Test 4 Flashcards
(132 cards)
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
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
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)
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).
5
Q
Gestational Diabetes-
A
Diabetes during pregnancy usually subsides after delivery. They are at greater risk for type 2 diabetes.
6
Q
True or false
Being diabetic, you are 4-5 times more likely to have a heart attack and microvascular complications
A
true
7
Q
Name three short term complications of diabetes.
A
- Hyperglycemia
- Hypoglycemia
- Ketoacidosis- potentially fatal
8
Q
Name some Hyperglycemia symptoms
A
polyuria polydypsia sluggish/sleepy polyphagia blink a lot weight loss
9
Q
polyphagia
A
increased hunger
10
Q
polydypsia
A
increased thirst
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.
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)
13
Q
Macrovascular disease-
A
large vessel disease. Causes heart attacks and strokes.
14
Q
Microvascular disease-
A
damage to small vessels and capillaries.
15
Q
Retinopathy-
A
1 cause of blindness in our country
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.
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
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
19
Q
Amputations-
A
Diabetes is responsible for 50% of lower limb amputations in America
20
Q
impotence-
A
Diabetes causes blood vessel injury and nerve damage to their sexy time organs
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
22
Q
OSA- Obstructive Sleep Apnea-
A
Occurs Especially with type 2 diabetics.
23
Q
Random plasma glucose more >______ mg/dl (with symptoms)- thirsty, polyuria is used to diagnose diabetes.
A
200
24
Q
Another diagnostic tool is a FPG level > or = _______mg/dl (repeat on separate day)
A
126
25
2 hour OGTT> __________ mg/dl (repeat on separate day) Pregnant women have to do this
200
26
Hemoglobin A1C- _______% or greater is diagnostic
6.5%
27
Name some Risk factors type 2 diabetes.
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
28
True or False
The lower a patients A1C, the less likely they will experience a hypoglycemic event?
FALSE
the lower the A1C, the MORE likely they are to experience a hypoglycemic event
29
Treatment targets
A1C < 7%
Fasting 70-100
2 hours after a meal= < 100
< 130/80 BP JNC guideline s
30
Self monitoring of blood glucose (SMBG)
IDDM- ___________ x per day-
A lot
frequent monitoring by pt on insulin correlates with success
Knowing sugar trend keeps them from going low.
31
Self monitoring of blood glucose (SMBG)
NIDDM ________x per day (controversial)
not a lot
no correlation between frequent monitoring and sucess
32
Urine Glucose Monitoring-
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
33
Glycosylated Hemoglobin (HBA1)
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.
34
Hemoglobin is glycosylated in presence of glucose. RBCs have life span of aprox ______ days
120
35
Frucosamine-
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.
36
Insulin (anabolic hormone) builds _______.
Muscle. Therefore it can be an abused substance
37
Insulin is produced by ________
beta islet cells of pancreas
38
What are the anabolic effects of insulin?
insulin facilitates glucose uptake- inhibits glycogenolysis, and glucogenesis
39
Glycogenolysis
is the breakdown of glycogen to glucose
40
Glycogenesis
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.
41
What are the Catabolic Effects of insulin?
body breaks down itself to make more sugar = insulin deficient
42
Rapid Acting NOVALOG- (Aspart)
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
43
Regular Insulin
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
44
NPH (HUMULIN)-
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.
45
What is the peak of NPH (Humulin)
8-10 hours
Dose at breakfast and at bedtime, clear before cloudy, roll it in your hands to agitate it.
46
Insulin Detmir (LEVIMIR)
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
47
Insulin Glargine
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
48
Name a rapid acting insulin
Novalog (Aspart)
49
Name a Slower acting shorter duration insulin
Regular Insulin
50
Name a Intermediate Acting Insulin
NPH Humalin
or
Insulin Detemir Levimir
51
Name a long acting Insulin
Insulin Glargine
52
When do you give 70/30 insulin
before breakfast and before supper
53
Where do you administer insulin
Site- Abdomen- central to core, bloodflow, less pain, more surface area, easily accessible
54
How do you mix insulin
Mixing- pull up REGULAR/ NOVALOG first, 70/30 vs 70/25 vs 50/50 fixed combos
55
How is insulin stored
storge- unopened in fridge, do not freeze, Vial in use can be stored at room temp for 28 days
56
How can insulin be delivered
Delivery- jet/pen injectors, pumps, syringes
pumps- delivers basal and bolus. Sets must be changed Q 3 days
57
Intensive Conventional therapy
QID dosing, dosing is adjusted based on preprandial SMBG measurements. Uses Rapid acting + insulin glargine
58
Continuous SC insulin
similar to ICT except with a pump
59
Dosage ranges from ________ unit/Kg/d and up
0.1 unit
60
Tight control vs loose control-
DCCT and UKPDS
Does not reduce heart attacks and strokes but does reduce microvascular complications
61
What are the signs and symptoms of stage 1 hypoglycemia
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
What are the signs and symptoms of stage 2 hypoglycemia
ii-stage 2- cognition-confusion-AMS, dnt make sense, alert family if pt says something that doesn’t make sense.
63
What are the signs and symptoms of stage 3 hypoglycemia
Iii- stage 3 coma, death, SZ- medical emergency
64
What are Sulfonylureas and how do they work
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
Name the 2nd generation sulfonylureas
Glypizide/glyburide/glimepiride
66
What are the side effects and cautions that pertain to sulfonylureas
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
What is the treatment for hypoglycemia? (rule of 15)
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
Name the two short acting sulfonylureas
Nateglinide (STARLIX)
Repaglinide (Prandin)
69
MOA of
Nateglinide (STARLIX)
Repaglinide (Prandin)
MOA Stimulates beta islet cells of the pancreas to release insulin
Dosing: prior to each meal
Adverse effects: hypoglycemia, wt gain
70
Metformin (Glucophage) MOA
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
Metformin (Glucophage) ADE
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
Pre-diabetics= 100-_____ fasting BG
126
73
MOA of Glitazones
–activating the peroxisome proliferator-activated receptor gamma (PPAR-gamma)
PPAR-gamma improves insulin resistance
So Glitazones decrease insulin resistance
74
NAME THE Glitazones
TROGLITAZONE (removed from market),
PIOGLITAZONE (ACTOS),
ROSIGLITAZONE (AVANDIA)
75
ADE of Glitazones
Fluid retention
Raises plasma lipid levels
Liver toxicity
76
** ACARBOSE (PRECOSE) and miglitol (Glyset) are __________.
Alpha Glucosidase Inhibitors- Delays absorbtion of complex carbs
77
What is the MOA of ** ACARBOSE (PRECOSE) and miglitol (Glyset)
(Alpha Glucosidase Inhibitors-)
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
ADE of ** ACARBOSE (PRECOSE) and miglitol (Glyset)
| Alpha Glucosidase Inhibitors-
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
PRAMLINITIDE (SYMLIN) MOA
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
Therapeutic usage of PRAMLINITIDE (SYMLIN)
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
ADE of PRAMLINITIDE (SYMLIN)
Side effects decrease
hypoglycemia
nausea
82
EXENATIDE (BYETTA) AND SITAGLIPTAN (Januvia) are ____________.
Incretin mimetic agents-
83
MoA of EXENATIDE (BYETTA) AND SITAGLIPTAN (Januvia)
| Incretin mimetic agents-
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
ADE of EXENATIDE (BYETTA) AND SITAGLIPTAN (Januvia)
| Incretin mimetic agents-
Adverse effects GI (nausea, vomiting) especially with exenatide- weight neutral
85
DKA- Diabetic Ketoacidosis
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
Treatment of DKA
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
What is Glucagon
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
Hypothalamus produces TRH (thyrotropin releasing hormone)-> which stimulates the__________
Pituitary->
89
The Pituitary stimulates __________
THS (thyroid stimulating hormone)----->
90
THS (thyroid stimulating hormone) stimulates the ________
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
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)
PEROXIDASE
92
Which is more potent, T3 or T4
T3
T4 converted to t3 in many tissues- supplier for t3
93
What is T3
liothyronine
94
What is T4
levothyroxine
95
rising t4 and t3 supresses TSH =
Negative feedback loop
96
What is Iodine deficiency-
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
What causes HYPOthyroidism
```
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
What is the adult presentation for HYPOthyroidism
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
Hypothyroidism during pregnancy
- 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
Hypothyroidism presentation in infants
(creatinism) mental retardation, short dwarf-like stature, large protruding tongue, potbelly
101
Hyperthyroidism (Graves disease and toxic nodular Goiter) Presentation
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
What is Thyrotoxic crisis (thyroid storm)-
extremely high levels of thyroid hormone, hyperthermia, tachycardia, profound weakness, LIFE THREATENING
103
Lab monitoring for thyroid issues
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
What drug is used for hypothyroidism?
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
What drug is used for Hyperthyroidism
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
What are the adverse effects of Propylthiouracil (PTU)
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
What is the MOA for radioactive Iodine
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
WHAT are the primary uses for radioactive iodine
graves disease- destroys thyroid tissue
thyroid cancer- only a select number of cancers can be treated this way
diagnostic use- lights up thyroid
109
Caution for iodide products
Iodide products****** iodide in HIGH CONCENTRATIONS has a paradoxical suppressant effect on thyroid.
Typically, the effects are short lived.
Rarely used long term.
110
What is the active form of thyroid hormone?
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
List symptoms of hypothyroidism
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
List symptoms of hyperthyroidism
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
List 2 drugs that interact with thyroid hormone
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
How should patients receiving propythiouacil by councelled?
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
What are symptoms of graves disease?
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
What lab tests are used to diagnose thyroid disease?
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
What is the MOA of NSAIDS
inhibit cyclooxygenase (COX) an enzyme that converts arachidonic acid into prostaglandins and related compounds like prostacyclin, thromboxane A2, etc.
Used for inflammation
118
What are the two forms of COX
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
What are the consequences of COX 1 and 2 inhibition
COX 1 – gastric erosion, ulceration, bleeding, renal impairment, MI/CVA protection
COX2- suppression of inflammation, pain relief, decreased fever, renal impairment.
120
NSAIDS
asprin- (acetylsalicylic acid, or ASA) is an _________ inhibitor of COX 1 and 2
******* IRREVERSIBLE
121
What are the therapeutic uses for Asprin
Anti inflammatory
Analgesics
Antipyretic
Dysmenorrhea
**suppression of platelet aggregation: by irreversible inhibition of COX1
122
Dysmenorrhea
painful periods, can be caused by asprin use
123
adverse side effects of asprin
Gi toxicity- inhibits COX1
Bleeding- by inhibiting platelet aggregation
Renal impairment-
REYES Symdrome- in children post virus
Hypersensitivity- develops in about 0.3%
124
REYES Symdrome-
asprin causes a rare but serious illness of childhood that carries a 20-30% mortality rate- follows a viral infection or breakout
125
Drug interactions of asprin
risk of bleeding with warafin (clotting cascade), glucocorticoids, alcohol- risk of GI ulceration
126
1st generation NSAIDS / non- ASA:
Prototypes will be IBUPROFEN, and NAPROXIN
What are their MOA
Moa- REVERSIBLE inhibition of COX 1 and 2
No platelet effects
Comparison: all equivalent- patients all different
Patient variability
127
2nd generation NSAIDS- Coxibs- prototype- CELECOXIB (Celebrex)
What is the MOA
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
What is the MOA of acetaminophen
Moa unlike other NSAIDS, limited to CNS- good for pain and fever.---not for inflammation
129
ADE of acetaminophen
liver injury in over dosage,
does not cause GI issues, renal impapirment does not promote bleeding, no link to reyes syndrome
130
LIVER DAMAGE pertaining to acetaminophen
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
What is Glutathione-
our bodys own antidote for acetaminophen poisoning
132
acetylcysteine (mucomyst) helps reduce tylenol overdose by
Acetylcysteine may protect against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione.
