Lecture 7+8 Flashcards

1
Q

mannitol

A

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

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2
Q

clinical app. of osmotic diuretic

A

• Increase urine flow in patients with acute renal
failure
• Reduce increased intracranial pressure & treatment of cerebral edema
• Promote excretion of toxic substances

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3
Q

AE / contraindications of osmotic diuretics

A

• Extracellular water expansion (can lead to
hyponatremia)
• Tissue dehydration

Contraindications:
• Congestive Heart Failure
• Pulmonary edema

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4
Q

ADH antagonists

A

conivaptan

this drug works at the V1 and V2 receptors in the collecting duct

ADH controls permeability of collecting duct to water

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5
Q

V1R vs V2R

A

V1R = increases smooth muscle contraction

V2R = increases H20 permeability and reabsorption (more aquaporins)

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6
Q

Clinical app. of ADH antagonists

A

HR (only if benefits outweighs risk)

Euvolemic and hypervolemic hyponatremia

SIADH

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7
Q

AE of ADH antagonist

A
  • Infusion site reactions
  • Thirst
  • Atrial fibrillation
  • GI & electrolyte disturbances
  • Nephrogenic diabetes insipidus
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8
Q

contraindications of ADH antagonists

A
  • Hypovolemic hyponatremia

* Renal failure

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9
Q

first line treatments for hypertension

A

ACE-inhibitors, ARBs, calcium channel blockers, thiazide diuretics

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10
Q

second line treatments for hypertension

A

b-blockers, aldosterone antagonists

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11
Q

what are examples of ACE inhibitors

A

Captopril / Enalapril / Lisinopril

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12
Q

ACE inhibitors MOA

A
INHIBIT ACE (angiotensin converting enzyme) that
cleaves angiotensin I to form angiotensin II

DECREASE peripheral vascular resistance
DECREASE Na+ & H20 retention
INCREASE BRADYKININ levels

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13
Q

clinical app. of ACE inhibitors

A

hypertension

preserve renal function in those with diabetes nephropathy

effective in chronic HF

used following MI

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14
Q

ACEI’s / ARB’s

A

preserve renal function

prevents glomerular HTN

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15
Q

AE of ACE inhibitors

A
• Dry hacking cough
• Hyperkalemia
• Hypotension
• Angioedema (rare but life-threatening)
• Acute renal failure (patients with bilateral renal artery
stenosis)
• Rash, fever, altered taste
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16
Q

contraindications of ACE inhibitors

A

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

17
Q

concentric hypertrophy

A

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

18
Q

eccentric hypertrophy

A

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

19
Q

HF and the types

A

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
20
Q

systolic dysfunction

A

inability to contract properly
myocyte loss in MI

pressure overload (HTN)

volume overload (regurgitation)

Decreased contractility like in myocarditis, dilated
cardiomyopathy

21
Q

diastolic dysfunction

A

Inability of the heart to relax and fill properly

Massive ventricular hypertrophy
Myocardial fibrosis
Amyloidosis (extracellular deposition of amyloid)
Constrictive pericarditis

22
Q

left sided heart failure

A

left ventricle is failing

systemic hypertension
mitral or aortic valve disease
ischemic heart disease
cardiomyopathy

23
Q

right sided heart failure

A

right ventricle is failing

Intrinsic disease of the lung parenchyma/vasculature

Chronic obstructive pulmonary disease (COPD),

pulmonary hypertension

24
Q

high output failure

A

Occurs due to increased tissue demands
(anemia, hyperthyroidism and pregnancy)

symptoms of HF will occur even though the heart is well functioning

systolic dysfunction

25
low output failure
Decreased cardiac output Majority of cardiac diseases result in a low output cardiac failure
26
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
27
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
28
compensated HF
Dilated ventricle is able to maintain the cardiac output to maintain the needs of the body
29
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
30
left ventricular failure features
* Dyspnea * Orthopnea * Paroxysmal nocturnal dyspnea (PND)
31
right ventricular failure symptoms
* Systemic venous congestion * Distended neck vein * Enlarged tender liver * Soft tissue edema
32
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
33
right heart failure morphology
Liver: Chronic passive congestion, Nutmeg liver Spleen: Enlargement and congestion of spleen Pleural and Pericardial spaces: Effusions Soft tissue edema
34
Ischemic Heart Disease (IHD)
imbalance between cardiac blood supply (perfusion) and myocardial oxygen and nutritional requirements also known as coronary artery disease (CAD)
35
pathogenesis of IHD
1. Chronic progressive atherosclerotic narrowing of the epicardial coronary arteries 2. Variable degrees of superimposed acute plaque change, thrombosis and vasospasm