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Med 1 UBC Fall 2019 > Week 14 Diabetes > Flashcards

Week 14 Diabetes Flashcards

1
Q

Early manifestations of hypoglycemia

A
  • palpitations, tachycardia
  • diaphoresis, anxiety
  • weakness, hunger, nausea
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2
Q

diaphoresis

A

profuse perspiration

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3
Q

Manifestations of prolonged/severe hypoglycemia

A
  • hypothermia
  • confusion, hallucinations
  • seizure, coma
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4
Q

hyperglycemia: early and later manifestations

A

Early:

  • polydipsia, polyuria
  • altered vision
  • weight loss, mild dehydration

Late:

  • cardiac arrhythmias
  • coma
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5
Q

Location of the pancreas

A

behind the stomach between the spleen & the duodenum

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6
Q

Functions of the pancreas

A

Mostly exocrine: pancreatic juice contains enzymes for protein digestion 1-3% is islets - endocrine - insulin/glucagon secretion from islets of langerhans scattered throughout exocrine pancreas

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7
Q

Beta Cells

A

Secrete insulin. 65-80% of islet endocrine cells

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8
Q

Alpha cells

A

Secrete glucagon; 15-20% of the total islet;

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9
Q

Delta cells

A

Secrete somatostatin; 3-10% of islet endocrine ;

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10
Q

Role of somatostatin

A

inhibits both insulin & glucagon

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11
Q

pancreatic polypeptide cells

A

PP cells; secrete pancreatic polypeptide 3-5% of islet endocrine cells; Reduces appetite and food intake, thus regulating blood sugar.

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12
Q

Parasympathetic innervation of pancreatic islets

A

Parasympathetic innervation via Vagus nerve; Primary NT is ACh –> stimulates insulin release

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13
Q

Sympathetic innervation of pancreatic islets

A

Postganglionic fibres of the celiac ganglion; Primary NT is NE –> inhibits insulin secretion

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14
Q

Insulin synthesis and structure

A

Insulin is synthesized as proinsulin - mainly in the beta cells, but also in the brain. It is synthesized in RER, processed in golgi and then stored in secretory granules for hours or days before secretion. Proinsulin has A and B chain linked by disulphide bonds with a C peptide.

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15
Q

Regulation of insulin secretion

A
  • Glucose is the major stimulator
  • there are also neural, hormonal, and nutrient stimulants, but these are also considered glucose-dependent in order to protect agains inappropriate stimulation of insulin and hypoglycemia.
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16
Q

Key hormones that stimulate release of insulin

A

GIP GLP-1 Glucagon (sounds paradoxical, but it does)

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17
Q

glucotoxicity & lipotoxicity

A

prolonged glucose and free fatty acid exposure may cause apoptosis of B cells

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18
Q

Mechanism of insulin release from the B cell

A
  1. Glucose enters through a GLUT2 channel
  2. Glucokinase cleaves glucose to G6P
  3. G6P inhibits an ATP-dependent K+ channel, which stimulates influx of Ca2+ through a voltage-gated Ca2+ channel
  4. Influx of Ca2+ stimulates exocytosis of granules containing proinsulin.
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19
Q

Biological actions of insulin (conceptually)

A
  • anabolic; promotes energy storage
  • Targets muscle, fat, and liver
  • critical role in growth and development
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20
Q

Action of insulin on muscle and adipocytes

A
  1. Insulin binds receptor on muscle cells and adipocytes
  2. Signalling pathway stimulates translocation of vesicles with GLUT 4 transporters to cell surface
  3. Glucose enters cells
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21
Q

Outcomes of insulin in adipose tissue

A

Lipogenesis (decreased lipolysis)

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22
Q

Outcomes of insulin in striated muscle

A

Glycogen and protein synthesis

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23
Q

Outcomes of insulin in the liver

A

Glycogen synthesis;

Lipogenesis (decreased gluconeogenesis)

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24
Q

The insulin receptor

A

A tyrosin kinase; 2 alpha subunits and 2 beta subunits.

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25
Q

Glucagon synthesis

A
  • Synthesized as proglucagon in intestinal L cells and in pancreatic cells
  • Proglucagon contains other glucagon-related peptides (GLPs)
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26
Q

Action of glucagon

A
  • major site of action is in the liver (in contrast to insulin, which works on many tissues)
  • Stimulates glycogenolysis and gluconeogenesis
  • Aims to maintain blood glucose during fasting and exercise
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27
Q

where is glucagon cleared?

A

in the renal capillary bed

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28
Q

Stimulants of glucagon (hormonal, neural, nutrients)

A
  • Hormonal: GIP and CCK
  • Neural: ACh and NE
  • Nutrients: low glucose and Ala or Arg
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29
Q

Action of cortisol in carbohydrate metabolism

A
  • counterregulatory to insulin action (works like glucagon)
  • Increases hepatic gluconeogenesis to maintain plasma glucose during fasting
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30
Q

Action of growth hormone in carbohydrate metabolism

A

Counterregulatory to insulin action and inhibits insulin.

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31
Q

Action of the sympathetic nervous system in carbohydrate metabolism

A

can directly stimulate hepatic glucose output

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32
Q

action of the parasympathetic nervous system in carbohydrate metabolism

A

can directly stimulate hepatic glucose uptake via the vagus nerve.

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33
Q

Macrovascular outcomes of diabetes

A
  1. Cardiovascular: MI, angina, heart failure
  2. Cerebrovascular: Stroke
  3. Peripheral vascular: foot ulceration, ischemia/gangrene, amputation, Charcot foot
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34
Q

Microvascular outcomes of diabetes

A
  1. Retinopathy: proliferative, hemorrhage, retinal detachment, blindness
  2. Nephropathy: Microabuminuria, GFR decline, end-stage renal disease
  3. Neuropathy: peripheral numbness or pain, cranial
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35
Q

How does insulin act on cells to help them take up glucose?

A

Insulin binds receptor (a tyrosine kinase), stimulating a cascade involving PI-3, which causes vesicles containing GLUT4 transporters to be translocated to the cell surface so that glucose may enter the cell.

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36
Q

Triggers for GLUT4 translocation

A

Insulin and exercise

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37
Q

2 modes of insulin secretion

A

the ‘basal-bolus’ concept

Basal - consistent release of insulin to suppress glucose between meals and overnight.

Prandial - spikes of insulin to facilitate glucose uptake after meals

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38
Q

Compare human basal, analogue basal, human bolus, and analogue bolus insulin (2)

A

Human basal insulin has a peak midway, whereas analog basal is much more steady throughout the day. With this in mind, human basal is not ideal for T1D because hypoglycemia may occur and they may not sense the warning signs. Analogue bolus acts much faster than human bolus, so it is preferred.

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39
Q

Random blood glucose result for diagnosing diabetes

A

> 11.1 mmol/L

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40
Q

Screening for diabetes (2)

A

Anyone who is high risk

  • Age > 40 years or high risk screen every 3 years
  • first degree relative or very high risk for another reason, screen every 6-12 months.
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41
Q

What kinds of exercise have been shown to improve glycemic control and lower morbidity in people with diabetes? How much and what type of exercise is recommended for people with diabetes?

A
  • 150 minutes of moderate-to-vigorous aerobic exercise per week
  • include resistance exercises 2 or more times a week
  • set physical activity goals and involve a multidisciplinary team if available
  • minimize uninterupted sedentary time
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42
Q

Should we aim for weight loss in diabetes?

A
  • the goal is to prevent weight gain, promote weight loss, and prevent weight re-gain
  • Weight loss of 5-10% (in CDM slides for the rest)
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43
Q

Serum osmolality equation

A

2[Na] + [HCO3] + [urea]

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44
Q

Actions of Incretin Agents

A
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45
Q

Differences in effects of GLP-1 agonists and DPP-4 Inhibitors

A
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46
Q

Compare and Contrast GLP-1 R Agonists and DPP-4 Inhibitors

  • administration
  • GLP-1 concentrations made available
  • targets of action
  • activating portal glucose sensor
  • increasing insulin and/or glucagon secretion
  • Effects on gastric emptying, weight loss, GIT symptoms
A
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47
Q

TZD Actions

A
  • reduces insulin resistance by sensitizing insulin receptors
  • modify adipocyte differentieation –> reduced Leptin levels –> increased appetite –> increased wt
  • Inhibits VEGF-induced angiogenesis
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48
Q

AIC Targets for people who have diabetes in different contexts (4)

A
  • < 6.5 for adults with type II diabetes to reduce risk of chronic kidney disease and retinopathy if at low risk of hypotension
  • <7 for most adults with Type I or Type II diabetes
  • 7-8.5 if recurrent hypoglycemia and/or unaware of hypoglycemia warning signs, limited life expectancy, frail/elderly
  • No A1C measurement recommended at end of life

tight glycemic control minimizes risk of microvascular complications, though this is not the case for macrovascular risk.

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49
Q

Which two families of diabetes drugs pose CV benefits?

A

GLP-1 agonists and SGLT2 inhibitors

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50
Q

Diabetes Canada recommendations for T2D management

A
  • Start with metformin +/- other therapies
  • Individualize therapy choices
51
Q

Insulin Regular

A

aka Humilin, Novolin

A bolus insulin - meaning it is taken prandially/after meals with short action

52
Q

Insulin NPH

A

Pre-mixed short-acting and intermediate-acting insulin that has a cloudy appearance.

53
Q

When to start pharmacological management of diabetes

A

If AIC is <1.5% over target then initiate health behaviour interventions and start metformin (either immediately or if target is not reached within 3 months.

If AIC > 1.5% over target then start metformin with health behaviour interventions and consider add a second concurrent agent.

54
Q

When to start a T2D pt immediately on insulin +/- metformin

A

When they present with symptomatic hyperglycemia and/or metabolic decompensation.

Symptoms of these:

  • polyuria
  • polydipsia
  • weight loss*****(this is the big one)
  • volume depletion
55
Q

where is angiotensinogen made? where does it go when it’s made?

A

the liver then it circulates around int he blood until cleaved by renin

56
Q

Where is ACE?

A

It’s an enzyme on the surface of endothelial cells in general, but especially those in the lungs.

57
Q
A
58
Q
A

a

59
Q
A

B

1st degree relatives increase risk for T2D

60
Q
A

D

61
Q

What are the different classes of diabetes? (5)

A

T1D

T2D

Gestational Diabetes

Monogenic diabetes (i.e., MODY)

Secondary Diabetes

62
Q

Secondary diabetes causes (4)

A

Medication- & drug-related diabetes

Exocrine pancreas-related diabetes

Endocrinopathy-related diabetes

Infection-related diabetes

63
Q

In simple terms, etiology of T1D & risk factors

A

Autoimmune OR non-autoimmune-mediated destruction of beta cells (usually immune-mediated, but can be idiopathic).

Risk factors: genetic predisposition + env factors

64
Q

Where is T1D more prevalent?

A

Finland > USA > China and some parts sout america

65
Q
A
66
Q

Etiology of T2D

Risk factors

A

Etiology: insulin resistance due to obesity, abnormal insulin receptors, adipokines, inflammation, beta cell dfects, and metabolic syndrome

Risk factors: highly genetic, family history, ethnicity, obesity, poor diet, sedentary, smoking

67
Q

Prevalence of Diabetes

A

6.4% worldwide, with greatest prevalence in USA

68
Q

Etiology of gestational diabetes

A

insulin resistance develops due to placental secretion or diabetogenic hormones, such as GH, CRH, and hPL, hPGH. Pancreas may already be predisposed to diabetes and is unable to keep up with insulin demand

69
Q

Risk factors for gestational diabetes

A
  • maternal age >37
  • ethnicity
  • Pre-pregnancy weight > 80kg
  • FHx diabetes in 1st degree relative
  • Hx macrosomia, polyhydramnios, unexplained stillbirth, PCOS
70
Q

Etiology of monogenitc diabetes

A

Single gene variants that cause defects in glucose-induced insulin release

71
Q

What medications may cause diabetes? (4 groups)

A
  • Cyclosporin, phenytoin, thiazides - can interfere with release from beta cells
    • glucocorticoids, niacin, anti-virals - can induce insulin resistance
  • anti-psychotics - can cause weight gain and sometimes beta cell dysfuctions
  • PD-1 and CTLA-4 inhibitors (cancer treatments) - can block inhibitory immune system
72
Q

How may exocrine pancreas-related diabetes develop?

A
  • Genetic conditions that cause destruction of pancreatic parenchyma (i.e., CF, hemochromatosis)
  • Acquired conditions that can cause destruction of pancreatic parenchyma (i.e., pancreatitis, trauma, infection, cancer, prancreatectomy)
73
Q

List 5 endocrinopathy-related diabetes

A
  • Acromegaly (aka gigantism) - due to excess GH
  • Cushing’s syndrome - excess cortisol (any cause)
  • Cushing’s disease - excess ACTH from pituitary gland
  • Ectopic Cushing’s syndrome - excess SCTH from a non-pituitary source)
  • Pheochromocytoma - excess catecholamines
74
Q

Should we screen for T1D?

A

No. No evidence for interventions to prevent or delay T1D.

75
Q

Screening recommendations for T2D?

A
  • Fasting plasma glucose and/or A1C every 3 years in individuals >40 years old or in individuals at high risk according to a risk calculator (33% chance of developing diabetes over 10 years)
76
Q

Groups that are considered high risk and should therefore be screened earlier/more frequently for T2D (6)

A
  1. Age > 40
  2. 1st degree relative with T2D
  3. HIgh risk population (african, arab, asian, hispanic, indigenous, south asian, low SES)
  4. Hx pre-diabetes (IGT, IFG, or A1C 6.0-6.4%)
  5. Hx GDM
  6. Hx delivery of macrosomic infant
  7. End organ damage
    • Microvasacular - retinopathy, neuropathy, nephropathy
    • Macrovascular - coronary, cerebrovascular, peripheral
  8. Vascular risk factors (low HDL, high TG, overweight, central obesity, smoking)
  9. Associated diseases (PCOS, HIV, OSA, CF, etc)
  10. Use of meds (glucocorticoids, atypical antipsychotics, HAART, etc)
77
Q

A took for screening diabetes risk

A

Canadian Diabetes Risk Questionnaire (CANRISK)

78
Q

HOw is type 2 diabetes diagnosed?

A
  • Fasting plasma glucose > 7.0
  • A1C > 6.5 (in adults)
  • 2 hour plasma glucose in an oral glucose tolerance test (OGTT) > 11.1 mM
  • Random plasma glucose (without regard for last meal time) > 11.1 mM
79
Q

Differentiate glucose levels for pt deemed normal, at risk, prediabetes, and diabetes

A
  • Normal: FPG or A1C < 5.6
  • At risk: FPG or A1C 5.6-6.0
  • Prediabetes: FPG 6.1-6.9 or A1C 6.0-6.4 (screen more often)
  • Diabetes: FPG > 7 or A1C > 6.5
80
Q

Define prediabetes

A

IFG (impaired fasting glucose) or IGT (impared glucose tolerance) or AIC 6.0 to 6.4%, which places these pts at high risk of developing diabetes and its complications

81
Q

What is metabolic syndrome?

A
  • Obesity, HTN, dyslipidemia, diabetes.
  • If they have 3 you should watch closely for the 4th
  • These pts are at high risk fo developing CVD
82
Q

Describe the socio-economic distribution of diabetes

A

3/4 of people with diabetes live in low-to-middle income countries. The prevalence has risen faster in this countries than in high income countries.

83
Q

How much does diabetes canada predict diabetes to increase between 2019 and 2029?

A

by 31%

84
Q

Describe the food insecurity obesogenic pathway

A

In the context of food insecurity, individuals may be driven to purchas inexpensive, high-calorie, low-nutrient foods. There are metabolic adaptations to nutritious food deprivations that can manifest in overweight and obesity. Anxiety and stress may also lead to disordered patterns of eating that exacerbate this pattern.

85
Q

What is an obesogenic environment?

A

One that promotes sedentary lifestyles and access to high-energy foods and presents barriers to accessing healthy food markets.

86
Q

What are some key reasons for higher diabetes rates in indigenous populations in canada?

A

Diabetes is an exemplar disease of colonization. High rates due to loss of land, culture, food security, among other factors.

87
Q

What s cultural food secruity?

A

the ability of Indigenous peoples to access important traditional/cultural foods through traditional harvesting methods to ensure the survival of their cultures.

88
Q

How are adverse chidlhood experiences related to diabetes?

A

Risk of obesity incrases 20-50% for several adversities.

Stress-DM Association Theory posits that chronic activation of the HPA axis can lead to hormone imbalances that oppose insulin action and cause adiposity (which is a contributor to insulin resistance)

89
Q

What are some approaches to diabetes management that may be especially effective in Indigenous communities?

A
  • Strong therapeutic alliance/relationship
  • Address stress factors first
  • Concurrent support for food secruity and meal planning
  • Consider traditional activites that may support wellbeing
  • Work with patient one-on-one, with family unit, with community support systems
  • Diet and exercise prescription only helpful in highly resoured communities
90
Q

activism vs agency

A

Activism is action that brings about change. Supporting agency is to support people in navigating systems when they would envounter challenges of barriers if they acted independently.

91
Q

What are the molecular mechanisms of diabetic complications?

A

Not entirely understood. May have to do with toxicity associated with intracellular hyperglycemia.

92
Q

Intracellular hyperglycemia toxicity

A

Toxicty via

  1. polyol (aldose reductase) pathways activation
  2. Advanced glycosylation end product formation
  3. PKC activation
  4. Hexosamine pathway activation

The big problem is builtup of reactive oxygen species, which case DNA damage. GAPDH (a key enzyme) levels fall and the result is activation of the 4 above pathways.

93
Q

What was the DCCT trial

A

Diabetes control and complications trial. Showed that strict control of sugars reduced incidence of complications.

94
Q

Pathophysiology of diabetic nephropathy (4)

A
  • Main driver is podocyte changes and dysfunction.
    • Podocytes effact, loss of glomerular BM, thus undermining filtration barrier.
  • Alterations to mesangial cells
    • Proliferation, hypertrophy, more EC matrix proteins, expansion leading to glomerular HTN
  • Inflammatory cell recruitment
  • Renal tubule damage
    • Increased glucosel causes tubule hypertrophy in an attempt to absorb more glucose. But Na is absorbed with glucose, so there is less glucose getting to macula densa, therefore less tubuloglomerular feedback and more glomerular pressure.
    • Fibrosis eventually results
95
Q

Screening for diabetic nephropathy

A

Start screening at diagnosis of T2D and at most 5 years after diagnosis of T1D

  • Creatinine and eGFR yearly
  • Spot urine ACR yearly
  • Urinary albumin (typically estimated from ACr; can do 24h urine collection)
96
Q

Stages of diabetic nephropathy progression

A
  1. Hyper filtration (increased GFR)
  2. SIlent
  3. Microalbuminuria
  4. Macroalbuminuria (overt nephropathy)
  5. Uremia (end stage renal disease)
97
Q

Management/prevention of diabetic nephropathy

A
  • Strict glucose control <7
  • BP control (under 130/80)
    • Use RAAS inhibitors
  • Lipid control
  • Smoking cessation
98
Q

Microcascular complications of diabetes (3)

A

Diabetic nephropathy, retinopathy, neuropathy

99
Q

Prevalence of dibatic retinopathy

A

~50-60% in T2D

Up to 90% of T1D patients if not receiving comprehensive treatment.

100
Q

Pathophysiology of diabetic retinopathy (stages; 3)

A
  • Retinal damage is the result of neurodegeneration due to increase in excitatory factors and decrease in neuroprotective factors
  • Nonproliferative microvascular changes include thickened basment membrane and loss of pericytes (supportive cells around blood vessels). Increased vasular permeability, inflammatotion, proliferation of endothelial cells.
  • Pre-proliferative changes include endothelial damage, vasoconstriction, hypoxia, and ischemia. Eschemia may promote angiogenesis of vessels that are leaky and fragile.
  • Proliferative = sever hypoxia casing angiogenesis (promoted by VEGF) of vessels thar are prone to bleeding
101
Q

Classification of diabetic retinopathy (3)

A
  1. Diabetic retinopathy
    1. Nonproliferative
    2. Proliferative
  2. DIabetic macular edema
102
Q

Diagnosing diabetic retinopathy

A
  • Dilated retinal exam
    • Nonprolferative DR: Look for microaneuysms, cotton wool spots, irregularities of vasculature, hard exudates
    • Proliferative DR: neovascularization
  • Optical coherence tomography to assess for dibaetic macular edema
103
Q

When may vision loss occur in diabetes?

A

In cases of vitreous hemmorrhage, traction retinal detachment, diabetic macular edema, and neovascular glaucoma.

104
Q

Treatment of diabetic retinopathy (3)

A
  1. Intravitreal injections of anti-VEGF Abs (works for macular edema too)
  2. Laser photocoagulation
  3. Virectomy (in case of non-clearing vitreal hemorrhage)
105
Q

Screening for diabetic retinopathy (how and when)

A
  • Annual dilated retinal exam (more or less frequent based on findings)
  • Start at diagnosis or T2D and at 5 years after T1D diagnosis.
106
Q

Pathophysiology of diabetic neuropathy

A

Not completely understood

  • Changes in peripheral sensory neurons (first in cells bodies and axons and then in myelination)
  • Some experience pain due to hyperexcitatbility and central sensitization

Different types of diabetic neuropathy, but most common is distal symmetric polyneuropathy, which has the stocking-gloving distribution (feet –> legs –> hands).

107
Q

Screening for diabetic neuropathy

A
  • History (numbness, paresthesias [=tingling], pain)
  • Clinical examination using 10 gram microfilament on feet, tuning fork, and other things.
108
Q

Management of diabetic neuropathy

A

Most for painful neuropathy

  • Gabapentin (nerve pain(
  • SNRI antidepressants
  • Tricyclic antidepressants
  • Narcotics
109
Q

Macrovascular disease outcomes of diabetes (3)

A

cardiovascular disease

  • coronary artery disease, MI
  • cardiomyopathy

cerebrovacular disease

  • stroke
  • Transient ischemic attack (TIA)

periphreal vascular disease

  • skin, hair nail changes
  • claudication, foot ulcers
  • limb amputation
110
Q

Pathophysiology of vascular disease in diabetes (4)

A
  • Hyperglycemia and insulin resistance leads to increased prevalence of FFAs, which lead to production of reactive oxygen species
  • Dyslipidemia also increases free fatty acids, TGs, LDL, and decreases HDL - contributes to atherosclerotic plaque formation.
  • Hypertension
  • Endothelial dysfunction, coagulationd isturbances, inflammation, oxidative stress
111
Q

Management of vascular disease in diabetes

A

ABCDES

  • A: A1c <7%
  • B: BP < 130/80
  • C: Cholesterol LDL < 2mM
  • D: drugs to protect heart
    • Ace inhibitors
    • Statins
    • ASA
    • SGLT2 inhibitors or GPL1 agonists
  • E: exercise and healthy eating
  • S: smoking cessation, stress managment, screening
112
Q

Etiology of diabetic foot and possible outcomes.

A

Due to peripheral vascular disease and diabetic neuropathy,

Charcot neuroarthropathy: repetitive trauma, fracture, bone remodeling leading to deformity and a hot/smollen foot in a pt with neuropathy (can’t feel it).

COnsequences include ulceration, infection, limb amputation

113
Q

Management of diabetic foot

A
  • Regular examination
  • offloading pressure, proper foot wear
  • Wound care, treat infections
  • Nail care, moisturize to prevent dryness
114
Q

Erectile dysfunction in diabetes

A
  • Multifactorial
    • vascular disease, endothelial dysfunction, smoking
    • autonomic neuropathy
    • low T
  • Occurs in 30-70% of diabetes pts
115
Q

Management of erectile dysfunction in diabetes

A

Assess for other vascular disease and check testosterone level;

PDE5 inhibitors (i.e., nitrates) and other more invasive treatments as needed;

116
Q
A
117
Q

Diabetic Ketoacidosis: Main cause and 3 primary clinical characteristics

A

Metabolic decomposition (usually in T1D) usually resulting from an absolute insulin deficiency.

Characertized by (1) hyperglycemia, (2) ketonemia, (3) metabolic acidosis.

+/- volume depletion

118
Q

Clinical presentation of Diabetic Ketoacidosis

A

Polydipsia, polyuria, weakness

Nausea, vomiting, abdominal pain

Volume depletion -> hypotension, tachycardia, cerebral edema

Tachypnea (Kussmaul breathing - rapid, deep inspiration)

Acetone breath

Myalgia

119
Q

Basic pathophysiology of Diabetic Ketoacidosis:

A

Loss of insulin leads to loss of glucagon suppression. Excess glucagon leads to gluconeogenesis and ketogenesis. Beta-oxidation of FFA leads to developments of ketones.

120
Q

Management of Diabetic Ketoacidosis:

A

Volume repletion, insulin infusion, K+ repletion (when volume is normalized), monitor closely

121
Q

serum characteristics for Diabetic Ketoacidosis compred to HHS

A

DKA has hyperglycemia, hyper ketonemia, and metabolic acidosis

HHS has VERY HIGH hyperglycemia (>33.3 mM), very high serum osmolality, and little/no acidosis or ketonemia)

122
Q

Hyperglycemic Hyperosmolar Syndrome: Definition and 3 primary characteristics

A

Metabolic decomposition (usually in T2D) resulting from relative insulin deficiency and severe hyperglycemia leading to hyperosmolality and volume depletion

Characterized by (1) severe hyperglycemia, (2) hyperosmolality, (3) volume depletion

123
Q

Clinical presentation of Hyperglycemic Hyperosmolar Syndrome

A
  • Older person
  • polydipsia, polyuria
  • weakness, confusion, lethargy
  • poor fluid intake
  • lethargy, stupor, coma
  • hypothermia

Med 1 UBC Fall 2019 (16 decks)

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