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Pharmacology > Week 6/7: Cardiovascular System > Flashcards

Week 6/7: Cardiovascular System Flashcards

1
Q

Hemophilia A: Definition, treatments

A

Factor VIII deficiency

Treatments:
- Factor VIII concentrate
- Desmopressin (DDAVP)
- Monoclonal antibody therapy
- Gene therapy

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2
Q

How does desmopressin treat hemophilia A?

A

Releases stored factor VIII form the endothelium. Used for mild hemophilia A

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3
Q

How does monoclonal antibody therapy treat hemophilia A?

A

Binds together two factors in the clotting cascade (IXa & X) that would normally be where factor VIII would work. Can’t be used for an acute bleeding episode.

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4
Q

How does gene therapy treat hemophilia A?

A

Reconstruction/repair of genetic material in patient’s body
Very expensive

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5
Q

Hemophilia B: Definition, treatment

A

Factor IX deficiency

Treatment: Factor IX concentrate

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6
Q

Microcytic anemia

A

Anemia characterized by small, abnormally shaped RBCs

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7
Q

Normocytic anemia

A

Anemia characterized by normal-shaped RBCs, but low RBC count

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8
Q

Macrocytic anemia

A

Anemia characterized by large RBCs

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9
Q

Nutrients/hormones essential for proper RBC formation (4)

A
  1. Iron
  2. Vitamin B12
  3. Folate
  4. Erythropoietin
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10
Q

PK/PD of iron (4 points)

A
  1. Absorbed in small intestine
  2. Stored as ferritin or binds transferrin for distribution
  3. Sent to bone marrow for use in Hgb
  4. Highly recycles, very minimal iron leaves the body
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11
Q

Iron deficiency: Cause, results, treatment

A

Cause: Due to uptake/demand imbalance
Results in dec. O2 carrying capacity (fatigue, pallor, tachycardia)
Treatment: PO iron supplement

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12
Q

PK/PD of vitamin B12 (4 points)

A
  1. Required for DNA synthesis and cell growth/division
  2. Catalyzes folic acid to active form, which is required for DNA synthesis
  3. Requires intrinsic factor from parietal cells of stomach for absorption
  4. Stored in liver, slow eleimination
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13
Q

Vitamin B12 deficiency: Cause, results, treatments

A

Cause: Usually due to lack of intrinsic factor
Results in the suppression of rapidly dividing cell groups (bone marrow and GI tract mucosa). Also results in neuronal demyelination of CNS
Treatments: Usually PO, IV if severe
- AE: HypoK

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14
Q

PK/PD of folic acid (4 points)

A
  1. Required for DNA synthesis and cell division/growth
  2. Must be converted into an active form (two pathways, one includes B12 and one doesn’t)
  3. Absorbed in small intestine
  4. Stored in liver
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15
Q

Folic acid deficiency: Cause, results, treatments

A

Cause: Poor diet (alcohol overconsumption) or malabsorptive disease
Results in suppression of rapidly dividing cell groups, can inc. colorectal CA + atherosclerosis risk, but no neuronal injury.
- Can cause neural tube defect in early fetus
Treatments:
- Correct underlying cause
- PO folic acid (inactive form)
- PO folinic acid (active form)
- Severe: IM folic acid and B12 injections followed by PO folic acid

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16
Q

PK/PD of erythropoietin (EPO) (3 points)

A
  1. Endogenous glycoprotein released by kidneys in response to hypoxia detection
  2. Results in stimulation of RBC production in bone marrow
  3. Response is limited if folate/B12/iron is low
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17
Q

Epoetin alpha and Darbepoetin alpha: Indications, AE

A

Indications: Lack of RBCs
AE:
CV events (MI, HTN, CVA)
Be careful if hemoglobin > 11 OR hemoglobin increased rapidly past 2 weeks

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18
Q

Darbepoetin alpha: What’s unique?

A

Slower clearance = longer 1/2 life, can administer less frequently

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19
Q

G-CSF Filgrastim: Indications, AE

A

Indications: Lack of WBC
AE:
Leukocytosis
Bone pain

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20
Q

Thrombopoietin receptor agonists: Indications

A

Lack of platelets – stimulate platelet production

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21
Q

PK/PD of cholesterol (3 points)

A
  1. Responsible for the flexibility of cell membranes and organelles
  2. Required for hormone synthesis
  3. Primarily manufactured in liver, but some dietary intake is also required
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22
Q

PD of lipoproteins (3 points)

A
  1. Transport cholesterol & triglycerides in the blood
  2. Contain apolipoproteins: recognition sites for
    cell surface receptors.
  3. Binding allows for cellular ingestion (endocytosis) & for metabolism
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23
Q

VLDL: Core hormone, associated apolipoproteins, actions, AE

A

Triglycerides as core
B-100
Actions: Delivers TGs from liver to adipose & muscle tissue
AE: Probably contributes to atherosclerosis

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24
Q

First line therapy for cholesterol management

A

Lifestyle modifications

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25
LDL: Core hormone, associated apolipoproteins, actions, AE
Cholesterol as core B-100 Actions: Delivers cholesterol from liver to nonhepatic tissue - Increased cellular demand for cholesterol -> increased LDL receptor # AE: GREATEST contribution to atherosclerosis - ASCVD probability is directly correlated w/ LDL levels
26
HDL: Core hormone, associated apolipoproteins, actions, AE
Cholesterol as core A-II, A-I Actions: Delivers cholesterol from peripheral tissues back to liver (i.e. promote removal) Not an AE but protects against atherosclerosis
27
Statins: Class, indications (1), MOA, AE (2), PK (4)
Class: HMG-CoA Reductase Inhibitors Indications: High cholesterol blood lvl MOA: Inhibits HMG CoA reductase → inc. LDL receptor proliferation → inc. LDL uptake into cell AE: All rare, generally well tollerated - Myopathy (rhabdomyolysis) - Hepatotoxicity PK - PO at night - Hepatic metabolism - Biliary excretion - Rosuvastatin is not well metabolized in Asian heritage
28
Statins and myopathies: Prevalence, symptoms, guidelines
Prevalence: Rare (5-10% of patients) Symptoms: - Aches - Tenderness - Weakness - Can progress to myositis w/ increased creatine kinase & K+ Guidelines: Measure creatine kinase upon start of therapy and again if symptomatic. Discontinue statin if creatine kinase >10x original
29
Colesevelam // Colestipol // Cholestyramine: Class, indications, MOA, AE
Class: Bile acid sequestrants Indications: High cholesterol blood lvl MOA: Nonabsorbable from GI tract → binds to bile acid → dec. reabsorption and inc. excretion of cholesterol - Ultimately inc.s LDL receptors in the liver AE: GI disturbance (constipation)
30
Ezetimibe: Indications, MOA, AE (4), PK (3)
Indications: High cholesterol blood lvl MOA: Act on brush border enzyme → prevents dietary cholesterol absorption and inhibits reabsorption of cholesterol secreted in the bile AE: - Myopathy - Hepatitis - Pancreatitis - Thrombocytopenia PK: - PO - Converted to active metabolite ezetimibe glucuronide - Biliary elimination
31
Gemfibrozil // Fenofibrate: Class, indications, MOA, AE (4)
Class: Fibric acid derivatives (fibrates) Indications: To lower VLDL levels MOA: Inhibits hepatic extraction of free fatty acids → liver cannot synthesize as many triglycerides → dec. VLDL AE: GI disturbances are most common Gallstones Myopathy Hepatotoxicity
32
Monoclonal antibody (PCSK9) inhibitor: Indications, MOA, AE (2), PK (3)
Indications: High cholesterol blood lvl MOA: PCSK9 is a protein that binds LDL receptors in the liver - Inhibition of PCSK9 = freed receptors = inc. LDL uptake AE: - Hypersensitivity - Immunogenicity PK: - SubQ only - Dosing Q2 weeks - Long half-life
33
Monoclonal antibody (PCSK9) inhibitor: What's unique?
Used in combination with statins in patients with very high risk of morbidity/mortality
34
ACL inhibitor: Indications, MOA, AE (2), PK (3)
Indications: High cholesterol blood lvl MOA: Inhibit ACL → dec. cholesterol synthesis → inc. LDL receptor proliferation → inc. LDL cell uptake AE: - Increase uric acid (gout risk) - Increase tendon rupture risk PK: - PO - Converted to active metabolite - Excreted renally
35
Most effective and lease effective drugs for lowering LDL and total cholesterol
Most effective: Statins
36
2 general steps of blood coagulation
1. Platelet plug 2. Fibrin mesh production
37
Steps of platelet plug formation (3)
1. When platelets contact surface of damaged blood vessel, they adhere 2. Platelet receptors activate when exposed to an agonist 3. Fibrinogen binds to activated platelet receptors 'bridging' between platelets
38
Platelet agonists (5)
1. ADP 2. TXA2 3. Thrombin 4. Collagen 5. Platelet aggregation factor
39
Steps of fibrin mesh (2)
1. Intrinsic pathway: Triggered by contact with collagen of an injured blood vessel 2. Extrinsic pathway: Triggered by thromboplastin, which is released by vascular wall trauma
40
Coagulation factors that depend on vitamin K for synthesis (4)
II (2), VII (7), IX (9), X (10)
41
Degradation of clots is through _______
Plasmin (precursor: plasminogen)
42
Heparin // LMWH: Class, indications (5), MOA, AE (3), PK
Class: Antithrombin activator Indications: - DVT/PE - Open heart surgery - Dialysis - Disseminated intravascular coagulation (DIC) - Acute MI MOA: Activate antithrombin → inhibit coagulation factors to prevent AE: - Hemorrhage - Heparin-induced thrombocytopenia (HIT) - Hypersensitivity PK: Hepatic metabolism/renal excretion
43
Describe the PK difference between Heparin and LMWH
1. Size - Heparin is large & polar = no PO absorption, no placenta crossing - LMWH is smaller 2. Protein binding - Heparin: Varied protein binding -> heparin plasma concentrations require lab monitoring (PTT) - LMWH: Dec. protein binding due to smaller size 3. 1/2 life - Heparin: 1.5hrs - LMWH: 1.5 x 6 = 9hrs (slower liver clearance) 4. Bleeding - Bleeding is less common with Heparin
44
Describe the PD difference between Heparin and LMWH
Heparin suppresses thrombin = factor Xa LMWH suppresses factor Xa > thrombin
45
Heparin-induced thrombocytopenia (HIT): Prevalence, actions, presentation, treatment/guidelines
Prevalence: Rare (0.2-5%) Actions: The body produces antibodies against heparin-platelet protein complexes Presentation: - Decreased platelets via consumption & destruction (thrombocytopenia) - Increased platelet activation (increase in thrombotic events – stroke, MI, etc.) Treatment: Discontinue heparin & use alternatives. - Supportive care
46
Warfarin: Class, indications (3), MOA, AE (3), PK (7)
Class: Vitamin K inhibitor Indications: - DVT/PE - Thromboembolism in prosthetic heart valves - MI/stroke risk MOA: Inhibits enzyme that activates vitamin K → prevents synthesis of factors 2, 7, 9, 10 → dec. fibrin formation AE: - Hemorrhage - Infant hemorrhage (caution in breastfeed) - Fetus hemorrhage (contraindicated in pregnancy) PK: - PO - 99% protein bound - Free drug crosses membranes (placenta, breastmilk) - CYP450 hepatic metabolism - Renal/fecal excretion - Peak effects take several days - ½ life = 1.5-2 days
47
Warfarin: Clinical considerations
Requires lab monitoring by PT/INR
48
Warfarin OD: Presentation, treatment
Presentation: Anaphylactoid responses Treatment: - IV/slow admin - FFP, plasma concentrates of vitamin K dependent factors
49
Dabigatran // Bivalirudin // Desirudin // Argatroban: Class, indications (2), MOA, AE (2), PK (5)
Class: Direct thrombin inhibitors Indications: Prevent thrombosis - DVT/PE MOA: Inhibit thrombin → dec. conversion of fibrinogen to fibrin and activation of factor XIII → prevents fibrin mesh formation AE: GI upset - Hemorrhage PK: - PO - Peak 1-3hrs (food affects absorption rate) - Low protein binding - Renal elimination, no liver metabolism (no interactions w/ CYP450 inducers/inhibitors) - ½ life 13hrs (normal renal function) → 18hrs (mod renal dysfunction
50
Whats unique about direct thrombin inhibitors?
- Rapid onset - No need to monitor lab values: predictable responses = reliable dosing - Few food-drug interactions - Lower risk of major bleeding
51
What's unique about Bivalirudin?
Unique AEs: Hypotension, back pain, headache Unique PK: continuous IV infusion * Immediate onset * Eliminated by renal excretion & proteolytic cleavage -> ½ life = 25mins (normal renal function)
52
Rivaroxaban: Class, indications (3) , MOA, AE (2), PK (3)
Class: Direct factor Xa inhibitors Indications: - DVT/PE - Prevent thrombosis - CVA MOA: Inhibit factor 10a → prevent fibrin mesh formation AE: Maternal hemorrhage & fetal risk (not approved in pregnancy) PK: - PO - Peak 2-4hrs - CYP450, 35% unchanged in urine
53
Rivaroxaban: What's unique?
- Rapid onset - Fixed dosage - Lower bleeding risk - Few drug interactions - No lab monitoring required
54
Rivaroxaban OD: Treatment
No specific antidote but: - Can give activated charcoal to avoid further absorption - Hemorrhage = factor VIIa or factor II (prothrombin)
55
Asprin: Class, indications (5), MOA, AE (3), PK
Class: COX inhibitor (irreversible) Indications: - Acute MI - CVA - TIA - Chronic stable angina - Stents MOA: Inhibit COX → dec. platelet activation/aggregation, dec. TXA2 mediated vasoconstriction → inhibit platelet plug AE: - Bleeding (general) - GI bleed - Hemorrhagic stroke PK: Effects last the lifetime of platelet
56
Clopidogrel // Prasugrel // Ticagrelor: Class, indications, MOA, AE (2), PK (3)
Class: P2Y12 ADP receptor antagonists Indications: Prevention of stent thrombosis & thrombotic events MOA: Antagonize P2Y12 receptor so ADP can’t bind → dec. platelet activation/aggregation → inhibit platelet plug AE: - Bleeding - TTP PK: - PO - Hepatic metabolism - Effects in 2hrs
57
Ticagrelor: What's unique?
It's reversible
58
Vorapaxar: Class, indications, MOA, AE, PK (5)
Class: PAR-1 antagonist Indications: Use with aspirin/clopidogrel in reduction of thrombotic events MOA: Reversible binding to PAR-1 receptors on platelet surface → dec. effects of thrombin → dec. platelet activation/aggregation AE: Bleeding (general) PK: - PO - Effects in 1hr - Hepatic metabolism - Fecal excretion - Long ½ life
59
Abciximab: Class, indications, MOA, AE, PK
Class: GP IIb/IIIa receptor antagonists Indications: Short term to prevent ischemic events in those w/ ACS or undergoing PCI MOA: Blocks IIb/IIIa receptors on platelet  inhibition of final common step in platelet aggregation - Inhibits aggregation from all factors (collagen, TXA2, ADP, thrombin, platelet activation factor)
60
Abciximab: What's unique?
Part of the most powerful class of anti-platelet drugs
61
Alteplase (tPA) // Tenecteplase // Reteplase: Class, indications, MOA, AE, PK
Class: Thrombolytic drugs Indications: Remove already formed clots - Acute MI - Acute stroke - Acute massive PE MOA: Binds to plasminogen -> plasmin - Plasmin breaks down already-formed clot AE: Special handling - Avoid manipulation of patient - Avoid SQ/IV inject - Avoid invasive procedures - Minimize use of other blood thinners
62
Acute severe hemorrhage caused by thrombolytic drugs: Treatments (3)
1. Whole blood replacement 2. FFP (plasma with clotting factors) 3. Aminocaproic acid (prevents plasminogen activation)
63
3 ways blood pressure is regulated
1. IMMEDIATE: SNS (α1 = vasoconstriction, β1 = HR & contractility increase) - β1 also stimulates renin release 2. SHORT/MEDIUM TERM: RAAS (renin release due to decreased RBF/blood volume) 3. LONG TERM: Kidney (decreased GFR promotion of fluid retention)
64
3 ways the body tries to adapt to dec. EF
1. Cardiac dilation (occurs due to increased venous pressure & decreased contractility) = increased diastolic filling 2. Increased SNS tone (occurs due to baroreceptors) = increased HR/contractility/venous tone/arteriolar tone 3. Retention of blood volume (due to low RBF/GFR & B1 agonism -> RAAS activation & decreased GFR) = H2O/Na+ retention
65
Determinants of O2 supply (2) and demand (3)
O2 supply: Myocardial blood flow 1. Coronary dilation 2. HR O2 demand 1. HR 2. Contractility 3. Intramyocardial wall tension
66
STEMI: Pathophysiology (3) and effects (3)
Pathophysiology: - CAD (atherosclerotic plaque) rupture - Platelet aggregation + vasoconstriction in the area - Cessation of blood flow to the myocardium that the vessel feeds Effects: - Death of cardiac myocytes = decrease contractility, release of H+/K+. - K+ = dysrhythmia risk - Longer term, collagen deposition & remodeling (angiotensin II & aldosterone) = increased HF & death risk
67
Diuretics: Mechanisms and 4 classes
Mechanism: Increase UOP and alter electrolyte excretion 4 classes: work on different areas of the nephron * Loop * Thiazide * K+ sparing * Osmotic
68
Furosemide: Class, indications, MOA, AE (3)
Class: Loop Diuretics Indications: HTN MOA: Blocks Na/Cl/K cotransporter in ascending LoH → excrete Na+/K+/2Cl- in urine followed by water AE: - HypoK - HypoNa+ - HypoCl- - Ototoxicity - Dehydration/hypotension - Drug interactions with other ototoxic drugs - Drug interactions with digoxin
69
Hydrochlorothiazide (HCTZ): Class, indications, MOA, AE (6), PK
Class: Thiazide Diuretics MOA: Block Na/Cl/K reabsorb @early distal convoluted tubule → these are excreted in urine followed by water AE: - HypoK - HypoNa+ - HypoCl- - Dehydration/hypotension - Increase uric acid lvl (gout risk) - Ineffective in kidney disease PK: Excreted unchanged in urine
70
Hydrochlorothiazide (HCTZ): What's unique? (3)
- The first line for HTN - Much lower max diuresis than loop diuretics - Not effective when GFR is too low
71
Spironolactone: Class, indications, MOA, AE (3), PK
Class: K+ Sparing Diuretics MOA: Blocks aldosterone - Decrease prod of Na/K exchange protein transporter - K+ retention, Na+/H2O excretion @late distal convol tubule - Dec. remodeling of CV system AE: - HyperK - Endocrine: Menstrual irregularities, gynecomastia PK: Onset in 48 hrs
72
Mannitol: Class, indications, MOA, AE (3), PK
Class: Osmotic Diuretics MOA: Freely filtered in GFR, stays in filtrate → draw water out to be excreted in urine AE: Fluid overload/edema - HF - Pulmonary edema PK: Excreted unchanged in urine
73
Mannitol: What's unique?
Strong diuresis, used for rapid excretion of volume in increased ICP/IOP
74
Treatment of low body fluid volume is based on whether there is... (3)
1. Equivalent H2O & solute loss (isotonicity is maintained) 2. More H2O lost than solute lost (blood is now hypertonic) 3. More solutes are lost than H2O lost (blood is now hypotonic)
75
HypoK: Treatment and administration guidelines
Treatment: K+ salts ROA: IV or PO Guidelines for IV admin: - Dilute + infuse slowly - Rapid infusion = cardiac arrest - Irritating to veins
76
HypoMg: Treatment and administration guidelines
Treatment: - PO for prophylaxis = Mg oxide - IV for severe deficiency = Mg sulfate Guidelines for IV admin: - Dilute + infuse slowly - Monitor for s/s hyperMg
77
HyperK: Treatment and guidelines
Treatment - Avoid K+ heavy foods - Avoid K+ sparing drugs - May require hemodialysis (HD) or peritoneal dialysis (PD) Guidelines: - Protect against K+ induced cardiotoxicity
78
HyperMg: Treatment
Treatment: May require hemodialysis (HD) or peritoneal dialysis (PD)
79
Angiotensin-converting enzyme (ACE) inhibitors (-pril): Indications, MOA (5ish), AE (8), PK (3)
Indications: HTN MOA: Inhibits ACE = Inhibition of ANG2 formation - Inc. vasodilation - Inc. diuresis, excrete out more Na - Dec. SNS response = dec. myocardial O2 supply - Prevention of CV remodeling AE: - HypoTN (first dose especially) - HyperK - Dehydration - Cough - Fetal injury - Renal failure - Rare: Angioedema, neutropenia PK: PO (except enalapril, which is IV) - All prodrugs (except lisinopril) that are converted in small intestine - Long 1/2 life
80
Angiotensin II receptor blockers (ARBs) (-artan): Indications, MOA, AE (8), PK
Indications: HTN MOA: Blocks the effects of ANG2 at the receptor - Inc. vasodilation - Inc. diuresis, excrete out more Na - Dec. SNS response = dec. myocardial O2 supply - Prevention of CV remodeling AE: - HypoTN - HyperK - Dehydration - Cough - Fetal injury - Renal failure - Rare: Angioedema, neutropenia PK: All PO
81
Compare ACE inhibitors to ANG2 receptor blockers, how are they different? Which is preferred?
MOA: - ACE inhibitors: Inhibits ACE = Inhibition of ANG2 formation - ARBs: Blocks the effects of ANG2 at the receptor Effects: - ARBs - Don't block kinase 2 = lower cough/angioedema risk - Dec. aldosterone release = lower hyperK risk - Less evidence that they reduce CV morbidity/mortality Preferred: ACE inhibitors
82
Aliskiren: Class, indications, MOA (5ish), AE (3), PK
Class: Direct renin inhibitor Indications: HTN MOA: Inhibit release of renin = block entire RAAS - Inc. vasodilation - Inc. diuresis, excrete out more Na - Dec. SNS response = dec. myocardial O2 supply - Prevention of CV remodeling AE: - HypoTN - HyperK - Dehydration PK: PO, high-fat meals impact absorption
83
Actions of beta blockers on CV (3) and kidneys (1)
CV: - Dec. HR - Dec. contractillity - Dec. AV node conduction velocity Kidneys: Dec. renin release = dec. ANG2/aldosterone production
84
Actions of calcium in the cardiac system (2)
1. Vascular smooth muscle + cardiac muscle - Inc. vasoconstriction and contractility 2. Pacemaker cells of the heart - Dec. action potential (SA node) and conduction velocity (AV node)
85
Classes of Ca2+ channel blockers (2)
1. Dihydropyridines: Mainly act on vascular smooth muscle @ therapeutic doses - Arteriole vasodilation - Reflex tachycardia/contractility inc. 2. Nondihydropyridines: Act on vascular smooth muscle and the heart - Arteriole vasodilation - Dec. HR - Dec. AV node conductivity - Dec. contractility
86
Verapamil // Dilitiazem: Class, indications (4), MOA, AE (9)
Class: Ca channel blockers - Non-dihydropyridines Indications: - HTN - Angina - Dysrhythmias - SVT MOA: Blocks Ca2+ @ vascular smooth muscle and the heart - Dec. HR, contractility, AV node conduction - Artery vasodilation → decrease afterload, coronary artery vasoconstriction AE: - Constipation - Dizziness - Facial flushing - Edema - Bradycardia - Heart block - Dec. contractility, dec. CO - Hypotension - HF
87
Nifedipine: Class, indications (2), MOA (3), AE (6), PK
Class: Ca channel blockers - Dihydropyridines Indications: - Prinzmetal angina - HTN MOA: Blocks Ca2+ vascular smooth muscle - Vasodilation of coronary arteries - Dec. afterload - Inc. contractility AE: - Reflex tachycardia - Peripheral edema - Flushing - Dizziness - Headache - Inc. myocardial O2 demand PK: PO
88
Compare the effects of vasodilation on arteries to veins
Arterioles: - Dec. afterload = inc. CO and tissue perfusion Veins: - Dec. preload = dec. ventricular filling and contractility, which dec. CO and tissue perfusion
89
AE of vasodilation (3)
1. Orthostatic hypotension (venodilation > arteriole dilation) 2. Reflex tachycardia (arteriole dilation > venodilation) 3. Expansion of blood volume with long term use * Decreased BP = increased renin release = increased aldosterone = retention of Na+/H2O
90
Hydralazine: Class, indications, MOA, AE
Class: Vasodilator Indications: HTN Actions: Dec. afterload MOA: Unknown - Direct arteriole vasodilation AE: - Fluid retention with long-term use - SLE-like syndrome - Headache - Dizziness - Fatigue - Hypotension - Reflex tachycardia
91
Sodium nitroprusside: Class, indications, MOA, AE, PK
Class: Vasodilator Actions: Dec. preload Indications: - Prinzmetal angina - HTN MOA: Vasodilate veins via NO AE: - Tolerance can develop rapidly - Can’t be used with other hypotensives - Long-term infusion can result in thiocyanate toxicity PK: - PO has insane first pass effect - IV onset is immediate
92
Sodium nitroprusside: What's unique?
Extremely potent and works faster than any other vasodilator, drug of choice for HTN emergencies
93
Digoxin: Class, indications, MOA, actions (3), AE (8)
Class: Cardiac glycoside Indications: HTN MOA: Selectively inhibits Na/K/ATPase pump - Build up of Ca2+ intracellularly = inc. actin/myosin interactions - Inc. contractility Actions: - Dec. HR - Slowed AV node conduction - Inc. electrical excitability in ventricles AE: - Cardiac dysrhythmias - GI: Anorexia, nausea/vomiting - CNS: Fatigue, visual disturbances * GI + CNS AE precede dysrhythmias = can be a warning sign Contraindications: - AV heart block - Symptomatic bradycardia - Caution in renal impairment - Caution in electrolyte disturbances
94
Nitroglycerin: Class, indications, MOA, AE, PK
Class: Organic nitrates Indications: HTN - Angina MOA: Uptake into vascular smooth muscle, conversion into NO (active form) - NO activates guanylyl cyclase, which catalyzes cGMP formation - cGMP = dephosphorylation of light chain myosin in vascular smooth muscle - Thus, cannot interact w/ action = relaxation = vasodilation AE: - Caution with drugs that cause hypotensive effects - Tolerance develops rapidly - Avoid abrupt withdrawal to avoid coronary vasospasm PK - Highly lipid soluble - Lots of ROA: Sublingual, buccal, transdermal, PO, IV
95
Treatment of HTN: Considerations, first-line therapy, HTN emergency, HTN of pregnancy
Considerations: - Cause of HTN - Comorbid conditions First-line therapy: Thiazide diuretics HTN emergency: Sodium nitroprusside or labetalol HTN of pregnancy: Labetalol or methyldopa
96
Classes of antidysrhythmic medications
Class I: Na+ channel blockers Class II: Beta blockers Class III: K+ channel blockers Class IV: Ca2+ channel blockers
97
Quinidine // Procainamide: Class, indications, MOA (3), AE
Class: IA antidysrhythmic - Na+ channel blocker Indications: Atrial and ventricular arrhythmias MOA: Blocks Na+ channel - Inc. AP - Inc. ERP - Inc. QT interval AE: Anticholinergic
98
Lidocaine: Class, indications (2), MOA (2), AE
Class: IB antidysrhythmic - Na+ channel blocker Indications: - Post MI - Ventricular arrhythmias MOA: Blocks Na+ channel - Dec. AP - Dec. ERP AE: Toxicity at high doses
99
IC antidysrhythmics: Class, indications (2), MOA, AE
Class: Na+ channel blockers Indications: - SVTs - Afib MOA: Blocks Na+ channel - Inc. ERP in AV node (but not ventricular tissue) AE: Can induce life-threatening VT
100
Metoprolol // Esmolol: Class, indications (3), MOA (3), AE (3)
Class: Beta blockers Indications: - SVT - VT - Post-MI MOA: Dec. HR, contractillity, AV node conduction AE: - Bradycardia - HypoTN - Can’t be given with CCB
101
Amiodarone: Class, indications, MOA (4), AE (8), PK
Class: K+ channel blocker Indications: VT MOA: Blocks K channel - Delay repolarization - Inc. AP duration - Inc. ERP - Prolongs QT AE: - Pulmonary fibrosis - Hypothyroidism - Hepatotoxicity - Prodysrhythmic: torsades, bradycardia, AV block - Corneal microdeposits - Skin discoloration PK: Extremely long half life (25-60 days)
102
Adenosine: Class, indications, MOA, AE (4), PK
Class: Class V antidysrhythmic Indications: VT MOA: Binds adenosine receptor in cardiac tissue → open K+ channel → hyperpolarize → prevent next contraction / temporary heart stop AE: - Flushing - Transient hypotension - Transient chest pain - Transient flat line PK: Extremely short half life (10 secs) → needs to be given w saline flush
103
Atropine: Class, indications, MOA, AE (3)
Class: Anti-cholinergic Indications: Symptomatic bradycardia MOA: M antagonism - Inc. HR AE: - Decreased GI/GU activity - Mydriasis - Dry mouth

Pharmacology (15 decks)

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