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(C) CM 1A: Heme/Onc/Endo > Lecture 27: DM Comorbidities/Complications > Flashcards

Lecture 27: DM Comorbidities/Complications Flashcards

1
Q

What usually qualifies as hypoglycemia?

A

Serum < 60 mg/dL

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2
Q

What are the symptoms of hypoglycemia due to?

A
  • NE release/Epi release
  • Neuroglycopenia
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3
Q

How often is a hypoglycemic episode?

A
  • T1DM: 2x/week
  • T2DM: less likely, unless on insulin or sulfonylureas.
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4
Q

How does the body compensate for increasing hypoglycemia?

A
  1. Decreasing insulin secretion
  2. Increasing glucagon secretion
  3. Increasing epinephrine secretion
  4. Increased cortisol and GH (if sustained for hours)
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5
Q

What are the usual DM drug causes of hypoglycemia?

A
  • Exogenous insulin
  • Insulin secretagogues (Sulfonylureas, meglitinides)
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6
Q

What are the common etiologies of hypoglycemia not related to DM drugs?

A
  • ALCOHOL
  • BBs
  • ACEIs
  • Quinolones/quinines
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7
Q

Why does alcohol cause hypoglycemia?

A

Inhibition of hepatic gluconeogenesis.

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8
Q

What severe illnesses/conditions can cause hypoglycemia?

A
  • Sepsis: inhibited gluconeogenesis and increased usage of glucose.
  • CKD: Impaired renal gluconeogenesis
  • Chronic liver disease: Impaired hepatic gluconeogenesis
  • Malnutrition
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9
Q

What hormonal deficiency typically can result in hypoglycemia?

A

Cortisol deficiency.

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10
Q

Why is an insulinoma so dangerous?

A

Increased insulin secretion will also impair glucagon secretion.

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11
Q

What is the most concerning comorbidity in DM that should be treated just as urgently?

A

HTN!

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12
Q

What is the goal BP for a DM pt with < 15% 10-year ASCVD risk? > 15%?

A
  • < 15%: 140/90
  • > 15%: 130/80
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13
Q

When is lifestyle modification indicated for DM in regards to BP?

A

Anything above 120/80.

Add pharmacotherapy if above 140/90 via ACEI/ARB

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14
Q

When is HLD tx concerning in regards to DM pts?

A
  • TG > 150 OR HDL < 40 (men) OR HDL < 50 (women) = intensify lifestyle changes, esp exercise.
  • Fasting TG > 500 = evaluate for secondary hypertriglyceridemia and consider meds to prevent pancreatitis.
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15
Q

What is the consensus with regards to statins increasing DM risk?

A

Benefit of CV risk reduction > DM risk.

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16
Q

What is the ideal kcal deficit for an obese pt with DM?

A

500-750 kcal/day

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17
Q

When is bariatric surgery indicated for DM pts?

A

BMI >= 35

Usually results in euglycemia with little to no med use.

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18
Q

What are the characteristics of DKA and HHS?

A
  • Severe hyperglycemia (>250)
  • Volume depletion
  • Relative/total lack of insulin
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19
Q

What findings are common in DKA?

A
  • Metabolic acidosis
  • Glucose 250-600, rarely > 800
  • pH = 6.8-7.3
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20
Q

What findings are common in HHS?

A
  • Minimal ketones
  • Glucose > 600-1000 usually
  • pH usually normal, with bicarb > 20
  • Greater dehydration than DKA.
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21
Q

What are the primary pathophysiologies of DKA?

A
  • Insulin deficiency
  • Glucagon excess
  • Body keeps trying to make glucose since cells are lacking it, breaking down FFAs and producing ketones.

At normal pH, ketones are ketoacids and get neutralized by bicarb.

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22
Q

How does DKA usually present?

A
  • T1DM pt
  • Fruity/acetone breath
  • Polyuria
  • Polydipsia
  • Hypotensive
  • Tachypnea/SOB
  • Kussmaul respirations
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23
Q

What are Kussmaul respirations?

A
  • Deep, labored breathing
  • Seen in DKA and severe metabolic acidosis as body attempts to correct acidosis.
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24
Q

What happens to potassium levels in DKA? Sodium?

A
  • Increases serum-wise due to an extracellular shift with acidosis.
  • Hyponatremia ensues to compensate osmolality from excess glucose.
25
Q

What test is best to determine the presence of ketones?

A
  • Serum test, because beta-hydroxybutyrate is the most common ketone.
  • Not measured in a urine test.
26
Q

What is the first step in managing DKA?

A

Rapid NS infusion for 1-2 hours

27
Q

What is the second step in DKA management?

A

IV regular insulin following NS

Aiming for 75 mg/dL/hr

Bolus, followed by infusion.

28
Q

What two electrolytes must be monitored for DKA? Why?

A
  • Potassium: drops as acidosis improves, but can cause massive EKG changes.
  • Bicarb: Only given for pH < 7.0 (potentially harmful still)
29
Q

What is the pathophysiology of HHS?

A

Relative insulin deficiency with inadequate fluid intake.

Also mainly seen in T2DM, but it is rarer than DKA in general.
DKA is usually T1DM.

30
Q

What generally can trigger HHS?

A
  • Low hormone levels of counterregulation
  • Greater insulin than DKA
  • Physiologic stress (infections, infarctions, decreased water)
31
Q

Why are middle/eldery pts more common for HHS?

A

Decreased water intake since they aren’t as thirsty.

32
Q

What is the classic presentation of HHS?

A
  • Elderly T2DM pt
  • Several days of polyuria, polydipsia
  • weakness
  • decreased oral intake
  • weight loss
  • lethargy
  • hypotensive
  • tachycardic
  • LACK OF N/V, abd pain, acetone breath, or Kussmaul’s
33
Q

What are the abnormal labs seen in HHS?

A
  • Serum glucose 600-1200
  • Prerenal azotemia
  • Serum osmolality > 350
  • Everything else pretty mild/normal.
34
Q

What is prerenal azotemia?

A
  • Increased BUN/creatinine
  • Decreased GFR

Damage prior to the kidney, MC in hospitalized pts.

35
Q

What is the first step in HHS management?

A
  • Rapid NS, with extra (more than DKA)
36
Q

What kind of insulin is used for HHS management? What can be added once glucose is stabilized?

A
  • IV regular insulin following fluid replacement.
  • Change to IV dextrose for fluids to prevent cerebral edema.

DKA typically uses more insulin than DKA.

Aiming for 50-75mg reduction per hour.

37
Q

Why is potassium infusion recommended even though HHS has normal K levels?

A
  • Insulin treatment will decrease potassium.
  • 10 mEq/hr recommended to prevent hypokalemia.
  • Caution in CKD patients, who can develop hyperK more easily.
38
Q

What are the microvascular complications of DM?

A
  • Retinopathy
  • Nephropathy
  • Neuropathy
39
Q

Why is diabetic retinopathy a concern?

A

Leading cause of blindness in the US for adults.

40
Q

Describe the first stage of diabetic retinopathy.

A
  • Non-proliferative/background retinopathy
  • Occurs generally late first decade of disease or later.
  • Retinal capillaries leak proteins, lipids, and red cells.
41
Q

What are the characteristic lesions seen in the first stage of diabetic retinopathy?

A
  • Microaneurysms
  • Dot hemorrhages
  • Retinal exudates
  • Retinal edema
42
Q

Describe the 2nd stage of diabetic retinopathy.

A
  • Proliferative retinopathy
  • Growth of new capillaries and fibrous tissue within the retina and vitreous chamber.
  • Small vessel disease => retinal hypoxia => VEGF release.
43
Q

What are the characteristic lesions of proliferative retinopathy?

A
  • Nonproliferative retinopathy findings
  • Cotton-wool spots
  • Neovascularization
44
Q

How do we manage proliferative retinopathy?

A
  • Ophthalmology consult
  • Laser photocoagulation
  • Anti-VEGF intraocular injections
45
Q

Who is diabetic nephropathy MC in?

A

T1DM.

46
Q

What is the initial manifestation of diabetic nephropathy? What is the MC test to check for it?

A
  • PROTEINURIA
  • Ideally through spot urine albumin/creatinine ratio in the morning.
  • Most accurate: 24hr urine collection, but impractical.

Separate from an UA.

UA cannot detect early proteinuria.

47
Q

How do we manage diabetic nephropathy?

A
  • Glycemic control
  • Low protein diet
  • BP control (ACEI/ARB)
  • SGLT2 inhibitor
48
Q

What are the characteristics of nephrotic syndrome?

A
  • Massive proteinuria
  • Edema
  • Hyperlipidemia
  • Hypoalbuminemia
49
Q

What is the MC type of peripheral neuropathy in DM pts?

A

Distal symmetrical polyneuropathy

50
Q

How does distal symmetrical polyneuropathy present?

A
  • Sensory involvement, followed by motor.
  • Distributes via a stocking-glove pattern (foot then hands)
51
Q

How do feet change in distal symmetrical polyneuropathy?

A
  1. Denervation of foot musculature
  2. Toe clawing and displaced metatarsal fat pads
  3. Increased plantar pressures
  4. Charcot arthropathy risk and calluses.

ulcer will generally appear at the bottom of the foot, below the 2nd metatarsal.

52
Q

What is charcot foot?

A

Rounded heel.

53
Q

How do we manage distal symmetric polyneuropathy?

A
  • Glycemic control
  • Podiatry referral
  • Debridement/wound care/abx for ulcers
  • TCAs/gabapentin/duloxetine if severe
54
Q

What characterizes autonomic neuropathy in DM pts?

A
  • Gastroparesis: delayed emptying (metoclopramide/erythro)
  • Diarrhea: ABX
  • Constipation: stimulant laxatives
  • N/V: antiemetics
  • Urinary: incomplete emptying
  • Orthostatic hypotension
  • ED

Multi-organ involvement.

55
Q

What CV risks are increased in DM pts?

A
  • PAD/CAD/MI/CHF
  • CVA
  • PAD: gangrene 30x more likely

Amputation ):

56
Q

When is aspirin indicated for DM?

A

> = 10% ASCVD risk.

Prevent silent ischemia.

57
Q

Why do DM pts get more frequent and severe infections?

A
  • Hyperglycemia impairs phagocytosis
  • Hyperglycemia is food for fungi
  • Vascular disease => impaired blood flow to sites of infection
  • Impaired cytokine production
58
Q

What skin conditions are DM pts more susceptible to?

A
  • Candida (esp. intertrigo)
  • Eruptive cutaneous xanthomas
  • Pigmented pretibial papules/diabetic dermopathy/shin spots
  • Acanthosis nigricans
  • Necrobiosis lipoidica diabeticorum

(C) CM 1A: Heme/Onc/Endo (28 decks)

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