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intrinsic
activates in response to injury
extrinic
activated when blood leaks out of vessel and enters tissue space
vitamin k is required
for the liver to make four of the clotting factors
thrombus
stationary clot
embolus
travelling clot
patients at risk for clots
surgical procedures, indwelling catheters, A Fib, mechanical heart valves
Thrombocytopenia
platelet count falls below 150,000 (due to decreased production or increased destruction of platelets)
hemophilia
genetic deficiencies in specific clotting factors
von Willebrand’s Disease
most common inherited coag disorder (decrease in that factor which is responsible for proper platelet aggregation)
promotion
inhibits fibrin destruction (hemostatics) or provides missing clotting factor (clotting factor concentrates)
removal
clot dissolves by drug ( thrombolytic)
prevention
inhibit specific clotting factors (anticoags) or inhibit platelet action (antiplatelet)
anti platelets
lengthens clotting time and prevents clots from forming or growing larger
ADP receptor blockers
irreversibly alters plasma membrane of platelet to interrupt the ability of ADP to bind to the receptor
anticoagulants
prevention of new clots from forming
preventing growth of existing clots
when is PTT necessary
heparin iv; not necessary for subq
enoxaparin air bubble
the air bubble helps push all of the medication out of the syringe and into the subq tissue
it creates a small air lock in the tissue, preventing the med from leaking back up the injection track to skin surface, thereby helping to reduce bruising
memory trick WARF
w-watch INR levels
a-avoid foods high in vitamin k )kale,spinach)
r-report any unusual bleeding or bruising
f- follow up regularly with healthcare provider
what affects INR levels
increases: antibiotics, amiodarone, HF, COPD, decreased vitamin K consumption, alcohol, grapefruit juice
decreases: oral contraceptive, malignancy, diarrhea, increased vitamin K consumption, alcohol
memory trick heparin works fast
heparin starts in a hurry but is gone in a hurry
memory trick warfarin
warfarin is a weaker start and takes up to a week to work
thrombolytics
promotes process of fibrinolysis by converting plasminogen to enzyme plasmin
must be given within 12 hours of MI symptoms and 3 hours of thrombotic stroke
antifibrinolytics
opposite action of anticoagulants
shorten bleeding time to slow blood flow
used to prevent and treat excessive bleeding following surgical procedures
all prevent fibrin from dissolving to enhance the stability of the clot
use cautious in patients with a history of thromboembolic disease
parietal cells
help kill viruses and bacteria
produce and secrete cells (surface epithelial cells)
primary site of action for many acid-controller drugs
mucoid cells
protector
protector
mucus-secreting cells (surface epithelial cells)
provide a protective mucous coat
protect against self-digestion by HCI
hydrochloric acid (HC1)
secreted by parietal cells when stimulated by food
maintains pH of 1-4
secretion stimulated by
large fatty meals
excessive amounts of alcohol
emotional stress
PUD
erosion of the GI mucosa
risk factors
#1: H.Pylori
meds: steroids, NSAIDS
lifestyle: stress/smoking/ETOH
Family hx
helicobacter pylori (H.pylori)
bacteria
responsible for 90% of duodenal ulcers
risk factor for stomach cancer if left untreated
testing for H.pylori
non-endoscopic
urea breath test
stool fecal antigen test
blood test for antibodies
Endoscopic
direct culture/PCR
PUD- gastric ulcers
less common
symptoms: gnawing, sharp pain, anorexia, weight loss
pain may be worse after eating
may be associated with gastric cancer
PUD- duodenal ulcers
more common
symptoms: no s/s or burning pain
younger ages 30-50
pain improves after eating
many heal spontaneously
GERD
caused by weak (LES)
alcohol, tobacco, caffeine, peppermint, medications, fatty foods,chocolate, obesity, hiatal hernia
s/s: heartburn, upper abdominal pain, regurgitation/hypersalivation, respiratory symptoms
Proton pump inhibitor
reduce the secretion of acid in the stomach by binding to enzyme
heal 90% of ulcers within 4-8 weeks
H2 Blockers
blocks the effect of histamine at H2 receptors in the parietal cells of the stomach inhibiting gastric acid secretion
H2 blockers
acts by blocking H2 receptors in stomach to decrease acid production
should be administered with meals and okay to take with antacids but not at the same time
antacids
neutralizes stomach acid
otc (chewable, liquid, or pill form