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Lisinopril by Mind Map: Lisinopril

1. Topic 1: Pharmacokinetics and Pharmacodynamics of Lisinopril

1.1. distribution

1.1.1. believed to have little to no tissue accumulation

1.1.2. 25% absorbed and excreted in kindeys

1.1.3. crosses BBB poorly

1.2. adsorption

1.2.1. lipid solubility

1.2.2. peak serum concentrations at 7 hours after oral dose

1.2.3. peak effect related to saturation of avaliable ACE

1.2.4. Not affected by food

1.2.5. Steady state is achieved in 2-3 days

1.2.5.1. little accumulation

1.2.5.2. Significant accumulation occurs in patients with severe renal impairment

1.3. excretion

1.3.1. Half life: 12 hours

1.3.2. eliminated via the kidneys

1.3.2.1. glomerular filtration, tubular secretion, and tubular reabsorption

1.3.3. not metabolized

1.4. Doseage

1.4.1. Hypertension

1.4.1.1. 5 to 10 mg once daily up to 40mg

1.4.2. Heart failure with reduced ejection fraction

1.4.2.1. Titrate up to goal of 40mg daily

1.4.3. interesting note: no change in dose if patient has liver failure

1.4.4. Benzyl alcohol and derivatives must be avoided in neonates

1.4.5. 2.5 mg, 5 mg, 10 mg, 20 mg, 30 mg and 40 mg tablets for oral administration

1.5. Toxicicities

1.5.1. risk of hypotension

1.5.1.1. risk of injury from hypotension related events

1.5.1.2. chronic hypotension

1.5.1.2.1. oxygen deprivation

1.6. Pharmacodynamics

1.6.1. Side effects

1.6.1.1. Weakness

1.6.1.2. cough

1.6.1.2.1. dry, hacking, nonproductive cough

1.6.1.3. headache

1.6.1.4. fatigue

1.6.1.5. hyperkalemia

1.6.1.5.1. Most frequently seen with renal impairment, diabetes mellitus, and use of potassium-sparing diuretics,

1.6.1.5.2. Seen in patients using potassium supplements or potassium sparing diuretics

1.6.1.6. renal impairment

1.6.2. Physiology behind Lisinopril

1.6.2.1. RAAS Mechanism Review

1.6.2.1.1. Angiotensinogen>Angiotensin I > Angiotensin II > Aldosterone

1.6.2.1.2. Effects of RAAS mechanism

1.6.2.2. Off- label uses

1.6.2.2.1. Proteinuric chronic kidney disease

1.6.2.2.2. Posttransplant erythrocytosis (renal transplant recipients)

1.6.2.2.3. Non-ST elevation acute coronary syndrome

1.6.2.3. range of BP reductions is 11-15% in systolic and 13-17% in diastolic

1.7. Drug action

1.7.1. synthetic peptide derivative

1.8. Drug effect

1.8.1. inhibition of ACE

1.8.1.1. decreased plasma angiotensin II

1.8.2. Treatment of . hypertension and heart failure

1.9. Drug Structure

1.9.1. ** I can not add graphics in this mind map software but I would add the chemical structure here

1.9.2. Chemical formula: C21H31N3O5

1.10. Doseage for adults

2. Topic 2: Dental applications and considerations of Lisinopril

2.1. Anxiety management

2.1.1. Barbiturates

2.1.1.1. may enhance the hypotensive effect

2.2. Considerations before treatment

2.2.1. No special considerations for bleeding

2.2.2. No special considerations before local annesthesia or vasoconstrictor use

2.2.3. dry, hacking, nonproductive cough can potentially interfere with dental treatment

2.3. Adverse effects

2.3.1. Side effect: Hyperkalemia

2.3.1.1. Seen in patients using potassium supplements or potassium sparing diuretics

2.3.2. orthostatic hypotension

2.3.2.1. Occurs when patient stands up after laying down during an appointment

2.3.2.2. Use extra caution when changing positions

2.3.2.3. Allow time for patient to adjust to upright position and watch carefully

2.3.3. Xerostomia

2.3.3.1. increased risk of caries

2.4. Pain management

2.4.1. NSAIDS- decreased lisinopril effect

2.4.1.1. Patients on ACEi should not take NSAIDS for more than 5 days since the NSAIDS may decrease the effect of the anti-RAAS medication (olin 2007)

2.4.2. Aspirin- decreased lisinopril effect

2.4.3. general anesthesia

2.4.3.1. hypotension may occur

2.5. Dental Surgery

2.5.1. If hypotension is a large risk, consider stopping lisinopril 24 hours prior to surgery

3. Topic 3: General Clinical Considerations

3.1. Indications

3.1.1. Mild to moderate hypertension

3.1.2. Acute MI

3.1.3. Congestive heart failure

3.1.3.1. increases cardiac output, and decreases pulmonary capillary wedge pressure and mean arterial pressure

3.1.4. Hypertension

3.1.4.1. 130 / 80 mmHg

3.2. Contraindications

3.2.1. ACE inhibitor allergy

3.2.1.1. Angiotensin II receptors are a viable alternative

3.2.1.2. Angioedema is a potentially life threatening response

3.2.1.2.1. effects on immunologic mediators

3.2.1.3. highest frequency in the first 3 months

3.2.1.4. ACE inhibitors may cross-react immunologically

3.2.2. renal impairment

3.2.2.1. Particularly in pediatric patients

3.2.3. Pregnancy

3.2.3.1. Fetal toxicity is a box warning

3.2.4. Normal blood pressure

3.2.4.1. 120 / 80 mmHg

3.3. Drug Interactions

3.3.1. NSAIDS- decreased lisinopril effect

3.3.2. Lithium- increased lithium levels andtoxicity risk

3.3.3. Aspirin- decreased lisinopril effect

3.3.4. Cyclosporine- increased risk of hyperkalemia

3.4. Brand names in the US

3.4.1. Prinivil

3.4.2. Qbrelis

3.4.3. Zestril

3.5. Most common adverse reactions

3.5.1. Hypotension

3.5.2. Dizziness

3.5.3. Increased serum creatinine

3.5.4. Syncope

3.5.5. Cholestatic jaundice

3.5.6. Renal function deterioration

3.5.6.1. increases in BUN and serum creatinine

4. PB Regulation mechanisms

4.1. Diuretics

4.1.1. increase excretion of salt and water

4.1.2. Acts on

4.1.2.1. Proximal tubule

4.1.2.1.1. Acetazolamide

4.1.2.1.2. Mannitol

4.1.2.2. loop of Henle

4.1.2.2.1. Furosemide

4.1.2.3. distal convoluted tubule

4.2. Adrenergic blockers

4.2.1. a1 blocker

4.2.1.1. Prazosin

4.2.1.2. peripheral resistance reduced

4.2.1.3. Some times used in combination with other agents

4.2.2. b blocker

4.2.2.1. non selective blocker

4.2.2.1.1. propanolol

4.2.2.1.2. reduces stroke volume and heart rate

4.2.3. Centrally acting drugs

4.2.3.1. sympathetic nerve firing frequency is reduced

4.2.3.1.1. caused by activation of a2 receptors

4.2.3.2. Clonidine

4.3. Ca Blockers

4.3.1. Dihydropyridines

4.3.1.1. selective for smooth muscle relaxation

4.3.1.1.1. nifedipine

4.3.1.1.2. amlodipine

4.3.2. Benzothiazepines

4.3.2.1. effect vascular smooth muscle and cardiac muscle

4.3.3. Phenylalkylamines

4.3.3.1. effect vascular smooth muscle and cardiac muscle

4.4. Vasodilators

4.4.1. Directly acting vasodilator

4.4.1.1. reduce BP

4.4.2. reduce BP

4.4.3. Nitroprusside releases NO

4.5. Anti RAAS system

4.5.1. Lisinopril

5. References

5.1. Hogg RJ, Delucchi A, Sakihara G, et al. A multicenter study of the pharmacokinetics of lisinopril in pediatric patients with hypertension. Pediatr Nephrol. 2007; 22(5):695-701.[PubMed 17216247]

5.2. Lancaster, S. G., & Todd, P. A. (1988). Lisinopril. Drugs, 35(6), 646-669.

5.3. Os, I., Bratland, B., Dahlöf, B., Gisholt, K., Syvertsen, J. O., & Tretli, S. (1994). Female preponderance for lisinopril-induced cough in hypertension. American journal of hypertension, 7(11), 1012-1015.

5.4. Prinivil (lisinopril) [prescribing information]. Whitehouse Station, NJ: Merck and Co Inc; October 2018.

5.5. Zestril (lisinopril) [prescribing information]. Wilmington, DE: AstraZenca Pharmaceuticals; July 2017.

5.6. Leicomp for Dentistry- Lisinopril

5.7. Olin, B. R., Hebel, S. K., & Dombek, C. E. (2007). Drug interaction facts. St Louis, Mo: Facts and Comparisons Inc.