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CRS > Lecture 7+8 > Flashcards

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
Q

low output failure

A

Decreased cardiac output

Majority of cardiac diseases result in a low output cardiac failure

26
Q

forward failure

A

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
Q

backward failure

A

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
Q

compensated HF

A

Dilated ventricle is able to maintain the cardiac output to maintain the needs of the body

29
Q

decompensated HF

A

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
Q

left ventricular failure features

A
  • Dyspnea
  • Orthopnea
  • Paroxysmal nocturnal dyspnea (PND)
31
Q

right ventricular failure symptoms

A
  • Systemic venous congestion
  • Distended neck vein
  • Enlarged tender liver
  • Soft tissue edema
32
Q

left heart failure morphology

A

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
Q

right heart failure morphology

A

Liver:
Chronic passive congestion, Nutmeg liver

Spleen:
Enlargement and congestion of spleen

Pleural and Pericardial spaces:
Effusions
Soft tissue edema

34
Q

Ischemic Heart Disease (IHD)

A

imbalance between cardiac blood supply (perfusion) and myocardial oxygen and nutritional requirements

also known as coronary artery disease (CAD)

35
Q

pathogenesis of IHD

A
  1. Chronic progressive atherosclerotic narrowing of the epicardial coronary arteries
  2. Variable degrees of superimposed acute plaque change, thrombosis and vasospasm

CRS (16 decks)

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