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Pharmacology 1 > Test 4 > Flashcards

Test 4 Flashcards

1
Q

Type 1- (IDDM, juvenile diabetes).

A

Auto immune process that destroys insulin producing cells in the pancreas.

–Insulin dependent diabetes

5 - 10% of the diabetes population

usually happens in the first 1-2 decades of life

these people are thin and fragile

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2
Q

Type 2 (NIDDM, adult onset diabetes)-

A

Non autoimmune, lifelong progression.

Non insulin dependant diabetes.

Very strong genetic predisposition.

begins typically in the 5th or 6th decade of life and is a mix of insulin deficiency and insulin resistance.

when first diagnosed you will have approximately 50% of your beta islet cells left. and over time you will continue to lose these cells

you will eventually need insulin.

these people are fat

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3
Q

Latent Auto immune Diabetes of Adulthood (Diabetes 1 and ½- LADA)

A

Typically manifests between 3rd and 4th decade of life-

Looks more like type 1 diabetes- very thin- they need insulin very quickly.

is autoimmune, so attacks the beta islet cells

oral therapy helps at first, but usually have to go to insulin very quickly (within about a year)

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4
Q

Pre-Diabetes-

A

IGT (OGTT with 2 hr. PP at 140-199 mg/dl) and/or IFG (FPG b/w 100 and 125).

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5
Q

Gestational Diabetes-

A

Diabetes during pregnancy usually subsides after delivery. They are at greater risk for type 2 diabetes.

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6
Q

True or false

Being diabetic, you are 4-5 times more likely to have a heart attack and microvascular complications

A

true

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7
Q

Name three short term complications of diabetes.

A
  1. Hyperglycemia
  2. Hypoglycemia
  3. Ketoacidosis- potentially fatal
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8
Q

Name some Hyperglycemia symptoms

A 
polyuria
polydypsia
sluggish/sleepy
polyphagia
blink a lot
weight loss
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9
Q

polyphagia

A

increased hunger

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10
Q

polydypsia

A

increased thirst

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11
Q

Diabetes control and complications trial (DCCT)-

A

Type 1 diabetic population.

one group kept 9% on A1C and sugars less than 200 (less controlled)

other group kept 70-100 blood sugars and 7% A1C (tightly controlled)

results were:

were able to substantially reduce microvascular complications, but were NOT able to reduce heart attacks or strokes.

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12
Q

UKPDS

A

type 2 population- loosely controlled( A1C 7.9%) and tightly controlled A1C 7%. Cannot reduce the risks of macrovascular (heart attacks and strokes)

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13
Q

Macrovascular disease-

A

large vessel disease. Causes heart attacks and strokes.

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14
Q

Microvascular disease-

A

damage to small vessels and capillaries.

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15
Q

Retinopathy-

A

1 cause of blindness in our country

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16
Q

Nephropathy

A

Compromised filtration of the kidneys.

start spilling protein into the urine.

Earliest indication of kidney damage b/c albumin/ protein is too large to fit in the filtration system.

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17
Q

Neuropathy-

A

Blood supply to the nerves is damaged.

leads to very painful nerve pain. Usually starts in distal appendages like the feet.

Sheets will hurt their feet and toes so they will sleep without covers over their feet

Do diabetic foot exams and vibration test

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18
Q

Autonomic Dysfunction-

A

injury to autonomic nerves that control GI motility and baroreceptor reflex.

Makes your food move through you more slowly (gasteroporesis)

pts become orthostatic, erectile dysfunction, tachycardia, bradycardia, cant sweat well

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19
Q

Amputations-

A

Diabetes is responsible for 50% of lower limb amputations in America

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20
Q

impotence-

A

Diabetes causes blood vessel injury and nerve damage to their sexy time organs

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21
Q

immune dysfunction-

A

sick often and wounds wont heal

Blood glucose increases when sick and 180-200 begins not to be able to fight infections

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22
Q

OSA- Obstructive Sleep Apnea-

A

Occurs Especially with type 2 diabetics.

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23
Q

Random plasma glucose more >______ mg/dl (with symptoms)- thirsty, polyuria is used to diagnose diabetes.

A

200

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24
Q

Another diagnostic tool is a FPG level > or = _______mg/dl (repeat on separate day)

A

126

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25
Q

2 hour OGTT> __________ mg/dl (repeat on separate day) Pregnant women have to do this

A

200

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26
Q

Hemoglobin A1C- _______% or greater is diagnostic

A

6.5%

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27
Q

Name some Risk factors type 2 diabetes.

A

1st degree relative with type 2 dm

Obesity (BMI > or = to 27

African American, Hispanic American, Native American, Asian, Pacific Islander

Age 45 or greater

History of IFG or IGT (Impaired fasting glucose, or Impaired glucose tolerance)

HTN

HDL-C < or equal to 35 mg/dl and/or TGs > or equal to 250 mg/dl

History of delivering a baby over 9 lbs or having gestational DM

OSA (obstructive sleep apnea)

HX of gestational diabetes

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28
Q

True or False

The lower a patients A1C, the less likely they will experience a hypoglycemic event?

A

FALSE

the lower the A1C, the MORE likely they are to experience a hypoglycemic event

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29
Q

Treatment targets

A

A1C < 7%

Fasting 70-100

2 hours after a meal= < 100

< 130/80 BP JNC guideline s

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30
Q

Self monitoring of blood glucose (SMBG)

IDDM- ___________ x per day-

A

A lot

frequent monitoring by pt on insulin correlates with success

Knowing sugar trend keeps them from going low.

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31
Q

Self monitoring of blood glucose (SMBG)

NIDDM ________x per day (controversial)

A

not a lot

no correlation between frequent monitoring and sucess

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32
Q

Urine Glucose Monitoring-

A

Dip stick in urine, depending on how much sugar is in urine- not used much at all- obsolete

Albumin to creatinine ratio <30

if greater than 30 indicates positive for microalbuminurea

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33
Q

Glycosylated Hemoglobin (HBA1)

A

glucose control over last 2-3 months (report card) Avg of glucoses over 2-3 mo.

Goal 7%

Best test for DM- AVG BG for 120 days. If its elevated- that’s bad! Long term elevation is what we worry about.

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34
Q

Hemoglobin is glycosylated in presence of glucose. RBCs have life span of aprox ______ days

A

120

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35
Q

Frucosamine-

A

glycosylation of albumin gives indication of BG over 1 month. Good test for end stage renal disease pts. – no erythropoeiten, low rbcs, sickle cell, hem A1C not accurate for these.

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36
Q

Insulin (anabolic hormone) builds _______.

A

Muscle. Therefore it can be an abused substance

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37
Q

Insulin is produced by ________

A

beta islet cells of pancreas

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38
Q

What are the anabolic effects of insulin?

A

insulin facilitates glucose uptake- inhibits glycogenolysis, and glucogenesis

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39
Q

Glycogenolysis

A

is the breakdown of glycogen to glucose

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40
Q

Glycogenesis

A

is the process of glycogen synthesis, in which glucose molecules are added to chains of glycogen for storage.

This process is activated during rest periods following the Cori cycle, in the liver,

and also activated by insulin in response to high glucose levels, for example after a carbohydrate-containing meal.

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41
Q

What are the Catabolic Effects of insulin?

A

body breaks down itself to make more sugar = insulin deficient

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42
Q

Rapid Acting NOVALOG- (Aspart)

A

Shorter acting insulin- take right before you eat!

Administration- bolus insulin,( fast acting, in and out quickly)

Purpose Prandial or bolus insulin always used in combo with basal to match carbohydrate intake

Continuous infusion for basal and bolus for prandial in PUMPS.

Also used for sliding scale

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43
Q

Regular Insulin

A

SLOWER ACTING- clear

Regular-clear insulin- short duration, can be given iv, available in U-100 or U500

Route- sc, or IV, inhaled (EXUBERA) no longer available

Purpose- prandial insulin

Timing of injections: works 30-40 min before you eat

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44
Q

NPH (HUMULIN)-

A

INTERMEDIATE ACTING- cloudy

protamine suspension (mixed with regular) . Protamine retards absorbtion of RHI-> delays onset of action- makes insulin last longer

Onset 1-2 hrs

*******Peak- 8-10 hrs- give 2x a day

Purpose: basal insulin with some prandial properties at peak. Typically dosed BID.

Appearance- cloudy

Mixing- Dose at breakfast and at bedtime, clear before cloudy, roll it in your hands to agitate it.

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45
Q

What is the peak of NPH (Humulin)

A

8-10 hours

Dose at breakfast and at bedtime, clear before cloudy, roll it in your hands to agitate it.

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46
Q

Insulin Detmir (LEVIMIR)

A

INTERMEDIATE ACTING

dose dependant pharmacodynamics- tweener- between NPH and Lantus.

Once or 2 x a day.

Basal insulin- Cant mix with other insulins.

Peak 18 hrs

Purpose basal insulin

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47
Q

Insulin Glargine

A

LONG DURATION insulin

long acting, no peak, dosed at bedtime, 24 hr coverage,

clear like reg insulin

Purpose basal insulin (Peakless)

Inject only SC

DO NOT mix with other insulins

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48
Q

Name a rapid acting insulin

A

Novalog (Aspart)

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49
Q

Name a Slower acting shorter duration insulin

A

Regular Insulin

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50
Q

Name a Intermediate Acting Insulin

A

NPH Humalin

or

Insulin Detemir Levimir

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51
Q

Name a long acting Insulin

A

Insulin Glargine

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52
Q

When do you give 70/30 insulin

A

before breakfast and before supper

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53
Q

Where do you administer insulin

A

Site- Abdomen- central to core, bloodflow, less pain, more surface area, easily accessible

54
Q

How do you mix insulin

A

Mixing- pull up REGULAR/ NOVALOG first, 70/30 vs 70/25 vs 50/50 fixed combos

55
Q

How is insulin stored

A

storge- unopened in fridge, do not freeze, Vial in use can be stored at room temp for 28 days

56
Q

How can insulin be delivered

A

Delivery- jet/pen injectors, pumps, syringes

pumps- delivers basal and bolus. Sets must be changed Q 3 days

57
Q

Intensive Conventional therapy

A

QID dosing, dosing is adjusted based on preprandial SMBG measurements. Uses Rapid acting + insulin glargine

58
Q

Continuous SC insulin

A

similar to ICT except with a pump

59
Q

Dosage ranges from ________ unit/Kg/d and up

A

0.1 unit

60
Q

Tight control vs loose control-

A

DCCT and UKPDS

Does not reduce heart attacks and strokes but does reduce microvascular complications

61
Q

What are the signs and symptoms of stage 1 hypoglycemia

A

Same symptoms as fight or flight-

I –stage 1- body- tachycardia, sweat, nervous, shaking, visual changes

Alpha 1 comes out, sympathetic… when older pts don’t notice or feel it as much.

62
Q

What are the signs and symptoms of stage 2 hypoglycemia

A

ii-stage 2- cognition-confusion-AMS, dnt make sense, alert family if pt says something that doesn’t make sense.

63
Q

What are the signs and symptoms of stage 3 hypoglycemia

A

Iii- stage 3 coma, death, SZ- medical emergency

64
Q

What are Sulfonylureas and how do they work

A

1st oral agents

A1c reduction-large 1-2%- cost effective

MOA-stimulates beta islet cells to release insulin

Therapeutic use- type 2 diabetics only- bc type 1 diabetics don’t have islet cells

65
Q

Name the 2nd generation sulfonylureas

A

Glypizide/glyburide/glimepiride

66
Q

What are the side effects and cautions that pertain to sulfonylureas

A

ADE-hypoglycemia. Caution is severe sulfa allergy

Do not take if you have a sulfa allergy

Anything that works through insulin pathway can cause hypoglycemia

Pregnancy-avoid- teratogenic in animals- Avoid if breastfeeding as well

67
Q

What is the treatment for hypoglycemia? (rule of 15)

A

Treatment of hypoglycemia: rapid form of glucose vs glucogon.

Rule of 15 if hypoglycemic- eat 15 carbs and in 15 min recheck. If above 70, youre good to go, if not repeat.

68
Q

Name the two short acting sulfonylureas

A

Nateglinide (STARLIX)

Repaglinide (Prandin)

69
Q

MOA of

Nateglinide (STARLIX)

Repaglinide (Prandin)

A

MOA Stimulates beta islet cells of the pancreas to release insulin

Dosing: prior to each meal

Adverse effects: hypoglycemia, wt gain

70
Q

Metformin (Glucophage) MOA

A

is a BIguanides- approved in 1994

MOA Decreases production of glucose in the liver and enhances utilization by the muscle

DOES NOT CAUSE HYPOGLYCEMIA

A1C reduction- 1-2%

Place in therapy- now considered drug of choice for initial use. Also has a role in pre-diabetes

***Diabetes Prevention Program: all pre-diabetics received either intensive lifestyle changes or metformin therapy or placebo

71
Q

Metformin (Glucophage) ADE

A

Adverse drug effects: GI issues- diarrhea

Lactic Acidosis. (inhibit the mitochondrial oxidation of lactic acid and could lead to lactic acid buildup). Very rare. 3 cases in 100,000 pts a year. 50% mortality rate. Caution in pts with compromised RFx and pts at greater risk for lactic acidosis. Radiographic dye study done 1-2 days prior

(happens when metformin is renally eliminated of serum creat 1.4 or greater for females or 1.5 for males- you may no longer use it

72
Q

Pre-diabetics= 100-_____ fasting BG

A

126

73
Q

MOA of Glitazones

A

–activating the peroxisome proliferator-activated receptor gamma (PPAR-gamma)

PPAR-gamma improves insulin resistance

So Glitazones decrease insulin resistance

74
Q

NAME THE Glitazones

A

TROGLITAZONE (removed from market),

PIOGLITAZONE (ACTOS),

ROSIGLITAZONE (AVANDIA)

75
Q

ADE of Glitazones

A

Fluid retention

Raises plasma lipid levels

Liver toxicity

76
Q

** ACARBOSE (PRECOSE) and miglitol (Glyset) are __________.

A

Alpha Glucosidase Inhibitors- Delays absorbtion of complex carbs

77
Q

What is the MOA of ** ACARBOSE (PRECOSE) and miglitol (Glyset)

(Alpha Glucosidase Inhibitors-)

A

MOA complex carbs have to be reduced to monosaccharides ay alpha-glucosidase (enzyme located in the brush border of sm. Intestine). These drugs inhibit this enzyme.

A1C reduction ½ %

PK: minimally absorbed- stays in GI tract- if not absorbed, it goes to bowel and bacteria breaks it down

78
Q

ADE of ** ACARBOSE (PRECOSE) and miglitol (Glyset)

Alpha Glucosidase Inhibitors-

A

ADE: substancial GI flatulence, cramps, abd distention, borborygmi, diarrhea, rare liver toxicity.

Hypoglycemia- you need glu tablets, sandwich wont work fast and will delay the absorbtion

GI tract issues minimized after time

79
Q

PRAMLINITIDE (SYMLIN) MOA

A

New class of drugs (amylin mimetics) used to complement the effects of insulin

Amylin- hormone produced by pancreas, used in conjunction w/ insulin, released in conjunction w/ insulin- slows digestive tract

MOA decreases post plandial glucose- delays gastric emptying

80
Q

Therapeutic usage of PRAMLINITIDE (SYMLIN)

A

Therapeutic usage- injected along with prandial insulin (type 1 and 2)- cant be mixed

A1C reduction- 50%

If you get 3 novalog injections youll need 3 symlin injections= 6 injections daily

81
Q

ADE of PRAMLINITIDE (SYMLIN)

A

Side effects decrease

hypoglycemia

nausea

82
Q

EXENATIDE (BYETTA) AND SITAGLIPTAN (Januvia) are ____________.

A

Incretin mimetic agents-

83
Q

MoA of EXENATIDE (BYETTA) AND SITAGLIPTAN (Januvia)

Incretin mimetic agents-

A

GLP-1is a peptide hormone that’s released from the cells of the GI tract in response to carb containing meal. GLP-1 slows gastric emptying, stimulates beta islet cells to release insulin, inhibits glucogon release, and increases satiety.

Exenatide is a synthetic GLP-1 and sitgliptan blocks the enzyme responsible for breaking down endogenous GLP-1

A1C reduction 0.8%

84
Q

ADE of EXENATIDE (BYETTA) AND SITAGLIPTAN (Januvia)

Incretin mimetic agents-

A

Adverse effects GI (nausea, vomiting) especially with exenatide- weight neutral

85
Q

DKA- Diabetic Ketoacidosis

A

dehydrated sugar high inter vascularity

Pathogenesis- Altered fat metabolism, Aleteration in glucose metabolism

DKA results from a shortage of insulin; in response the body switches to burning fatty acids and producing acidic ketone bodies that cause most of the symptoms and complications.

86
Q

Treatment of DKA

A

insulin replacement (drip)- plasma glucose goal 200 mg/dl

bicarbonate- if PH <6.9 (watch K+ levels with PH shift)

fluids/ K+ replacement- give K+ even if high because, (insulin drives k+into cells) which would cause it to be low.

glucose normalization- when acidosis resolves and insulin given, glucose will quickly rush into glucose depleated cells. May need to give glucose or glucogon if hypoglycemia occurs

87
Q

What is Glucagon

A

Hormone produced by alpha cells of the pancreas

Effects are opposite to the effects of insulin

It produces breakdown of glycogen, stimulates gluconeogenesis

USES_ injectable drug to REVERSE EMERGENCY HYPOGLYCEMIA QUICKLY (IM,SQ,IV)

Provided in a powder form that must be reconstituted

88
Q

Hypothalamus produces TRH (thyrotropin releasing hormone)-> which stimulates the__________

A

Pituitary->

89
Q

The Pituitary stimulates __________

A

THS (thyroid stimulating hormone)—–>

90
Q

THS (thyroid stimulating hormone) stimulates the ________

A

thyroid gland—–>to produce t3 and t4 and synthesized by iodide

So, Hypothalamus produces TRH (thyrotropin releasing hormone)-> which stimulates the Pituitary-> which stimulates THS (thyroid stimulating hormone)> thyroid gland> t3 and t4 and synthesized by iodide

91
Q

Iodide uptake- TSH stimulates thyroid to grow and take up more iodide—> iodide oxidated to iodine by ____________ which leads to formation of t3 (liothyronine) or t4 (levothyroxine)

A

PEROXIDASE

92
Q

Which is more potent, T3 or T4

A

T3

T4 converted to t3 in many tissues- supplier for t3

93
Q

What is T3

A

liothyronine

94
Q

What is T4

A

levothyroxine

95
Q

rising t4 and t3 supresses TSH =

A

Negative feedback loop

96
Q

What is Iodine deficiency-

A

not enough t3 and t4 production —–> increases tsh, stimulates thyroid to be big= goiter

gets bigger to soak up all the iodine that it can

97
Q

What causes HYPOthyroidism

A 
autoimmune thyroiditis 
lack of iodine
surgery
radioactive ablation
radiation (radioactive iodine) exposure in utero
TSH deficiency (pituitary)
TRH deficiency (hypothalmus)
Non developed thyroid in infants
98
Q

What is the adult presentation for HYPOthyroidism

A

skin— cold,dry—always cold

hair- brittle and possible alopecia

cardiac- bradycardia

body temp-lowered

psyche-depression, lethargy, AMS, malaise

metabolism-low-unexplained wt gain

99
Q

Hypothyroidism during pregnancy

A
  • if occurs in 1st trimester, can result in severe neuropsychological problems in the baby later on.

Screening is important. Treatment should begin early.

Also, for women taking thyroid supplements, generally while pregnant, THEIR DOSAGE GOES UP APROX 30-50%.

100
Q

Hypothyroidism presentation in infants

A

(creatinism) mental retardation, short dwarf-like stature, large protruding tongue, potbelly

101
Q

Hyperthyroidism (Graves disease and toxic nodular Goiter) Presentation

A

Graves disease- 2nd-4th decade mostly

Presentation- (thyrotoxicosis)

skin- warm, moist

cardiac- tachycardia, arrhythmias (afib)

CNS excitation- insomnia, excitable rapid speech,

weak muscles

metabolism- increases- wt loss

thermoregulation- increased temp, always feel hot

Exophthalmos (eyeball protrusion)

102
Q

What is Thyrotoxic crisis (thyroid storm)-

A

extremely high levels of thyroid hormone, hyperthermia, tachycardia, profound weakness, LIFE THREATENING

103
Q

Lab monitoring for thyroid issues

A

TSH- most sensitive screen to detect hypothyroid disease

T3 more useful to detect hyperthyroid disease

t4- confirms diagnosis of hypothyriod and can be used along with tsh to guide replacement therapy

104
Q

What drug is used for hypothyroidism?

A

Levothyroxine- (T4) (Synthroid)-

makes more sensitive to warfin

Uses- hypothyroidism, previously used at wt loss agent- causes arrhythmias,

7day ½ life, 28 day steady state.

Adverse effects- if overdosed sxs of thyroid toxicosis

Therapeutic interchange- narrow

Goal- to become euthroid

105
Q

What drug is used for Hyperthyroidism

A

Propylthiouracil (PTU)

MOA: Blocks thyroid hormone synthesis by preventing oxidation of iodide by peroxidase

kinetics- short ½ life- give 3-4 x a day

106
Q

What are the adverse effects of Propylthiouracil (PTU)

A

adverse effects-

**causes agranulocytosis- rare- 3 cases per 100,000 (stop drug immediately if jaundice, or fever/chills, sore throat, bleeding gums occur) Need to monitor CBC for drop in WBCs (neutrophils to be exact)

rash

hypothyroid state

pregnancy- Crosses the placenta and enters breast milk. Can cause hypothyrois state in neonate

107
Q

What is the MOA for radioactive Iodine

A

MOA concentrated in the thyroid. Emmission of beta particles destroys thyroid tissue. Beta particles have a very limited ability to penetrate tissues, thus it doesn’t usually go outside the thyroid. Very specific to the thyroid

radioactive iodine- can destroy thyroid

For graves disease, or thyroid cancer- lights up thyroid

108
Q

WHAT are the primary uses for radioactive iodine

A

graves disease- destroys thyroid tissue

thyroid cancer- only a select number of cancers can be treated this way

diagnostic use- lights up thyroid

109
Q

Caution for iodide products

A

Iodide products**** iodide in HIGH CONCENTRATIONS has a paradoxical suppressant effect on thyroid.

Typically, the effects are short lived.

Rarely used long term.

110
Q

What is the active form of thyroid hormone?

A

The thyroid hormones, (T3) and (T4), are tyrosine-based hormones produced by the thyroid gland that are primarily responsible for regulation of metabolism.

Iodine is necessary for the production of T3 and T4. A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as goitre.

The major form of thyroid hormone in the blood is (T4), which has a longer half-life than T3.

T4 is converted to the ACTIVE T3 (three to four times more potent than T4)

111
Q

List symptoms of hypothyroidism

A

skin— cold,dry—always cold

hair- brittle and possible alopecia

cardiac- bradycardia

body temp-lowered

psyche-depression, lethargy, AMS, malaise

metabolism-low-unexplained wt gain

Infants- (creatinism) mental retardation, short dwarf-like stature, large protruding tongue, potbelly

112
Q

List symptoms of hyperthyroidism

A

skin- warm, moist

cardiac- tachycardia, arrhythmias (afib)

CNS excitation- insomnia, excitable rapid speech, weak muscles

metabolism- increases- wt loss

thermoregulation- increased temp, always feel hot

Exophthalmos (eyeball protrusion)

113
Q

List 2 drugs that interact with thyroid hormone

A

Levothyroxine- (T4) (Synthroid)-
Uses- hypothyroidism, previously used at wt loss agent- causes arrhythmias, 7day ½ life, 28 day steady state.

Propylthiouracil (PTU)
Used for hyperthyroidism. MOA: Blocks thyroid hormone synthesis by preventing oxidation of iodide by peroxidase

114
Q

How should patients receiving propythiouacil by councelled?

A

MOA: Blocks thyroid hormone synthesis by preventing oxidation of iodide by peroxidase

short ½ life- give 3-4 x a day

**causes agranulocytosis- rare- 3 cases per 100,000 (stop drug immediately if jaundice, or fever/chills, sore throat, bleeding gums occur) Need to monitor CBC for drop in WBCs (neutrophils to be exact)

rash

hypothyroid state

115
Q

What are symptoms of graves disease?

A

Graves disease- 2nd-4th decade mostly

skin- warm, moist

cardiac- tachycardia, arrhythmias (afib)

CNS excitation- insomnia, excitable rapid speech, weak muscles

metabolism- increases- wt loss

thermoregulation- increased temp, always feel hot

Exophthalmos (eyeball protrusion)

116
Q

What lab tests are used to diagnose thyroid disease?

A

TSH- most sensitive screen to detect hypothyroid disease

T3 more useful to detect hyperthyroid disease

t4- confirms diagnosis of hypothyriod and can be used along with tsh to guide replacement therapy

117
Q

What is the MOA of NSAIDS

A

inhibit cyclooxygenase (COX) an enzyme that converts arachidonic acid into prostaglandins and related compounds like prostacyclin, thromboxane A2, etc.

Used for inflammation

118
Q

What are the two forms of COX

A

COX 1- good one- promotes housekeeping chores- renal blood flow- protects gastric mucosa

COX 2- bad one- produced mainly at sites of tissue injury- the one we want to wipe out

119
Q

What are the consequences of COX 1 and 2 inhibition

A

COX 1 – gastric erosion, ulceration, bleeding, renal impairment, MI/CVA protection

COX2- suppression of inflammation, pain relief, decreased fever, renal impairment.

120
Q

NSAIDS

asprin- (acetylsalicylic acid, or ASA) is an _________ inhibitor of COX 1 and 2

A

*** IRREVERSIBLE

121
Q

What are the therapeutic uses for Asprin

A

Anti inflammatory
Analgesics
Antipyretic
Dysmenorrhea

**suppression of platelet aggregation: by irreversible inhibition of COX1

122
Q

Dysmenorrhea

A

painful periods, can be caused by asprin use

123
Q

adverse side effects of asprin

A

Gi toxicity- inhibits COX1

Bleeding- by inhibiting platelet aggregation

Renal impairment-

REYES Symdrome- in children post virus

Hypersensitivity- develops in about 0.3%

124
Q

REYES Symdrome-

A

asprin causes a rare but serious illness of childhood that carries a 20-30% mortality rate- follows a viral infection or breakout

125
Q

Drug interactions of asprin

A

risk of bleeding with warafin (clotting cascade), glucocorticoids, alcohol- risk of GI ulceration

126
Q

1st generation NSAIDS / non- ASA:

Prototypes will be IBUPROFEN, and NAPROXIN

What are their MOA

A

Moa- REVERSIBLE inhibition of COX 1 and 2

No platelet effects

Comparison: all equivalent- patients all different
Patient variability

127
Q

2nd generation NSAIDS- Coxibs- prototype- CELECOXIB (Celebrex)

What is the MOA

A

Moa – selectively inhibits COX2

Uses- analgesia, inflammation

Adverse drug effects- GI ulcers, CV events, renal impairment, sulfa allergy…increased risk of stroke and heart attack

128
Q

What is the MOA of acetaminophen

A

Moa unlike other NSAIDS, limited to CNS- good for pain and fever.—not for inflammation

129
Q

ADE of acetaminophen

A

liver injury in over dosage,

does not cause GI issues, renal impapirment does not promote bleeding, no link to reyes syndrome

130
Q

LIVER DAMAGE pertaining to acetaminophen

A

produces metabolites that eats liver

saturable pathway- non toxic metabolite

alternative pathways- toxic metabolites

***Glutathione- our bodys own antidote

acetylcysteine (mucomyst) replaces depleted glutathione levels, spares liver

131
Q

What is Glutathione-

A

our bodys own antidote for acetaminophen poisoning

132
Q

acetylcysteine (mucomyst) helps reduce tylenol overdose by

A

Acetylcysteine may protect against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione.

Pharmacology 1 (6 decks)

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