Lecture 7+8 Flashcards
mannitol
osmotic diuretic
Raises osmotic pressure of the plasma thus draws
H20 out of body tissues & produces osmotic diuresis
does not impact Na directly
increases urine volume
MOA: everywhere along the nephron
clinical app. of osmotic diuretic
• Increase urine flow in patients with acute renal
failure
• Reduce increased intracranial pressure & treatment of cerebral edema
• Promote excretion of toxic substances
AE / contraindications of osmotic diuretics
• Extracellular water expansion (can lead to
hyponatremia)
• Tissue dehydration
Contraindications:
• Congestive Heart Failure
• Pulmonary edema
ADH antagonists
conivaptan
this drug works at the V1 and V2 receptors in the collecting duct
ADH controls permeability of collecting duct to water
V1R vs V2R
V1R = increases smooth muscle contraction
V2R = increases H20 permeability and reabsorption (more aquaporins)
Clinical app. of ADH antagonists
HR (only if benefits outweighs risk)
Euvolemic and hypervolemic hyponatremia
SIADH
AE of ADH antagonist
- Infusion site reactions
- Thirst
- Atrial fibrillation
- GI & electrolyte disturbances
- Nephrogenic diabetes insipidus
contraindications of ADH antagonists
- Hypovolemic hyponatremia
* Renal failure
first line treatments for hypertension
ACE-inhibitors, ARBs, calcium channel blockers, thiazide diuretics
second line treatments for hypertension
b-blockers, aldosterone antagonists
what are examples of ACE inhibitors
Captopril / Enalapril / Lisinopril
ACE inhibitors MOA
INHIBIT ACE (angiotensin converting enzyme) that cleaves angiotensin I to form angiotensin II
DECREASE peripheral vascular resistance
DECREASE Na+ & H20 retention
INCREASE BRADYKININ levels
clinical app. of ACE inhibitors
hypertension
preserve renal function in those with diabetes nephropathy
effective in chronic HF
used following MI
ACEI’s / ARB’s
preserve renal function
prevents glomerular HTN
AE of ACE inhibitors
• Dry hacking cough • Hyperkalemia • Hypotension • Angioedema (rare but life-threatening) • Acute renal failure (patients with bilateral renal artery stenosis) • Rash, fever, altered taste
contraindications of ACE inhibitors
pregnancy (During 1st trimester due to risk of congenital malformations and during 2nd and 3rd trimesters because of risk of fetal hypotension, anuria & renal failure)
Patients with bilateral renal artery stenosis
concentric hypertrophy
Occurs in pressure overload on ventricles like in Hypertension and Aortic Stenosis
New sarcomeres are added in-parallel to existing sarcomeres
Increases wall thickness and decreased diameter of cavity
eccentric hypertrophy
Occurs in volume overload on ventricles like in Aortic regurgitation
New sarcomeres are added in-series with existing sarcomeres
Muscle mass increases proportional to chamber dilatation
There can be significant hypertrophy without any increase in thickness of the walls
HF and the types
inability of the heart, working at normal or elevated filling pressure, to pump enough blood to meet the metabolic demands of the body.
types: systolic and diastolic high output and low output left sided and right sided forward and backward compensated and decompensated
systolic dysfunction
inability to contract properly
myocyte loss in MI
pressure overload (HTN)
volume overload (regurgitation)
Decreased contractility like in myocarditis, dilated
cardiomyopathy
diastolic dysfunction
Inability of the heart to relax and fill properly
Massive ventricular hypertrophy
Myocardial fibrosis
Amyloidosis (extracellular deposition of amyloid)
Constrictive pericarditis
left sided heart failure
left ventricle is failing
systemic hypertension
mitral or aortic valve disease
ischemic heart disease
cardiomyopathy
right sided heart failure
right ventricle is failing
Intrinsic disease of the lung parenchyma/vasculature
Chronic obstructive pulmonary disease (COPD),
pulmonary hypertension
high output failure
Occurs due to increased tissue demands
(anemia, hyperthyroidism and pregnancy)
symptoms of HF will occur even though the heart is well functioning
systolic dysfunction
low output failure
Decreased cardiac output
Majority of cardiac diseases result in a low output cardiac failure
forward failure
Decreased output to the systemic circulation
Leads to renal hypoperfusion = activation of RAAS pathway = water and Na retention = edema
Patient will present with low blood pressure, fatigue,
syncope, shock
backward failure
Pulmonary congestion
leads to pulmonary edema = pulmonary HTN
leads to RHF = venous congestion
Patient presents with edema, ascites, raised jugular venous pressure (JVP), congested liver
compensated HF
Dilated ventricle is able to maintain the cardiac output to maintain the needs of the body
decompensated HF
Despite the compensator mechanisms, the failing
myocardium is no longer able to propel sufficient blood to meet the needs of the body even at rest
left ventricular failure features
- Dyspnea
- Orthopnea
- Paroxysmal nocturnal dyspnea (PND)
right ventricular failure symptoms
- Systemic venous congestion
- Distended neck vein
- Enlarged tender liver
- Soft tissue edema
left heart failure morphology
LV is hypertrophied and dilated
Brain: Hypoxic encephalopathy
Kidney: Acute tubular necrosis
Lungs:
heavy and wet. frothy mixture of fluid and blood
histo:
Congestion of pulmonary alveolar capillaries
Edema fluid in alveolar spaces
Persistent cases – brown induration of lungs
right heart failure morphology
Liver:
Chronic passive congestion, Nutmeg liver
Spleen:
Enlargement and congestion of spleen
Pleural and Pericardial spaces:
Effusions
Soft tissue edema
Ischemic Heart Disease (IHD)
imbalance between cardiac blood supply (perfusion) and myocardial oxygen and nutritional requirements
also known as coronary artery disease (CAD)
pathogenesis of IHD
- Chronic progressive atherosclerotic narrowing of the epicardial coronary arteries
- Variable degrees of superimposed acute plaque change, thrombosis and vasospasm
