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LMCC - Medicine > Endocrinology - Diabetes > Flashcards

Endocrinology - Diabetes Flashcards

1
Q

Differentiate between macrovascular and microvascular complications with diabetes

A 
Macrovascular
- medium and large size blood vessels involved
- CAD, MI, stroke, PAD
Microvascular
- involve small capillaries
- retinopathy, nephropathy, neuropathy
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2
Q

Discuss the stages of diabetic retinopathy

A

Non-proliferative
- asymptomatic but could have impaired vision due to macular edema
- progressive blood vessel change including microaneurysm, hemorrhage, hard exudate
Pre-proliferative
- macular edema
- venous shunts and possible bleeding
- intra-retinal microvascular abnormalities
Proliferative
- neovascularization (abnormal BV growth) and fibrous scarring
- blindness due to vitreous hemorrhage or retinal detachment

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3
Q

Discuss the presentation and management of diabetic retinopathy

A 
Presentation
- asymptomatic
- blurry vision
- darkening or distorted vision due to macular edema
- cotton wool spots
- exudates
Management
- follow with ophthalmologist
- glycemic control
- control HTN and lipids
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4
Q

Discuss the stages of diabetic nephropathy

A 
- nephrotic syndrome
Stage 1
- hyperfiltration (increased GFR) where kidney may increase in size
Stage 2
- microalbuminuria due to damage of glomeruli
- ACR 2-20 male or 3-28 in female
Stage 3
- increased albumin excretion (macroalbuminemia), rising creatinine and increased BP
- ACR >20 male or >28 female
Stage 4
- GFR <75 with proteinuria
 Stage 5
- end stage renal disease, GFR <10
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5
Q

Discuss the management of diabetic nephropathy

A
  • glycemic control
  • blood pressure control
  • ACEi or ARB to reduce albuminemia
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6
Q

Discuss the presentation of different types of diabetic neuropathy

A

Peripheral Sensory Neuropathy
- Neuropathic pain, numbness, paresthesia
- decreased tactile sensation (glove and stocking)
Motor Neuropathy
- muscle weakness
- reversible cranial palsy
Autonomic Neuropathy
- alternating constipation and diarrhea due to gastroperesis
- urinary retention
- erectile dysfunction

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7
Q

Discuss the presentation, investigations and management for diabetic foot ulcer/cellulitis

A 
Presentation
- infected ulcer (erythema, warmth, swelling, pain) or pus
- necrotizing if soft tissue gas, skin discoloration or foul odor
Investigation
- wound swab
- CBC, blood glucose, ESR/CRP
- blood culture
Management
- Surgical
     - debridement and cleaning
     - revascularization
     - osteomyelitis then amputation
- Wound care
     - relieve pressure on ulcer
     - wound cleaning and dressing
- Glycemic Control
- Antibiotic
     - Mild: Keflex
     - Moderate: Septra plus Amox-Clav or Clindamycin
     - Moderate with deep tissue: IV Pip-Tazo, Meropenem, Moxifloxacin, Flagyl + Ceftriaxone
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8
Q

Discuss classification of infection and risk for osteomyelitis for diabetic foot ulcer

A

Classification
- Infected if >=2 of purulence, erythema, pain, warmth, swelling
- Mild if erythema extends <=2cm around ulcer
- Moderate: erythema extends >2cm around ulcer or involvement of deep tissue
- Severe: systemic toxicity or instability
Risks for Osteomyelitis
- Large ulcer
- deep ulcer, probing to bone
- visualization of bone
- ESR >70
- MRI to r/o

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9
Q

Discuss the pathophysiology, benefits, risks and dosing of biguanides

A 
Pathophysiology
- increase sensitivity of the cell to insulin
Benefit
- A1c lowering of 1-1.5%
- low risk of hypoglycemia
- improved cardiovascular risk
Risks
- contraindicated with eGFR <30 (increase risk of lactic acidosis)
- GI side effects
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10
Q

Discuss the pathophysiology, benefits, risks and dosing of incretins

A 
Pathophysiology
- secreted in the gut and result in increased insulin secretion from the pancreas
- glucagon like peptide-1
- glucose dependent insulinotrophic peptide
Benefit
- increase satiety and decrease gastric emptying which reduces weight gain
- increase insulin secretion
Benefits
- A1c lowering of 1%
- significant weight loss
- low risk of hypoglycemia
- some cardiovascular benefit
Risks
- GI side effects
- subcutaneous injection required
- rare cause of pancreatitis
- increase parafollicular hyperplasia
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11
Q

Discuss the pathophysiology, benefits, risks and dosing of DDP-IV inhibitors

A 
Pathophysiology
- amplify incretin pathway by inhibiting breakdown of endogenous GLP and GIP
Benefits
- A1c lowering of 0.7%
- low risk of hypoglycemia
- improve post-prandial control
- GI side effects
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12
Q

Discuss the pathophysiology, benefits, risks and dosing of SGL2-inhibitors

A

Pathophysiology
- block glucose transport in proximal renal tubule leading to urinary exretion
Benefits
- glycosuria:
- negative caloric balance and weight loss
- decrease A1c
- increase uric acid release
- natriuresis
- decrease blood pressure resulting in decrease arteriolar stiffness
- decrease plasma volume resulting in decreased myocardial stretch
- increase tubulo-glomerulo fedback and afferent arteriole constriction
Risks
- increase risk of UTI
- osmotic diuresis leading to hypotension
- ketoacidosis in euglycemic individual

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13
Q

Discuss the pathophysiology, benefits, risks and dosing of sulfonylurea

A 
Pathophsyiology
- bind to sulfonylurea receptor inhibiting efflux of K -> depolarization and increase in Ca entry into cell -> increase insulin release
Benefits
- A1c lowering of 0.8%
- rapid glucose lowering
Risks
- may cause hypoglycemia
- weight gain
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14
Q

Discuss the pathophysiology, benefits, risks and dosing of meglitinide

A 
Pathophysiology
- same as sulfonylurea as is a secretague 
Benefit
- A1c lowering of 0.7%
- rapid glucose lowering with lower risk of hypoglycemia due to shorter half-life
- safe with renal impairment
Risks
- weight gain
- hypoglycemia
- interaction with plavix
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15
Q

Discuss the pathophysiology, benefits, risks and dosing of acarbose-glucosidase inhibitor

A 
Pathophysiology
- inhibit intestinal enzymes alpha-glucosidase and pancreatic alpha-amylase resulting in reduced digestion of carbohydrates
Benefits
- A1c lowering of 0.6%
- rare hypoglycemia
- GI side effects
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16
Q

Discuss the pathophysiology, benefits, risks and dosing of thiazolidinediones

A 
Pathophysiology
- increase sensitivity of tissues to insulin by activation of ppar-gamma receptor
Benefit
- longer duration of monotherapy
- Mild blood pressure lowering
- A1c lowering 0.8%
- low risk of hypoglycemia
Risks
- weight gain
- increased peripheral edema and heart failure
- increased risk of fractures
17
Q

Discuss the pathophysiology of insulin therapy

A
  • bind to tyrosine kinase receptor on myocytes, hepatocytes, adipocytes to activate P13K -> PIP3 -> PDK/Akt signalling to ellicit
    - increased glycogenesis, lipogenesis and triglyceride synthesis
    - decreased lipolysis, glycogenolysis, and ketogenesis
    - increase glucose uptake from blood
    - liver and muscle increase glycogenesis and protein synthesis
    - adipocytes inhibit lipolysis
18
Q

Discuss the correction scale for insulin

A
  • bolus prescribed by correction scale
    - determine correction factor 100/TDI (0.3units/kg or number of total daily units of insulin receiving)
    - if BG 4-8 no insulin
    - if BG (8 - 8+CF) then one additional unit
    - if BG (8+CF) - (8+2CF) then two additional units
19
Q

Discuss the general principles of managing diabetes in hospital

A
  • Type require insulin even if NPO
  • diabetic diet
  • BG monitoring at before meals, at night and prn
  • Continue with pre-admission treatment and change if
    - NPO or decreased PO intake
    - HbAIc >8%
    - measured BG >10
    - frequent episodes of hypoglycemia
20
Q

Discuss management of type 2 diabetic patients in hospital

A

Patients newly diagnosed (add in order below)
- Max dose oral agent
- add new oral agent from another class
- Start basal insulin
- 0.2-0.3 units/kg long acting (Glaring, Determir) at night or NPH before breakfast and at night
- Add meal time insulin
- discontinue all oral agents except metformin
- 0.1-0.2 units/kg of fast acting at breakfast, lunch supper if long acting or before breakfast and supper if on NPH
- Use corrective insulin sliding scale
- Adjust insulin based on glucose pattenr
- hypoglycemia: decrease at time before noticed
- adjust insulin to get pre-prandial breakfast into range
- correct insulin to correct for high insulin during the day
Patients on Insulin (add in order)
- start basal insulin (same as above)
- add meal time insulin (same as above)
- use corrective insulin sliding scale
- adjust as needed

21
Q

Discuss the management of diabetic patients that are NPO or cannot take oral agents due to renal failure

A

Discontinue all oral agents
NPO/Clear Fluids
- CBG Q6H
- IV D5W 100cc/hr
- discontinue meal time insulin
- NPO >2days or peri-operative then IV protocol
- previously on oral agents/diet and not on insulin
- use corrective scale
- if >8 units after 2 days then start basal
- previously on insulin
- switch basal to 1/2 to 2/3 basal insulin dose
- use corrective

22
Q

Discuss insulin use for patients on steroids

A
  • cause hyperglycemia 5-12 hrs after steroid intake
    Morning Steroid Only
  • NPH 0.2-0.4units/kg before breakfast
    Steroid BID-QID
  • NPH 0.2-0.4 units/kg before breakfast and dinner
23
Q

Discuss the presentation and management of hypoglycemia

A 
Presentation
- autonomic/adrenergic symptoms
      - hunger
      - diaphoresis
      - tremulousness, tingling
      - palpitation
      - anxiety
- Neuroglycopenic symptoms
      - dizziness
      - unusual behaviour
      - seizure
      - visual changes
- late type 1 and type 2 there is hypoglcyemia unawareness so less symptoms
Diagnosis
- Whipple's triad: blood glucose <2.8 with symptoms that is corrected with food or glucose
Management
- conscious eat food or drink with carbohydrate or 15-20g glucose tablet
      - should improve in 5-10 and complete in <20
- Unconscious glucagon 1mg SC/IM or 50mL D50W
- thiamine 100mg IM
24
Q

List the 5 I’s of diabetic ketoacidosis

A 
Insulin Deficiency
- inadequate dose
- omission of insulin
- new diagnosis
Infection
- most common
Ischemia
- MI
- stroke
Intra-abdominal process
- pregnancy
- pancreatitis
Intoxication
- drugs or alcohol
25
Q

Discuss the pathophysiology of diabetic ketoacidosis

A

Severe Insulin Deficiency
- stress increase insulin demand that is not matched by pancreas
- decrease peripheral glucose utilization and uptake, leading to hyperglycemia
- K shift out of cell leading to hyperkalemia with low body store of K
Severe Cell Starvation
- liver produce and release glucose -> hyperglycemia
- adipose tissue release free fatty acids which are converted to ketones by liver
- peripheral muscle decrease glucose utilization leading to weakness
Ketone Bodies
- cause metabolic acidosis, which can be compensated by breathing
Hyperglycemia and Ketone Bodies
- cause osmotic diuresis
- dehydration
- electrolyte depletion
- hyperosmolality (hyponatremia and cerebral dehydration)

26
Q

Discuss the presentation, investigation and diagnosis of DKA

A 
Presentation
- sleepiness, LOC
- blurry vision
- N/V
- polyuria, polydipsia
- Kaussmaul breathing
- hypovolemic
- fruity ketone breath
Investigation
- CBC, electrolytes, creatinine BUN
- blood glucose
- serum osmolality
- serum ketone
- VBG
- urine analysis
- ECG
Diagnosis (all of the following)
- metabolic acidosis with increased anion gap
- serum and urine ketone bodies
- hyperglycemia
27
Q

Discuss the management of DKA

A

Q2-4H electrolytes, anion gap, glucose, creatinine, plasma osmolality, LOC
IV Fluids for decreased Effective Circulating Volume
- Severe shock give NS 1-2L/h until hypotension correction and then switch to NS 500mL/hr for 4hr then 250mL/hr for 4 hr
- mild to moderate start at 500mL
- Once euvolemic
- Na is normal/high or rate of plasma osmolality fall is <3 switch to 0.45NS
- Na is low or rate of plasma osmolality fall >=3 then continue with 0.9%NS
- Once plasma glucose reaches 14 add D5W to IV fluids to maintain glucose 12-14
Serum K
- <3.3 then give 40mmol/L KCl and no insulin until K >=3.3
- >=3.3 and less 5-5.5 then 10-40KCl
Acisosi
- if K <3.3 correct hypokalemia before insulin
- if K >=3.3 administer IV short acting insulin 0.1unit/kg/h
- adjust rate of insulin based on anion gap resolution
- if pH <7.0 then NaHCO3 1 amp/h until pH >=7

28
Q

Discuss the screening for Diabetes

A
  • screen every 3 years for those over 40
  • If screen positive for diabetes must do confirmatory test unless symptomatic (polydipsia, polyphagia, polyuria, weight loss, blurry vision)
    FPG <5.6 or A1c <5.5%
  • normal rescreen in 3 years
    FPG 5.6-6.6 and/or AIc 5.5-5.9%
  • no risk factors then rescreen more often
  • risk factors then go to 75g OGTT
    FPG 6.1-6.9 and/or A1c 6.0-6.4%
  • go to 75g OGTT
    • fasting <6.1 and 2h <7.8
      • if A1c <6% then rescreen more often
      • if A1c 6-6.4% then prediabetes
    • fasting <6.1 and 2h 7.8-11 then impaired glucose tolerance and prediabetes
    • fasting 6.1-6.9 and 2h <7.8 then impaired fasting glucose and prediabetes
    • fasting 6.1-6.9 and 2h 7.8-11 then prediabetes
    • fasting >7 or 2h >11.1 then diabetes
      FPG >7.0 and/pr A1c >6.5% then diabetes
29
Q

Discuss the monitoring for diabetes

A 
Fasting Blood Glucose
- 4-7
2hr Post Prandial
- 5-10 or 5-8 if not achieving A1c target
- HbA1c <7.0% done every 3 months
Blood Pressure
- <130/80
Lipids
- LDL <=2 or >=50% reduction
- apoB <0.8 or non-HDL <=2.6
- done yearly
Chronic Kidney Disease
- Normal ACR <2.0
- normal eGFR >60
- type 1 screen at 5 year and then yearly
- type 2 at diagnosis then yearly
Retinopathy
- type 1 5 years after diagnosis then yearly
- type 2 at diagnosis then 1-2 years
Neuropathy
- screen with 10g monofilament (until bends) at 1st, 3rd, and 5th metarsal head and base of great toe
- type 1 at 5 years then yearly
- type 2 yearly
Waist Circumference/BMI
- Maintain WC <102cm in males and <88cm in females
- BMI between 18.5-24.9
Lifestyle Modification
- 150minutes/week of aerobic exercises
30
Q

Discuss screening following adding antihyperglycemic agent

A
  • make timely increase in dose or add drug from different class in order to reach A1C target in 3-6 months
  • if A1c is <1.5 above target of 7% then begin with lifestyle for three months before switching to metformin
  • if A1c is >1.5 above target of 7 begin metformin right away and possibly other drug
31
Q

Discuss when to initiate insulin therapy

A 
Suboptimal control with oral agents
Marked Hyperglycemia at Presentation
- A1c >9%
- require basal-bolus regimen
Stress on Body
- infection
- pregnancy
32
Q

List risk factors for diabetes

A
  • First degree relative with type 2 diabetes
  • history of prediabetes
  • history of gestational diabetes
  • metabolic syndrome
  • PCOS
  • aconthosis nigricans
  • OSA
  • glucorticoids
  • atypical antipsychotics
  • retroviral therapy
33
Q

List factors that can alter A1c

A 
Increase A1c
- B12 or iron deficiency
- chronic renal failure
- hyperbilirubinemia
- EtOH or opioids
Decrease A1c
- use of EPO, iron or B12
- reticulocystosis
- ASA
- Vitamin C or E
- hemoglobinopathies
- Splenomegaly
- rheumatoid
34
Q

Discuss the algorithm for starting insulin

A
  • can be combined with oral agent
    Basal (glargine or detemir)
  • start at 10 units or 0.2units/kg at bedtime
  • check fasting glucose daily and increase by 2 units every 3 days until in in fasting range
    - if FBG >10 then can increase by 4 units every 3 days
    Second Injection
  • If A1c >=7% after 2-3 months then add bolus (lispart or aspart) at pre-lunch, -dinner, -bed
    - if pre-lunch high then do at breakfast, etc
  • if after 2 months A1c still out of range then check 2h post-prandial
35
Q

Discuss when to add additional therapy to diabetes

A 
ACEI or ARB
- clincal macrovascular disease
- age >55
- age <55 and microvascular disease
Statin
- clinical macrovascular disease
- age >=40
- age <40 and diabetes duration >15yr, microvascular complication or cardiovascular risk factor
Low Dose ASA
- for those with cardiovascular disease
36
Q

Discuss causes and pathophysiology hyperosmolar hyperglycemic state

A

Causes
- Sepsis
- Stroke
- Mi, CHF
- Renal failure
Pathophysiology
- partial or relative insulin deficiency decrease glucose utilization in muscle, fat, liver leading to hyperglycemia and liver glucose production
- small amount of insulin prevents ketosis
- Have more severe dehydration to DA due to gradual onset and increased duration of metabolic decompensation

37
Q

Discuss the presentation, investigations, and manageemtn of HHS

A
  • hyperglycemia (44-133), hyperosmolality, dehydration without ketosis
  • More common in T2DM
    Presentation
  • Polyuria, polydipsia leading to weakness
  • decreased fluid intake
  • decreased LOC
    Investigation
  • Increase BG
  • Hyponatremia in mild dehydration (every 10 increase in BG have 3 decrease in Na)
    - Hypernatremic in severe
  • Increase osmolality
    Management
  • Rehydration
    - 500mL/h x4h then 250mL/h for 4h then 0.45% NS when euvolemic unless corrected Na is low or rate of osmolality fall is >=3
    - Switch to D5W when BG at 14
  • K replacement
    - K <3.3mmol then give 40mEq/L and hold insulin until K>3.3
    - K 3.3-5 then start insulin with 10-40 of K
    - K >5 then recheck in 2hrs
  • Insulin
    - Monitor plasma osmolality

LMCC - Medicine (40 decks)

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