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PHARMA > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Insulin

A

Stimulates synthesis of glycogen and helps glucose enter the cells of striated muscle and adipose tissue

Promotes protein synthesis and helps the body store fat by preventing its breakdown for energy.

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2
Q

Beta Cells in Pancreas

A

secrete 0.2-0.5 units/kg/day of insulin ex- someone weighing 150lbs will secrete on an average of 15-35 units per day

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3
Q

Lipodystrophy

A

when the body can’t maintain fat tissue and
why a diabetic should change injection sites

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4
Q

Rapid acting Insulin

A

-Names of Drugs: Aspart, Glulisine, Lispro, Inhaled

-Fast acting: 5-15mins
-Peak: 45-75 mins
-Duration: 2-4 hours
-Deadliest insulin
-Always monitor for hypoglycemia

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5
Q

Short acting Insulin
(regular)

A

given 30 mins before meals

Short Acting: 30-60min
Peak: 2-4 hours
Duration: 5-8 hours

If Regular insulin (clear) is mixed with NPH human insulin (cloudy), the Regular insulin should be drawn into the syringe first.

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6
Q

Intermediate-Acting Insulin
or NPH (neutral Protamine Hagedorn)

A

-also called ‘isophane’
-2X daily 70/30 mixture pen
room temp for 10 days

Acting: 1-2hours
Peak: 4-12
Duration: 18-24 hours

(Provide basal insulin overnight)

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7
Q

Long actin insulin

A

Onset - 2 hours
Peak-3-9 or none
Duration- 24 hours

Types: Glargine & Determir

-even absorption no peaks or valleys

-used in both Type 1 and 2 (common in 2)

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8
Q

Doses of Insulin

A

0.6-0.8ukg/day
2/3-AM and1/3-PM

-Start with 1 unit of insulin per 15 grams carbs, adjust while checking glucose levels

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9
Q

Keytones

A

Caused by high glucose

Altered process of aerobic and anaerobic metabolism

Breakdown of fat into free fatty acids and glycerol; for energy.

Converted into ketones by the liver
Are strong acids that accumulate in the blood and can lead to metabolic acidosis

Gluconeogenesis occurs instead of Krebs or citric acid cycle

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10
Q

Hypoglycemia

A

Blood glucose > 60

Symptoms: Sweating, clammy, confused, hungry, lightheaded, dizzy, blurred vision, seizures, coma

Common causes: Excessive exercise, alcohol, poor food intake, too much insulin, stress, surgery, and medications.

Epinephrine and Glucagon are released causing activation of the SNS which is responsible for most of the signs and symptoms

As hypoglycemia continues, epinephrine and glucagon promote glycogenolysis and gluconeogenesis in the liver

“I’m sweaty, cold, clammy, give me some candy”

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11
Q

Atherosclerotic

A

Glucose sticks to proteins in blood vessel’s making them hard and form plaque.
Leads to heart disease, stroke, hypertension, infections, poor eye sight

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12
Q

Diabetic ketoacidosis
(DKA)

A

Is a hyperglycemic emergency

-burning of ketones for energy (diabetes type 1)
- leads to acid in blood

Characterized by: Metabolic acidosis, dehydration, and electrolyte loss

Diagnosis:
Serum glucose >250mg/dl
Ketonemia and urine
Low pH
Low HCO3

Three main causes of DKA
-Infection or illness
-Lack of Insulin
-Undiagnosed or undertreated diabetes

Symptoms: thirsty, rapid breathing (getting rid of extra co2), fruity breath

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13
Q

Hyperglycemia hyperosmolar nonketotic syndrome
HHNS

A

Increase blood sugar without burning ketones. (Type 2 diabetes)

Symptoms: dehydration, thirsty, high BS, mental status changes

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14
Q

3 ps

A

Polyuria- increase urination
Polyphagia- increase in appetite
Polydipsia-increase in thirst

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15
Q

Clinical Manifestations of DKA

A

Presenting Symptoms:
The 3 P’s and weight loss
Abdominal pain
Severe nausea and vomiting, and fatigue

Extreme Dehydration
Poor skin turgor
Dry mucous membranes
Tachycardia
Hypotension

Acetone breath,
Kussmaul respirations (similar to hyperventilation) respirations
Changes in Level of consciousness

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16
Q

Treatment for DKA

A

Fluid replacement first!
-To restore intravascular volume
-To clear ketones
-To correct electrolyte imbalances

Insulin – regular-considered short acting

Need to monitor for cerebral edema as fluid shifts back to the cells

Hyponatremia and Hyperkalemia are most common electrolyte issues

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17
Q

Morning Hyperglycemia
(Dawn Phenomenon)

A

Increase in fasting blood glucose and/or insulin requirements during the early morning hours

Occurs naturally in everyone

Is the result of circadian variations in hormone secretion

18
Q

Somogyi Effect

A

Nocturnal hypoglycemia followed by rebound hyperglycemia.

The hypoglycemia triggers the release of counter-regulatory hormones: releasing glycogen from the liver; epinephrine, cortisol and growth hormone

Occurs due to too much or too little insulin at bedtime or skipped nighttime snack

Treat by decreasing insulin dose or changing time of adm

19
Q

Type 1

A

Autoimmune
Types:
Type 1A (90-95%)
Type B (idiopathic,no autoimmune)

Requires exogenous insulin to stop the catabolic process, lower the BS and prevent ketosis.

Has circulating autoantibodies (humoral immunity) to islet cells of the pancreas, insulin and other enzymes needed for insulin production

Macrophage & lymphocytic infiltration of the beta cells leads to cytokine production and ultimate apoptosis of the beta cells

Ketosis: When there is no insulin, no lipolysis, body uses Fat For Atp for energy

20
Q

Other Blood Tests for Type 1

A

C-peptide
-Detects natural insulin secretion, C-peptide released when pancreas able to secrete insulin

Islet Cell Autoantibodies (ICA)
-Often detected in those with Type 1 DM

Insulin Autoantibodies (IAA)
-Looks for the antibodies targeting insulin.

Insulinoma-Associated-2 Autoantibodies (IA-2A)
-Looks for antibodies mounted against a specific enzyme in beta cells. Both the IA-2A and GADA tests are common T1D antibody tests.

Zinc Transporter 8 (ZnT8Ab)
-Looks at antibodies targeting an enzyme that is specific to beta cells.

Glutamic Acid Decarboxylase Autoantibodies (GADA or Anti-GAD)
-Looks for antibodies built against a specific enzyme in the insulin-producing pancreatic beta cells.

21
Q

C-peptide Test

A

Detects natural insulin secretion, C-peptide released when pancreas able to secrete insulin

22
Q

Islet Cell Autoantibodies (ICA) Test

A

Often detected in those with Type 1 DM

23
Q

Insulin Autoantibodies (IAA) Test

A

Looks for the antibodies targeting insulin.

24
Q

Insulinoma-Associated-2 Autoantibodies (IA-2A) Test

A

Looks for antibodies mounted against a specific enzyme in beta cells. Both the IA-2A and GADA tests are common T1D antibody tests.

25
Q

Zinc Transporter 8 (ZnT8Ab) Test

A

Looks at antibodies targeting an enzyme that is specific to beta cells

26
Q

Glutamic Acid Decarboxylase Autoantibodies (GADA or Anti-GAD)

A

Looks for antibodies built against a specific enzyme in the insulin-producing pancreatic beta cells.

27
Q

Glycogenesis

A

Process of glycogen formation when glucose supplied excess need for ATP synthesis

Glucose is stored in cells to a saturation point for about 12-24 hours.

Stored mainly in the liver and muscle

Reverse process of glycolysis

Genesis=Formation

28
Q

Glycogenolysis

A

Breakdown of stored glycogen to make glucose

Process occurs when the glucose levels become too low (i.e. prolonged starvation)

Process occurs in the liver and muscle tissue in response to hormonal and neural signals
-Epinephrine
-Glucagon
-Insulin

Process also inhibits glucogenesis

29
Q

Gluconeogenesis

A

Synthesis of glucose by the liver from non-carbohydrate sources

Process primarily occurs in liver

Amino acids (protein) and fats are converted to glucose

From stored fat to fatty acids and/or glycerol
Amino acids to lactic acid

Can lead to the development of ketones

Happens when there is not enough glucose to meet the needs for the body

Also play a role in maintaining acid-base balance

30
Q

Functions of the Pancreas

A

Exocrine acini -> digestive juices -> duct -> duodenum

Endocrine Islets of Langerhans -> hormones
-> blood

Beta cells—>Insulin, amylin
Alpha cells—> Glucagon
Delta cells —>Somatostatin (which is a growth hormone)
F/PP cells—> Pancreatic polypeptide

31
Q

Insulin Hormone

A

Required by the body cells to initiate active transport of glucose into the cell

-Skeletal cells – store glucose as glycogen
-Adipose tissue – stops release of fatty acids
-Liver – stops gluconeogenesis, starts producing glycogen and fat

Brain does not require insulin for glucose uptake

Insulin stimulates the uptake, use, and storage of glucose

32
Q

Ancanthosis Nigricans-

A

signs of insulin resistance:
Darkening and thickness of skin on armpits and neck

33
Q

Why Does Obesity Cause Insulin Resistance?

A

Causes increases in adipose and free fatty acids

Induces inflammation and release of the associated inflammatory mediators

Increases stress on pancreatic B cells as insulin is increased

Results in liver increase glucose in the blood (impaired suppression)

34
Q

Why Does A Sedentary Lifestyle Increase Insulin Resistance?

A

NO EXERCISE
- have decreased intracellular enzymes such as pyruvic acid

EXERCISE
-Increases mitochondrial enzymes,
-Increases insulin sensitivity
-TG get broken into FFA to use for fuel
-Decrease BS, decrease insulin
-Increase glucagon
-Causes uptake of glucose from circulation

35
Q

Glycated Hemoglobin A1C

A

Used to diagnose or monitor diabetes

Glucose does not normally go into the RBC but the membrane is very permeable.

When the glucose level is chronically high, it will move into the RBC.

Once glucose is in the RBC, it can not leave

The HgbA1C measures the amount of glucose over 120 days (3 month period)

36
Q

Somatic neuropathy

A

Diminished perception: vibration, pain, temperature

Hypersensitivity: light touch; occasionally severe “burning” pain

37
Q

Autonomic neuropathy

A

Defects in vasomotor and cardiac responses

Urinary retention

Impaired motility of the gastrointestinal tract

Sexual dysfunction

38
Q

Hyperosmolar Hyperglycemic Syndrome (HHS)

A

Only seen in type 2

Characterized by severe hyperglycemia (>600), hyperosmolality, and dehydration caused by insulin resistance

At same time, the cells are not absorbing glucose

Sets up the same hyperosmolarity as in DKA.

ECF increases and there is intracellular dehydration
Because there is some insulin there is
NO KETONE formation

Causes: Infection, non-compliance with diet or medications, undiagnosed, substance abuse, alcohol, etc.

Symptoms: extreme glucose level, rapid/thread pulse, hypotension, profound dehydration, polydipsia, polyuria, confusion, disorientation, possible seizure, or coma

Treatment:
Hydration (given first)
IV insulin- rehydrate the cells (GIVE before INSULIN)
Electrolyte replacement (Potassium, Intercellular)

39
Q

Why is it necessary for a person to maintain blood glucose no lower than 70?

A

To improve insulin secretion

To allow beta cells to have periods of rest

To maintain a continuous supply of glucose for energy

To avoid too much glucagon from being broken down in the liver

40
Q

Glucagon

A

Hormone secreted by alpha cells
Causes liver to breakdown stored glycogen
Activates gluconeogensis

PHARMA (13 decks)

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