Endocrinology (MS and DM) -IM Plat 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
Overview of management for Type 2 DM
**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
26
3 major components of exogenous insulin therapy
* Basal * Bolus * Correctional
27
Basal insulin
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**
28
Bolus Insulin
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 min**s. before meals
29
Correctional Insulin
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
30
Rapid Acting insulin
**Lispro Aspart Glulisine** * Onset: \<15 mins * Peak: 30-90 mins * Duration: 2-4 hours
31
Short Acting Insulin
**Human Regular** * Onset: 30-60 mins * Peak: 2-3 hours * Duration: 3-6 hours
32
Intermediate Acting Insulin
**Isphane/ Human NPH** * OnsetL 2-4 hours * Peak: 4-10 hours * Duration: 10-16 hours
33
Basal Insulin Analogs
**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
Insulin Secretagogues
**Increases insulin secretion** SE: hypoglycemia and weight gain Sulfonylureas Non-sulfonyureas
35
Sulfonylureas
* **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
Non-sulfonylureas (insulin secretagogues)
* **Repaglinide** 0.5-16 mg/d PO * **Nateglinide** 120 mg/d PO
37
Insulin Sensitizers
* Biguanides * Thiazolidinediones
38
Biguanides
**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
Thiazolidinediones
Decrease insulin resistance, increases glucose utilization Benefit in NASH **Pioglitazone** 15-45 mg OD PO SE: Edema, weight gain, OSTEOPOROSIS, anemia, CHF
40
Intestinal Absorption inhibitors
Inhibits intestinal absorption of sugars SE: weight loss, diarrhea, flatulence * Alpha-glucosidase inhibitors * Lipase Inhibitors
41
Alpha-glucosidase inhibitors
* **Acarbose** 25-100 mg TID PO * **Miglitol** 25-100 mg TID PO
42
Lipase inhibitors
**Orlistat** * 120 mg TID PO
43
Incretin-Related Drugs
**Prolongs endogenous GLP-1 action** * DPPV-IV inhibitors (DPP4) * GLP-1 agonists (parenteral)
44
DPP4 inhibitors
* **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
GLP-1 agonists (parenteral)
* **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
Na-glucose co transporter-2 inhibitors (SGLT2i)
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
Amylin Agonist (Parenteral)
Slows gastric emptying.Decrease glucagon * **Pramlintide** 15-20 mcg OD SC SE: Nausea and hypoglycemia
48
Bile Acid sequestrants
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
Dopamine 2 agonists
Activates dopaminergic receptors and modulates hypothalamic regulation of metabolism * **Bromocriptine** 0.8-4.8 mg/d PO SE: Dizziness, nausea, fatigue, rhinitis
50
Initiating Antihyperglycemic Therapy at Diagnosis of DM
* 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
Metformin
high efficacy low hypoglycemic risk, neutral effect or decrease in weight and low cost ## Footnote **CONTRAINDICATED with eGFR \<30**
52
TRIPLE THERAPY
consider **if A1C target not achieved even after 3 months of dual therapy** AND **patient not markedly symptomati**c Metformin + lifestyle modifications, PLUS a combination of the following
53
Combination Injectable Therapy
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
Drugs and their primary Areas of Control
55
`Monitoring Response of Treatment for DM
**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
Self Monitoring of Blood Glucose
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
Goals of treatment
HbA1c (Primary goal) : \<7.0% Preprandial Capillary plasma glucose: 80-130 mg/dl Peak postprandial capillary plasma glucose: \<180 mg/dl
58
Etiopathogenesis of hyperglycemic crises in diabetes
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
precipitating factors for hyperglycemic crisis
* **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
Diabetic Ketoacidosis
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
Hyperosmotic hyperglycemic State
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
Diagnosis of Hyperglycemic Crisis in Diabetes
63
General Management of Hyperglycemic crises in Diabetes
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
Specific Treatment Hyperglycemic Crisis
65
Criteria for resolution
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
Complications of hyperglycemic crisis
* **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
Etiopathogenesis Diabetic Foot Ulcer
Development is attributed to: neuropathy, ischemia, infection, and immune impairment NEUROPATHY: most common underlying etiology of foot ulcer
68
Classification of Diabetic Foot Ulcers
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
University of Texas System Diabetic foot ulcer classification
* 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
Etiopathogenesis of Hypoglycemia
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
Physiologic Response to Hypoglycemia
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
Classification of Hypoglycemia
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
Whippl'es Triad
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
Management of Hypoglycemia
* 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