Endocrinology (MS and DM) -IM Plat Flashcards
1
Q
BMI
A
Weight in kg/ Height in m2
Curvilinear relation with percent body fat mass
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
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
4
Q
etiopathogenesis of Metabolic syndrome
A
Insulin resistance
Central adiposity is the key feature
Hypertriglyceridemia is an excellent marker of insulin resistance
5
Q
BMI classification (ASIA-PACIFIC)
A
- Underweight :<18.5
- Overweight :18.5-22.9
- Obese 1: 23-24.9
- Obese II: >30
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
7
Q
Orlistat
A
Lipase inhibitor
60-120 mg TID
Adverse Effect: Abdominal discomfort oily stool, flatulence Malabsorption of fat-soluble vitamins
8
Q
Lorcaserin
A
Selective serotonin 2C receptor agonist
10 mg BID
Adverse effect: Hypoglycemia headache, fatigue, bradycardia serotonin syndrome
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
10
Q
Naltrexone/bupropion
(For Metabolic Syndrome)
A
Opiod antagonist/ aminoketoneantidepressant combination
8-32 mg/ 90-360 mg OD
Adverse effect: Nausea Constipation Headache
11
Q
Liraglutide
A
Glucagon-like peptide 1 receptor agonist
3 mg SC OD
Adverse Effect: Hypoglycemia Nausea Bowel movement changes Headache
12
Q
Etiopathogenesis of Diabetes Mellitus
A
Hyperglycemia
defined as the level of glycemia at which diabetes-specific complications occur
13
Q
Type 1 DM
A
Due to autoimmunity B-cell destruction,usually leading to absolute insulin deficiency
14
Q
Type 2 DM
A
Due to a progressive loss of B-cell insulin secretion frequently on the background of insulin resistance
15
Q
Impaired Glucose Homeostasis
A
- FBS:100-125 mg/dl
- Oral glucose challenge: 140-199 mg/dl
- HBA1c: 5.7-6.4%
16
Q
Diabetes Mellitus
A
FBS: >126 mg/dl
Oral glucose challenge: >200 mg/dl
HBA1c: >6.5%
17
Q
Manifestations of DM
A
Classic symptoms: Polyuria, Polydipsia, Polyphagia, Nocturia, Weight Loss
Others: Fatigue weakness BOV Frequent superficial infections Poor wound healing
18
Q
Mirovascular complications of DM
A
- Retinopathy
- Neuropathy
- Nephropathy
19
Q
Macrovascular complications of DM
A
- Coronary artery disease
- Peripheral artery disease
- Cerebrovascular disease
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
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
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
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
24
Q
Pramlintide
A
Amylin analog
Induces weight loss and lowers insulin dose
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
