pharm unit 4

phases of hemostasis

primary and secondary

primary hemostasis

forms platelet plug, quick fix, body prevents blood loss by sticking to injury then together

secondary hemostasis

coagulating and clotting, proteolytically activated, activation of fibrin to reinforce protein meshwork

extrinsic pathway for clot formation

tissue damage —> tissue factor and factor VII become factor VII complex —>factor X to activated factor X

intrinsic pathway for clot formation

contact with a damage blood vessel (release of collagen) —> factor XII —>factor XI —> factor IX —> factor X

thrombosis in an extremity

DVT

thrombosis in the trunk/lungs

embolism

virchows triad

stasis, hypercoagulability, vessel wall injury 

stasis: clot formation

inactive muscles, venous stasis

hypercoagulability: clot formation

imbalance in alto mechanism, overproduction of fibrin (smoking, estrogen, genetic mutation)

vessel wall injury: clot formation

start of clotting cascade (fall, burns, diabetes, sepsis)

pt the highest risk for clot formation

women >35 yr old, smoker, on estrogen replacement therapy

aspirin MOA

irreversibly blocks COX in platelets to block TXA2 formation (platelet aggregation)

aspirin indications

TIA, ischemic stroke, chronic stable angina, acute MI, previous MI

aspirin ADRs

bleeding, hemorrhagic stroke, EC may not reduce GI bleeding

aspirin contraindications

kids, pregnancy, other anticoagulants

pt teaching for anti platelets

anti platelets may bruise/bleed more easily or take longer to stop, notify PCP of unexpected bleeding, blood in urine/stool, idiopathic bleeding, notify PCP of all meds and stop before surgery

clopidogrel MOA

inhibits ADP reducing platelet activation and aggregation

clopidogrel indication

stops blockage of coronary artery stents, decrease thrombotic events, secondary prevention of MI/ischemia

clopidogrel ADRs

bleeding, hemorrhagic stroke, EC may not reduce risk of GI bleeding

why is clopidogrel less frequently RX

the PCP has to provide with evidence of why aspirin doesn’t work so insurance covers it

limitations of anticoagulants

they have no direct effect on a formed clot, only prophylaxis

heparin characteristics

natural substance=cheap, preferred in pregnancy, 1-2 hr ½ life, monitor with a PTT, a double check medication

heparin MOA

inhibit thrombin and factor Xa to suppress coagulation 

heparin indication

PE/DVT, evolving stroke, renal dialysis, open heart surgery

heparin contraindication

thrombocytopenia, during/after eye, brain, spinal cord injury

heparin ADRs

hemorrhage, HIT, spinal epidural/hematoma

heparin antidote

protamine sulfate

enoxaparin characteristics

lower molecular weight than heparin, SUBQ, expensive, once a day injection, longer ½ life

enoxaparin MOA

inhibits factor Xa, more predictable

enoxaparin indication

prevent/treat DVT, prevent ischemic issues

enoxaparin contraindication

epidural catheter within 2hr

warfarin MOA

blocks factors II, VII, IX, and X (vitamin K clotting factors)

warfarin indications

long term prophylaxis of thrombosis due to Afib, prevent thromboembolism

warfarin characteristics

PO only, goes into liver to inhibit production of factors, ORIGINALLY RAT POISON, not predictable, measure with a PTINR once a PTT is in range (therapeutic 2-3), varried dose

warfarin contraindications

pregnancy X

warfarin ADRs

hemorrhage, teratogenesis, skin necrosis

warfarin antidote

vitamin K, boost production of factors, no warfarin for 7 days after admin

warfarin interactions

1. vitamin k

2. amiodarone

3. fluconazole

4. metronidazole

5. sulfa drugs

6. aspirin

7. acetaminophen

8. anticoagulants

9. otc: garlic/ginko biloba, St Johns wart

dabigatran MOA

direct inhibition of thrombin (free and bound clots)

dabigatran indiction

A fib, post op (not Ortho surgery)

dabigatran contraindications

anticoagulants

dabigatran ADRs

GI bleed, GI disturbances

dabigatran antidote

praxbind

dabigatran advantages

no monitoring, fewer interactions

rivaroxaban MOA

binds directly with factor Xa to cause inactivation and inhibition of thrombin

rivaroxaban indictions

prevent DVT/PE, after hip/knee replacement (ortho indication), prevent stroke in Afib

rivaroxaban contraindications

anticoagulants

rivaroxaban ADRs

spinal hematoma/epidural, increase risk of thrombosis (taper off)

rivaroxaban antidote

Andexxa (BBW for increased risk of CVA, stroke, sudden cardiac death)

rivaroxaban advantage

no monitoring (more common)

Patient teaching for anticoagulants

1. S/S of hemorrhage

2. avoid excess ETOH

3. wear med alert bracelet

4. use soft toothbrush

5. notify PCP

6. avoid all drugs not approved

alteplase MOA

binds with plasminogen to form plasmin (an enzyme that digest fibrin meshwork of clots)

—> fibrinogen, factors V, VII, XII

alteplase indication

active MI, ischemic stroke, massive PE, shunt occlusion

alteplase ADRs

bleeding, GI effects

alteplase antidote

aminocaproic acid

alteplase advantage

short ½ life (5 min), give IV over an hour and look for quick reversal (watch IV site)

thyroid gland parts

parafolicular cells and follicular cells

parafollicular cell function

calcitonin, pushes excess Ca into the bones for storage

follicular cell function

thyroxine (t4) and triiodothyronine (t3) production

what does T3 and T4 affect

brain, eyes, heart, lungs, liver, digestive/reproductive/musculoskeletal system

parathyroid gland

secretes parathyroid hormone to increase bone reabsorption to release into vasculature

thyroid gland feedback loop

hypothalamus —> TRH —> anterior pituitary—> TSH—> thyroid —>T3/T4

function of T3/T4

float freely in the body and make things metabolically active

hyperthyroidism clinical findings

low TSH, high T4

hypothyroidism clinical findings

high TSH, low T4

hyperthyroidism causes

Grave’s disease, multi nodular disease, thyroid storm, pituitary tumor, thyroid cancer

hyperthyroidism physical exam findings

metabolic overdrive, goiter, exophthalmos, irregular menses, gynecomastia, prolonged fight/flight symptoms, tired/weka, hyperactive DTR, SOB, increased respiratory rate, increased appetite with weight loss, enlarged spleen/liver, heat intolerance, thin brittle nails, tremor, V/D

thyroid crisis: thyroid storm

excessive hormones, life threatening, caused by increased stressor/meds (amiodarone/lithium), can cause seizures, coma, fever, vomit, achy 

antithyroid drugs MOA

inhibit thyroid hormone synthesis, impedes formation thyroid hormone, blocks combining ATP and iodine

• decrease release=decrease metabolic function

• CANT DEACTIVATE T3/T4

• delayed onset (4-8 weeks for full effect)

methimazole characteristics

first line antithyroid

• doesn’t destroy existing thryoid hormones

• 3-12 weeks to reach euthyroid

methimazole ADRs

agranulocytosis, S/S hypothyroidism 

methimazole effects in pregnancy

neonatal hypothyroidism, avoid in 1st trimester, avoid breastfeeding

propylthiouracil (PTU) characteristics

inhibit thyroid hormone synthesis, 2nd line, full benefits may take 6-12 months, pregnancy D except in 1st trimester

propylthiouracil ADRS

severe liver injury, agranulocytosis, S/S hypothyroidism 

radioactive iodine effect

damages/kills thyroid tissue so it can no longer produce T3.T4 and PTH (monitor Ca)

radioactive iodine advantages

cheap, easy access, works well, don’t have to adjust meds/dose

radioactive iodine disadvantages

longer ½ life, increased risk of thyroid cancer

education for radioactive iodine

oral care (prevent dry mouth/infection), watch out for s/s of hypothyroidism

hyperthyroidism during pregnancy

• NEVER take radioactive iodine

what may a patient being on after causing a hypothyroid state

methimazole or PTU, beta blockers, synthetic T3/T4

antithyroid drug nursing implications

assess allergies, contraindications, or any interactions

• obtain VS and weight

• cautious use advised for patients with cardiacc disease and HTN and for pregnany women

types of hypothyroidism

• primary: common, radioactive idoine, thyroid gland issue

• secondary: pituitary issue

• tertiary: hypothalamus issue

cretinism 

born with hypothyroidism

• decreased T3/T4 in youth=decreased development

• sexual development off

• decreased metabolism 

• mental/physical delay 

• proturuding abdomen/tongue 

myxedema ad

adulthood

• decreased metabolism

• decreased mental and physical stamina

• yellow skin

• hair losss

triiodothyronine

synthetic T3, liothyronine,

• short half life

• works faster

• more expensive

thyroxine, tertaiodothyronine 

synthetic T4, levothyroxine (synthroid)

• more common

• convert T3 for biological use

• onset delayed by food (take 30-60 min before breakfast)

• mcg

• once a day (PO/IV), require blood work monitor (test TSH)

• NO MILK

thyroid monitoring on thyroid replacement horomone

decreased S/S, increased energy and mental/physical stamina

• ADRS: cardiac dysrhythmia

antithyroid monitoring on thyroid repla

cement hormone no hyperthyroidism

• ADRs: leukopenia, fever, sore throat, lesions

thyroid replacement hormone MOA

achieve euthroid and speed up metabolic rate 

• works the same way as endogenous thyroid 

thyroid replacement hromone ADRs

• cardiac dysrhythmia

• tachycardia/palpitations

• angina

• tremors, headache, anxiety N/D

• menstral issues

• weight loss

• sweating heat intolerance

• fever

thyroid replacement  hormone contraindications

hyperthyroidism, adrenal insufficiency 

thyroid replacement drug interactions

reduce levothyroxine: proton pump inhibitors, antacids, calcium, iron supp

drugs that accelerate levothyroxine metabolism : seizure drugs

warfarin (recheck TSH and PTINR)

complementary and integrative medicine

traditional and alternative meds,

• alternative medicine system

• mind-body interventions

• biologically therapies

• manipulative and body based methods

• energy theory

quality control 

FDA set guidelines, but not regulated or do tests (done by private organization) 

• test quality, manufacturing, purity, identity, potency, dissolution

what CAT labels can’t claim

cure, treatment, protection

ADRs for CAT products

alteration in m metabolism, compete for receptor site as drugs, CV issues, interfere with clotting

Black Cohosh 

gynecological issues, improves menopause S/S

• MOA: unknown

• adrs: minimal with routine use, avoid long term, estrogenic effeorts, liver toxicity, metabolic regulation 

• interacts: BP, hypoglycemics 

cranberry juice

UTI prophylaxis, decreased odor

• MOA: prevent bacteria from adhering to urinary wall

• ADRs: no data, interact with warfarin