diabetes diagnosis
>7.0 mM
79
A1C diabetic diagnosis cutoff
>6.5%
80
2hPG in 75 g OGTT amount for diabetes
>11.1 mM
81
Random PG for diabetes diagnosis
>11.1 mM
82
FPG and A1C amounts for normal, at risk, pre-diabetes and diabetes
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
What is prediabetes ?
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
What is the significance of patients with metabolic syndrome?
Significant risk of developing CVD and diabetes
85
>/=3 of which criteria are required for the diagnosis of metabolic syndrome ?
``` 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
When should pregnant women be screened for GDM?
24-28 weeks | High risk: before 24 and if negative again from 24-28 weeks
87
What is diabetic ketoacidosis?
Metabolic decompensation resulting from an absolute insulin deficiency
88
What is diabetic ketoacidosis characterized by?
Hyperglycaemia Ketonemia Metabolic acidosis Volume depletion
89
Clinical features of DKA?
``` Prodrome (1-2 days) Volume depletion Tachypnea Acetone breath Myalgia Normal temp/hypothermia ```
90
What is prodrome?
Polydipsia, polyuria, weakness (early) | Nausea, vomiting, abdominal pain (later)
91
What is Kussmaul breathing and what is it a classic symptom for?
Rapid, deep inspirations | DKA
92
Precipitating conditions for DKA
``` Acute illness - infection - CVA/stroke - MI - acute pancreatitis New onset diabetes Insulin under dosing Drugs ```
93
Triad of DKA
Hyperglycaemia, metabolic acidosis, ketones
94
What is the mechanism behind DKA?
- 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
Formula for anion gap
AG= [Na+] - ([Cl-]+[HCO3-])
96
What is a wide anion gap
>16 mEq/L
97
Causes of wide anion gap acidosis
CAT MUDPILES | D= DKA
98
Steps in DKA management
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
What is a complication sometimes seen with paediatric DKA?
Cerebral edema
100
Signs and symptoms of cerebral edema in paediatric DKA
``` Mental status changes Focal neurological deficits Age-inappropriate incontinence Headache Cushing’s Triad Hypoxemia ```
101
What is Cushing’s triad?
Hypertension, bradycardia, irregular resp | —> signs of increased intracranial pressure
102
Management of suspected cerebral edema
``` Elevation of the head of the bed Reduce IV fluids by 1/3 Mannitol 3% hypertonic saline Might require intubation and ventilation ```
103
What is hyperglycaemic hyperosmolar state?
Metabolic decompensation (T2D) resulting from relative insulin deficiency, severe hyperglycaemia leading to hyper osmolality and volume depletion
104
What is hyperglycaemic hyperosmolar state characterized by?
Hyperglycaemia Hyperosmolality Volume depletion
105
Clinical features of hyperglycaemic hyperosmolor state
``` Often >60 Prodrome Poor fluid intake Volume depletion Lethargy/stupor/coma Hypothermia ```
106
Plasma osmolality equation
2[Na]+[glucose]+[urea] | Normal 285-295 mosm/L
107
Hyperglycaemic hyperosmolar state management
1. Volume repletion: 1/2 N saline 2. Normalize glucose: insulin 3. K+ repletion 4. Treat precipitating condition 5. Monitor
108
Checks in DKA and HHS before discharge
1. Patient is eating and drinking well 2. Glucose controlled with SC insulin 3. Precipitating condition is treated 4. Instructions
109
Autonomic clinical features of hypoglycaemia
``` Perspiration Tachycardia Tremor Hunger Anxiety Feeling warm Nausea ```
110
CNS features of hypoglycaemia
``` Dizziness Weakness Blurred vision Drowsiness Confusion Seizure/coma ```
111
What happens to hypoglycaemia symptoms over time?
<5 years: normal adrenergic symptoms 5-15 years: gradual loss of adrenergic sx >15 years: increasing reliance on NGP sx
112
Where does CGM measure glucose level in?
Interstitial fluid
113
What steps are important in AGP graphic interpretation?
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
What is a glucose management indicator (GMI)?
An approximation of A1C, based on the average glucose from CGM readings for 14 or more days
115
What is the difference between bolus and basal glucose?
Bolus: - facilitates glucose uptake after meals Basal: - suppresses glucose production between meals and overnight
116
How os bolus starting insulin dose determined?
Calculate average daily CHP intake and divide this by total bolus insulin dose 500/TD
117
What is insulin sensitivity of correction factor?
Estimated decrease in blood glucose by 1 unit of rapid acting insulin 100/TD = insulin sensitivity factor
118
Insulin pump basal rate adjustments at night
``` 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
Insulin pump basal rate adjustments, daytime
``` 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
Bolus delivery options
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
What are some modifiable risk factors for diabetes?
``` Overweight Obesity Physical inactivity Unhealthy eating Smoking Literacy ```
122
ABCDES of diabetes care
``` 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
What are the benefits of aerobic exercise in regards to diabetes?
Inproved insulin sensitivity 150 min/week —> decrease A1C 0.5-0.9% Enhanced cardiovascular health
124
What are the benefits of resistance exercise in regards to diabetes?
60-90 min/week —> decrease A1C 0.5-1.0% Increased lean body mass Enhanced bone mineral density Reduced risk of sarcopenia, osteoporosis
125
Fuel metabolism in exercise
Liver: promotes glycolysis Muscle: promotes glucose uptake
126
What are the 2 glucose transporters?
GLUT1, GLUT4
127
What is necessary for insulin stimulated glucose uptake?
Translocation of glucose transporter GLUT4 to plasma membrane
128
What causes GLUT4 translocation independent of insulin?
Exercise
129
Hormonal changes during exercise
Enhance fuel availability for muscles Improve glucose transport to muscles Increased sensitivity of insulin receptors —> improved glucose uptake to support muscle activity
130
How does intracellular hyperglycaemia lead to toxicity ?
``` 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
End results of protein kinase C activation
- blood flow abnormalities - vascular permeability, angiogenesis - vascular and capillary occlusion - pro inflammatory gene expression
132
What are the primary micro vascular complications of diabetes?
Diabetic nephropathy Diabetic retinopathy Diabetic neuropathy
133
Pathophysiology of diabetic nephropathy
``` Podocyte changes and dysfunction —> loss of glomerular basement membrane Mesangial cell alterations —> glomerular hypertension Inflammatory cell recruitment Renal tubule damage ```
134
Risk factors for diabetic nephropathy
``` Hyperglycaemia Hypertension Dyslipidemia Insulin resistance Obesity Smoking Age Genetics and epigenetics ```
135
How is urinary albumin normally measured?
Estimated from spot urine ACR
136
What are the stages of diabetic nephropathy ?
``` Hyperfiltration Silent Microalbuminuria Macroalbuminuria Uraemia ```
137
What are the screening tests for diabetic nephropathy and when should they be done?
Creatinine and EGFR Spot urine ACR Start at diagnosis in T2DM Start after <5 years after diagnosis in T1DM
138
What is important for management/prevention of diabetic nephropathy ?
Glucose control BP control Lipid control Smoking cessation
139
Pathophysiology of diabetic retinopathy
Retinal damage Nonproliferative micro vascular changes More advanced pre-proliferation changes Proliferative diabetic retinopathy
140
Risk factors for diabetic retinopathy
``` Hyperglycemia Hypertension Genetics Pregnancy Puberty Dyslipedemia ```
141
Diagnosis of diabetic retinopathy
Dilated retinal exam | Optical coherence tomography
142
Diagnosis of non proliferative DR
``` Microaneurysms Cotton wool spots Intraretinal microvascular abnormalities Hard exudates Venous abnormalities ```
143
Loss of vision with DN
Vitreous hemorrhage Traction retinal detachment Diabetic macular edema Neovascular glaucoma
144
Treatments for diabetic retinopathy
Intravitreal injections of anti VEGF antibodies Laser photo coagulation Virectomy
145
What are the different types of diabetic neuropathy ?
Distal symmetric polyneuropathy Ridiculous/plexopathy Mononeuropathy Autonomic neuropathy
146
Risk factors for diabetic neuropathy
``` Hyperglycemia Metabolic syndrome Obesity Smoking Alcohol ```
147
Management for diabetic neuropathy
Gabapentinoids SNRI antidepressants Tricyclics antidepressants Narcotics
148
Macro vascular complications of diabetes
Cardiovascular disease Cerebrovascular disease Peripheral vascular disease
149
Diabetic foot examination
``` Inspection -overall -skin - nails Palpation - pulses, temp Neurological - 10 gram monofilament testing -128 Hz tuning fork -strength, reflexes, proprioception ```
150
Management of diabetic foot
``` Regular foot examinations Proper footwear Wound care as appropriate Treatment of infections Regular nail care Involve podiatry ```
151
Management for erectile dysfunction with diabetes
PDE5 inhibitors Assess for other vascular disease Check testosterone levels

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