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high yield concepts > Endocrinology (MS and DM) -IM Plat > Flashcards

Endocrinology (MS and DM) -IM Plat Flashcards

1
Q

BMI

A

Weight in kg/ Height in m2

Curvilinear relation with percent body fat mass

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2
Q

IBW

A
  • males: 106 lbs + (6lbs over inch over 5 ft)
  • females: 100 lbs + (5lbs per inch over 5 feet)

Does not show fat or muscle percentage in one’s body

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3
Q

Waist-Hip Ratio

A

Waist circumference should be measured at the midpoint between the lower margin at the last palpable rib and top of the iliac crest

HIP: around the widest portion of buttocks

Abnormals:

  • >0.9 in males
  • >0.85 in females
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4
Q

etiopathogenesis of Metabolic syndrome

A

Insulin resistance

Central adiposity is the key feature

Hypertriglyceridemia is an excellent marker of insulin resistance

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5
Q

BMI classification (ASIA-PACIFIC)

A
  • Underweight :<18.5
  • Overweight :18.5-22.9
  • Obese 1: 23-24.9
  • Obese II: >30
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6
Q

Diagnostic Criteria for Metabolic Syndrome

A
  • Central Obesity (weight circumference)
  • Hypertriglyceridemia (>150 mg/dl)
  • Low HDL (Males: <40 Females: <50)
  • Hypertension
  • FBS >100mg/dl
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7
Q

Orlistat

A

Lipase inhibitor

60-120 mg TID

Adverse Effect: Abdominal discomfort oily stool, flatulence Malabsorption of fat-soluble vitamins

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8
Q

Lorcaserin

A

Selective serotonin 2C receptor agonist

10 mg BID

Adverse effect: Hypoglycemia headache, fatigue, bradycardia serotonin syndrome

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9
Q

Phentermine/topiramate ER

(For Metabolic Syndrome)

A

Sympathomimetic amine/anticonvulsant combination

3.75-15 mg/23-92 mg OD

Adverse effect: Paresthesia COnstipation Headache Dry mouth

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10
Q

Naltrexone/bupropion

(For Metabolic Syndrome)

A

Opiod antagonist/ aminoketoneantidepressant combination

8-32 mg/ 90-360 mg OD

Adverse effect: Nausea Constipation Headache

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11
Q

Liraglutide

A

Glucagon-like peptide 1 receptor agonist

3 mg SC OD

Adverse Effect: Hypoglycemia Nausea Bowel movement changes Headache

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12
Q

Etiopathogenesis of Diabetes Mellitus

A

Hyperglycemia

defined as the level of glycemia at which diabetes-specific complications occur

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13
Q

Type 1 DM

A

Due to autoimmunity B-cell destruction,usually leading to absolute insulin deficiency

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14
Q

Type 2 DM

A

Due to a progressive loss of B-cell insulin secretion frequently on the background of insulin resistance

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15
Q

Impaired Glucose Homeostasis

A
  • FBS:100-125 mg/dl
  • Oral glucose challenge: 140-199 mg/dl
  • HBA1c: 5.7-6.4%
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16
Q

Diabetes Mellitus

A

FBS: >126 mg/dl

Oral glucose challenge: >200 mg/dl

HBA1c: >6.5%

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17
Q

Manifestations of DM

A

Classic symptoms: Polyuria, Polydipsia, Polyphagia, Nocturia, Weight Loss

Others: Fatigue weakness BOV Frequent superficial infections Poor wound healing

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18
Q

Mirovascular complications of DM

A
  • Retinopathy
  • Neuropathy
  • Nephropathy
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19
Q

Macrovascular complications of DM

A
  • Coronary artery disease
  • Peripheral artery disease
  • Cerebrovascular disease
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20
Q

Criteria for the Diagnosis of DM

A
  • HBA1c : >6.5%
  • FBS: >126 mg/dL
  • 2 hour 75g OGTT: >200 mg/dL
  • Random Blood Sugar: >200 mg/dL

Fasting: defined as no caloric intake for at least 8 hours

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21
Q

Criteria for testing diabetes or prediabetes in asymptomatic adults

A

Begin at age 45 years, then every 3 years

Screen at earlier age if they are overweight + 1 risk factor

  • AIC >5.7%, IGT, or IFG on previous testing
  • First-degree relative with diabetes
  • High risk ethnicity
  • GDM
  • Hypertension or history of CVD
  • HDL <35 mg/dl and/or TG >250 mg/dl
  • Physical inactivity
  • PCOS
  • Other conditions with insulin resistance
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22
Q

Staging of Type 1 DM

A

STAGE 1

  • with autoantibodies
  • Normoglycemia

STAGE 2

  • with autoanibodies
  • IFG: FPG 100-125 mg/dl OR
  • IGT: 2 h PG 140-199 mg/dl OR
  • HbA1c: 5.7-6.4% or >10% increase

STAGE 3

  • with clinical symptoms DM by standard criteria
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23
Q

Overview of management with TYPE I

A

multiple daily injections of prandial and basal insulin Insulin is the mainstay of therapy

Starting insulin dose: 0.4-1.0 unit/kg/day

50% of computed value given as basal insulin

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24
Q

Pramlintide

A

Amylin analog

Induces weight loss and lowers insulin dose

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25
Q

Overview of management for Type 2 DM

A

Metformin is the preferred initial pharmacologic agent Consider insulin (with or without additional agents) in newly diagnosed T2DM who are

  • symptomatic and/or
  • have HbA1c >10% and/or
  • blood glucose >300mg/dL

after 3 months with HbA1c not achieved: add 2nd oral agent, a GLP-1 receptor agonist, or basal insulin

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26
Q

3 major components of exogenous insulin therapy

A
  • Basal
  • Bolus
  • Correctional
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27
Q

Basal insulin

A

Required to regulate metabolic processes even in the absence of meal

usually:

  • INTERMEDIATE (Given in portions 2/3 AM and 1/3 PM) or
  • LONG-ACTING
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28
Q

Bolus Insulin

A

Required to cover glycemic excursions following a meal

Usual:

  • SHORT or
  • RAPID ACTING

Rapid acting: given 15 min -20 mins or immediately before meals

Short acting: given within 30-45 mins. before meals

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29
Q

Correctional Insulin

A

Supplemental doses of short or rapid acting insulin given to correct elevations in blood glucose that occur despite the use of basal and bolus insulin

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30
Q

Rapid Acting insulin

A

Lispro Aspart Glulisine

  • Onset: <15 mins
  • Peak: 30-90 mins
  • Duration: 2-4 hours
31
Q

Short Acting Insulin

A

Human Regular

  • Onset: 30-60 mins
  • Peak: 2-3 hours
  • Duration: 3-6 hours
32
Q

Intermediate Acting Insulin

A

Isphane/ Human NPH

  • OnsetL 2-4 hours
  • Peak: 4-10 hours
  • Duration: 10-16 hours
33
Q

Basal Insulin Analogs

A

GLARGINE

  • Onset: 2-4 hours
  • Minimal peak activity
  • Duration: up to 24 hours

Detemir

  • Onset: 1-4 hours
  • Minimal Peak activity
  • Duration: up to 24 hours

Degludec

  • Onset: 30-90 mins
  • Minimal Peak Activity
  • Duration: >24 hours
34
Q

Insulin Secretagogues

A

Increases insulin secretion

SE: hypoglycemia and weight gain Sulfonylureas Non-sulfonyureas

35
Q

Sulfonylureas

A
  • Gliclazide 30-120 mg/d PO
  • Glibenclamide 2.5-20 mg/d PO
  • Glimepiride 1-8 mg/d PO
  • Glipizide 5-40 mg/d PO
36
Q

Non-sulfonylureas (insulin secretagogues)

A
  • Repaglinide 0.5-16 mg/d PO
  • Nateglinide 120 mg/d PO
37
Q

Insulin Sensitizers

A
  • Biguanides
  • Thiazolidinediones
38
Q

Biguanides

A

Decrease hepatic glucose production and slightly improves peripheral glucose utilization

Metformin 500-2000 mg/d PO

SE:weight loss, GI upset, Vit. B12 deficiency, metallic taste, lactic acidosis

39
Q

Thiazolidinediones

A

Decrease insulin resistance, increases glucose utilization Benefit in NASH

Pioglitazone 15-45 mg OD PO

SE: Edema, weight gain, OSTEOPOROSIS, anemia, CHF

40
Q

Intestinal Absorption inhibitors

A

Inhibits intestinal absorption of sugars

SE: weight loss, diarrhea, flatulence

  • Alpha-glucosidase inhibitors
  • Lipase Inhibitors
41
Q

Alpha-glucosidase inhibitors

A
  • Acarbose 25-100 mg TID PO
  • Miglitol 25-100 mg TID PO
42
Q

Lipase inhibitors

A

Orlistat

  • 120 mg TID PO
43
Q

Incretin-Related Drugs

A

Prolongs endogenous GLP-1 action

  • DPPV-IV inhibitors (DPP4)
  • GLP-1 agonists (parenteral)
44
Q

DPP4 inhibitors

A
  • Sitagliptin 25-100 mg OD PO
  • Saxagliptin 2.5-5 mg OD PO
  • Linagliptin 5 mg OD PO
  • Vidagliptin 50-100 mg BID PO

SE: Headache, nasopharyngitis, requires renal dose adjustment

45
Q

GLP-1 agonists (parenteral)

A
  • Exenatide 5-10 mcg BID SC
  • Liraglutide 0.6-1.8 mg OD SC
  • Albiglutide 30-50 mg weekly SC
  • Dulaglutide 0.75-1.5 mg weekly SC
  • Lixisenatide 10-20 mcg OD SC

SE: Skin irritation after injection, nausea

46
Q

Na-glucose co transporter-2 inhibitors (SGLT2i)

A

Increases urinary glucose excretion

  • Dapagliflozin 5-10 mg OD PO
  • Canagliflozin 100-300 mg OD PO
  • Empagliflozin 10-25 mg OD PO

SE: Urinary and vaginal infections, dehydration, Risk of fractures (CANAGLIFLOZIN)

47
Q

Amylin Agonist (Parenteral)

A

Slows gastric emptying.Decrease glucagon

  • Pramlintide 15-20 mcg OD SC

SE: Nausea and hypoglycemia

48
Q

Bile Acid sequestrants

A

Binds bile acids in intestinal tract, increasing hepatic bile acid and decreasing hepatic glucose production

  • Colesevelam 3.75 g/d PO

SE: constipation, hypertriglyceridemia, decreased absorption of other medications

49
Q

Dopamine 2 agonists

A

Activates dopaminergic receptors and modulates hypothalamic regulation of metabolism

  • Bromocriptine 0.8-4.8 mg/d PO

SE: Dizziness, nausea, fatigue, rhinitis

50
Q

Initiating Antihyperglycemic Therapy at Diagnosis of DM

A
  • A1C <9%: consider monotherapy
  • A1C >9% consider dual
  • A1C >10%, glucose >300 mg/dl or marked symptoms consider combination injectable therapy

MONOTHERAPY

Consider if A1C <9% and patient not markedly symptomatic

  • start with metformin + lifestyle modification

DUAL THERAPY

  • metformin and lifestyle modification PLUS one of the following drugs

Consider if A1C >9% and patient not markedly symptomatic, OR A1C target not achieved even after 3 months of Monotherapy

51
Q

Metformin

A

high efficacy low hypoglycemic risk, neutral effect or decrease in weight and low cost

CONTRAINDICATED with eGFR <30

52
Q

TRIPLE THERAPY

A

consider if A1C target not achieved even after 3 months of dual therapy AND patient not markedly symptomatic

Metformin + lifestyle modifications, PLUS a combination of the following

53
Q

Combination Injectable Therapy

A

Consider this if:

  • Baseline A1C >10%
  • FBS > 300 mg/dl
  • Patient markedly asymptomatic
  • A1C target not achieved even after 3 months of triple therapy

Possible regimens

  • If already on oral combination: add basal insulin or GLP-1RA
  • If already on GLP-1 RA : add basal insulin
  • If already on optimally-titrated basal insulin: add GLP-1RA on mealtime insulin

Metformin should be maintained while other oral agents may be discontinued on an individual basis to avoid unnecessarily complex or costly regimens

54
Q

Drugs and their primary Areas of Control

A
55
Q

`Monitoring Response of Treatment for DM

A

Sulfonylureas

  • Peak effect: 1-2 weeks
  • FPG at 2 weeks, HbA1C at 3 months

Meglitinides

  • PEak effect: 1-2 weeks
  • FPG at 2 weeks, HbA1C at 3 months, PPG at initiation

Metformin

  • peak effect: 2-3 weeks
  • FPG at 2 weeks, HbA1C at 3 months

Acarbose

  • Peak effect: 2-4 weeks
  • HbA1C at 3 months, PPG at initiation

TZD

  • Peak effect: 1-2 months
  • FPG at 4 weeks, HbA1C at 3-6 months

DPP4 Inhibitors

  • Peak effect: 2 weeks

FPG at 2 weeks, HbA1C at 3 months, PPG at initiation

56
Q

Self Monitoring of Blood Glucose

A

Should be performed on multiple dose insulin or insulin pump

  • Prior to meals and snacks, occasionally postprandially, and at bedtime
  • Prior to exercise or critical tasks such as driving
  • When they suspect low blood glucose
  • After treating low blood glucose until they are nomoglycemic
57
Q

Goals of treatment

A

HbA1c (Primary goal) : <7.0%

Preprandial Capillary plasma glucose: 80-130 mg/dl

Peak postprandial capillary plasma glucose: <180 mg/dl

58
Q

Etiopathogenesis of hyperglycemic crises in diabetes

A

Associated with absolute or relative insulin deficiency combined with counterregulatory hormone excess, volume depletion, and acid-base abnormalities

Decrease insulin-glucagon ratio promotes gluconeogenesis, glycogenolysis and ketogenesis

59
Q

precipitating factors for hyperglycemic crisis

A
  • Infection: most common
  • Discontinuation of or inadequate insulin therapy
  • Comorbidities such as pancreatitis, MI, stroke
  • Restricted water intake
  • Drugs
    • steroids
    • thiazideds
    • Sympathomimetic agents
    • pentamidine
    • antipsychotics
60
Q

Diabetic Ketoacidosis

A

Results from increased glucogenogenesis and glycogenolysis, and impaired glucose utilization by peripheral tissues

Ketones (Indicator of DKA) should be measured in individuals with DM type 1 when glucose is >300 mg/dl

  • SYMPTOMS
    • nausea, vomiting
    • Thirst, polyuria
    • Abdominal pain, dyspnea
  • Signs
    • Tachycardia, tachypnea, dehydration
    • Kussmaul respirations
    • Abdominal tenderness
    • Decreased sensorium
  • Course
    • Develops over 24 hours
    • triad of uncontrolled hyperglycemia, metabolic acidosis, and increased total bod ketone concentration
61
Q

Hyperosmotic hyperglycemic State

A

Greater degree of dehydration and higher endogenous insulin secretion compared with DKA

Primarily seen with T2DM

  • SYMPTOMS
    • Polyuria, weight loss
    • Diminished oral intake
    • Mental confusion, lethargy, coma
  • SIGNS
    • Profound dehydration, hypotension, tachycardia
    • Altered mental status
    • No nasuea, vomiting, abdominal pain, kussmaul respiration, unlike DKA
  • COURSE
    • ​Develops within several weeks
    • Severe hyperglycemia, hyperosmolality, and dehydration
    • Absence of significant ketoacidosis
62
Q

Diagnosis of Hyperglycemic Crisis in Diabetes

A
63
Q

General Management of Hyperglycemic crises in Diabetes

A

Admit to ICU

Measure CBG every 1-2 hours

Monitor every 1- 4 hours

  • BP
  • Pulse
  • Respirations
  • Mental status
  • fluid intake and output

Assess serum electrolytes, ABG, and renal function

64
Q

Specific Treatment Hyperglycemic Crisis

A
65
Q

Criteria for resolution

A

DKA

  • Plasma glucose <200 mg/dL and two of the following:
    • Serum bicarbonate level >15 mEq/L
    • Venous pH >7.3
    • Calculated anion gap <12 mEq/L

HHS

  • Normal serum osmolality
  • Improvement of normal mental status
66
Q

Complications of hyperglycemic crisis

A
  • Hypoglycemia and hypokalemia
    • overzealous treatment of DKA with insulin and bicarbonate
  • Hyperchloremic Non-Anion Gap Acidosis
    • durng recovery phase of DKA
    • loss of ketoanions plus excess infusion of chloride-containing fuids during treament
  • Cerebral Edema
    • treated with mannitol and mechanical ventilation
67
Q

Etiopathogenesis Diabetic Foot Ulcer

A

Development is attributed to: neuropathy, ischemia, infection, and immune impairment

NEUROPATHY: most common underlying etiology of foot ulcer

68
Q

Classification of Diabetic Foot Ulcers

A

Wagner Classification

  • Grade 0 : Pre or post-ulcerative lesion, completely epithelized
  • Grade 1: Partial/full thickness ulcer, superficial wound
  • Grade 2: Penetrates the tendon or capsule
  • Grade 3: Deep with osteitis
  • Grade 4: Partial foor gangrene
  • Grade 5: Whole foor gangrene
69
Q

University of Texas System Diabetic foot ulcer classification

A
  • Grade 0 : Pre or post ilceraive lesion, completely epithelized
  • Grade 1: Superficial wound
  • Grade 2: Wound penetrates tendon or capsule
  • Grade 3: wound penetrates bone and joint
  • Stage A: Clean wound
    • No ischemia
    • No infection
  • Stage B: Non ischemic infected wound
    • No ischemia
    • with infection
  • Stage C: Ischemic non-infected wound
    • With ischemia
    • No infection
  • Stage D: ischemic infected wound
    • with ischemia
    • with infection
70
Q

Etiopathogenesis of Hypoglycemia

A

glucose <55 mg/dL with symptoms that are relieved promptly after the glucose level is raised

Hepatic glycogen stires usually only last for 8 hours

71
Q

Physiologic Response to Hypoglycemia

A

1st line of defense

  • Decreased insulin (Primary glucose regulatory factor)

2nd Line of Defense

  • Increased glucagon (primary glucose counterregulatory factor)

3rd Line of Defense

  • Increased epinephrine (critical when glucagon is deficient)

Other defenses

  • Increased cortisol and growth hormone
72
Q

Classification of Hypoglycemia

A

Glucose Alert Value

  • <70 mg/dL
  • Sufficient low for treatment with fast acting carbohydrate and dose adjustment of glucose-lowering therapy

Clinically Significant Hypoglycemia

  • <54 mg/dl
  • Sufficiently low to indicate serious, clinically important hypoglycemia

Severe Hypoglycemia

  • No specific threshold
  • Hypoglycemia associated with severe cognitive impairment requiring external assistance for recovery
73
Q

Whippl’es Triad

A

Symptoms consistent with hypoglycemia

  • Neuroglycopenic symptoms: behavioral changes, confusion, fatigue, seizures, loss of consciousness
  • Adrenergic symptoms: palpitations, tremors, anxiety, sweating

Low Plasma glucose measured with a precise method

Relief of symptoms after the plasma glucose level is raised

74
Q

Management of Hypoglycemia

A
  • If awake and conscious
    • 15-20 g oral glucose, then repeat SMBG after 15 mins.
  • If unconscious or unwilling
    • Parenteral glucose 25 g
    • SC or IM glucagon (1.0 mg adults)
  • Manage Primary reason for hypoglycemia

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