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LDL (BAD) - HDL (GOOD)
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We don’t know the causes of ASCVD but what is it linked to and what is the treatment?
linked to hyperlidemia (metabolic syndrome)
Tx -> 3-6 months diet change
What are the 5 major factors that increase the risk of ASCVD
Abdominal obesity
high blood pressure
high blood triglycerides
low levels of HDL
cholesterol and insulin resistance.
Fats are broken down into smaller parts in the “blank“ and the “blank“. The “blank“ stimulates (via the high cholesterol content) the “blank“ to release bile salts, which break them down into smaller parts the fat molecules
Fats are broken down into smaller parts in the stomach and the duodenum. The duodenum stimulates (via the high cholesterol content) the gallbladder to release bile salts, which break them down into smaller parts the fat molecules
Which class of fats is HDL and LDL apart of and are they lipoprotiens?
A) Triglycerides
B) Phospholipids
C) Cholesterol
C) Cholesterol and YES
Define and what are some causes (5)
Rhabdomyolysis
muscle damge releases proteins like myoglobin and electrolytes into the bloodstream, which can harm the kidneys and heart
causes: not moving,drugs, toxins, infections, and genetics
What are the 3 steps in Blood coag process? elaborate on the last step and what’s included in that step.
Vasoconstriction
Platelet Aggregation (Platelet Plug Formation)
Clotting factors
Intrinsic Pathway (damage within the blood vessel)
trigger by exposed collage
Extrinsic Pathway (damage within the tissues)
Tiggered by Tissue factor (TF)
Which clotting factor and vitamin are involved just before activation of the common pathway, and do the intrinsic and extrinsic pathways both lead into the common pathway?
factor X and Vitamin K (VIII)
YES
What happens in the common pathway
conversion of prothrombin → thrombin, and then fibrinogen → fibrin (stablizes the clot)
Where is vit.K made and what drug OD is it used for?
Liver and Warfarin
Define this bleeding disorders and what speific info she talked about them for each
Hemophilia
Vitamin K deficiency
von Willebrand Disease (vWD)
Disseminated Intravascular Coagulation (DIC)
Hemophilia – A Recessive genetic missing or defective clotting factor
Hemo A (VIII) Hemo B Hemo C
IT ONLY AFFECTS THE INTRINSIC PATHWAY
Vitamin K deficiency – affects production of clotting factors (II, VII, IX, and X )
EFFECTS ALL 3 PATHWAYS
Please eat dark leafy greens; spinach
Vit. K is administered to newborns, b.c immature livers
von Willebrand Disease (vWD) - dominant genetic dysfunction of von Willebrand factor (vWF).
Affects Platelet Aggregation (Platelet Plug Formation)
Disseminated Intravascular Coagulation (DIC)
Abnormal clots + bleeding, thus using up the clotting factors
Tx. -> Heparin - Plasma - IV blood
Define
Thrombocytopenia
Immune thrombocytopenic purpura (ITP)
Thromboembolic Disorders and what are the s/sx of this one
Thrombocytopenia
Low platelet count.
Immune Thrombocytopenic Purpura (ITP)
Autoimmune destruction of platelets.
Thromboembolic Disorders
Conditions where abnormal blood clots form and block vessels.
Hypoxia -> Anoxia -> Tissue necrosis
What are 2 natural plasma proteins that are used to breakdown clots?
Antithrombin III
Inhibits thrombin, preventing fibrin formation, helps control excessive clotting
Plasmin
The main enzyme responsible for breaking down fibrin
define
PT & INR
PTT
PT (Prothrombin Time) & INR (International Normalized Ratio)\
Test Extrinsic pathway and vit K lvl (liver fxn)
Monitor warfarin therapy
PTT (Partial Thromboplastin Time)
Measures clotting via the intrinsic pathway
Monitor heparin therapy
screen for many bleeding disorders
Class
Action
Adverse
D2D
Cholestyramine
Class → Bile Acid Sequestrants
Action → The bile acids pull the LDL from the bloodstream to bind to it in the intestine, thus dec the LDL lvl
Adverse:
Fatigue, HA
GI- constipation, hemorrhoids, GI upset.
Musculoskeletal-muscle aches and pains
D2D:
delay absorption- thiazide diuretics, digoxin, OCPs
Administer 1 hour prior to or 4-6 hours after the bile sequestrant
Class
Action
Tx
Adverse
D2D
Atorvastatin
Class → HMG-CoA Reductase Inhibitors
Action → blocks enzyme HMG-CoA reductase, dec LDL and Inc HDL lvls
Tx:
high cholesterol and LDL as an adjunct to diet and exercise
prophylaxis for MI in at-risk CAD patients
Adverse:
CNS- insomnia, HA
GI flatulence, abdominal cramp
D2D:
Erythromycin- increased risk of rhabdomyolysis
Digoxin and grapefruit juice - increase the risk of toxicity
Class
Action
Adverse
D2D
Ezetimibe
Class → Cholesterol Absorption Inhibitors
Action → Dec the absorption of cholesterol, used with stains ot HMG-CoA
Adverse → mild abdominal pain, diarrhea, muscle aches/pains
D2D:
admin 2 hours before or 4 after bile sequestrant,
With statins, myopathy, liver issues
With warfarin, increase levels, monitor- PT, PTT, INR
Class
Action
Tx
Adverse
Evolocumab
Class → PCSK9 Inhibitors
Action → stops PCSK9 from destroying liver LDL receptors, so your liver can clear more LDL from the blood.
Tx:
short term HF if no response to (digoxin, vasodilators, diuretics)
Emergent situations
Adverse → Flu-like s/sx
Class
Tx
Adverse
Contraindications
Aspirin (ASA)
Class → Antiplatelets
Tx → CV diseases (PVD, MI ….)
Adverse → bleeding, ASA-GI irritation, risk of ulcers, and tinnitus
Contraindications → known bleeding disorder, closed head injuries
Class
Adverse
Contraindications
D2D
Heparin
Class → Anticoagulants
Adverse:
Heparin-induced thrombocytopenia
bleeding
Contraindications
Known bleeding disorder, recent trauma, and or surgery, GI ulcers
D2D:
Salicylates, cephalosporin/ PCN inc bleeding risk
Decreased anticoagulation with nitroglycerin
Antidote for herparin OD is…
Protamine sulfate
Class
Tx
Adverse
Contraindications
D2D
Alteplase
Class → Thrombolytics
tx → MI, PE, clear IV and CVP lines
Adverse:
Bleeding (monitor Hgb and Hct)
arrythmias
Contraindications:
Known bleeding disorder, recent trauma, and or surgery, GI ulcers
D2D
anticoagulants, antiplatelets, watch for increased risk of bleeding
Class
Adverse
Contraindications
D2D
Aminocaproic acid
Class → Hemostatic Agents
Adverse → Prevent systemic clot breakdown, prevent blood loss
Contraindications:
dizziness, hallucinations (from changes in brain blood flow)
nausea, cramping
D2D
OCP
Action
Adverse
Antihemophilic Factor
Action → Replaces the missing VIII clotting factor in hemophilia A (classic)
Adverse → Risk use with blood products causing allergic rx s/sx