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Preclerkship > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Diagnostic criteria for DM

A

Fasting plasma glucose of 7.0 + on 2 separate occasions
Random glucose of 11.1+ w/ symptoms of hyperglycemia
2-hr glucose of 11.1+ on 75g OGTT
HbA1C of 6.5% +

(and/or)

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2
Q

What blood sugar = impaired glucose tolerance/prediabetes?

A

FPG of 6.1-6.9 mmol/L = impaired fasting glucose

A1C 6.0-6.4 = prediabetes

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3
Q

Family history in T1DM?

A

Not usually family Hx (vs type 2 usually has FmHx)

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4
Q

Recommended screening for T1DM & T2DM?

A

T1DM not recommended (educate parents about signs of hyperglycemia such as polydipsia/polyuria)
T2DM: every 3 yrs for adults >40 or high risk (33% chance in 10 years)
If very high risk (50% in 10 years), screen every 6-12 mo

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5
Q

A1C% targets?

A

<6.5 if low risk of hypoglycemia (e.g. meds, pt characteristics)
<7.0 for most adults w/ T1DM/T2DM
7.1-8.5 if hypoglycemia issues, limited life expectancy, frail/elderly/dementia

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6
Q

HbA1C averages sugars over how long?

A

3 months (lifespan of RBCs)

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7
Q

FPG and 2-hr postprandial PG targets

A

FPG: <7 mmol/L

2-hr PP PG: <10

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8
Q

Upon diagnosis of T2DM, what is the threshold for starting metformin in addition to just lifestyle mods?

A

A1C >1.5% above target
(if less, just try lifestyle mods for 3 months before starting metformin if not reached target by then)
**if symptomatic hyperglycemia/metabolic decompensation –> Insulin +/- metformin

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9
Q

How do biguanides work? Example? Benefits? Can you use in pregnancy?

A 
Improve insulin sensitivity @ liver
Metformin = 1st line drug!!
Doesn't cause hypoglycemia, improves lipid profile, weight-loss
CV benefit 
Useful in pregnancy
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10
Q

What are 2 classes of meds that cause insulin secretion via diff mechanisms?

A

1) Affect K+ channels on B cells (sulfonylureas, meglitinides) glucose-mediated insulin release (DPP IV inhibitors or GLP-1 agonists)

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11
Q

Secretagogues (Sulfonylureas & meglitinides): examples, pros/cons, contraindications

A

Sulf: glyburide, gliclazide, glimepiride
Meglitinides: repaglinide, nateglinide, mitiglinide

Pros: rapid onset of action, lower postprandial glucose
Cons: hypoglycemia, weight gain
Contraindications: renal/liver disease (?? but some sulfonylureas recommended in severe DKD)

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12
Q

Incretin-based therapies: examples, route of admin, pros/cons, contraindication

A

DPP-IV inhibitors (gliptins): oral; Sitagliptin, Saxagliptin, Linagliptin
GLP-1 agonists: injection;Liraglutide, Semaglutide (Ozempic), etc; weight loss!! (also used to treat obesity) + nausea; CV benefits

No hypoglycemia! (glucose-DEPENDENT insulin secretion; incretins are endogenous)

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13
Q 
SGLT2 inhibitors:
Examples
Mechanism of action
Pros
Cons
Contraindications
A

Canagliflozin, Dapagliflozin (Forxiga), Empagliflozin (Jardiance)
Inhibit glucose reuptake in PCT by blocking Na-glucose co-transporter
Pros: better CV/renal outcomes, weight loss, lower BP (diuretic)
Cons: polyuria/dehydration, GU infections, DKA (rare)
Contraindications: moderate renal insufficiency, insulin-dependent DM

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14
Q 
Alpha-glucosidase inhibitors:
Example
Mechanism of Action
Why is use limited?
Contraindications?
A

Acarbose
Inhibits enzyme that breaks down complex carbs so not absorbed
GI side effects due to undigested sugar in bowels (–> gas/bloating/diarrhea)
Contraindications: renal/liver disease

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15
Q

Thiazolidinediones:
Examples
Mechanism of action
Why is use restricted?

A

Rosiglitazone, Pioglitazone
Improve insulin sensitivity
Concerns of CV events (retracted, but can mess with fats, cause edema/weight gain, reduce hematocrit
Contraindicated if liver disease or CHF

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16
Q

2 types and examples of bolus insulin

A

Rapid-acting (just before eating): Lispro, Aspart

Short-acting (30 min before eating): Regular, Toronto

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17
Q

2 types and examples of basal insulin

A

Intermediate (12-16 hrs w/ peak): NPH

Long-acting (~24 hrs, no peak): glargine, detemir

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18
Q

In what situations might insulin be used initially in T2DM

A

Severe weight loss
Renal/hepatic disease prevent pills
Acute illness
Severe hyperglycemia (FPG >13.9), glucose toxicity

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19
Q

In T2DM insulin is usually administered how?

A

1 dose of long-acting before bed (endogenous usually sufficient for meals)

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20
Q

When pt w/ diabetes had illness w/ vomiting/diarrhea, what meds should be held until able to eat/drink normally?

A 
SANDMANS
Sulfonylureas & other secretagogues
ACE-inhibitors
Diuretics, direct renin inhibitors
Metformin
Angiotensin receptor blockers
NSAIDs
SGLT2 inhibitors
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21
Q

If pt with diabetes becomes pregnant, what are 3 things you should stop and 3 things you should start?

A

Stop:

  • non-insulin antihyperglycemic agents (except metformin and/or glyburide)
  • *most experts believe that intensive insulin therapy is the only means of achieving the degree of glycemic control desirable throughout pregnancy in women with type 1 and type 2 diabetes.
  • statins
  • ACEi/ARB (stop pre-conception if possible)

Start:

  • Folic acid 1mg/day (start 3 months before conception if possible)
  • Insulin if target A1C (<6.5%) not achieved on metformin or glyburide (T2DM)
  • other hypertensive agents safe for pregnancy (e.g. labetalol)
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22
Q

ABCDESSS of diabetes care

A

A1C <7 (or 6.5 to reduce CKS/retinopathy)
BP <130/80
Cholesterol: LDL-C <2mmol/L or 50% reduction
Drugs for CVD risk reduction (ACEi/ARB, stains, ASA, SGLT2i/GLP1ra, as indicated)
Exercise + healthy eating
Screening for complications (ECGs, feet, kidney, retinopathy)
Smoking cessation
Self-management, stress, barriers

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23
Q

Which CV protection meds are indicated for patients with…
CV disease (cardiac ischemia, peripheral arterial disease, cerebrovascular/carotid disease)?
if also not at glycemic target?

A

Statin +
ACEi/ARB +
ASA

If not at glycemic target –> + liraglutide (GLP-1ra), empagliglozin or canagliflozin (SGLT-2 inhibitors)

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24
Q

Which CV protection meds are indicated for patients with…

No CV disease but microvascular disease (retinopathy, kidney disease, neuropathy)

A

Stain +

ACEi/ARB

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25
Q

Which CV protection meds are indicated for patients with…

No CV disease or microvascular disease but age 55+ w/ CV RFs

A

Statin + ACEi/ARB

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26
Q

Which CV protection meds are indicated for patients with…
No CV disease or microvascular disease
Age 40+ or 30+ w/ diabetes 15+ years

A

Statin

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27
Q

Name 4 drug classes that lower PG immediately & 2 that lower PG over weeks

A

Secretagogues, GLP-1 receptor agonists/DPP-IV inhibitors, alpha-glucosidase inhibitors, SLGT2 inhibitors

Delay for biguanides (metformin), thiazolidinediones

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28
Q

Name 5 diabetes drugs that don’t directly cause hypoglycemia

A 
Biguanides
Thiazolidinediones
SGLT2-inhibitors
Incretin therapies (GLP-1ras/DPP-IVi)
Alpha-glucosidase inhibitors
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29
Q

Hypoglycemia = blood glucose of what? Associated with what meds?

A

<4 mmol/L

Insulin, secretagogues (sulfonylurea)

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30
Q

What leads to recurrent hypoglycemia w/ unawareness?

A

Hypoglycemia-associated autonomic failure

Reduced adrenomeduallary epi responses –> defective glucose counterregulation
Reduces symp neural responses –> hypoglycemia unawareness

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31
Q

What are the symptoms of hypoglycemia (2 categories)

A

Adrenergic: tremor, sweating, anxiety, palpitations, nausea, tingling (can be lacking w/ autonomic neuropathy)
Neuroglycopenia: headache, confusion, behaviour changes, weakness, drowsiness/coma, seizure, vision changes

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32
Q

What type of sugar can be administered and is identical to D-glucose (biologically active form of glucose found in plasma)

A

Dextrose

D50w = Dextrose 50% in water

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33
Q

Treatment for hypoglycemia

A

15g carbs as single sugars (e.g. 1/2 glass juice)

If reduced LOC and can’t eat –> IV D50w push or IM/SC glucagon

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34
Q

What med can mask hypoglycemica symptoms?

A

Beta blockers (stop tremor, palpitations, etc; catecholamine-mediated Sx)

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35
Q

Name 3 microvascular & 3 macrovascular complications of diabetes

A

Micro: neuropathy, nephropathy, retinopathy
Macro: CAD, CVD (TIA, stroke), peripheral vascular disease (amputation!)

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36
Q

What is the most common form of diabetic neuropathy?

A

Distal symmetric sensorimotor polyneuropathy
- distal sensory loss & pain (50% asymptomatic); glove-and-stocking distribution
- numbness/tingling/burning in feet, spreads proximally
Loss of protective sensation & motor defects may develop
+PVD –> foot ulcers + amputation

37
Q

Name 4 manifestations of autonomic neuropathy

A

CV system: HR issues, tachycardia, orthostatic hypotension, sudden death
GU: gastroparesis, bladder-emptying issues
SNS: hyperhidrosis/anhirdosis
Reduced counterreg hormones (catecholamines) –> failure to sense hypoglycemia (hypoglucemia-associated autonomic failure)

38
Q

Name 3 reasons why infections common in uncontrolled diabetes

A

Sugars available for bact/fungi
Immune abnormalities
Diminished vascularization/poor wound healing

39
Q

How often are eye exams recommended in DM patients?

A

T1DM: annually
T2DM: annually or biannually

40
Q

___ and ___ are the best ways of preventing diabetic retinopathy
Once it develops, the best treatment is ___

A

Annual dilated fundoscopy
Glucose/BP control

Photocoagulation therapy for existing proliferative retinopathy (laser –> thermal burn of retinal tissue –> corrects ischemic hypoxia, minimizes neovascularization)
Also VEGF-inhibitors

41
Q

Describe proliferative retinopathy

A

New friable BVs on retina –> bleeding, vision impairment, can lead to retinal hemorrhage/detachment –> blindness

42
Q

2 types of diabetic retinopathy

A

Nonproliferative: retinal vascular microaneurysms, blot hemorrhages, cotton-wool spots
Proliferative: neovascularization response to retinal hypoxemia –> new vessel rupture easily –> hemorrhage, retinal detachment

Catch nonprolif early to PREVENT progression to proliferative

43
Q

Describe screening and progression of renal failure in DM

A

Yearly screening for microalbuminuria w/ urine albumine:creatinine
Microalbuminuria (smaller quantity) progresses to proteinuria; before progression much easier to treat, progression strongly associated w/ end-stage renal failure

44
Q

Name 3 prevention strategies for renal failure

A

1) BP control
2) ACEi/ARBs
3) Glycemic control

45
Q

LDL in diabetes should be controlled how?

A

<2mmol/L (aggressive control), even lower if very high risk
Statin therapy
LDL particulars in DM are more atherogenic (glycated, susceptible to oxidation)

46
Q

Target BP in DM

A

<130/80 (lower than Htn!)

47
Q

What is MODY? Inheritance pattern?

A

Mature Onset Diabetes of the Young
Distinct from type 1 & type 2
Genetic defects in B cell function, autosomal dominant inheritance

48
Q

What is LADA?

A

Latent Autoimmune Diabetes in Adults (often misdiagnosed as type 2!)

49
Q

What is C-peptide and how is it useful?

A

Substance secreted w/ insulin
Useful because can distinguish from synthetic insulin
Tumor in pancreas (insulinoma) would increase C-peptide with insulin level

50
Q

Define metabolic syndrome

A

3+ of…

1) BP >130/85 or on meds
2) FPG >5.6 or on meds (or 6)
3) TAGs >1.7 or on meds
4) HDL <1 in men, <1.3 in women
5) Large waist circumference

51
Q

Why does excess insulin secretion in T2DM lead to beta cell destruction?

A

B-cell fatigue +

Amylin co-released w/ insulin –> deposits on B-cells

52
Q

What is the most common cause of CKD?

A

Diabetic nephropathy

53
Q

Name 2 mechanisms leading to complications of DM?

A

1) Non-enzymatic glycation of proteins/lipids –> proinflamm molecules, hyaline arteriosclerosis –> reduces perfusion –> CAD, PAD, CVD, retinopathy, nephropathy
2) Glucose –> sorbital in cells that lack enzyme to convert –> osmotic cell death (demyelination of Schwann cells, lens of eye, tubular cells)

54
Q

The 6 “I”s of DKA

A

1) Reduced insulin supply (undiagnosed, not taking meds)
2) Infections
3) Inflammation
4) Intoxication (alcohol, cocaine, methamphetamines for ADHD)
5) Infarction (MI, stroke)
6) Iatrogenic (corticosteroids, surgery)
* *mostly increases in insulin demand or decreases in supply

55
Q

What is the triad of characteristics for DKA/HHS? Pathophys?

A

Stress –> SNS stimulation –> E/NE –> glucagon
Gluconeogenesis, glycogenolysis, lipolysis
–> hyperglycemia, glucosuria, osmotic diuresis, hyperosmolar state

Triad = ketoacidosis + dehydration + hyperosmolarity
DKA has mainly 1+2
HHS has 2+3

56
Q

What happens to potassium in DKA?

A

Acidosis –> H+ moves into cells, K+ into ECF
also insulin required for Na/K ATPase, so K influx reduced

Results = LOW total body K but normal/HIGH serum k!!
Arrhythmias –> palpitations, chest pain

57
Q

What type of respiration is seen in DKA?

A

Kussmaul respiration due to acidosis

58
Q

What type of acidosis is seen in DKA?

A

High anion gap metabolic acidosis

59
Q

What does HHS stand for?

A

Hyperglycemic hyperosmolar syndrome

60
Q

What is the issue with hyperosmolarity in HHS? How does it impact neurons/muscles?

A

Water moves out of cells into blood stream
Neurons: AMS –> seizures, coma
Muscles: weakness

61
Q

Serum glucose in DKA & HHS

A

DKA: >13.9

HHS > 33.3

62
Q

pH in DKA & HHS

A

DKA pH<7.3, can get VERY low

HHS >7.3

63
Q

HCO3- in DKA & HHS

A

DKA: low
HHS: normal

64
Q

Urine/serum ketons in DKA & HHS

A

DKA: high
HHS: negative

65
Q

Anion gap in DKA & HHS

A

DKA: high (>12)
HHS: normal, or slightly increased due to lactic acid

66
Q

Serum osmolality in DKA & HHS

A

DKA: variable
HHS: very high (>320 mOsm/kg)

67
Q

What is interesting about the way we measure ketones?

A

We measure acetoacetate even though B-hydroxybutyrate synthesized 3x as much
May appear to INCREASE during treatment because B-hydroxy gets converted to acetoacetate first

68
Q

DKA & HHS: which has worse prognosis and why?

A

HHS has much worse prognosis (15% mortality vs <1%) vs patients older, more likely life-threatening precipitating event, comorbitities

69
Q

___ is a possible severe complication during DKA treatment esp in kids
How to avoid?

A

Cerebral edema

Avoid quick correction of serum glucose, overreplacement of free water, bicarb admin unless absolutely necessary

70
Q

4 components of DKA treatment

A

1) Rehydration w/ 0.9% normal saline (may have to change to 0.45% half-normal or D5W if high Na or low glucose respectively)
2) Insulin
3) Potassium (insulin pushes K back into cells)
4) Bicarb only if pH really low
(also start w/ ABCs of course!)

71
Q

Describe translational hyponatremia in hyperglycemia

A

Water moves into ECF
No change in total body water but lower [Na] in serum
Will return to normal once plasma glucose corrected
Need to correct for Na measurements in this state

72
Q

Recommended physical activity per week

A

150 min moderate exertion

73
Q

Why might a diabetic patient by put on pip-tazo for an infected ulcer?

A

Because of higher likelihood of pseudomonas infection

74
Q

Meds for blood sugar in stage 4 and 5 DKD (no dialysis)

A

Stage 4 = GLP-1 (sulfonylureas possible)
Stage 5 = sulfonylureas (GLP-1 possible)
**need sulfonylureas with inactive metabolites and lower risk of hypoglycemia, because with CKD hypoglycemia is even more likely (reduced renal clearance of insulin)

75
Q

In hemodialysis pts, ____ is preferred

In peritoneal dialysis pts, ___ is preferred (for glycemic control)

A

Hemo –> insulin

PD –> sulfonylureas (may also require Subq insulin)

76
Q

____ should NOT be used in pts w/ advanced CKD

A

Metformin

77
Q

SGLT2 inhibitor DKD paradox

A

Not effective for glycemic control in advanced DKD

BUT prescribed due to cardiorenal protective effects in pts w/ declining GFR

78
Q

Why might ESKD patients not present “typically” w/ severe hyperglycemia?

A

Anuria (no glycosuria/volume depletion)

79
Q

6 key things to monitor in DKD patients

A 
Blood pressure
Volume status
eGFR
A1C
UACR
Serum K
80
Q

In pt w/ T2DM who needs insulin, what regime should you start with and why?

A

Basal rather than prandial

Because more convenient for patient, better adherence, less hypoglycemia

81
Q

The possibility of _____ should be considered in diabetic patients with foot wounds associated with signs of infection in the deeper soft tissues and in patients with chronic ulcers, particularly those overlying bony prominences that do not heal after several weeks of wound care and off-loading

A

Exogenous osteomyelitis

82
Q

Empiric Abx in pt with osteomyelitis (adult)

A

IV Vancomycin PLUS either antipseudomonal cephalosporins (ceftazidime, cefepime) OR antipseudomonal fluoroquinolones (ciprofloxacin, levofloxacin)

83
Q

Diagnosis of osteomyelitis (definitive)

A

isolation of bacteria from a sterilely obtained bone biopsy sample with histologic evidence of inflammation and osteonecrosis

84
Q

If bone biopsy isn’t possible, what clinical findings related to diabetic foot ulcer support diagnosis of osteomyelitis

A

●Grossly visible bone or ability to probe to bone
●Ulcer size larger than 2 cm2
●Ulcer duration longer than one to two weeks
●Erythrocyte sedimentation rate (ESR) >70 mm/h

Do x-ray, if it doesn’t show it do MRI

85
Q

Amputation indicated if…

A

Critical limb ischemia (PAD) w/out option of revascularization
Severe infection w/ extensive soft tissue or bony destruction

86
Q

Most commonly recommended Abx prophylaxis for vascular surgery/limb amputation

A

Cefazolin (1st gen IV cephalosporin)

=”Ancef”

87
Q

What ankle-brachial index indicates arterial disease?

A

<1

0.5-0.9 = mild-mod, <0.5 = severe

88
Q

There is a strong, interdependent association between diabetes and what other endocrine disorder?

A

Thyroid dysfunction (hyper & hypo)

Preclerkship (25 decks)

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