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Year 1: Patho/Pharm > Diabetes PATHO > Flashcards

Diabetes PATHO Flashcards

1
Q

Type 1 DM
Prevalence

A

Canada has one of the highest prevalence’s in the world

Men = women

10% of all diabetes diagnoses

Most common chronic paediatric illness

Diagnosis 11-13 years (rare < 1 years, > 30 years)

White people 2x > than ethnic minorities

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2
Q

Type 1 DM
Risk Factors

A
  • virus
  • formulae feeding
  • cow milk allergies
  • genetics (family history, 50% twins)
  • HLA-DR (autoimmune disorders: thyroid (graves, hashimoto), adrenal (addisons), ceilac disease)
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3
Q

Type 1 DM
Pathophysiology

A
  1. Auto-immune
  2. Idiopathic

Genetic predisposition x environment

  • formation auto-antibodies against
    1. Islet antigen 2 antibodies (IA-2A)
    2. anti-glutamic acid decarboxylase (GADA) antibodies
  • Activation macrophages, cytotoxic T cells, humoral immune response (antibody production)
  • Destruction of beta cells (insulin producing cells)
  • No insulin released
  • No GLUT4, no uptake of glucose in fat/muscle/liver
  • No inhibition of glucagon
  • No amylin release
  • No inhibition glucagon, gastric emptying is not slowed, saiety is not supressed
  • removed inhibition glucagon
  • increase blood glucose (counter-regulatory hormone)
  • liver breaks down glycogen, makes glucose from a.a and FFA
  • adipose tissue breaks down fat
  • muscle breaks down protein
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4
Q

Type I DM
Onset & Screening

A

Slow onset

80-90% beta cell destroyed before detected

No screening for T 1 DM
- cannot prevent / delay diagnosis

If diagnosed screen for other auto-immune diseases (HLA-DL)
- Thyroid (graves, hashimoto)
- Celiac
- Addison’s disease

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5
Q

Type 1 DM
Clinical Signs and Symptoms

A

Polyuria
- osmotic diuresis
- glucosuria pulls water out of body

Polydipsia
- Hyperosmolarity of blood
- low blood volume
- triggers hypothalamus thirst center

Polyphagia
- breakdown of glycogen, muscle, fat stores

Underweight

Diabetic ketoacidosis:
- ketones detected in urine, breath, and blood
- liver oxidizing FFA for energy produces ketone bodies
- metabolic acidosis (hyperventilation, lethargy, coma)

Electrolyte imbalances:
- hyponatremia
- hypokalemia

Cellular dehydration
- seizures

No C-Peptide
- no endogenous insulin production

+/-
- IA-2A antibodies
- GADA antibodies

Blurred vision
- hyperglycemia in lens of eye, pulls water in

Genital Pruritis

Infection, poor wound healing
- hyperglycemia
- micro/macrovasular damage from hyperglycemia

Cardiovascular complications
- parasethesias
- chest pain
- extremity pain

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6
Q

Type 1 DM
Etiology

A
  1. Idiopathic
  2. Auto-immune *HLADR
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7
Q

Type 2 DM
Prevalence

A

90% Type 2 DM

> 40 years of age

ethnic minorities > white
(indigenous > african, hispanic, asian)

Obesity * (and metabolic syndrome)

men > women

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8
Q

Type 2 DM
Risk Factors

A

Age
> 40 years

obesity* (primary driver)

metabolic syndrome (dylipidemia, hypertension, abdominal girth, hyperglycemia)
- BP > 130
- TG > 1.7
- Waist circumference > 102cm males, > 88cm females

pre-diabetes (impaired FG, impaired GTT, elevated A1C)
- IFG 6.1-6.9mmol/L
- IGTT 7.8-11.0mmol/L
- 6.0-6.4% A1C

ethnic minorities

Males > females

PCOS

Sleep apnea

NAFLD

neuropsychiatric medications

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9
Q

Insulin Receptor Sensitivity
Modulating factors

A
  • age
  • weight
  • HTN
  • dyslipidemia
  • stress
  • exercise
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10
Q

Type 2 DM
Clinical Signs and Symptoms

A
  1. Silent hyperglycemia
    - hyperinsulinemia results in silent hyperglycemia
  2. Symptomatic hyperglycemia (HHS)
  • Polyuria (osmotic diuresis)
  • polydipsia
  • polyphagia
  • fatigue
  • glucosuria
  • albuminuria
  • hyperglycemia
  • blurred vision
  • hyperosmolarity blood
  • cellular dehydration, seizures
  • electrolyte imabalances: hypokalemia, hyponatremia
  • infections, impaired wound healing, genital pruritis
  • microvascular and macrovascular complications: CVE, MI, paraesthesias, retinopathy, nephropathy
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11
Q

Type 2 DM
Pathophysiology

A
  1. Obesity results in peripheral insulin resistance
    - adipokines, pro-inflammatory cytokines
    - increased insulin resistance
    - increased demand on beta cells
    - cytotoxic to beta cells
  2. beta cells hyper secrete insulin (hyperinsulinemia)
    - increase beta cell secretion insulin
    - beta cell dysfunction
    - adipokines are also cytotoxic to beta cells
    - silent hyperglycemia
    - microvascular and macrovascular damage continues
  3. beta cells begin to dysfunction
    - adipokines are cytotoxic
    - increased demand, decreased function
    - decrease 1. insulin 2. amylin
    - decrease response to incretins (GLP1 and GIP) which results in decrease insulin secretion
  4. Decreased insulin and amylin removes negative inhibition on glucagon
    - increase gluconeogenesis, and breakdown of fat, protein and glycogen
    - increases blood glucose
  5. decreased function amylin
    - no saeity
    - increased GI motility
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12
Q

Type 2 DM
Screening

A

Everyone is screened at 40 years, every 3 years

Screen earlier if risk factors present and screen every 6-12 months

*CANRISK calculator

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13
Q

Gestational DM
Prevalence

A

3-20% of pregnancies

  • all mothers screened at 24 weeks
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14
Q

Gestational DM
Risk Factors

A

80% have pre-diabetes
1. insulin resistance
2. beta cell dysfunction
at baseline prior to pregnancy

  • advanced maternal age
  • obesity
  • ethnic minorities
  • family history, personal history (genetics)
  • PCOS
  • pre-diabetes
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15
Q

Gestational DM
Clinical Manifestations

A
  1. Silent hyperglycemia
    - asymptomatic
    - all mothers screened at 24 weeks
  2. Symptomatic
    - polyuria, polydipsia, polyphagia, fatigue, hyperglycemia, weight loss
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16
Q

Gestational DM
Preferred vs. Alternate screening

A

50g OGTT
- 2 hour mark BG > 9.0mmol/L

then

75g OGTT
- 2 hour mark BG > 8.5mmol/L

*lower threshold as fetus eats the glucose

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17
Q

Gestational DM
Complications of hyperglycemia

A
  • still birth
  • spontaneous abortions
  • teratogenic (congenital abnormalities)
  • pre-eclampsia
  • retinopathy

Tighter glycemic control
- A1C < 6.1%
- Hypoglycemia < 3.7mmol/L

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18
Q

Gestational DM
Pathophysiology

A

Placent causes insulin resistance
- estrogen, progesterone, cortisol, GH, lactogen
- increase maternal resistance to insulin
- increases glucose in blood for the baby

Maternal counter-regulatory hormones released
- glucagon increases blood glucose

beta cell hyperplasia and hypertrophy
- hyperinsulinemia
- increased fetal uptake of glucose

80% of GDM have beta cell dysfunction at baseline along with insulin resistance

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19
Q

Gestational DM
Patient Education Post-Partum

A
  1. breast feed
    - immediately (prevent hypoglycemia)
    - until 4 months (prevent DM in baby and mother)
  2. Re-check FPG at 6 weeks and 6 months
    - type 2DM?
  3. montior thyroid dysfunction
    - higher risk for post partum thyroiditis
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20
Q

Diabetes Mellitus
Immediate Complications

A
  1. Diabetic Ketoacidosis (DKA)
    - diabetic coma syndrome
    - Type I DM
  2. Hyperosmolar Hyperglycemic Syndrome (HHS)
    - Type 2 DM
  3. Hypoglycemic shock
    - Insulin shock
    - Insulin reaction
    - Type 1 or 2 DM
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21
Q

Diabetic Ketoacidosis (DKA)
Risk factors

A
  1. Undiagnosed Type 1 DM
  2. Trigger - Sick, Trauma, Drug reaction (cocaine, SGLT2, anti-psychotics), thyrotoxicosis
    - release of counter-regulatory hormones (cortisol)
  3. Missed Insulin
  4. Insulin antagonists
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22
Q

Diabetic Ketoacidosis
Laboratory Results

A

BG > 14mmol/L
anion gap
low bicarbonate
high lactate (low pH)
plasma and urine ketoacids (beta hydroxybutyrate, acetoacetone, acetone)

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23
Q

Diabetic Ketoacidosis
Pathophysiology

A
  1. No insulin (relative insulin deficiency)
  2. Activation counter-regulatory hormones
    - rise in cortisol
    - increase blood glucose
    - site of action: 1. liver 2. muscle 3. fat
    - Liver: breaks down glycogen, gluconeogenesis from oxidation fat
    - Muscle: breakdown protein
    - Fat: lipolysis, FFA
  3. FFA oxidation by liver produces ketoacids
    - beta hydroxybutyrate
    - acetoacetate
    - acetone
  4. Reduction pH leads to metabolic acidosis
    - bicarbonate low, anion gap formation
    - kaussmaul respirations
  5. Hyperglycemia -> clinical signs and symptoms
    - polyuria - osmotic diuresis
    - dehydration
    - hyperosmolality and CNS dehydration
    - polydipsia
    - polyphagia
    - electrolyte imbalances: hyponatremia, hypokalemia
    - N/V/D, arrhythmias, abdominal pain etc.
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24
Q

Hyperosmolar Hyperglycemic non-ketotic Syndrome
Risk Factors

A
  1. Type 2 DM undiagnosed
  2. Insulin antagonists
    - Illness, trauma, drugs (corticosteroids)
  3. Pancreatitis
    - no insulin released
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25
Q

Hyperosmolar Hyperglycemic (HHS)
Laboratory results

A

BG > 33.5mmol/L
Osmolality > 320mmol/L
BUN:Cr > 20:1
NO KETONES

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26
Q

Hyperosmolar Hyperglycemic Syndrome (HHS)
Pathophysiology

A

Absolute or relative decrease in insulin

Hyperglycemia
- reduced insulin, blood glucose remains in blood

Silent hyperglycemia
- onset slow
- body has insulin to take up glucose
- progresses silently
- level hyperglycemia much more severe than DKA

Clinical S&S
- polyuria
- polydipsia
- severe dehydration
- severe electrolyte imbalances (N/V/abdominal pain, weakness): hyponatremia, hypokalemia
- poor skin turgor, dry lips, mucous membranes
- hypotensive shock
- poor kidney perfusion leads to accumulation BUN:Cr
- hypothermia (CNS dysfunction), stupor, coma

27
Q

Higher mortality rate
DKA or HHS?

A

HHS

28
Q

Hypoglycemic Shock
Risk Factors

A

Iatrogenic

  1. too much insulin
  2. too much insulin secretagogues
  3. Combination therapy
  4. Impaired awareness hypoglycemia (IAH) multiple hypoglycemic episodes (rapidly fluctuating BG)
  5. Exercise
  6. To little food with insulin therapy
  7. Alcohol
  8. Medications
    - beta blockers (mask hypoglycemia)
  9. Decline in insulin need
    - Chronic kidney disease (decrease insulin degredation)
    - post partum period (gestational DM)
29
Q

Individuals at high risk for
Hypoglycemic shock

A
  • age
  • longer duration diabetes
  • more hypoglycemic episodes (threshold hypoglycemia lower)
  • diabetic neuropathy (ANS not activated)
  • preschool
  • cognitive impairment
  • low health literacy
30
Q

Why are frequent hypoglycemic episodes bad

A

Re-set glucose counter-regulatory threshold
- lower BG required to stimulate SNS response
- Neuroglycopenic symptoms are the first signs (Level 3)
- too late and require assistance to treat
*very dangerous

31
Q

When are Type 1 DM more likely to experience hypoglcyemic shock?

A

Night time

Decreased sympathoadrenal repsonse to hypoglycemia
Level 3

*somogyi

32
Q

Clinical Signs and Symptoms
Hypoglycemia
Adrenergic (Autonomic)

A
  • trembling
  • sweating
  • palpitations
  • pale
  • anxiety
  • nausea
  • tingling
  • hunger
33
Q

Clinical Signs and Symptoms
Hypoglycemia
Neuroglycopenic

A
  • Fatigue
  • confusion
  • slurred speech
  • blurred vision
  • weakness
  • sensory and motor changes
  • HA
  • dizziness
  • coma
  • death
34
Q

Classifications of Hypoglycemia

A

Level 1
BG 3.0-3.9mmol/L (< 4.0mmol/L)
Autonomic symptoms

Level 2
BG < 3mmol/L
Neuroglycopenic symptoms (able to self treat)

Level 3
BG < 3mmmol/L
neuroglycopenic symptoms
unable to self treat

35
Q

Hypoglycemia
Laboratory diagnostics

A

Normal blood glucose adult 4.0-7.0mmol/L

Neonate < 1.7mmol/L

Adult < 3.9mmol/L

Pregnant adult < 3.7mmol/L

36
Q

Hypoglycemic Shock
Pathophysiology

A

Too much insulin
- Trigger: too much insulin, combination therapy, excerise, alcohol, not enough food, sleep
- uptake of BG into cells

Counter-regulatory hormones released
- Cortisol increases: gluconeogenesis, glycogenolysis, lipolysis, proteolysis
- SNS activated: adrenergic symptoms

Insufficient counter-regulatory response
- neuroglycopenic symptoms: CNS depression, confusion, HA, coma, death

37
Q

Long term Hypoglycemia
Complications

A

Hypoglycemia is pro-inflammatory

  • platelet aggregation
  • fibrosis

Long term consequences of hypoglycemia

  • Fear of hypoglycemia (keep blood glucose high increase micro and macrovascular complications)
  • IAH (impaired awareness hypoglycemia)
  • Scaring of the brain (intellectual development, alzheimer’s disease, pontine dysfunction, hemiparesis)
38
Q

Treatment of Hypoglycemia

A
  1. switch from intermediate to long acting insulin
    - degludec > glargine > detemir
  2. check insulin regularly at night (impaired awareness hypoglycemia)
  3. continuous glucose monitoring and continuous subcutaneous insulin infusions
  4. Increase glucose target for 3 months
    - re-sets the adrenergic hypoglycemic set point
    - avoidance hypoglycemia for 2 days or 3 months
  5. Avoid drinking
  6. Exercise
    - reduce pre-prandial insulin
    - reduce basal insulin at night
    - increase carbohydrate intake before exercise
    - weights before cardio
    - sprints in between cardio
  7. patient and family education

*prevention is easier than treatment

39
Q

Laboratory Values
Predict what chronic complications

A

A1C
- CVD, CVE, progression to T2DM

FPG and OGTT
- microvascular complications

40
Q

Chronic complications of DM

A

Microvascular complications (capillaries)
1. neuropathy
2. retinopathy
3. nephropathy

Macrovascular complications (major arteries, cerebral arteries)
1. Cardiovascular disease
2. Cerebrovascular disease
3. Peripheral vascular disease

41
Q

Microvascular complications
Pathophysiology

A

Hyperglycemia -> glycation end products -> inflammation -> atheroscelerosis -> scaring, narrowing -> ischemia -> necrosis

42
Q

Retinopathy & DM

A

DM leading cause of blindness world wide

  1. non-proliferative stage
    - inflammation, increased premeability retina capillaries
  2. pre-proliferative stage
    - ischemia, infarcts
  3. proliferative stage
    - neovascularization, retinal detachment, blindness

Other:
- blurred vision (lens swelling)
- cataracts
- glaucoma

43
Q

Nephropathy & DM

A

DM leading cause of ESRD
50% individuals with DM

  1. Glomeruloscelerosis
    - hyperglycemia damages the glomerular membrane
    - inflammation -> scaring -> loss of negative charge and filtration slits
    - proteinuria
  2. Acute tubular necrosis
    - hyperglycemia damages the epithelium of the nephron tubulse
    - cannot reabsorb or secrete (perform functions)
44
Q

Neuropathy & DM

A

Most common complication of DM
DM leading cause of nephropathy in the west

demylination of nerves
slows conduction

  1. sensory nerves
    - loss sensation, pain, temperature, vibration, pressure, etc.
  2. motor nerves
    - loss of motor funciton
    - Charcot Arthropathy - degeneration joints in foot
  3. Autonomic nerves
    - gastric paresis
    - insensible hypoglycemia
    - silent MI
    - etc.
45
Q

Macrovascular Complications
DM

A
  1. Cerebrovascular disease (strokes)
  2. cardiovascular disease (CAD, MI, etc.)
  3. peripheral vascular disease (ex. gangrene and amputations)
46
Q

Cardiovascular disease (CAD) and DM

A
  1. CAD
  2. HF
  3. CAD
    Coronary Artery disease leading cause of morbidity and mortality in DM

Hyperglycemia –> glycated end products –> inflammation endothelial lining –> recruitment neutrophils and macrophages -> oxidative damage LDL –> engluphed –> fatty streak / atheroscelerotic plaque –> unstable plaque –> thrombosis

narrow lumen –> ischemia –> infarct –> necrosis

  1. HF
    Atheroscelerosis increases BP
    Increase pressure heart pumps against
    L ventricular remodelling
    Diastolic compliance decreases
    HFpEF - heart failure preserved ejection fraction
47
Q

Peripheral artery disease and DM

A

Hyperglycemia -> demylination nerves -> slow/no conduction -> injury -> ulceration -> infection -> amputation

48
Q

Impaired fasting glucose
Pathophysiological changes

A

6.1-6.9mmol/L
Impaired fasting glucose

*Predicts microvascular complications

PRO
- fast
- easy
- predicts microvascular complications

CON
- variable
- one point in time
- fasting 8 hours

49
Q

Impaired oral glucose tolerance
Pathophysiological changes

A

7.8-11.0mmol/L

*predicts microvascular complications

PRO
- fast
- easy
- measure any time of day

CON
- unpalitable
- high cost
- high variability
- one time point

50
Q

Impaired A1C
Pathophysiology changes

A

A1C 6.1-6.4%

*predicts microvascular changes
*predicts type 2 DM
*predicts CVD and all cause mortality

PRO
- predictor micro and macrovascular changes
- Predictor type 2 DM advancement
- reflects 120 days glucose management

CON
- not for diagnosis in children or adolescents
- altered values in hemoglobinopathies, age, ethnicity, liver and kidney disease

51
Q

Pre-Diabetes
Diagnostic Classification

A

Impaired fasting glucose 6.1-6.9mmol/L
impaired oral glucose tolerance 7.8-11.0mmol/L
impaired A1C 6.1-6.4%

52
Q

Goal of Treatment
DM

A

Maintain A1C in target range
- Tight control is not recommended (<6.5%) as associated with higher mortality, no CV benefit (only microvascular benefit)

Individualized based on age: children, adolescent, adult, pregnant, elderly ; and health status

Minimize fluctuations in BG

Minimize hypoglycemic episodes
- more episodes = higher mortality, cardiovascular complications, and IAH

Multifactorial treatment
- BG
- HTN
- dyslipidemia
- exercise
- smoking cessation

53
Q

Glycemic Targets
Adults

A

Fasting plasma glucose 4.0-7.0mmol/L
2 hour post prandial glucose 5.0-10mmol/L
A1C < 7%

54
Q

Glycemic Targets
Pregnancy

A

A1C < 7% (at minimum)
A1C < 6.5% (goal)
A1C < 6.1% (third trimester)

Prevention
- miscarriage, still birth, spontaneous abortion
- congenital abnormalities
- pre-eclampsia
- retinopathy

55
Q

Glycemic Targets
Children and Adolescents

A

A1C < 7.5%
- prevention hypoglycemia (inflammatory scarring of brain and negative impact congitive development and IQ)
- prevention IAH development

Fasting plasma glucose 4.0mmol/L - 8.0mmol/L

2 hour post prandial glucose 5.0mmol/L-10mmol/L

56
Q

Glycemic Targets
Functional dependence, IAH, frailty, palliative care

A

A1C 7.1-8.5%

Functional dependence
- unable to notify S&S of hypoglycemia
- IAH and high risk death

Frailty and palliative care
- hypoglycemia = degredation of glycogen, muscle, fat stores
- decreased implication of CV and microvascular damage

IAH
- loosen glycemic control
- re-set counter-regulatory threshold

57
Q

Laboratory screening
DM

A
  • A1C
  • urinalysis (nephropathy)
  • retinopathy
  • neuropathy
  • dyslipidemia
  • blood pressure
  • vaccinations yearly (influenzae, COVID19)
  • smoking, alcohol cessation
  • pregnancy planning
  • autoimmune disorders (thyroid, celiac, addisons)
58
Q

Self Monitoring
DM

A

Blood glucose at minimum TID
A1C levels for glycemic control over 120 days
Ketone monitoring when sick, stressed, trauma

59
Q

Initiation insulin therapy
Children T2 DM

A

A1C > 9 %
- insulin and metformin

9% > A1C > 7%
- metformin
- diet, exercise

60
Q

Nonpharmacological Management
DM

A
  1. Exercise (weight loss)
  2. Diet
61
Q

Dietary Considerations
DM

A
  • portion control (40-60% carbs, 15-20% protein, 20-35% fat)
  • DASH, Mediterranean, Nordic, Vegetarian diets
  • whole wheat, nuts, legums/beans/pulses, omega fats, fish, vegetable proteins, vegetables, fruits, high fibre
  • low glycemic index carbohydrates
  • regular spacing of meals throughout the day
  • physical activity
  • weight loss
62
Q

Physical activity
DM

A

150minutes per week moderate-high intensity aerobic exercise

3x per week resistance training

No more than 2 days rest

63
Q

Physical exercise induced
Hypoglycemia vs. hyperglycemia

A

PE induced hypoglycemia
- reduce bolus insulin
- eat before exercise
- reduce basal insulin 20% (exercise long lasting effect)
- cardio before weights
- sprints between weights

PE induced hyperglycemia
- weights and sprints induce counter-regulatory hormones which breakdown lipids, muscle, and glycogen stores to raise glucose levels

Year 1: Patho/Pharm (39 decks)

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