This document discusses ACE inhibitors, which are medications that lower blood pressure by inhibiting the renin-angiotensin-aldosterone system. It describes how ACE inhibitors work to decrease blood pressure by blocking the conversion of angiotensin I to angiotensin II. Common uses of ACE inhibitors include treatment of hypertension, heart failure, myocardial infarction, diabetic nephropathy, and type 2 diabetes. Potential side effects include first-dose hypotension, dry cough, hyperkalemia, and renal failure. Drug interactions and considerations for use such as lifestyle changes and monitoring are also reviewed.
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RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
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Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
2. ACE Inhibitors
ACE Inhibitors are medications that belong in the
class of medications known as antihypertensive
medications.
ACE Inhibitors work on the Renin-Angiotensin-
Aldosterone System
3. Renin-Angiotensin-Aldosterone System
A system which works to increase blood pressure
when the pressure within the kidneys drops.
As a result of low blood pressure and/or oxygenation
in the nephron, renin is released from the
juxtaglomerular cells.
Renin travels to the liver via the cardiovascular system
and combines with angiotensinogen to form
angiotensin I.
Angiotensin I travels through the cardiovascular
system and arrives at the lungs where it is changed
into Angiotensin II.
The alveoli use Angiotensin Converting Enzyme also
known as kinase II to cause this conversion.
4. Renin-Angiotensin-Aldosterone System cont.
Angiotensin II is a powerful vasoconstrictor which
causes a rise in peripheral resistance and
increases pressure.
Angiotensin II works to increase the release of
aldosterone from the adrenal glands.
Aldosterone causes renal retention of sodium and
water, which further increases blood pressure by
increasing volume.
5.
6.
7. Mechanism of Action for ACE Inhibitors
ACE Inhibitors work in the lungs to inhibit
Angiotensin Converting Enzyme from turning
Angiotensin I into Angiotensin II.
These medications cause an increase of bradykinin,
which inhibits kinase II, another name for
Angiotensin Converting Enzyme.
Blood Pressure is decreased due to a decrease in blood
volume, peripheral resistance, and cardiac load.
ACE Inhibitors, inhibit vasoconstriction and release
of aldosterone which inhibits the retention of sodium
and water.
8. Indications For Use
Hypertension-used especially for malignant
hypertension and hypertension secondary to renal
arterial stenosis.
Benefits of Using an ACE Inhibitor as they:
Do not interfere with cardiovascular reflexes
Do not interfere with patients who have asthma, like
beta-blockers do.
Do not decrease potassium levels.
Do not cause lethargy, weakness and sexual
dysfunction.
“ACE inhibitors reduce the risk of cardiovascular
mortality caused by hypertension.”
9. Indications For Use cont.
Heart Failure
By decreasing arteriolar tone region blood flow to the
heart improves.
By decreasing afterload, cardiac output increases.
Venous dilation increases causing a decrease in
pulmonary congestion and peripheral edema.
Dilates the vessels of the kidneys increasing renal flow
and helps to excrete sodium and water. This helps to
decrease edema and blood volume.
Prevents pathologic changes in the heart that result from
reducing the angiotensin II levels in the heart.
10. Indications For Use cont.
Myocardial Infarction (MI)
Decreases the chance of heart failure after an MI.
Should be given for 6 weeks post MI. If heart failure
occurs it should be considered for permanent use.
Nephropathy
Slows renal disease of diabetic or nondiabetic origins
Decreases glomerular filtration pressure.
11. Indications For Use cont.
Type 2 Diabetes
Decreases morbidity in high risk patients.
Increased levels of angiotensin II have a correlation to
type 2 diabetes.
ACE inhibitors increase kinin levels, which increase
production of prostaglandins and nitric oxide.
Prostaglandins and nitric oxide improve muscular
sensitivity to insulin.
May preserve pancreatic function and prevent onset of
diabetes especially with people who have hypertension.
13. Benazepril: 10 mg once daily in patients initial dose (not on a
diuretic). Usual dose: 20-40 mg in a single or 2 divided doses.
Captopril: HFrEF (Heart failure with reduced ejection fraction)/
HTN/Left ventricular dysfunction after myocardial infarction (LVD
after MI): 6.25-12.5 mg three times a day (with diuretic) with goal
of 50 mg three times a day for HFrEF. Diabetic nephropathy: 25 mg
three times a day.
Enalapril: HFrEF/HTN: 2.5-5 mg once or twice daily, increased up
to 40 mg/day every 1-2 weeks in 2.5 mg intervals. IV : 1.25 mg/dose
every 6 hours
Fosinopril: HFrEF/HTN: 10 mg daily initially, then titrate to effect
(max dose 40 mg daily). Usual dose: 20-40 mg daily.
14. Moexipril: Hypertension: 7.5 mg once daily (not on a diuretic) or
3.75 mg once daily (when combined with a diuretic). Administer 1
hr prior to meal. Maintenance: 7.5-30 mg daily in 1-2 divided
doses
Perindopril: HTN: Initial: 4 mg daily; titrate to desired effect
every 1-2 weeks to a max dose of 16 mg/day. Usual dose 4-8
mg/day in 2 divided doses. Stable coronary artery disease (CAD):
Initial: 4 mg once daily for 2 weeks then increase to 8 mg once
daily as tolerated.
Quinapril: HTN: 10-20 mg daily initially. Initial dose may be
reduced to 5 mg daily (if patient on a diuretic). Range: 10-40 mg
once daily. HFrEF: 5 mg once or twice daily; titrate to desired
effect every week to a dose of 20-40 mg daily in 2 divided doses.
15. Lisinopril: HTN: Initial 10 mg daily (no diuretic) or 5 mg daily
(if on diuretic). Dose range: 10-40 mg daily. HFrEF: Initial: 2.5-5
mg once daily; titrate by 10 mg increments every 2 weeks to
target of 20-40 mg/day. Acute MI: 5mg immediately, uptitrated
to 10mg daily
Ramipril: HTN: 2.5-5 mg once daily (max dose of 20 mg/day).
Left ventricular dysfunction (LVD) post-MI: 2.5 mg twice-daily;
titrate to 5 mg twice daily as tolerated. Reduced risk of stoke, MI
and death Initial: 2.5 mg once daily for first week, then 5 mg
once daily for weeks 2-4, then titrate to 10 mg once daily as
tolerated.
Trandolapril: CHF/LVD Initial: 1 mg/day, titrate to 4 mg/day as
tolerated. HTN: 1 mg/day initially (may use 2 mg/day in black
patients) max dose=8mg/day; titrate to desired effect in 1 week
intervals.
16. Side effects:
Altered sense of taste (Metallic taste)
Allergic skin rashes
Fatigue
Dizziness
Dry cough
Headaches
17. Adverse Effects
First-Dose Hypotension
Usually occurs with initial dose.
Worse in patients with severe hypertension, or are on
diuretics, or are sodium or volume depleted.
Cough
“Persistent, dry, irritating, nonproductive cough can
develop with all ACE inhibitors.”
Due to rise in bradykinin which occurs due to inhibition
of kinase II.
Occurs in 5-10% of patients and is more common in
women and the elderly.
18. Adverse Effects cont.
Hyperkalemia
Potassium levels rise due to the inhibition of aldosterone,
which causes potassium to be retained by the kidneys.
Renal Failure
Can cause renal insufficiency in people who have bilateral
renal artery stenosis, because dropping the pressure in the
renal arteries in these patients can cause glomerular
filtration to fail.
Fetal Injury (Teratogenicity)
In the second and third trimesters a fetus can experience
hypotension, hyperkalemia, skull hypoplasia, renal failure,
and death. Recent evidence also implies 1st trimester
exposure has increased teratogenic risk.
19. Drug Interactions
Antihypertensive agents
Can cause an increased effect of medications especially with
diuretics.
Potassium increasing medications
Cause an increased risk of hyperkalemia due to the
suppression of aldosterone. (ACEIs, NSAIDs, ARBs &
Potassium-sparing diuretics )
Lithium
Increases to risk of lithium toxicity.
Allopurinol
Increases hypersensitivity to medication
NSAIDS (Ibuprofen, Naproxen)
Reduce antihypertensive effects of medication.
20. Considerations
Encourage lifestyle changes
Weight loss
Quit smoking
Decrease alcohol intake
Encourage exercise to help lower blood pressure
Monitor Renal Function
BUN, Creatinine, and Potassium levels
Monitor for decreased fluid volume which can bottom our
blood pressure
Excessive sweating
Diarrhea
Vomiting
Dehydration
21. Considerations cont.
Monitor for 1st-dose hypotension
May have to stop other antihypertensive medications at
initiation of ACE inhibitors.
May have to give these medications in lower doses going
forward.
Discontinue diuretics for 2-3 days prior to starting an ACE
inhibitor.
Monitor BP for several hours and if patient becomes
hypotensive lay patient supine and consider discussing IV
bolus of saline with the MD.
Educate Patient
Educate the patient about the medication including name
adverse effects, drug interactions.
Educate the patient about the signs of hypotension,
hyperkalemia, and renal failure. If patient is taking lithium
discuss the signs of lithium toxicity.
22. References
Karch, A. (2011). Focus on nursing pharmacology (5th
ed.). Philadephia, PA: Wolters Kluwer | Lippincott
Williams & Wilkins.
Lehne, R. (2007). Pharmacology for nursing care (6th ed.).
St. Louis, MO: Saunders|Elsevier.
Solski, L. V. & Longyhore. (2008). Prevention of type 2
diabetes mellitus with angiotensin-converting-
enzyme inhibitors. American Journal of Health-
System Pharmacy, 65(10): 935-40.
Waterfield, J. (2008). ACE inhibitors: use, action, and
prescribing rationale. Nurse Prescribing, 6(3): 110-4.