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Pharmacology 1 > Exam 1-Midterm > Flashcards

Exam 1-Midterm Flashcards

1
Q

Insulin Administration via SubQ injections

A

Syringe size: 0.3-1mL
Needle Gauge: 25-31
Needle length 3/16- 5/8
Insertion Site: Upper arm, anterior or lateral portion of thigh, buttock and abdomen

Angle of insertion: 45-90*
Method: Pinch an Inch

Volume 0.5-1 mL

Concentrations of units/mL

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2
Q

Short duration Rapid Acting Insulins

A 
Insulin Lispro (Humalog)
Insulin Aspart  (Novalog)
Insulin Glulisine (Apidra)
(best given with food, so you don’t bottom out or elevated bgc; breakfast, lunch, dinner)
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3
Q

Short Duration Slower Acting

A 
Regular insulin ( Humulin R, Noluin R)
(provides more a long-term relief for bgc levels that tend to rise up; usually used between doses of rapid acting to maintain)
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4
Q

Intermediate duration

A 
NPH insulin ( Humalin N, Novulin N)
¬	(lasts longer, a pt. may only require a shot in the AM and PM, allows tailoring for specific pt. needs) Can be mixed with all above; NPH is the only one that can be mixed with short acting insulins

Regular drawn up first into the same syringe, then short durations

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5
Q

Long duration

A 
Insulin Glargine (Lantus)
Insulin Detemir ( Levemir)

(steady; attempt to do 1 injection a day)

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6
Q

Insulin Lispro

A

AKA: Humalog
Short duration rapid acting insulin

  • SQ 15 min before or just after meals
  • SQ cont infusion with bolus just before meals

Onset: 15-30 min
Peak: 30 min-2.5 hr
Duration: 3-6 hrs

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7
Q

Insulin Aspart (Novalog)

A

AKA: Novalog

  • SQ 5-10 minutes before meals
  • SQ infusion cont with bolus 5-10 min before meals
  • Approved IV but rarely used

Onset: 10-20 min
Peak: 1-3 hr
Duration: 3-5 hrs

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8
Q

Insulin Glulisine

A

AKA: Apidra

  • SQ within 15 min before or within 20 min after meals
  • Approved IV but rarely used

Onset: 10-15 min
Peak: 1-1.5 hr
Duration: 3-5 hrs

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9
Q

Regular insulin

A

AKA: Humulin R, Noluin R

  • SQ 30 min before or after meals
  • SQ infusion cont with bolus 20-30 min before meals
  • IV for emergencies
  • IM approved but rarely used

Onset: 30-60 min
Peak: 1-5 hr
Duration: 6-10 hrs

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10
Q

NPH insulin

A

Humalin N, Novulin N

*SQ twice daily at the same time each day: gently agitate before use

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11
Q

Insulin glargine

A

AKA: Lantus

*SQ once daily at the same time each day

Onset: 70 min
Peak: None
Duration: 18-24 hrs

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12
Q

Insulin detemir

A

AKA: Levemir

*SQ twice daily or once daily

Onset: 60-120 min
Peak: 12-24
Duration: varies

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13
Q

Diabetes Mellitus

A

Disorder of carbohydrate metabolism

Deficiency of insulin (Type I) (destruction of pancreatic beta cells = no insulin created)

Resistance to action of insulin (Type II) (impaired insulin secretion)

S/S : Sustained hyperglycemia polyuria (increased urine), polydipsia (increased thirst), polyphagia( increased hunger), ketonuria, and weight loss

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14
Q

Type I DM

A

o Destruction of pancreatic beta cells
o Decreased insulin levels early in disease which eventually fall to zero
o Risk for ketoacidosis

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15
Q

Type II DM

A

o Insulin resistance
o Impaired insulin secretion
o Over time hyperglycemia leads to reduced beta cell function
o Little risk of ketoacidosis

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16
Q

Short-term complications

A

hyper and hypo glycemia

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17
Q

Long-term Complications

A

Macrovascular Damage

  • Heart disease
  • Hypertension
  • Stroke

Microvascular Damage

  • Retinopathy
  • Nephropathy
  • Neuropathy
  • Gastroparesis ( delayed gastric emptying)
  • Amputations
  • Erectile dysfunction
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18
Q

Diagnosis of DM

A

Excessive plasma glucose is diagnostic of diabetes.;Patient must be tested on two separate days, and both tests must be positive.

Three test:

  1. Fasting Plasma glucose > 126
  2. Casual plasma glucose >200 + sxs of diabetes
  3. oral gluocse tolerance test (OGTT) - 2 hr plasma glucose >200
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19
Q

Hemoglobin A1c

A

Monitors longterm glycemic control
determines average blood glucose levels over a period of 2-3 months
- value of 6.5% or higher is considered diagnostic for DM

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20
Q

Treatment

A

Primary goal for both Type 1 and Type 2 is prevention of complications
Maintaining glycemic control
70-130 before meals
and target level of <7% (equivalent to an estimated average blood glucose of 154mg/dL or less)

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21
Q

Type 1 treatment

A

Diet
Exercise
insulin replacement
monitoring treatment ( self monitoring blood glucose levels)

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22
Q

Type II treatment

A

diet
exercise
glycemic control
monitoring treatment

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23
Q

Insulin

A

Two types of insulin

  • Natural (Regular)
  • modified (changed slightly from what our natural insulin does, works faster)
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24
Q

SubQ injection types

A
  • Syringe and needle
  • Pen injectors
  • Jet injectors
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25
Q

SubQ infusions

A

portable or implantable insulin pumps

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26
Q

Storage of insulin

A
  • Unopened vials should be stored in the refrigerator
  • Open vials in use can be stored up to one month without significant loss of activity – check institutional policy
  • Time and date the vial when opened

If a vial is open and not labeled, DISCARD, DO NOT USE

Pre-filled syringes should be stored in refrigerator /needle up
-Agitate gently prior to administration to re-suspend the insulin

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27
Q

Tight Glucose control

A

Act of maintaining glucose levels in normal range
-benefits: prevent longterm complications
drawbacks- takes a long time to figure out because there are so many factors at play in order to balance glucose control ( diet, exercise, etc)

28
Q

Dosage

A

Total Daily Dosages may range from 0.1 units/kg of body weight to more than 2.5 units/kg of body weight

29
Q

What might cause the need for increased Insulin use in DM

A
  • increased caloric intake
  • infection
  • obesity
  • stress
  • adolescent growth spurt
  • pregnancy AFTER 1st Trimester
30
Q

What might cause the need for decreased Insulin use in DM

A
  • decreased caloric intake or a missed meal
  • increased levels of physical activity
  • 1st trimester of pregnancy
31
Q

What is needed to maintain tight contorl

A
  • attention to entire treatment program
  • defined glycemic target
  • motivation
  • extensive education
32
Q

Hypoglycemia

A

Causes:

  • missed meals
  • exercise after ingestion
  • lack of tight control
S/S:
#1 TACHYCARDIA
shakes
weakness/fatigue
body sweats
irritability

Drug interactions:
o Hyperglycemic agents
o Hypoglycemic agents
o Beta-Adrenergic Blocking Agents (decrease heart rates, often hide the first signs of hypoglycemia)

33
Q

Biguanides (GLUCOSE SUPPRESSANTS)

A

( First line of fire for a type II diabetic- nearly always)
METFORMIN

Drug Choice for initial therapy

  • Started immediately upon diagnosis
  • Used alone or in combination

Mechanism of Action

  • Inhibits glucose production in liver
  • Slightly reduces glucose absorption in GI tract
  • Sensitizes insulin receptors in target tissues (increases the cells ability to take in glucose whenever insulin is present)
  • Does not stimulate release of insulin form the pancreas so it does not drive BG levels down

Pharmacokinetics

  • Absorbed from small intestine
  • Excreted unchanged by the kidneys

Side Effects

  • Decreased appetite
  • Nausea
  • Diarrhea
  • Decreased B12 and folic acid deficiency

Toxicity
-Lactic Acidosis

Drug Interactions
-Alcohol
-Metformin and IV dye (contrast) together cause nephrotoxity
48 hours after/before metformin- you can have dye

34
Q

Sulfonylureas (Insulin secretory agents)

A

Second Generation

  • **Glipizide (Glucotrol)****
  • Glyburide (DiaBeta, Micornase)
  • Glimepiride (amaryl)

Mechanism of Action

  • Stimulate release of insulin from pancreatic islets
  • Insulin release is glucose dependent

Therapeutic Use

  • Type II
  • Can be combined with other hypoglycemic drugs

Pharmocokinetics

  • Hepatic metabolism
  • Renal excretion

Side Effects

  • Excessive lowering of blood glucose
  • CV toxicity

Drug-Drug Interactions

  • Alcohol
  • Beta blockers
  • Other hypoglycemic agents
35
Q

Meglitinides (Glinides) ( insulin secretory agent)

A

**Repaglinide [Prandin]***
Nateglinide [Starlix]

Mechanism of Action
-Promotes insulin release

Pharmocokinetics

  • Hepatic metabolism
  • Billiary excretion

Side Effects
-Hypoglycemia

**Administered with meals

36
Q

Thiazolidinediones (Glitazones) (Insulin sensitizers)

A

makes insulin more effective- does not create insulin but makes it more potent

Rosiglitazone [Avandia]
Pioglitazone [Actos]

Mechanism of Action
-Decrease insulin resistance

Administration
-With or without meals

Adverse effects

  • Fluid retention
  • Elevation of lipid levels
37
Q

Combination Oral products for Type II

A
  • Glyburide/metformin
  • Glipizide/metformin
  • Rosiglitazone/metformin
38
Q

Diabetic Ketoacidosis

A

Manifestation of Insulin deficiency

Give regular IV insulin

Altered glucose metabolism

  • Hyperglycemia
  • Water loss
  • Hemoconcentration

Altered fat metabolism
-Ketoacids

Ultimately leads to…

  • Acidosis
  • Coma
  • Death

Treatment

  • Correct hyperglycemia and acidosis
  • Insulin replacement
  • IVFs
  • Start with .9 NSS (8-10 liters)
  • Potassium replacement
  • Monitor K+ and replace as needed
  • IV replacement
  • Bicarbonate
  • May be needed for acidosis
  • Most of the time when you correct the fluids and hyperglycemia you will correct the acidosis without needing bicarbonate
39
Q

Hypoglycemic Patient

A

Causes

  • Insulin levels exceed insulin needs
  • Overdose of insulin
  • Reduced food intake,
  • Vomiting
  • Diarrhea
  • Excessive alcohol consumption
  • Intense exercise
  • Childbirth

What does it look like…

  • If glucose levels fall rapidly, activation of SNS
  • Tachycardia
  • Palpitations
  • Sweating
  • Nervousness

If glucose levels fall gradually then symptoms are CNS in origin

  • HA
  • Confusion
  • Drowsiness
  • Fatigue
  • If hypoglycemia persists risk irreversible brain damage
  • Severe hypoglycemia can lead to coma, convulsions, and death
40
Q

What does Rapid Treatment Look like

A

If pt is conscious

  • Fast acting oral sugars
  • Glucose tablets, OJ, sugar cubes, non-diet soda

If unconscious…

  • IV glucose – immediate action
  • Parenteral glucagon
41
Q

Glucagon

A
  • Hormone produced by alpha cells of the pancreas
  • Breaks down glycogen stores
  • Opposite effects of insulin
  • Used in emergencies if IV glucose cannot be given
  • In unconscious patient, produces arousal in 20 minutes
  • Cannot correct hypoglycemia due to starvation
  • Given IV, SQ, or IM
42
Q

Diuretics

A

Increase the output of urine (creating a byproduct)

Therapeutic Uses

  • Hypertension (reduce fluid volume)
  • Mobilization of fluid:
    - Heart failure
    - Cirrhosis (ascites)
    - Kidney disease (create urine)
  • Prevent renal failure
  • different classes of Diuretics, work on different parts of the nephron*
43
Q

Basic Anatomy of the Kidney

A

Basic functional unit: Nephron

  • Glomerulus
  • Proximal convoluted tubule
  • Loop of Henle
  • Distal convoluted tubule
  • Collecting ducts
44
Q

Function of the kidney

A
  • Cleansing of ECF and maintenance of ECF volume and composition
  • maintain acid-base balance
  • excretion of metabolic wastes and foreign substances
45
Q

Renal Process

A

filtration
reabsorption
active secretion

46
Q

Filtration

A

All small molecules in plasma are filtered

Most prevalent: Sodium and chloride ions
Others :Bicarbonate and potassium ions

Large molecules (lipids & proteins) stay in the blood

47
Q

Reabsorption

A

** the mechanism that diuretics mess with the most***

  • > 99% of water, electrolytes, nutrients are reabsorbed
    - Sodium (Na++) and Chloride (Cl-) are the predominant solutes
  • Occurs through active transport
  • Water follows passively due to osmotic gradient
  • Amount of reabsorption varies along site on the nephron
  • Most diuretics act by interfering with reabsorption
48
Q

Active Tubular Secretion

A
  • “Pumps” in the kidney transport compounds from plasma to the nephron
  • This action causes excretion of metabolic wastes, drugs, toxins
49
Q

Sodium- Potassium Exchange

A

-Aldosterone stimulates reabsorption of sodium from distal nephron and causes potassium to be secreted
o This is viewed as an exchange mechanism

-Aldosterone stimulates cells of the distal nephron to synthesize more of the pumps responsible for sodium potassium exchange

50
Q

How do Diuretics work

A

Cause a blockade of sodium ad chorlide reabsorption

-creates osmotic pressure that PREVENTS passive water reabsorption

51
Q

What are the 4 Types of Diuretics?

A
  1. high-ceiling( loop diuretics) MOST COMMON, most potent, acts on loop of henley
  2. Thiazide diuretics
  3. Osmotic diuretics
  4. Potassium-sparing agents ( 1. aldoseterone antagonists: block sodium reabsorption; 2. non-aldosterone antagonists)
52
Q

High-ceiling ( Loop Diuretics)

A

Site of action: Loop of Henle
o AKA: loop diuretics

The MOST effective diuretics available

  • Most frequently prescribed diuretic
  • Produce more loss of fluid and electrolytes
  • Prototype: Furosemide (Lasix)
53
Q

Furosemide (LASIX)

A

Mechanism of Action
-Blocks reabsorption of sodium and chloride

Administration

  • PO, IV, IM
  • PO administration: works in 60 min, lasts for 8 hours
  • IV administration: works in 5 min, lasts for 2 hours (push over 3-5 minutes)

Pharmacokinetics

  • Metabolized in the liver
  • Renal excretion

Therapeutic Uses

  • Pulmonary edema (fluid on the lungs)
  • CHF
  • Edema of hepatic, cardiac or renal origin not relieved by other less efficacious diuretics
  • HTN not relieved by other less efficacious diuretics
  • Severe renal impairment
  • *Can be used if GFR is low or oliguria
  • Can add thiazide to treatment if treatment alone is not sufficient

Adverse Effects
Hypokalemia :
-Monitor K+ esp. pre-administration Report CRITICAL values STAT, hold if needed
-Educate on diet (increase: dried fruits, nuts, spinach, citrus fruits, potatoes, bananas)
-Ensure potassium supplements when needed

Hyponatremia, Hypochloremia, Severe Dehydration
S/S of dehydration
-Dry mouth, unusual thirst, oliguria,

CONCERNS

  • Development of thrombosis & embolism (S/S: HA, pain in chest, calves, or pelvis)
  • Intervention
  • Monitor for above S/S & notify HCP if occurs, daily weights, monitor labs, I/O
Hypotension
-Loss of volume
-Reduced venous return to heart
S/S:
-Dizziness, lightheadedness, syncope

CONCERNS

  • Risk for injury
  • Intervention
  • Orthostatic hypotension precautions, monitor BP, orthostatic BP PRN, take BP prior to administration look at trends

Ototoxicity

  • Transient (temporary) hearing loss with Lasix
  • Other loop diuretics can cause irreversible hearing loss

Interventions
-Use with caution if given with other ototoxic drugs like aminoglycoside antibiotics (eg. Gentamycin)

Hyperglycemia (uncommon)
-Monitor glucose levels closely in diabetic patients

Hyperuricemia (frequent)
-Monitor for gout flares (tenderness, pain, swelling of joints)

*not all diuretics will work on kidneys if they’re not functioning well already, UNLIKE Furosemide!

Drug Interactions

  • Digoxin (Lanoxin)
  • Monitor K+ levels carefully
  • Monitor digoxin levels
  • Ototoxic drugs
  • Increased risk of furosemide induced hearing loss if used concurrently
  • Potassium Sparing diuretics
  • Reduce risk of hypokalemia
54
Q

Thiazide Diuretics

A

The thiazides comprise the largest group of diuretics.
They are related structurally to the antibacterial sulfonamides.
Similar to loop but…
oThe ability to cause diuresis is dependent on adequate kidney function
Mechanism of Action
-Increase renal excretion of Na+, K+, water, CL-
-Promote reabsorption of CA+
-Increase glucose and uric acid levels

55
Q

Hydrochlorothiazide (HCTZ)

A

A weak diuretic effect, because most of the sodium is reabsorbed before the distal tubule
-Ability of thiazides promoting diuresis depends on ADEQUATE kidney function
o Thiazides need high GFR to work
o Not effective in renal impairment

Therapeutic Uses
¬ Primary use: first choice for essential HTN
¬ Preferred drug for mild to moderate heart failure
o Cardio protective properties
¬ Edema
o heart failure, hepatic or renal disease
¬ Diabetes insipidus
o Paradoxical effect to reduce the overproduction of urine by 30% to 50%
¬ Protection ag. Postmenopausal osteoporosis

Adverse Effects

  • Moderate hyponatremia, hypochloremia, and dehydration
  • Hypokalemia
  • Hyperglycemia
  • Hyperuricemia (joint pain)

Drug Interactions

  • Digoxin (toxicity d/t hypokalemia)
  • Other antihypertensive drugs
  • NSAIDS can limit thiazide effects
  • MAY give with other ototoxic drugs
56
Q

Potassium-sparing Diuretics

A

works best with other diuretics; given primarily to reduce risk of hypokalemia

Produce a modest increase in urine production (maybe 10ml/hr- Veryyyy little)
-Rarely used alone to promote diuresis

2 categories:
o Aldosterone antagonists
-Spironolactone (Aldactone)
o Non-aldosterone antagonists
-triamterene (Dyrenium)

57
Q

Aldosterone Antagonist: spironalctone (Aldactone)

A

spironalctone (Aldactone)

Mechanism of Action
¬	Blocks aldosterone causing:
o	Sodium excretion
o	Potassium retention
¬	Scanty diuresis, most fluid filtered prior to site of action
¬	Delayed effect: up to 48 hours

Therapeutic Uses

  • HTN and edema
  • Most commonly used in combination with thiazide or loop diuretic
  • Main purpose: to counteract the potassium-depleting effects of the more powerful diuretics
  • Heart failure
  • Reduces mortality & hospital admissions
  • Protective benefits on heart & blood vessels

Adverse Effects

  • Hyperkalemia
  • Endocrine effects
  • Gynecomastia, menstrual irregularities, impotence, hirsuitism, deepening of the voice
Drug Interactions
D/T hyperkalemia risk use with caution:
-Angiotensin-converting enzyme (ACE) inhibitors
-Angiotensin receptor blockers (ARBS)
-Direct renin blockers
58
Q

Non-aldosterone Antagonist: triamterene (Dyrenium)

A 
Direct inhibitor of the sodium-potassium pump causing:
o	Sodium excretion
o	Potassium retention
 Acts quicker than spironolactone
o	Works in hours v. days
¬	Scant diuresis
Therapeutic Uses
•	HTN and edema
•	Adverse effects
•	Hyperkalemia
•	Nausea, vomiting, leg cramps. Dizziness
59
Q

Osmotic Diuretic: mannitol (Osmitrol)

A

ONLY osmotic diuretic in use in US
• IV administration only
• Filtered by glomerulus
• Has minimal reabsorption causes passive reabsorption of water
• Degree of diuresis directly related to concentration of drug

Effects start 30-60 min lasts 6-8 hours

Therapeutic Uses:
•	Prophylaxis of renal failure
•	Reduction of intracranial pressure
•	Adverse effects:
•	Edema
•	Use extreme caution with CHF and Pulmonary edema
60
Q

Key points for EXAM (diuretics)

A 
¥	Vital signs
¥	Intake and output
¥	Daily weights
¥	Monitor for dehydration
¥	Orthostatic hypotension
¥	Monitor for drug interactions
¥	Slow IV push
61
Q

Discharge teaching ( diuretics)

A
  • Take in the am (no later than 4pm)
  • Daily weights
  • s/s of dehydration
  • Managing orthostatic changes
  • Diet
62
Q

IV therapy

A

Fluid Replacement

- isotonic
- hypotonic	
- hypertonic (rarely ever given)
63
Q

Potassium Replacement

A

Potassium salts

  • **Potassium chloride PO or IV
  • Potassium phosphate IV
  • Potassium bicarbonate IV
64
Q

IV Potassium for Hypokalemia

A

Primarily KCL

  • Used for severe hypokalemia or NPO patients
  • NEVER IV PUSH = DEATH
  • Use IV pump
  • Infuse slowly
  • No faster than 10 mEq/hr
  • telemetry monitoring check policy
  • Causes vein irritation
  • Must be diluted
65
Q

PO Potassium Replacement

A

-KCL
K-Dur (PO form)
-Sustained-release tablets preferred
-Klor-con, Micro-K

Adverse Effects

  • GI irritation, N/V/D
  • Take with meals or full glass water
66
Q

Regulation of Potassium Levels

A

Hyperkalemia Treatment
Mild or moderate: Kayexalate PO or PR (makes you have severe diarrhea)
-Absorbs potassium

Severe: Dextrose and Insulin IV

If acidosis present:
-Sodium bicarbonate infusion

Calcium gluconate IV
-Offset effects on heart

Dialysis

67
Q

Magnesium Replacement

A

Magnesium hydroxide

  • Tablets
  • Liquid (MOM) milk of magnesia

Severe

  • IV Magnesium sulfate
  • AVOID with pts that have AV heart block

Adverse effects:

  • Excessive amts: neuromuscular blockade
  • Have calcium gluconate ready as antidote

Pharmacology 1 (4 decks)

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