Complication of diabetes Flashcards

1
Q

DKA vs HHS (hyperosmolar hyperglycemic state)
Who is it more common in

A

DKA
- common in young people with type 1

HHS
- adult or elder with type 2

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2
Q

DKA vs HHS
Glucose levels?

A

DKA
- normal-high glucose
- 14+ (or sometimes lower)

HHS
- Higher glucose >22

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3
Q

DKA vs HHS
Symptoms?

A

DKA
- SOME reduced level of consciousness, hypokalemia, kussmal breathing, fruity breath

HHS
- SEVERELY reduced level of consioussness, hypokalemia
NO kussmal breathing or fruity breath, or positive urine acetone test

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4
Q

DKA vs HHS
onset/mortality

A

DKA
- Fast onset
- Lower mortality rate

HHS
- Slow onset
- Higher mortality rate

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5
Q

DKA vs HHS
pathophysiology

A

DKA
- Absolute insulin deficiency
- increased glucagon
- milder hyperosmolarity

HHS
- relative insulin deficiency
- no ketones present
- minimal acid-base problem

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6
Q

DKA vs HHS
Treatment

A

DKA
- MUST use insulin
- IV fluids, Serum K+, Insulin

HHS
- MAY use insulin
- Hydration, Serum K+, +/- insulin

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7
Q

What are common features of DKA vs HHS

A

Insulin deficiency –> hyperglycemia –> urinary loss of water + electrolytes
- volume depletion + electrolyte + hyperosmolarity

Both will be fluid depleted

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8
Q

Is it possible that a patient with no diabetes get HHS?

A

Yes

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9
Q

Which groups of people should you assess for DKA if symptoms are present but BG is not elevated

A

Pregnancy & SGLT2 use

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10
Q

What specific test should be ordered to identify DKA and ketones in the blood?

A

B-hydroxy butyrate

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11
Q

What are conditions that can make DKA diagnosis difficult (3)

A
  1. Conditions that inc bicarb (eg. vomiting)
  2. Significant osmotic diuresis –> loss of keto anions = normal anion gap
  3. Pregnancy and SGLT2i –> mildly inc glucose
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12
Q

What are common causes/precipitating factors of DKA

A
  • Insulin omission
  • New diagnosis of diabetes
  • infection/sepsis
  • MI
  • Thyrotoxicosis
  • Drugs
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13
Q

How to prevent DKA in type 1 and type 2 diabetes

A

Type 1
- education around sick day management
- continuation of insulin EVEN when not eating (dose may need adjustment)
- frequent monitoring when ill

Type 2
- education around sick day management
- Frequent monitoring when ill

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14
Q

SADMANS acronym

A

Solfunylurea
ACEi
Diuretics
Metformin
ARB
NSAIDs
SGLT2i

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15
Q

How often should you check blood or urine ketones and BG when you’re sick?

A

Every 2-4 hours

or if symptoms of DKA are experienced (

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16
Q

When should you seek your primary care provider or emergency when you’re sick with diabetes?

A
  • If vomiting occurs twice or more within 12 hours
  • on going diarrhea or getting worse
  • or when symptoms of DKA are experienced (nausea, vomiting or abdominal pain)
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17
Q

If you cannot tolerate solid food when you are sick how much CHO should you aim for?

A

15g of CHO every hour

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18
Q

Define microvascular, macrovascular and mixed complications

A

Microvascular: small BV
- Retinopathy
- Nephropathy
- Neuropathy

Macrovascular: large BV
- Atherosclerosis
- lipid abnormalities
- CHD coronary heart disease
- Cerebrovascular and peripheral vascular disease CVD and PVD
- hypertension
- Heart failure

Mixed complications
- combination of micro and macro and/or neuropathic changes
ex. foot problems and ED can be both

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19
Q

What are symptoms of retinopathy?
Both eyes or one eye affected?

A
  • Seeing spots or floaters
  • Blurred vision
  • Having a dark/empty/black spots in the center of vision
  • Difficulty seeing well at night
  • Noticing colours appear faded or washed out losing vision

Both eyes

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20
Q

What are the 4 forms of retinopathy. Define them

A
  1. Macular edema
    - diffuse or focal vascular leakage at the macula
  2. Non-proliferative
    - Microaneurysms, intraretinal hemmorage, vascular tortuosity, and vascular malformation
    - Damaged BV leak fluids and fat into the retina
  3. Proliferative
    - abnormal vessel growth
    - BV to retina therefore retina produces new abnormal BV
  4. Retinal Capillary close
    - Limited profusion
21
Q

Most common cause of blindness among working age
in type 1
Type 2 on insulin
Type 2 not on insulin

A

Type 1:
- proliferative retinopathy

Type 2 insulin
- Macular edema

Type not on insulin
- Macular edema
- not as prevalent though

22
Q

When to initiate screening for retinopathy in type 1 and 2

A

Type 1: 5 years after diagnosis if 15+

Type 2: everyone at diagnosis

23
Q

How to prevent/delay getting retinopathy (3)

A
  1. Glycemic control: A1C 7 or under
  2. BP control: less than 130/80
  3. Lipid-lowering therapy: Fibrates
24
Q

Can retinopathy be treated? How?

A

Yes

Laser therapy (reduce blindness by 90% in non/proliferative retinopathy)
VEGF antagonists (pharmacologic options)
Surgery (removing vitreous humor)

25
Q

How to diagnose CKD?

A

ACR (albumin-creatine ratio) 2.0 mg/mmol+

and/or

eGFR <60

rescreen in 1 year

26
Q

Define nephorpathy. What is the first/best marker for this condition?

A

Nephropathy
- increase in proteinuria in people with longstanding diabetes, followed by declining function which can lead to end-stage

First/best marker = microalbuminuria

27
Q

What is the range for normal, microalbuminuria, overt nephropathy on a urine dipstick. (negative/positive)

A

Normal (negative)
- ACR under 2

Microalbuminuria (negative)
- ACR 2-20

Overt nephropathy/ macroalbuminuria (postive)
- ACR over 20

28
Q

What are potential causes of transient albuminuria/ when should you delay treatment?

A

Recent major exercise
UTI
Fever illness
Decompensated CHF
Menstruation
Acute severe elevation in BG/BP

29
Q

What is first line drug therapy for CKD and diabetes? in type 1 and type 2

A

Type 2:
- SGLT2i if eGFR over 20
- Metformin if eGFR 30+

Type 1 and 2:
- ACE/ARB if htn
- Statin

30
Q

Differentiate between glycemic control in micro vs macro albuminuria

A

Microalbuminuria
- intensive therapy (lowering A1C target) can bring you back to normal levels

Macro
- intensive therapy can prevent progression to CKD (not as much benefit)

31
Q

How to prevent progression of diabetic nephropathy?

A
  • optimal glycemic control
  • optimal BP control
  • ACEi/ARB
  • SGLT2i
  • Non-steroidal MRA if ACR over 3 (finerenone)
32
Q

Can you use ACEi and ARB to slow progression of nephropathy even in the absence of hypertension?

A

Yes

33
Q

What will you expect with Cr when you start ACEi/ARB?

A

Can go up to 30% in the beginning

Ok for renal function to go down a bit

34
Q

What does neuropathy cause you to have an increased risk for?

A
  • Foot ulceration and amputation
  • Neuropathic pain
  • Significant morbidity
  • Usage of healthcare resources
35
Q

What are risk factors for neuropathy

A
  • Elevated BG
  • elevated Triglycerides
  • High BMI
  • Smoking
  • Hypertesnion
36
Q

What are autonomic neuropathies that can effect other biologic systems

A
  1. GI
    - gastroparesis, constipation, diarrhea, esophageal dysmotility
  2. CV neuropathy
    - exercise intolerance, postural hypotension, tachycardio
  3. Genitourinary
    - incontinence, ED, female sexual dysfunction

Sudomotor
- sweating dysfunction, heat intolerance, dry skin

Pupillary
- pupil abnormalities

Metabolic
- hypoglycemia unawareness and unresponsiveness

37
Q

Give 2 examples of screening for diabetic neuropathy

A
  1. 10g semmes-weinstein monofilament
    - gauges the patients ability to perceive the sensation of a metal filament touching their big toe
  2. 128Hz vibration tuning fork
    - testing if they can sense vibration on the bone of their toe for 40 seconds
38
Q

What is first line, second line, and other options for treatment for neuropathic pain

A

First line
- anticonvulsants
- antidepressants

2nd line
- opioids

Other
- topical nitrate
- capsaicin
- transcutaneous electrical nerve stimulation

39
Q

What is the best anticonvulsant used for neuropathic pain approved? Other?

A

Pregablin (needs renal adjustment)

Other:
- gabapentin
- valproate

40
Q

What is the best antidepressant used for neuropathic pain approved? Other?

A

Duloxetine

Other
- amitriptyline
- venlafaxine

41
Q

Do people get full relief of neuropathy pain?

A

Yes, only a few people have complete relief

A 30-50% reduction in pain is considered meaningful (hard to get complete relief)

42
Q

Which method of CVD prevention was better in type 2 diabetes, intensive vs. conventional? What does it entail?

A

Intensive (BETTER)
- therapies to achieve targets in glycemia, lipids, BP, albuminuria
- follow-up q3months
- ASA and ACEi (independant of BP)

Conventional arm
- follow clinical practice guidelines

43
Q

Who should recieve statins (regardless of baseline LDL) (4)

A
  • Clinical CVD
  • Age 40+
  • Microvascular complications
  • Diabetes for over 15 years and age 30+
44
Q

Who shouldn’t be on a statin or ACE/ARB?

A

Women who are pregnant or trying to be.

45
Q

Who should recieve ACEi/ARB therapy regardless of baseline BP? (3)

A
  • Clinical CVD
  • Age 55+ with a CV Risk factor or end organ damage (albuminuria, retinopathy)
  • Microvascular complications
46
Q

Which drugs help in reduction in MACE (major adverse cardio events)

A

SGLT2i
GLP1-RA

47
Q

Which drugs reduce hospitalization for heart failure

A

SGLT2i

48
Q

Which drugs increase risk of hospitalization for heart failure

A

TZDs
Saxagliptin

49
Q

When should ASA be used in diabetes

A

For secondary prevention of CVD events

No overall benefit for primary prevention
- bleed risk outweighs benefits