Test Number 3

Endocrine
Definitions:

Glycogenolysis- breakdown of glycogen to glucose

Gluconeogenesis- formation of glucose from glycerol and proteins rather than

carbs.

Stress Feedback

stresshypothalmus to release CRH anterior pituitary release ACTHadrenal

cortex release glucocorticoids, estrogen, adrogens and cortisol. cortisol feeds back
to the hypothalamus to say stop making CRH and ant pit stop ACTH and stop
release glucocorticoids.

Adrenal Suppression oral gluc. Stop the release of CRH and ACTH which inhibts
the release of glucocort by the adrenals. IF give gluc. Long term ant pit gets lazy so
must TAPER dose! Prepare to give extra gluc. During times of stress. Withdrawl
(stop giving gluc): hypotension, hypoglycemia, fatigue

Adrenal Cortex makes 3 hormones:

1. Glucocorticoids (cortisone, prednisone)- influence carb and gluc metabolism

2. Mineralcorticoids (aldosterone) –renin- angio system.
3. Androgens – sexual character

Glucocorticoids”prednisone, methylprednisolone, prednisolone” increase the

availability of glucose causes hyperglycemia.

Pharmacologic high doses- high anti inflammatory and imuno suppressive actions
(thrush). Have little mineralocorticoid activity, don’t worry about Na , K loss.

- stimulates glucose and doesn’t allow glucose storage! Suppresses immune

system and inflammation, causes weight gain. Check out page 828 table 71-7
for list of gluc.
- Use for lupus, RA, neoplasm, allergic rxn.
- Adverse RXN: not so bad if u taper dose, 1. Adrenal insufficiency bc gets lazy
2. Osteoporosis Get Ca and vit D def. 3. Hyperglycemia 4. PCP infection 4 if
take high doses na and water retention and k loss. 5. Mood changes 6. PUD bc
eats up stomach 7. Iatrogenic Cushing= moon face, buffalo hump.

Pharm- cross placenta and enters breast milk BAD. DRUG inter: Watch out for
DIGOXIN, loop diuretics, NSAIDS, vaccine. Don’t give if have fungal infection.
CAN give it anyway.

Only give high doses if someone’s very sick.

 Mineralocorticoids( Fludrocortisone) aldosterone regulates K and Na and
H20 balance. Low BP, increase aldosterone. Renin ang- regulates salt balance.

DIABETES- resistance to insulin or def.

 Causes blindness, amputations, impotence, polyuria.

 Type One- see in kids – destruction of pancreatic beta cells. At risk for
ketoacidosis Type 2 see in obese people. Not really at risk for
ketoacidosis.
 Complications: have decrease blood flow so CHECK FEET,
macrovascular damage, heart disease microvascular damage to small
blood vessels, retinopathy, neuropathy tingling.

Tests

1. Fasting plasma glucose- at least 8 hrs after meal normal less than 100, if
greater 126 have diabetes.
2. Casual plasma glucose test anytime less than 200 and display signs
(polyuria, polydyspia, ketonuria and rapid wt loss).
3. Oral glucose tolerance- used when first 2 test were not definitive, give
gluc of 75 g and measure 2 hrs later normal less 140, diab. Above 200.

Limits: Want premeal 90-130. POstmeal below 180. Hg A1C below 7 percent- tests
for the past 3 months!

Prevention: diet, exercise, makes receptors more sensitive to insulin.

Type 2 prevention: dieat, exercise, drug, add insulin,

Insulin made by beta cells in pancreas. Aplha cells inhibit release of insulin.

Insulin deficiency: puts body in catabolic state (breakdown of complex molecules)

break down glycogen and have too much glucose.

Insulin stores glucose! Anabolic. If don’t have insulin then sugar just floats around.

Types of Insulin

Rapid acting/ short duration- lispro, aspart, glulisine (LAG) -humalog,

novolog, apidra. Bf meals

Slower acting/ short duration- Regular (bf meals)

Intermediate duration- NPH insulin Bed Time peak 6-14 hrs.

Long Duration- Glargine- given once daily

Insulin Short Duration/ Rapid acting lispro, aspart, glulisine (LAG)

- give before or right after meals, clear solution, require prescription. Don’t
give IV! Give in belly change injection sites (15-30 min onset).

Slower acting/ short duration- Regular only insulin given IV. Available without
prescription.

Intermediate duration- NPH (neutral protamine hagedorn), determir insulin

can stay out of fridge for 30 days. No prescription use twice daily, in btwn meals and
bed time. Determir req. prescription. Can mix with other insulin.

Long Duration- Glargine- clear, colorless, once daily sometimes twice. Less risk of
hyper/hypoglycemia. Req prescription. Don’t MIX.

Random Info:

-only one that’s not colorless= NPH, needs to be shaken up.

-only one can mix is NPH with short acting insulin’s (r, lispro, asp, gluli). Draw short
acting insulin into syringe first to avoid contamination of NPH vial. Good for 28 days
room temp, 1 month in fridge. Insulin should be given sub Q abdomen (fast) and
upper arm, thigh (slowest). Not by mouth! Rotate injection sites to reduce
lipohypertrophy fat patch.

ONLY regular insulin can be given IV! All patient with type 1 diabetes get insulin.

-Beta Blockers can mask the s/s of hypoglycemia.

Oral Hypoglycemic for Type 2 (to treat hyperglycemia), all side effects
hypoglycemia

Sulfonyureas (glipizide, glyburide) promote insulin secreation by pancreas and

increase tissue response to insulin. Avoid during pregnancy. Drug inter: Alcohol
antibuse.

Meglitinides ( nateglinide, repaglinide) promote insulin secretion by pancrease-

glucose dependent so need to eat no longer than 30 min after take drug!

Biguanide (metformin)- dec. glucose production by the liver and increase tissue
response to insulin. DOES NOT promote insulin release. (can be used for type 1).
Can be given alone or with sulfonylureas. Exctreted unchanged in kidneys CHECK
Creatnine clearance. Side effect- weight loss and lactic acidosis, life threatening.
Nausia! (careful those with CHF)

Thiazolidinediones rosiglitazone, pioglitazone decrease insulin resistance and

thereby increase glucose uptake by muscle and decrease glucose production by the
liver. Insulin must be present to work. Adverse: hepatoxicity and heart failure.
Alpha glucosidase – acarbose, miglitol- inihibit carb, digestion and absorption,
thereby dec. the postprandial rise in blood glucose. be careful with beano. Make sure
you eat! Can use with other drugs. Adverse effects: farts.

Hypoglycemia- below 50. Get from unaccostmed exercise, alcohol, diarrhea, Take
fast acting sugar.

Hypoglycemia

Glucagon produced by alpha cells in pancrease. Inc plasma levels of cglucose and
relaxes smooth muscle in GI. Prevent insulin! Elevates blood glucose levels following
insulin overdose. Promotes breakdown of glycogen. Given Sub Q and IV.

INJECTIBLES

Amylin Mimetics- pramlintide

Delays gastric emptying and suppress glucagon secretions. Also acts to inc sense of
satiety and can thereby lower caloric intake. Can be used in type one and type 2.
Makes feel full. Adverse: hypoglycemia. Give po drugs one hour bf injection bc it
slows motility.

Incretin Mimetics/ glucagon like peptide 1 agonist exenatide (byetta)

Makes feel full, also slows gastric empyting. Dont give to pts with renal ds. Drug
interactions oral contraceptives and antibiotics.

Ketoacidosis- severe manifestation of insulin def. see hyperglycermia production of

ketoacids and coma.

Thyroid- effects metabolism. Hyper- inc metabolism. T3 is more potent, T4 serves

as a source of T4. Body makes lots of T4 and its converted to T3. All protein bound.
So only a small amount of thyroid is free. Half life is shorter for t3 (1 day) than t4 (7
days). Usually take in the am half hour bf any food. Overdose – irritable
everything is sped up. Best not to give to pts with recent MI. Actions: Thyroid
hormone is a stimulant. Stimulates appetite, inc. production and release of other
hormones.

Clinical Features

Hyperthyroid- inc appetite, thinner, fine , nervous, diarhea

Hypothyroid- dec appetite, weight increases, lethargic, constipation.

Is a feedback mechanism. High tsh level, more hypothyroid bc means not getting
feedback to tell ant pituitary to stop making TSH

Less TSH , feedback is in action had too much so tell ant pit stop maing TSH.
Hyperthyroid.
Thyroid function test- use serum TSH test.

Hypothyroid MEDS desiccated thyroid (armour thyroid) has both T3 and T4

synthetic name for t3- liothyronine sytn name for t4- levothyroxine, . Mixture of
T3 and T4- liotrix. Usually give T4. Give in AM 30 min bf meal with glass water.

Pregnancy congenital or maternal hypothyrodism can cause mental retardation esp

during 1st trimester. 2 and 3 trimester baby can make on its own.

**Drugs that accelerate levothyroxine absorption: Phenytoin, carbamazapine,

rafampin, Sertraline, Phenobarbital.

***Warfin may need to be reduced if pt is taking levothyroxine bc accelerates

vitamin K absorption.

Hyperthyroidism: Antithyroid (propylthiouracil(PTU) take with food. (give for

pregnancy if need meds), usually 3 times day. methimazole

PTU is not as likely to cross placenta

Cardiovascular
Hypertension

Goals: maintain systolic <140 and diastolic <90 in stage 1 and 2. For patients with
diabetes target BP 130/80.

Normal 120/80

Prehyp 120-139/80-89 (lifestyle changes)

Stage 1- 140-159/90-99 (meds, lifestyle)

Stage 2 >160/>100 (more meds)

Arterial pressure (pump heart out) is the product of CO and peripheral

resistance.

CO is influences by 4 factors 1. HR 2. Myocardial contractility (force of contraction 3.

Blood volume 4. Venous return of blood to the heart.

DRUGS

Dec HR- beta blocker, verapamil, diltiazem (CCB)

Venodilators- reduce venous return

Arteriolar dilation counteract peripheral vascular resistance.

RAAS- kidney release rennin in response to reduce renal blood flow. Renin converts
Ang to Ang 1 and ACE converts this is to ANG 2 which causes constriction. RAAS also
release aldosterone in retention of Na and water. ( if have a cough switch from ACE
inhibitor (inc braedykinin) to ARB).

COnteract Renin- beta blockers, ARBS, Ace inhibitor.

Base Hptn on higher of 2 numbers.

2 kind hptn: Primary- no identifiable cause Secondary- is a cause that causes

HPTN

Risk of CV dz is doubled by INC systolic 20 mm Hg and diastolic 10 mm inc beg at

115/75. And ending at 185/155

Sites of Action for Hyp *if beta blocker is used as needed its not for BP

SYMP response- BP GOES Up bc have Vasoconstriction!

1. Brainstem (clonidine, methyldopa) suppress sympathetic outflow which

dec. HR, contraction and vasodilation. Clonidien is used as needed,
maintnance.
2. Sympathetic ganglia( mecamylamine) ganglionic blockade reduces
sympathetic stimulation of heart. Only used for SEVERE cases.
3. Terminals of adrenergic nerve( guanethidine, reserpine) s- dec release of
NE which dec sympathetic stim of heart and Blood vessels.
4. Beta 1 adrenergic rec on the heart- (atenolol, propranolol “olol”) beta 1 rec
blockers prevent symp stim of heart. HR and myocardial contractility
STimulate Beta Recp- INC BP.
5. 5) Alpha1 Adrenergic rec on blood vessels – blockade of alpha1 rec
promotes dilation of arterioles & veins which reduces peripheral resistance
& venous dilation reduces venous return to the heart (Prazosin, terazosin,
labetalol (beta blocker with alpha blocking activity))
6. Vascular Smooth Muscle – relaxation of vascular smooth muscle (Na+
nitroprusside & diazoxide) Used only in HTNsive emerganicies (Hydralazine)
get heada aches. used in chronic HTN
7. Renal Tubules (diuretics)– diuretics promote salt & H2O excretion which
causes blood vol to decline
8. Beta1 Rec on Juxtalgomerular Cells – Suppress release of renin which dec
angiotensin II levels which cause: peripheral vasodilation, renal vasodilation
& suppression of aldosterone-mediated volume expansion (Beta1 blockders)
9. Angiotensin-Converting Enzyme (ACE) (ACE inhibitors: captopril,
lisinopril) – suppress formation of angiotensin II which causes peripheral &
renal vasodilation & suppression of aldosterone-mediated volume expansion
10. Angiotensin II Rec Blockers ARB’s “sartans” Losartan)– prevents axn of
angiotensin II causing peripheral & renal vasodilation & suppression of
aldosterone-mediated volume expansion
 Aldosterone Rec Blockers – blockade of rec in kidney promotes excretion of
Na+ & H2O thus reducing blood volume (Eplerenone)

Look at page 502.

Antihypertensive Drugs

Thiazide diuretics hydroclorothiazide HCTZ- first line trtmnt reduce blood

volume and reduce resistance. Adverse effects: hypokalemia eat food rich in K+ but
not huge deal, dehydration hyperglycemia and hyperuricemia.

Loop Diuretics- Furosemide highest diuresis used for pts that need great diuresis
than thiazide and pts with low GFR (thiazide wont work if GFR too low) big prob:
hyperkalemia

K+ sparing diuretics spironolactone diuresis is small but K+ loss is also small

adverse: hyperkalemia (don’t mix with ACE inhibitor, ARBS or aldosterone ant bc
hyperkalemia).

Sympathilytics

Beta Blockers less effective in blacks than whites. Slow down Heart.
Adverse: can mask hypoglycemia. Bradycardia. Dec Av conduction.If not selective
will cause bronchochonstriction

Alpha1 blockers prevents stim. Of alpha 1 rec. preventing

vasoconstriction.not first line med. Adverse rxn: orthostatic hypotension.

Alpha/ Beta Blockers (carvedilol, labetalol) combo Alpha 1: blockade

promotes dialation of art. And veins. Beta 1 blockade reduce release of rennin advrs
rxn: Beta: bradycardia, asthma Alpha postural hypotension

Centrally Acting Alpha 2 Agonist (clonidine (as needed)- methylodopa

block sympathetic outflow in brainstem so vasodialtion will reduce BP. Advrs rxn:
dry mouth. Clonidine- can cause rebound HTN if stop abruptly. Methyldopa anemia
and liver probs.

( FYI Adrenergic Neuron Blockers- guanethidine

Direct acting Arterial Dialators dialation of arterioles (hydralazine, monoxidil)

rxn: tachycardia and rennin release fluid retention. Minoxidil can cause fluid
retention. Lots of hair growth (hypertrichosis).

Calcium Channel Blockers- both groups promote dilation of arterioles.

Dihydropyradines- (Nifedipine)

Non- dihydropyradines- (verapamil, diltiazem) works directly on the heart.

Ace Inhibitors- stop vasoconstriction prevent agn. 2 formation. Can cause
persistant cough/ causes bradykinin. Angioedema. HYPERkalemia. Don’t use in
pregnancy.

Ang. 2 rec blockers- ( losartan, ibersartan) same as ace inhibitor EXCEPT cough.

Aldosterone antagonist (spirinolactone, eplerterone) cause hyperkalemia

HTN first line drug: Thiazide, beta blockers, Ace inhibitors, CCB.

Stage 1: thiazide diuretic.

Stage 2: thiazide combines with beta Blocker, ace inhibitor CCB or ARB.

**if you give a vasodialtor give with beta blocker to prevent reflex tachycardia.

Special considerations: Renal dz. THiazide may not work in severe renal ds bc
low GFR so use loop dieretic. Targer BP 130/80

Thiazide and loop can promote hyperglycemia.

Sodium nitroprusside use for SEVERE HTN. Pregnancy: give Methyldopa

(maintnance). Eclampsia- MG+ sulfate. To lower BP right away hydralazine

DIURETICS see page 445 all can cause Hypotension (higher up go more diuresis and
loss of K+)

HIGH CEILING/LOOP (furosemide, Bumetadine, torsemide, ethacrynic acid) in loop

of henle, great diuresis give with K+ suppl. DON’T GIVE AT NIGHT, will pee a ton.
Works fast. Don’t want to start with this, try HCTZ first. Adverse: Hypotension.
Hyperglycemia. Be careful with digozin. Works at loop of henle

THIAZIDE (hydrochlorothiazide HCTZ) dital tubule higher up. Don’t give K+

supplements. Wont make you go like crazy so can take at night. DOC for essential
HTN!

OSMOTIC (Mannitol)- works high up by glomerulus need K+..lots of diuresis,

amount of dieuresis is directly correlated to amount of manitol in glomerulus. IV
ONLY, dec lots of fluid and intraocular pressure. Use if have renal failure.

K+ SPARING (at very end of kidney) mild diuresis advrs Hyperkalemia esp with
ACE

Aldosterone antagonist (spirnolactone)- opposite effect of aldosterone. Pee

out sodium. Takes longer to work.

Non aldosterone antagonist- (triamterine, (Amiloride))

CARBONIC ANHYDRASE INHIBITORS—used for high altitudes, used for intraocular

pressure.
ANGINA PECTORIS- happens before an MI. Get it if don’t have enough oxygen or you
need too much oxygen that cant get. Secondary ds. To atherosclerosis. Can give anti
cholesterol or anti platelet. DRUGS to prevent MI and angina pain: nitrates, Beta
blocker (propranolol) and CCB (verapamil) bc all dec. 02 demand. Also take an
antiplatelet- aspirin/ plavix. Variant- beta blockers are not as effective bc need more
02.

Nitrates- drug of choice for angina. Promotes vasodialtation. Can give most routes.
Dec angina pain. ADvrs: headache, hypotension, tachycardia. Let 8 hours pass of
drug free pd. ..transdermal patch.

Drug Class Stable Angina Variant Angina

Nitrates Dec. oxygen demand,
dialates veins decrease
pre-load.
Beta Blockers Dec. oxygen demand dec.
heart rate and
contractility
Calcium Channel Blockers Dec. oxygen demand
dialating arterioles, dec
afterload and dec heart
contractility
Inc oxygen supply by
relaxing coronary
vasospasm
Not used
Increases oxygen supply
by relaxing coronary
vasospasm.

Sublingual works fastest so if feel an attack take sublingual Nitrate. Sublingual only
good for a year, if opened only good for 3 months. Can take up to 3 doses 5 min
apart. Patch not for ongoing attack. RIGHT NOW- buccal, sublingual, spray.

Isosorbide mononitrate and dinitrate- same as NTG. Give PO. Amyl Nitrate- give for
acute episodes of angina pectoris.

Cardiovascular 2
CHF= a condition in which the heart can no longer pump enough blood to
the rest of the body.
*doesn’t allows have s/s of pulmonary or systemic congestion.

Stage A- no symptoms or structural abnormalities. TRT: Ace in or ARB. Change

lifestyle.

Stage B- no s/s but has structural heart dz, prob already had a heart attack. (LV)
TRT: same as stage A plus an ACE inh or ARB and a Beta Blocker is added for pts
with reduced ejection fraction, hx of MI or both.

Stage C: s/s and structural heart ds. Trt: diuretic, Ace in or ARB, BB, add digoxin if
Sx cant be controlled. If good renal function use thiazide if probs use loop. (can add
aldosterone anag only if good kindye function and normal K+. Avoid:
antidysrythmic, CCB’s, NSAIDS.

Stage D: very bad need heart transplant do same as stage C.

Drugs for CHF

-1. diuretics, 2. RAAS, 3. beta blockers 4. Digoxin, dopamine, hydralazine, nesiratide

S/S fatigue, SOB, exercise intolerance, due to volume overload. (venous distention,
edema). As art. Pressure falls, baroreceptors start a sympathetic reaction to inc
blood. Inc hr, contractility, venous tone, arteriolar tone.

Remodling- change in size, shape or function of the heart after injury of the
ventricles.

Starling effect- more blood comes into the heart more blood is ejected from the
heart in systole. Heart will inc in size to pump harder.

The kidneys will sense that there is less blood flow, urine is dec and h20 is retained
not excreted. HF activates RAAS and ang 2 is released to constrict vessels have inc
venous and arterial pressure. If still low blood eventually lead to pulmonary and
peripheral edema and death.

First line agent= diuretics, dec volume, dec pressure edema.

Thiazide- hydrochlorothiazide- used for long term tx of HF, edema not bad.
Not as effective if GFR is low and cant be used if CO is low. AE: Hypokalemia, which
inc risk of digoxin induce dysrhythmias.

Loop Diuretics furosemide- lots of diuresis so don’t give at night. DOC

severe HF, provide loss even with low GFR and CO low. AE Hypokalemia,
hypotension.

K+ Sparing Diuretics- spirinolactone, Triamterine- little diuresis, lowers

risk of digoxin toxicity. AE: hyperkalemia- don’t combne K+ sparing with an ARB
or ACE inhibitor.

Drugs that inhibit RAAS help stop remodling., ACE inh, ARBS and Aldosterone
Antagonist

ACE IN (catopril, enalpril, ramipril) “PRIL”- improves functional stat. and

prolonges life. If have HF= need ACE. Causes dialation and block release of
Aldosterone (excretes Na+ ad water causing retention of K+) AE hypotension,
hyperkalemia cough, don’t take with pregnancy, don’t use ACE if taking
triamterine or spirnolactone

ARBS- same thing without the cough bc don’t increase kinin. First try ACE if get
cough switch.
 BB- (carevidol, bisoprolol, metoprolol)- they improve left vent ejection and
PROLONG LIFE. Start does low so don’t reduce contractility too much.

DIGOXIN- (digoxin, lanoxin)- positive iontropic action: inc contractility which

inc CO by inhibiting Na/K atpase. Which promote Calcium build up of actin and
mysin (myocyes). Moniter K+ levels, if too high response of digoxin is reduced. If
too low, digoxin can be toxic. Normal range 3.5-5. Makes heart pump better 1. Symp.
Tone declines2. Urine production inc 3. Rennin release drops. Summary: 1. CO
improves 2. HR dec. 3. Heart size declines 4. Vasodialtation 5. H20 peed out. 6. Blood
vol dec 7. Edema drops 8. Exercise tolerance improves 9. Fatigue reduces 10 DOES
NOT PROLONG LIFE!!!

Neurohormonal system- altered due to alteration of electrical activity , DON’T

PROLONG LIFE, 2nd line agent. Can cause dysrhythmias. Benefits through electrical
activity: inhibits NA/K atpase. Makes barroreceptors more sensitive so signals CNS
to dec. sympathetic outflow. Can cause or treat dysartyhmias.

Toxicity: stop digoxin and K+ wasting diuretics. MOniter serum K+. Give activated
charcoal or cholestyramine binds to digoxin and prevent absorption. S/S
dystrythmia, blurred vision, halos.

AE: NARROW THERAPEUTIC DRUG keep within .5-.8. Hypokalemia may need to
give K+ supplements or spirinolactone.

Drug interactions: diuretics bc cause K+ loss. ACE inh and ARBS inc K+ levels.
Sympathomimetic drugs (inc heart rate), quinidine, verapamil inc plasma levels.

Crosses placenta,if HR is <60 beats stop digox.

Dysrhythmia can have 1. Tachy 2. Brady.

Best place to have is in SA node because easy to slow down.

DRUGS:

Class 1: Na+ channel Blockers: blocks Na channels slow impulse early on.(Quinidine,
procainamide, disopyramide,(strong anticholinergic) lidocaine (IV ONLY),
mexiletine, phenytoin), Flecainide, propafenone) adverse: thrombi

Class 2: Beta Blockers- reduce Ca+ entry, cardiac effects same as CCB’s. drugs:
propranolol, acebutolol, - both non selective beta 1 and 2 esmolol, sotalol, selec. Beta
1, Sotalol also blocks K+ channels. Used for life threatening.

Class 3: K+ channel blockers amiodarone (only for life threatening vent dys, don’t
take with grapefruit juice.), bretyllium , dofetilide, ibutilide, sotalol.

Class IV: CCBs: Verapamil and DIlitiazem ONLY DRUGS WORK DIRECTLY ON
HEART! Elevate digoxin levels, BB bc of inc bradycardia.
Other drugs: Digoxin, Adenosine (DOC for terminating paroxysmal SVT)

2 groups: supraventricular – give IV beta blocker, and warfarin to prevent stroke.

DRUGS short term: current conversion or IV ibutilide longterm: class 1- flecanide,
propafenone), class 3- amiodarone, sotalol, dofetilide) and give beta blocker,
verapamil or diltiazem to slow heart.and warfarin.

ventricular (more dangerous) im. Treatment: imed: cardioconversion is TX of

choice or IV amiodarone alternative are lidocaine and procainamide. Longterm:
amiodarone.

DIGOXIN induced dyst: TX: lidocaine and phenytoin. Torsades de pointes:

tachydysrthymias (life threatening). Na blocker and K+ blockers cause this. TX: IV
magnesium and cardioconversion.

Coagulation- damaged vessel= platelets come, contact with collagen and platelets
are activated and form bridges, thromboxan A2, thrombim collagen PAF and adp
bind to fibrinogen.

DRUGS used for Thromboembolic Disorders

1. anticoagulant (heparin, warfarin) – most effective against venous throm.

Heparin- enhance activity of antithrombin. Unfractioned: rapid acting given
by injection.
NOT given PO (only IV and SQ) Overdose: use protamine sulfate. AE:
hemorage, bruising. MOniter dose closely check APTT does nto go more than
double its supposed to. Can make adjustments is apt is >80 sec lower dose if
<60 sec raise dose. Low molecular weight Heparin enoxaprin, dalteparin,
tinzaparin. Does not req. moniter aPTT can be given at home. FIRst line
drug in DVTS given SQ based on body weight.
Anticoagulant Warfarin (PO) warfarin delayed onset of axn. NOT used for
emergency., long term use only.MONITER INR range within 2 to 4.5, (PT) If
using warfarin and heparon moniter levels no sooner than 5 h after IV or no
than than 24 hr after SQ inj.
OVERDOSE: give vitamin K 1 if doesn’t work give them new blood. DON’T
USE DURING PREG! DRUG interaction: heparin, aspirin acetominophen.
2. Antiplatelet (asprin, tirofiban) prevent arterial throm.
Aspirin- IRREVERISBLE inhibtion last life of platelet. TX: prevents MI,
prevents stroke. AE: GI bleeding, hemorrhagic stroke.
Adenosine Diphosphate rec. antagonist- Clopidogrel (MI), ticlopidine –
irreversible blockade of ADP
Glycoprtien IIB rec. ant- tirofiban, eptifibatide, abciximab most effective
antiplat. Drugs on market.
(dipyridamole, cilostazol)
3. Thrombolytic drugs (alteplase, streptokinase) lysis of fibrin. “clot busters”
Streptokinase, alteplase, tenectplace, reteplase, urikinase “ASE” Digest firbrin
clot, TX: acute coronary thom. DVT pulmonary emboli. Get within 4 to 6 hrs
of MI.