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DB Therapeutics > Lecture 5 (Complications of DM) > Flashcards

Lecture 5 (Complications of DM) Flashcards

1
Q

List some acute complications with DM

A

hypoglycemia
hyperglycemia (ketoacidosis, hyperglycemic hyperosmolar state)
infections (sick day management)

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2
Q

List some chronic complications with DM

A

Macrovascular (CVD, Dyslipidemia, HTN)
Microvascular (nephro, retino, neuropathy)
others (mental health, apnea, driving)

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3
Q

Define hypoglycemia

A

low BG levels (<4 mmol/L)
development of autonomic or neuroglycopenic symptoms
symptoms respond to the intake of carbs

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4
Q

What are some common causes of hypoglycemia?

A

not eating on time, not eating enough
unusual amount of physical exercise
taking too much of an anti-hyperglycemic meds
alcohol

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5
Q

Define and list symptoms of neurogenic hypoglycemia

A

usually occurs first at BG levels <4 mmol/L

Symptoms
trembling, palpitations, sweating, anxiety, hunger, nausea, tingling

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6
Q

Define and list symptoms of neuroglycopenic hypoglycemia

A

usually occurs when BG level <2.8 mmol/l
symptoms
difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking, headaches, dizziness

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7
Q

Define mild hypoglycemia

A

glucose <3.9 mmol/L and <3.0mmol/L
autonomic symptoms present
pt is able to self treat

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8
Q

Define moderate hypoglycemia

A

glucose <3
autonomic and neuroglycopenic sx present
pt is able to self treat

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9
Q

Define severe hypoglycemia

A

glucose usually <2.8
autonomic and neuroglycopenic sx
distinguished by unresponsiveness and unconsciousness
pt is not able to self treat

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10
Q

List some major risk factors of severe hypo in T1DM

A

Prior episode of severe hypoglycemia
Current low glycated A1C (< 6.0 %)
Hypoglycemia Unawareness
Long duration of diabetes
Autonomic neuropathy
Adolescence
Preschool-aged children unable to detect and/or treat mild hypoglycemia on their own

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11
Q

List some major risk factors of severe hypo in T2DM

A

Advancing age
Severe cognitive impairment
Poor health literacy
Food insecurity
Increased A1C
Hypoglycemia unawareness
Duration of insulin therapy
Renal impairment
Neuropathy

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12
Q

Define hypoglycemia unawareness

A

The inability to recognize the early warning signs of low BG levels; the first symptoms of hypoglycemia will often be confusion or loss of consciousness

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13
Q

What can occurs as a result of frequent lows (BG) due to?

A

A decrease in the hormonal response mechanisms that prevent hypoglycemia (i.e. epinephrine and glucagon)
A lowering of the threshold at which hypoglycemia symptoms are experienced
Beta blockers can also contribute to hypoglycemia unawareness
This puts people at increased risk for severe hypoglycemia, hence it is important to minimize hypos as much as possible

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14
Q

List the steps to address hypoglycemia

A
  1. recognize ANS or neuroglycopenic symptoms
  2. Confirm is possible (with CBG)
  3. treat with fast sugar (15 g)
  4. retest in 15 min to ensure BG>4.0 and retreat if needed
  5. eat usual snack or meal due at that time of day
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15
Q

Treatment of mild to modterate hypoglycemia

A

Eat or drink 15 g of a fast-acting carbohydrate
This will raise BG by ~ 2 mmol/L within 20 mins, with adequate symptom relief for most people

Wait 15 mins then check BG again. If it is still low, retreat with 15 g CHO.

Once BG > 4 mmol/L, eat within the hour (either a meal or a snack including a starch and protein)

Wait until BG > 5 mmol/L before driving; this may take around 40 minutes (“5 to Drive”)

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16
Q

What level should you be before you should drive with hypo?

A

above 5

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17
Q

Treatment for severe hypoglycemia (BG<2.8) if pt is conscious

A

Treat with with oral ingestion of 20 g carbohydrate, preferably as glucose tabs
This will raise BG by ~ 3.5 mmol/L over 45 mins
Wait 15 mins and retest BG
Retreat with another 15 g of glucose if the BG level remains < 4.0 mmol/L
Eat usual snack or meal due at that time of day or a snack with 15 g carbohydrate plus protein

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18
Q

Treatment for severe hypoglycemia (BG<2.8) if pt is not conscious

A
  1. Treat with glucagon
  2. Call 911
  3. Turn the pt into recovery position
  4. eat as soon as safety possible
  5. discuss with health care team
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19
Q

What are some examples of injectable glucagon?

A

glucagen
glucagon rDNA

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20
Q

What are some examples of nasal spray of glucagon?

A

baqsami

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21
Q

MOA of glucagon

A

makes the liver release storages of sugars into the body

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22
Q

What is pseudo-hypoglycemia?

A

A state in which an individual experiences symptoms of hypoglycemia despite having BG levels > 4.0 mmol/L

Usually occurs in individuals who are accustomed to having chronic high BG levels and have a rapid drop in BG levels once they start treatment

Once BG levels are under better control, the perception of symptoms at these higher BG levels will dissipate

Still treat if symptomatic

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23
Q

List some usual causes of hyperglycemia

A

Too little / omission of insulin
Illness (UTI, sepsis, pneumonia are common culprits of DKA) – see an increase in counter-regulatory hormones
Infection
Surgery
Injury
Stress; emotional or physical
Increased food
Exercise (in T1DM) with BG > 14 mmol/L and ketones

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24
Q

What are some characteristics of DKA?

A

Hyperglycemia (usually >14 mmol/L)
Ketonemia
Metabolic acidosis (venous pH <7.3 and/or serum bicarbonate <15mmol/L, anion gap >12 mmol/L)

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25
Q

When there is insulin deficiency, hyperglycemia causes …

A

significant loss of water and electrolytes through the urine and extracellular fluid volume depletion
also increase catecholamines stimulates lipolysis, the breakdown of TGs into FFAs that are converted into ketone bodies by the liver and released into circulation
this causes the acidosis

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26
Q

List some sx of DKA

A

Excessive thirst
Excessive urination
Fatigue / weakness
Blurred vision
Change in appetite
Abdominal pain, nausea, vomiting
Air hunger
Fruity acetone breath
Hyperventilation: Kussmaul Respiration
Confusion

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27
Q

Explain the treatment plan

A

Replacement of fluid loss (IV fluids (0.9% NaCl) - replete the Na deficit)

Replacement of potassium (if <5.0-5.5mmol/L) once diuresis has been started. If K+ is <3.3mmol/L, withhold insulin until it goes above this level

Correction of metabolic acidosis. Administer short-acting insulin IV 0.1 U/kg/hr. adjust based on anion gap resolution – and avoid hypoglycemia and hypokalemia

If patient is in shock or pH <7 , sodium bicarbonate may be added

Once BG reaches 14mmol/L, IV glucose should be added to target a BG of 12-14mmol/L to prevent hypo

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28
Q

What is hyperosmolar hyperglycemia syndrome?

A

Characterized by extremely high sugar, increased osmolality, significant dehydration, and minimal ketoacidosis

Infection or another medical illness is the usual precipitant

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29
Q

What is the management plan for HHS?

A

fluid resuscitation (individualized)
avoidance of hypokalemia
insulin administration
avoidance of rapidly falling osmolality (which could cause cerebral edema)
And search for the precipitating cause

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30
Q

What is the plan for prevention of DKA/HHS?

A

Education around sick day management
Adjust insulin dose as needed; continuation of insulin even when not eating
Frequent monitoring of BG when ill
Check for ketones

31
Q

What is the acromyn for sick day management?

A

SICK
S- blood sugar testing
i- insulin
C- Carbs and fluid
K-ketone testing

32
Q

What is SAD MANS mean?

A

if the pt is ill and unable to maintain fluid they should hold medications (just for a few days)
S-sulonylureas
A- ace
D-diuertics

M- metformin
A- angiotensin receptors blockers
N- NSAIDs
S-SGLT2 i

33
Q

What is ABCDESSS mean when used for risk reduction?

A

A-A1C
B-BP targets
C-cholesterol targets
D- drugs for CVD risk reduction
E-exercise
S-screening for complications
S-smoking cessation
S-self management

34
Q

Goal for HTN for DM

A

130/80

35
Q

What is first line for pt with CVD or CKD with DM?

A

ACEi/ARB

36
Q

When should ACEi and ARB used for vascular protection in DM?

A

sometimes if pt has
CVD
Age >55 with addition CV risk factors
microvascular complications

37
Q

Screening requirements for dyslipidemia for DM

A

should get baseline when diagnosed and checked at least 1/yr

38
Q

When are statins indicated for PWD?

A

age >40
Age > 30 & DM duration >15yrs
microvascular disease

39
Q

Lipid targets for DB

A

LDL <2
>50% reduction of LDL at current levels

40
Q

Monitoring plan for lipid for DM

A

repeat testing should be performed 3-6 months after tx intiaiton & periodically after (at least 1/yr)

41
Q

When should PWD be on ASA?

A

only recommended with secondary prevention (but are exceptions)

42
Q

What is the key to prevent microvascular complications for PWD?

A

tight control of BP, BG, and lipids

43
Q

List some risk factors of DB nephropathy

A

longer duration of DB
poor BG, BP and lipid control
obesity
smoking

44
Q

What is the leading cause of kidney disease in canada?

A

diabetes

45
Q

When should screening for CKD be done?

A

random urinary ACR and a serum creatinine levels
T1Dm - 5 yrs after diagnosis in adults (then annuallY)
T2DM - at diagnosis (then annually)

46
Q

What is treatment plan for DB nephropathy?

A

aimed to slow the progression of albuminuria and a decline in eGFR

optimize BG control
optimize BP control
Use of SGLT2i

47
Q

Define retinopathy

A

Diabetic retinopathy is a vascular complication of diabetes, It is caused by damage to the blood vessels of the retina that can cause them to bleed or leak fluid, distorting vision.

48
Q

Risk factors for retinopathy

A

Duration of diabetes
Glycemic control
HTN, dyslipidemia
Anemia
Nephropathy
Tobacco use
African American

49
Q

When should you screening for retinopathy for T1DM and T2DM?

A

T1DM: 5 yrs after diagnosis when ≥15yo (then annually)
T2DM: At diagnosis (then q 1-2yrs)

50
Q

What is prevention for retinopathy?

A

Optimize glycemic control
Optimize BP control

51
Q

What is treatment plan for retinopathy?

A

Varies based on the type of the ocular problem
Laser therapy, intraocular (local) injections (bevacizumab, ranibizumab, aflibercept, or steroids), and/or vitreoretinal surgery

52
Q

Define DB neuropathy

A

A type of nerve damage that can occur as a result of having diabetes
Nerve damage most commonly results from reduced blood flow to nerves, which is the result of damage to blood vessels caused by hyperglycemia
Chronic and often progressive; early recognition and management is ideal

53
Q

List the two types of DB neuropathy

A

distal symmetric poly-neuropathy (DSPN)
diabetic autonomic neuropathy (DAN)

54
Q

Define DSPN

A

distal symmetric poly-neuropathy
most common
involves the sensorimotor nervous system

55
Q

Define DAN

A

diabetic autonomic neuropathy
Involves the autonomic nervous system
Includes the heart (cardiac autonomic neuropathy), GIT, genitourinary system, sexual function, sudomotor abnormalities

56
Q

Risk factors for diabetic neuropathy

A

Elevated BG
Elevated triglycerides
High BMI
Smoking
Hypertension

57
Q

Screening for diabetic neuropathy

A

T1DM: After 5 years post-pubertal duration (then annually)
T2DM: At diagnosis (then annually)
Screening is assessed via loss of sensitivity to the 10g monofilament or loss of sensitivity to vibration at the dorsum of the great toe (128-Hz tuning fork)

58
Q

List type of autonomic neuropathy

A

Gastrointestinal - gastroparesis
CV
Genitourinary
Sexual dysfunction
metabolic
sudomotor

59
Q

List sx for CV DAN

A

resting tachycardia, exercise intolerance, orthostatic hypotension, silent MI. Risk factor for mortality

60
Q

List Sx for genitourinary DAN

A

bladder dysfunction, erectile dysfunction, retrograde ejaculation
Erectile dysfunction:
Affects up to 40% of males with diabetes
Both vascular and neurogenic causes
Important to ask about

61
Q

List Sx for sexual dysfunction DAN

A

Females may experience ↓vaginal lubrication, arousal, excitement, satisfaction, orgasm; increased dyspareunia
Males may experience erectile dysfunction

62
Q

List sx for metabolic DAN

A

hypoglycemia unawareness, hypoglycemia unresponsiveness

63
Q

List sx for sudomotor DAN

A

gustatory sweating, anhidrosis, heat intolerance, dry skin

64
Q

Explain what peripheral neuropathy

A

Most common type of neuropathy

Will develop within 10 years of the onset of diabetes in 40-50% of people with T1DM and T2DM (diabetes is the most common cause of peripheral neuropathy)

Often presents in feet first

Predisposes a patient to the development of foot ulcers, infection, gangrene, and ultimately amputation

65
Q

List some sx for peripheral neuropathy

A

Early symptoms as a result of small fibers
Pain
Burning and tingling sensation
Altered sense of temperature
Involvement of large fibers
Loss of protective sensation (LOPS)
Numbness

66
Q

Treatment plan for peripheral neuropathy

A

Optimize BG
May prevent or delay onset in T1
Can slow the progression in T2

67
Q

Pain management for peripheral neuropathy

A

A common complication of diabetes (>16% will experience it), yet about only half of patients receive treatment

Usually starts in the toes then makes its way up

Affects QOL, activity, productivity

68
Q

List some options for pain management for peripheral neuropathy

A

Oral:
Gabapentinoids (pregabalin, gabapentin)
SNRIs (duloxetine, desvenlafaxine)
Sodium channel blockers (valproic acid)
TCAs (amitriptyline)

Topical:
Capsaicin (8% and 0.075%) – small effect

Cognitive Behavioral Therapy

69
Q

What are the screening for foot care for PWD?

A

Annual foot examinations (or more frequent) including visual assessment, pedal pulses, and sensory foot exam with monofilament

70
Q

General preventive foot care education for PWD

A

Wash feet in warm water using a mild soap
Dry your feet carefully, especially between toes!
Thoroughly check feet and in between toes to ensure no cuts, cracks, ingrown toenails, blisters, etc. Can use hand mirror
Clean cuts with mild soap/water then cover with dressing
Trim your toenails straight across and file any sharp edges. Don’t cut the nails too short
Apply unscented lotion to heels and soles. Wipe off excess
Don’t put lotion between toes since this can promote infection
Wear clean socks and well-fitting shoes daily. Don’t ever go barefoot
Test bath water temperature with your hand before you step in to make sure the water is not too hot
Avoid sitting for long periods of time
Do not smoke

71
Q

What are the main points for foot care?

A

Educate about proper foot care
- Daily self exam and HCP at least once yearly

Foot care exams are not standard practice for pharmacists and likely not feasible, but we can do a 10 gram monofilament assessment

Identify those at high risk of foot ulcers and educate, assess more frequently, and consider appropriately fitted footwear

Refer persons with foot ulcers and other complications to those specialized in foot care

72
Q

Definition of OSA

A

Obstructive sleep apnea
Sleep disorder with repetitive episodes of cessation of breathing followed by awakening to restart breathing
OSA alters glucose metabolism & promotes insulin resistance

73
Q

Sx of OSA

A

Restless, non-refreshing sleep
Snoring
Breathing pauses
Awakenings (with gasping or paroxysmal nocturnal dyspnea)
Insomnia
Excessive daytime sleepiness of fatigue

DB Therapeutics (5 decks)

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