DIABETES MELLITUS Flashcards by Ila Sunio

a metabolic disorder characterized by glucose intolerance, caused by an imbalance between insulin supply and insulin demand.

DIABETES MELLITUS

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the body is not tolerating the increased amount of glucose in the blood because there is no insulin that will be able to metabolize the glucose

GLUCOSE INTOLERANCE

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Also referred as insulin dependent diabetes mellitus

TYPE 1

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Juvenile onset and is characterized as destruction of beta cell by autoimmune responses, Hereditary predisposition (human leukocyte antigen), and toxin and virus

TYPE 1

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Type of diabetes wherein there is little or absence of insulin

TYPE 1

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Also referred to is non insulin dependent diabetes mellitus

TYPE 2

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Adult onset and is characterized by insulin resistance due to obesity, hereditary predisposition, and environmental factors (toxins and virus)

TYPE 2

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Occurs in 2nd to 3rd trimester and due to hormone released during pregnancy (human placental lactogen)

GESTATIONAL DIABETES

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GDM can progress to _________ if untreated

TYPE 2 DM

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Complication of TYPE 1

DIABETIC KETOACIDOSIS

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Complication of TYPE 2 diabetes

HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC COMA

HYPERGLYCEMIC HYPEROSMOLAR SYNDROME

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Primary treatment for TYPE 1 DM

Insulin

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Primary treatment to type 2 DM

LIFESTYLE MODIFICATION (Diet and Exercise)

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If type 2 DM cannot be controlled by lifestyle modification, the patient will be on

OHA treatment

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Failure of entry of glucose inside the cell will cause

POLYPHAGIA

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Fluid goes into the blood vessels due to hyperglycemia will cause

POLYURIA

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Increase urination or polyuria will cause

POLYDIPSIA

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Acid base imbalance in patient with DKA

METABOLIC ACIDOSIS

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Patient with HHNS will have what electrolyte imbalance?

HYPOKALEMIA (low potassium)
Because of increase urination, potassium is excreted

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Patient with DKA will have what compensation to decrease acid in the blood

RESPIRATORY COMPENSATION
(KUSSMAUL BREATHING)

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What by-products is present in patient with DKA as a result of lipolysis

KETONES OR KETONE BODIES

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What is responsible for the acidic state of blood in patient with DKA

KETONES (acidic in nature)

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Explain the Differences between DM 1 and DM 2.

Type 1 DM or Juvenile onset DM is a form of DM that is dependent on insulin. The primary problem in this type of diabetes is the destruction of beta cell which is responsible for insulin production. Since beta cell are damage, there will be lack or no insulin at all present in this patient. Without insulin, the body will not be able to metabolize glucose or let it enter the cell, leading to increasing amount of glucose in the blood stream or HYPERGLYCEMIA. This is commonly associated with autoimmune response wherein the body immune cells mistakenly attack the pancreas or beta cell.

On the other hand, DM 2 also known as Adult onset DM is non insulin dependent . The main problem of this kind type of Diabetes is Insulin resistance, wherein cells are not just receptive to insulin. Because of this, there will be no glucose uptake or metabolism leading to increasing amount of glucose in the blood stream or HYPERGLYCEMIA). This is commonly associated with lifestyle factors such as obesity and sedentary lifestyle.

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Explain the differences between DKA and HHNS

Diabetic KetoAcidosis is a complication of type 1 DM. Its hallmarks includes
1). HYPERGLYCEMIA (300-800 mg/dL) due to decrease glucose uptake or metabolism associated with lack of insulin

2). KETOSIS due to fat breakdown or lipolysis associated with cell starvation and compensatory mechanism of our body for energy needs

3). ACIDOSIS due to the presence of ketones in the blood, which is acidic.

Hyperglycemic Huperosmolar Nonketotic Coma is a complication of type 2 DM and is characterized by

1). HYPERGLYCEMIA (600-2000 mg/dL) due to decrease glucose uptake or metabolism associated with insulin resistance

2). HYPEROSMOLARITY due to increase blood glucose level (600-2000 mg/dL)

3). PROFOUND DEHYDRATION due to osmotic diuresis associated with hyperosmolarity. The super increased blood glucose level moves fluid from the interstitial and cells into the vessels (Highly concentrated) leading to it being excreted along with excess glucose)

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What are 3ps of DM

POLYPHAGIA POLYURIA POLYDIPSIA

Usual target for diabetic px is to maintain an HBA1C of

6-7%

considered by doctors as the cornerstone of management among diabetic client because it directly controls the body’s major glucose source.

DIET

ADA RECOMMENDATION OF CALORIES DISTRIBUTION: Carbohydates

50-60%

ADA RECOMMENDATION OF CALORIES DISTRIBUTION: Fats

30-35% 20-30% (book)

ADA RECOMMENDATION OF CALORIES DISTRIBUTION: Protein

10-20%

ADA RECOMMENDATION OF CALORIES DISTRIBUTION: Fiber

25g

most common tool for nutritional management.

DIABETIC EXCHANGE LIST

Recommended frequency of exercise in a week

3 times

How many minutes is the recommended exercise for DM patient

20-45 min

What should the diabetic patient bring when exercising?

RESCUE CANDY

is a cornerstone of diabetes management

BLOOD GLUCOSE MONITORING

has dramatically altered diabetes care.

SELF MONITORING OF BLOOD GLUCOSE

Route of insulin therapy

SC IV - regular

Site for insulin injection

AAT ARMS ABDOMEN THIGH

Most preferred site for insulin injection because of fastest absorption

ABDOMEN

Recommended frequency of laboratory monitoring for patient with DM

3-6 months

Recommended diet for patient with DM should have _____ regular meals and _____snacks

3 regular meals 2 snack

TRUE OR FALSE diet for patient with DM requires omission or reduction in food intake

FALSE

Recommended duration of warm up and cool down for exercise

5 mins each

Injection of insulin should be rotated _____ inch apart

1 inch

TRUE OR FALSE In administering insulin, one should avoid heavily exercised site

TRUE

This method of insulin injection is ideal since it allows gradual release of insulin in the bloodstream

SC or SUBCUTANEOUS

TRUE OR FALSE One must shake insulin before aspiration and administration

FALSE ## Footnote roll only using palms

TRUE OR FALSE In administering insulin, after injection aspiration is a must

FALSE

TRUE OR FALSE Never massage after injection of insulin

TRUE

alternative method of insulin delivery wherein it is implanted towards the skin and releases Basal Rate and Bolus rate. It also acts as little pancreas

INSULIN PUMP

Expensive type of insulin. Pre-calibrated

INSULIN PENS (novomix)

allows the insulin to spread over the larger area. faster absorption of insulin to the bloodstream

JET INJECTIONS

Type of insulin that has rapid action and shorter time to attain its peak action

SHORT ACTING

What are examples of short acting insulin

LAG Lispro Aspart Glulisine RSH Regular Semilente Humulin R

Intermediate acting insulin examples

NLH NPH Lente Humulin N

Long acting insulin examples

GUD Glargine Ultralente Detemir

Any combination of different kinds of insulin

PREMIXED

Is the only insulin that can be administered IV

Regular insulin

First use of regular insulin should be placed in

Refrigerator

2nd and 3rd use of regular insulin should be placed in

ROOM TEMPERATURE

Sources of insulin

BEEF PORK HUMAN GENETICALLY ENGINEERED (bacteria)

TRUE OR FALSE Insulin is high alert medication

TRUE

TRUE OR FALSE One can use tuberculin insulin in administration

FALSE ## Footnote can cause hypoglycemic effects because it has different calibration

Purpose of rotation of insulin injection

Prevent lipodystrophy Prevent lipoatrophy

It refers to blood sugar less than 80 or 60 mg/dL

HYPOGLYCEMIA

Signs and symptoms of hypoglycemia

Diaphoresis Tachycardia Tremors

TRUE OR FALSE Only regular insulin has clear color or appearance

TRUE

Onset of Lispro

15-30 mins

Onset of Aspart

10-20 mins

Onset of Glulisine

10-15 mins

Onset of NPH

60-120 mins

Onset of Glargine

70 mins

Onset of detemir

60-120 mins

Onset of regular insulin

30-60 mins

Peak of lispro

0.5-2.5 hrs

Peak of aspart

1-3 hrs

Peak of Glulisine

1-1.5 hrs

Peak of NPH

6-14 hrs

Peak of Glargine

None

Peak of Detemir

12-24 hr

Peak of regular insulin

1-5 hrs

Duration of lispro

3-6

Duration of aspart

3-5

Duration of glulisine

3-5

Duration of NPH

16-24

Duration of regular

6-10

Insulin that is administered through inhalation

AFREEZA

Oral Hypoglycemic Agent is specifically used for patient with

TYPE 2 DM

OHA that triggers or stimulates pancreas to increase production of insulin

SULFONYLUREAS

OHA that stimulates liver to stop production of glucose. It inhibit Gluconeogenesis and Glycogenolysis

BIGUANIDES

Use for patient with type 2 DM and is having insulin injection but inadequate to control blood glucose. Patient who have HBA1C or 8 or above

THIAZOLADINEDIONES

OHA that delays absorption of glucose in the GI tract resulting in lower Post Pradial Blood Glucose

ALPHA GLUCOSIDASE INHIBITORS

Example of Sulfonylureas

GLIMEPRIDE GLYBURIDE TOLAZAMDE ## Footnote all ends with IDE

Examples of Biguanides

Metformin Phenformin ## Footnote all ends with MIN

Example of thiazoladinediones

ROSIGLITAZONE PIOGLITAZONE ## Footnote all ends with ZONE

Example of alpha glucosidase inhibitors

MIGLITOL ACARBOSE

Known as rebound hyperglycemia

SOMOGYI EFFECT

Refers to alternating periods of nocturnal hypoglycemia and hyperglycemia.

SOMOGYI EFFECT

Management for patient experiencing somogyi effect

DECREASE EVENING DOSE OF INSULIN INCREASE BED TIME SNACKS ## Footnote to prevent hypoglycemia and counteregulatory hyperglycemia

Refers to as early morning hyperglycemia that is caused by excessive early morning release of growth hormone and cortisol

DAWN PHENOMENON

Management for patient experiencing dawn phenomenon

INCREASE INSULIN DOSE CHANGE TIMING OF INSULIN

Refers to disappearance of symptoms on newly diagnosed client with DM.

HONEYMOON PHASE

Management for patient experiencing honeymoon phase

DO NOT STOP TREATMENT (medication) ABRUPTLY

Stimulate pancreatic beta cells to release insulin and Decrease gluconeogenesis by the liver.

ORAL HYPOGLYCEMIC AGENT

Criteria for prescribing OHA

>40 y.o Not pregnant (teratogenic) No hx of ketosis On <40 unit of insulin Has mild yo moderate symptoms of hyperglycemia

GI disturbances related to taking biguanides (metformin)

EPIGASTRIC PAIN

PTA refers to

Transplant of PANCREAS alone

PAK refers to

Transplant of PANCREAS after KIDNEY

PSK

Simultaneous PANCREAS and KIDNEY transplant

Develops when insufficient insulin levels result in cellular starvation and hyperglycemia.

DIABETIC KETOACIDOSIS

DKA usually stimulated or precipitated by

INFECTION STRESS MISSED INSULIN DOSE ## Footnote INFECTION STRESS leads to increase energy demands thus there will be glycogenolysis, gluconeogensis, and Ketogenesis

occur due to the increased concentration of the blood sugar in the blood and also because of the acidic state of the blood, body is trying to excrete the acid and excess sugar of the body through the kidney

OSMOTIC DIURESIS

common complication of diabetic ketoacidosis

HYPOKALEMIA

Hallmarks of DKA

HYPERGLYCEMIA KETOSIS ACIDOSIS DEHYDRATION

Blood glucose of patient with DKA

300-800 mg/dL

Evidence of ketoacidosis seen in laboratory and diagnostics examination

DECREASE PH, BICARBONATE, and PCO2 ## Footnote Decrease PCO2 signifies respiratory alkalosis which can be attributed to compensatory mechanism of the body to excrete acids.

MANAGEMENT FOR DKA: Reverse Acidosis

REGULAR INSULUN = 25ml/Hr

MANAGEMENT FOR DKA: Reverse Acidosis If Blood glucose is 250-300 mg/dL

D5NSS or D5 45% NSS

MANAGEMENT FOR DKA: Rehydration

PNSS 0.5-1 L/hr for 2-3 hrs

MANAGEMENT FOR DKA: Rehydration After 2-3 hours of first management

0.45% NS

MANAGEMENT FOR DKA: Rehydration Until bp is stable

PNSS 200-500 ml/hr

MANAGEMENT FOR DKA: Rehydration For blood glucose of 300 mg/dL or less

D5W

MANAGEMENT FOR DKA: electrolyte replacement

POTASSIUM ## Footnote *monitor ECG *check serum K every 2-4 hrs

TRUE OR FALSE If patient is unable to void one must HOLD potassium replacement

TRUE ## Footnote Patient who has oligria cannot excrete excess potassium thus it can lead to hyperkalemia and can pose problem in the heart

Comatose condition wherein the diabetic client produces insulin sufficient to prevent ketone bodies from forming but still inadequate to reduce hyperglycemia.

HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC COMA

Blood glucose level of patient with HHNC OR HHNS

600-2000 mg/dL

Characteristic of breath in patient with DKA

Acetone breath Fruity odor breath

MANAGEMENT FOR HHNC: Hyperglycemia

Insulin at slow rate

MANAGEMENT FOR HHNC: Rehydration

0.9% NSS or 0.45 NSS

MANAGEMENT FOR HHNC: Electrolyte Replacement

POTASSIUM

Onset of DKA is

SUDDEN

Onset of HHNC is

Gradual

Results from overdosage of insulin, omitting a meal while on insulin or OHA, Over exertion, Alcohol intake and Nutritional and fluid imbalance

HYPOGLYCEMIA

In mild hypoglycemia first indication would be

HUNGER GLUCOSE LEVEL OF <70 mg/dL

In moderate hypoglycemia______ signals that the brain cells are deprived of glucose

DROWSINESS

In severe hypoglycemia there will be

CNS FUNCTION IMPAIRED

If patient is hypoglycemic management would be

15 g of fast acting concentrated carbohydrates I mg of glucagon SC 25-50 ml of D50W (patient if unconscious or cannot swallow)

For patient who will undergo surgery insulin is administered how many units if blood glucose is 180-200 mg/dL

For patient who will undergo surgery insulin is administered how many units if blood glucose is 120-150 mg/dL

For patient who will undergo surgery insulin is administered how many units if blood glucose is 150-180 mg/dL

For patient in NPO monitoring of blood glucose is done how many times

3 times a day

For patient in NPO, if blood glucose Increases what should the nurse do?

Give insulin

For patient in NPO, if blood glucose decrease what should the nurse do?

Increase rate of D5

TRUE OR FALSE SC insulin should not be given intraoperatively

TRUE ## Footnote absorption of insulin if given intraoperatively is affected by body temperature, circulatory blood volume, and anesthetics.