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Endocrine > 398 DM Complications > Flashcards

398 DM Complications Flashcards

1
Q

A 56/M diabetic for 15 years on Empagliflozin+ Linagliptin 25/5 mg OD presents with 2 days diarrhea progressing to difficulty breathing and drowsiness. BP 110/60 mmHg, HR 116 bpm, RR 26 cpm, HbA1c of 6.8%, CBG is 120 mg/dl. ABG pH 7.26, HCO3 of 12 and ketonuria 4+. What is the likely diagnosis?

A

Euglycemic diabetic ketoacidosis

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2
Q 
43M DM was brought to ER for fever,cough and vomiting. PE drowsy, dry lips with poor skin turgor. BP 90/60. HR 112 bpm. RR 32 cpm. CBG 521 mg/dl. After assessing electrolyte and acid base status, which fluid must you infuse?
A. 0.9 Saline
B. D5 Normosol
C. 0.45 Saline
D. Lactated ringers
A

A. 0.9 Saline

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3
Q 
What is the recommended initial bolus dose of IV regular short acting, insulin in DKA and HHS?
A. 15 units/kg
B. 10 units/Kg
C. 1 unit/Kg
D. 0.1 unit/Kg
A

D. 0.1 unit/Kg

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4
Q

Most common and early complication of DM

A

Diabetic retinopathy

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5
Q

Refers to the rise of blood glucose after food intake

A

Glycemic index

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6
Q

Most physiologic way of administering insulin

A

1 basal and 3 pre prandial short acting insulin

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7
Q

Brand for insulin apart

A

NovoRapid

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8
Q

What is the target blood glucose for hospitalized patients

A

180 mg/dl

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9
Q

IV drug given for DM type 1 aside from insulin

A

Amylin antagonist

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10
Q

OHA that can be given to DM type 1

A

Alpha glucosidase: acarbose/voglibose

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11
Q

OHA known to decrease lipolysis

A

TZDs

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12
Q

Specific side effect of SGLT2 inhibitors

A

Genital infection

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13
Q

Why no ketosis in HHS?

A

Relative insulin deficiency

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14
Q

Add 5 more to the Ominous octet to make 13

A 
Decrease vitamin D
Decreased dopamine
Decreased testosterone
Kidney
GUT/incretin
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15
Q

Hormones responsible for DKA

A

Decreased insulin

Excess glucagon

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16
Q 
What test will you do to assess diabetic nephropathy?
A. Serum creatinine
B. EGFR using CKD EPI formula
C. Urine Creatinine: protein ratio
D. 24 hr urine protein excretion
A

C. Urine Creatinine: protein ratio

Micral test

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17
Q

Preferred over regular insulin the the managed of post prandial coverage

A

Aspart
Lispro
Glulisine

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18
Q

Covers for basal insulin requirement

A 
Long acting insulin such as
NPH
Glargine
Detemir
Degludec
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19
Q

What just the 70/30 in insulin pens mean?

A

70% NPH

30% regular insulin

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20
Q

When should insulin analogues injected before a meal? Regular insulin?

A

Insulin analogues less than 10 mins

Regular insulin 30-45 mins prior to a meal

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21
Q

What is the difference between insulin regimens versus endogenous insulin

A

Endogenous insulin: secreted into portal venous system

Insulin regimen: systemic circulation

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22
Q

How is prandial insulin dose computed

A

1 unit insult for ever 50 mg/dl over the preprandial glucose target

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23
Q

Another formula in formulating insulin to be given

A

Body weight in Kg x blood glucose - desired divided by 1500

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24
Q

How to avoid nocturnal hypoglycemia when using long acting insulin

A

Give long acting insulin at bedtime to that at the peak of the insulin action as glucose levels rise in the morning due to growth hormone and cortisol secretion

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25
Q

General assumptions in SMBG

A

fasting glucose determined by prior evening long acting
Pre lunch glucose determined by breakfast short acting insulin
Pre supper glucose is determined by morning long acting insulin
Bedtime glucose is function of pre supper short acting insulin

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26
Q

Dosage of long acting insulin

A

0.2-0.4 U/Kg per day

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27
Q

Ketone measure in blood

A

Beta hydorxybutarate

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28
Q

Ketone measured in urine

A

Acetone and acetoacetate

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29
Q

Indicator of DKA

A

Ketones

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30
Q

Prominent symptoms of DKA

A

Nausea and vomiting

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31
Q

Extremely serious complication of DKA

A

Cerebral edema

32
Q

When is bicarbonate supplementation done in DKA?

A

pH less than 7.0

33
Q

What is the fluid replacement in DKA?

A

2-3 L in first 3 hours or 10-20 ml/ Kg in first 3 hrs

PNSS

34
Q

Is there serum potassium level requirement in giving insulin?

A

Replace serum potassium if less than 3.3 ml/dl

35
Q

Why is PNSS replaced with D5. 045 if CBG equal to less than 250 mg/dl

A

To avoid hyperchloremia

36
Q

mechanism behind the chronic complications of hypeglycemia

A
  1. formation of advanced glycosylation end products and non enzymatic glycosylation of proteins 2. increased glucose metabolism via sorbitol pathway using the enzyme aldose reductase 3. increased formation of diacylglycerol leading to activation of protein kinase C 4. increased flux through the hexosamine
37
Q

unifying mechanism in chronic DM complications

A

increased production of reactive oxygen species or superoxide in the mitochondria

38
Q

play an important role in some diabetes related microvascular complications

A

growth factors

39
Q

Landmark trial provided definitive proof that reduction in chronic hyperglycemia can prevent complication of T1DM

A

DCCT

40
Q

trial the showed improvement of glycemic control reduced retinopathy, microalbuminuria, clinical nephropathy, and neuropathy

A

DCCT

41
Q

trial that showed continuous relationship between glycemic control and development of complications

A

UKPDS

42
Q

trial that showed that strict BP control reduce micro- and macrovascular complication greater than glycemic control

A

UKPDS

43
Q

trial that showed intensive lifestyle changes delayed the development of T2DM

A

Diabetes Prevention Program (DPP)

44
Q

trial that showed metformin delayed the development of T2DM by 31% compared to placebo

A

DPP

45
Q

classification of diabetic retinopathy

A

proliferative and nonproliferative

46
Q

what is the hallmark of proliferative retinopathy

A

appearance of neovascularization to retinal hypoxemia

47
Q

True or false. Non all individual with nonproliferative retinopathy go on to develop proliferative retinopathy. The more severe the nonproliferative disease, the greater chance of evolution to proliferative retinopathy

A

True.

48
Q

best predictor of retinopathy

A

duration of DM and degree of glycemic control

49
Q

most effective therapy for diabetic retinopathy

A

prevention

50
Q

treatment of proliferative retinopathy or macular edema

A

photocoagulation and or anti VEGF therapy

51
Q

when does nonproliferative DM retinopathy occur

A

late in first decade or early in the second decade of disease

52
Q

findings in non proliferative retinopathy

A

retinal vascular microaneurysm, blot hemorrhages and cotton wool spots

53
Q

True or false. There is paradoxical transient worsening retinopathy during the 6-12 months of improved glycemic control

A

True.

54
Q

Treatment for macular edema

A

focal laser photocoagulation

55
Q

treatment for proliferative retinopathy

A

panretinal laser photocoagulation

56
Q

True or false. Aspirin does not influence natural history of diabetic retinopathy

A

True.

57
Q

pathophysiology of DM nephropathy

A

GFR increases in first few years; thickening of glomerular basement membrane, mesangial expansion, and glomerular hypertrophy occur; after 5-10 years T1DM excrete small amounts of albumin in the urine

58
Q

stages of DM nephropathy

A

hyperfiltration, microalbuminura, macroalbuminuria

59
Q

define albuminuria

A

albumin creatinine ration more than 30 mg/g Cr

60
Q

when to screen for albuminuria

A

5 years from diagnosis of T1DM and at time of diagnosis for T2DM

61
Q

True or false. Once macroalbuminuria is present, GFR decline is steady

A

True.

62
Q

most common areas for T2DM to develop foot ulcer

A

great toe or metatasophalangeal areas

63
Q

most common site of ulceration on the foot

A

plantar surface

64
Q

most common pathogens of diabetic foot

A

aerobic gram postiive cocci (staphylococci MRSA, Group A and B streptococci)

65
Q

most specific modality in assessing diabetic foot ulcer

A

MRI

66
Q

interventions with demonstrated efficacy in diabetic foot ulcers

A

off loading, debridement, wound dressing, appropriate use of antibiotics, revascularization limited amputation

67
Q

antibiotics for diabetic foot ulcer

A

dicloxacillin,cephalosporin, amoxicillin/clavulanate

68
Q

studies that showed cardiovascular benefit with GLP1 samglutide

A

SUSTAIN 6

69
Q

studies that showed cardiovascular benefit with GLP1 liraglutide

A

LEADER

70
Q

studies that showed cardiovascular benefit with SGLT2 inhibitors empagliflozin

A

EMPA-REG

71
Q

studies that showed cardiovascular benefit with SGLT2 inhibitors canagliflozin

A

CANVAS

72
Q

age of diabetes that benefit from primary prevention of cardiovascular events with aspirin

A

men more than 50 and women more than 60

73
Q

Aspirin for primary prevention in DM

A

age more than 50; increased CV risk of more than 10% OR at least one risk factor (hypertension, dyslipidemia, smoking, family history, or albuminuria

74
Q

most common form of diabetic neuropathy

A

distal symmetric polyneuropathy which presents with distal sensory loss and pain

75
Q

treatment for diabetic neuropathy

A

tricyclic antidepressant, gabapentin, venlafaxine, carbamazepine, tramadol, topical capsaicin

76
Q

most common skin manifestation of DM

A

xerosis and pruritus

77
Q

begins as erythematous macule or papule that evolves into an area of circular hyperpigmentation

A

pigmented pretibial papules or diabetic skin spots

Endocrine (15 decks)

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