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NU734 Acute Care I > DM Type I and II > Flashcards

DM Type I and II Flashcards

1
Q

Hormonal Abnormality
Type I DM
Type II DM

A
  • **Hormonal Abnormality **
    Deviciency of the Insulin Hormone
    Insulin deficency maybe absolute or relative

**Type I DM **
Insulin Deficiency
Destruction of insulin -producing pancratic beta cells

**Type II DM
**Decreased sensitivity
Decreased of insulin produced by Beta cells **

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2
Q

Type I DM

A
  • Insulin Deficiency **
    **Destructio of insulin **-prodcing pancreatic **Beta Cells **
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3
Q

DM Type II

A
  • Decrease Sensitivity
  • Decrease of insulin produced by Beta cells
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4
Q

Insulin Function

A
  • Released from Beta Cells
  • Allows Cellular Glucose uptake
  • Facilitates** lipids and protein** Metabolism
    *
  • Promotes cell devision and growth

Insulin Aloud absorb glucose that in a blood stream; Glucose serves as energy to cells or can be converted to fat

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5
Q

Role of Insulin and Glucagon

A

* Low BG: Pancrease > Glucagon Released by Alpha Cells of Pancrease> Liver release **Glucose **into Blood = Achieve Normal Blood Glucose Level

* High Blood Glucose : > Pancrease > Insulin Released by** Beta Cells of Pancrease > Fat **Cells take in Glucose from Blood = Achieve Normal Blood Glucose Levels

Glycolysis : Break down of glucose

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6
Q

Type I DM

A

*** 5 to 10 % of all cases **
* **Autoimmune Predispostion **
* RElatively short onset weeks to months due to beta cells destruction
* Typical pateitn presentation is DKA

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7
Q

TYpe 2 DM

A
  • 90 to 95 % of all cases
  • Combination of insulin resistance and beta cell **dysfunciton **
  • Progressive disease over time
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8
Q

Typ I DM symptoms

**Type II DM **

A
  • **Hyperglycemia with DKA **
  • Polyuria
  • Polydipsia
  • Blurry Vision
  • Paresthesia ( sensation of tingling and numbness )
  • **Acetone breath **

No acone breath
HHS ( profound hypeglycemia )

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9
Q

DM Work Up

A

A1C
* FG
* Urinalysis **(Proteuria ) **
* C-Peptide ( Type I no insulin production will be little to none C-Peptide ; )
( II : Makes isulin pancrease not use well ; C-Pap Highter

  • Lipid Panel ( Hypelipedemia )
  • EKG
  • Foot Exam
  • Eye Exam
  • Weight loss when applicable
  • Education
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10
Q

Type II DM

A
  • Profound Hyperglycemia (HHS )
  • Polyuria
  • Polydipsia
  • Blurry Vision
  • Paresthesia
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11
Q

DM I lab and Dx

A
  • Hgb A1C >= 6.5 or
  • FBS >= 126 on 2 occasions or
  • 2 Hr plasma glucose >= 200 during OGTT
  • **Serum Ketones, eleveted BUN/CR , HYpokalemia, High Anion Gap
  • Ketoacidosis **
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11
Q

Typ 2 DM

A
  • Hgb A1C > = 6.5 or
  • FBS >= 126 on two occasion or
  • 2 hrs plasma glucose >= 200 durign OGTT
  • Renal insult over years, chronic elevation in BUN /Cr
  • Hyperosmolar non-ketosis
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11
Q

Prediabetes Dx

A
  • **Definition **: Impaired Glucose Homeostatis
  • Impaired Fasting Glucose (IFG)
  • Fasting Plasma Glucose (FPG) 100 to 125
  • Impaired Glucose Tolerance (IGT )
  • Two hour plasma glucose elevated after OGTT of >= 140 to < 200 and FPG <125

After oGTT >/= 140 to <200
FPG <125

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12
Q

Typ I Management

A

Insulin SQ
Long
Itermidiate
Short
Insulin Pump ( with insurance )
Lifestyle Modifications

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13
Q

Type II Managemenet

A
  1. Metormin is mainstay treatment
    * Maximize oral agents
    * 2 or more RX
    * Insulin
    * Consider Insulin
    * Lifestyle modification
    * Victoza avoid with cardiac problems
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14
Q

I and II DM Management

A

A1C <7.0 (By IDF) and AACE (,6.5)
Sugar Control
Weight Management
Lipid Control
CV risk Management
Smoking cessation
Optimize BP
Renal Function

15
Q

A1C and Glycemic Control for the Older and Elderly

A

**Individualize tx based on health factors
* A1C not always accurate wth chronic condition

Ages >65 years old **
* HgB A1C goal should be **<7.5 **
* with co-morbidities and expectancy >10 yrs

**Frail Elderly **
A1C goal < 8 wth co- morbidities and expectancy <10 yrs

**Hyperglycemia: **: Dehydration; Vision changes, Delayed cognition, infections

Hypoglycemia : traumatic falls, Syncope, altered mental status

16
Q

Biguanide

A
  • Metromin (Glucophage )
    *** 1st line agent **
  • Insulin Sensitizer
  • No Inherent Hypoglycemia risk
  • Can Impair Renal Function Hold for contrast
  • Can increase risk of Vitami B 12 deficiency
17
Q

Thiazolidinedione (TZD)

A

*** Pioglitazone (Actos ) Rosiglitazone (Avandia ) **
* Insulin Sensitizer
* No Inherent HYpoglycemia risk
* Advantages : Improves lipid profile
* Disadvanages **Fluid Retesion , HF, Weight GAin , bone Fx CV risk
**
Actos been associated with Bladder CA

18
Q
A
19
Q

Sulfonylurea

A
  • Glipizide ( Glucotrol ), Glyburide (Diabeta), Glimepiride (Amaryl )
  • Increase insulin release from beta cells
  • Advancage: **Fast Acting **
  • Disadantates: Weight Gain, HYpoglycemia
20
Q

Meglitinides

A
  • Repaglinide** (Pranding **), Nateglinid (Starlix )
  • Increase insulin release
  • Action works on postrprandial blood glucose only
  • Advangages: Rapidly effective
  • Disadang: Weight gain , TID, hypogly..
21
Q

Dipeptidyl Peptidase ( DPP 4 ) Inhibitor

A

Januvia; Onlyza; Tradjenta
increase insulin release
Advange: NO HYpoglycemia
Disa: **Pancreatic CA **
Dose need for renal impairment

22
Q

GLP I Receptor Agonist

A

**Victoza
Increase insulin release
Responses to blood glucose post meal
Small hypoglycemia risk
Adv: **weekly injetion, **reduction in manor adverse CV events weight loss
Dis: **Pancreatitis **
Do no prescribe with severe renal impairment

23
Q

Sodium Glucose contrasporter (SGLT 2)

A

Jardiance ( sodium in a jar )
Lowers plama glucose level
Increases amojnts of glucose excreted in urine
postprandial glucose effect
Advang: Reduces CV mortality, reduces SBP, imrove renal outcome
Disat:** AKI, DKA, UTI, **Vulvovaginal candidais

24
Q

Alpha Glucosidase Inhibitors

A

**Precose, Mglitol, Glyset

**Delays intestinal carbohydrate absorption

Acts on post prandial BG

Adv: small risk hypoglycimia

disa: Ileius, Hypatis, Flatulence

25
Q

A1C <7.5

A

)* Monotherapy: Metormin 1st line * Monotherapy: Metormin 1st line
* Consider other OPtions: DPP4 or GLP-1
* Dual Therapy:
* Triple therapy
* add insuling

2 to 3 wks b/w

26
Q

A1C >/= 7.5 to 9.0
Caution A1c 8.5 risk for hypoglycemia

A
  • **Metrormin+GLP-1 or
  • TZD or DPP4 or SU or Meglidine

treat 3 month

27
Q

A1C >9.0

A

Symptomatic: Insulin +/- other agents
Under tx and inadequate : insulin + other agents
Asymtomatic: Consider dual vs triple therapy

1 unit = 50 points

28
Q
A
29
Q

DKA

A

Present Ketoacidosis
Elevated anion
Low bicarb
Tx: Insulin 0.1 unit/kg ; elecrolyte Isotonic fluid replacement

30
Q

HHS

A

No ketoacidosis
Tx: reducy BG
Isotonic Solution
Replce electrolyte s

31
Q

Somogyi Effect

A

Hypoglycemia around 2 to 3 am

Adjust time for insulin
Eat snakc

32
Q

Dawn Phenomenon

A

Ricingn
Abnormal early mornign hypeglycemia ( 2 to 8 am )
Avoid carbs HS
adnjust meds
exercise after dinner

33
Q

Insulin

A
  • Humalog (Aspart ) : Once 15 mints
  • Peak 1to 2 hrs
  • Duration 4 to 6 hrs
    _________________________________________
    REgular : 30 to 60 mints ; 2 to 4 hrs ; 6 to 8 hrs
    NPH: 2 to 4 rhs ; 4 to 10 hours ; 12 to 20 hrs

NU734 Acute Care I (25 decks)

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