Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Internal Medicine (IM platinum) > Metabolic Syndrome and Diabetes (IM Platinum) > Flashcards

Metabolic Syndrome and Diabetes (IM Platinum) Flashcards

1
Q

BMI

A

Weight in kg/ Height in m2

Curvilinear relation with percent body fat mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

etiopathogenesis of Metabolic syndrome

A

Insulin resistance

Central adiposity is the key feature

Hypertriglyceridemia is an excellent marker of insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

BMI classification (ASIA-PACIFIC)

A
  • Underweight :<18.5
  • Overweight :18.5-22.9
  • Obese 1: 23-24.9
  • Obese II: >30
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Orlistat

A

Lipase inhibitor

60-120 mg TID

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Lorcaserin

A

Selective serotonin 2C receptor agonist

10 mg BID

Adverse effect: Hypoglycemia headache, fatigue, bradycardia serotonin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Naltrexone/bupropion

(For Metabolic Syndrome)

A

Opiod antagonist/ aminoketoneantidepressant combination

8-32 mg/ 90-360 mg OD

Adverse effect: Nausea Constipation Headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Liraglutide

A

Glucagon-like peptide 1 receptor agonist

3 mg SC OD

Adverse Effect: Hypoglycemia Nausea Bowel movement changes Headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Etiopathogenesis of Diabetes Mellitus

A

Hyperglycemia

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Type 1 DM

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Type 2 DM

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Impaired Glucose Homeostasis

A
  • FBS:100-125 mg/dl
  • Oral glucose challenge: 140-199 mg/dl
  • HBA1c: 5.7-6.4%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Diabetes Mellitus

A

FBS: >126 mg/dl

Oral glucose challenge: >200 mg/dl

HBA1c: >6.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Manifestations of DM

A

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

Others: Fatigue weakness BOV Frequent superficial infections Poor wound healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mirovascular complications of DM

A
  • Retinopathy
  • Neuropathy
  • Nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Macrovascular complications of DM

A
  • Coronary artery disease
  • Peripheral artery disease
  • Cerebrovascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pramlintide

A

Amylin analog

Induces weight loss and lowers insulin dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

3 major components of exogenous insulin therapy

A
  • Basal
  • Bolus
  • Correctional
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
58
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

59
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
60
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

61
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

62
Q

Diagnosis of Hyperglycemic Crisis in Diabetes

A
63
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
64
Q

Specific Treatment Hyperglycemic Crisis

A
65
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
66
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
68
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

70
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
71
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
72
Q

Etiopathogenesis Diabetic Foot Ulcer

A

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

NEUROPATHY: most common underlying etiology of foot ulcer

73
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
74
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
75
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

76
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
77
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
78
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

79
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

Internal Medicine (IM platinum) (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions