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Cardiovascular Diseases > Heart diseases > Flashcards

Heart diseases Flashcards

1
Q

What are the factors that cause artherosclerosis??

A

Causes:

  • HBP
  • High cholesterol and triglycerides
  • smoking
  • diabetes/obesity
  • hypertension
  • hereditary
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2
Q

How does artherosclerosis develop?

A

It develops by plaque (fats,cholesterol, and other substances) build up in the arteries. It decreases the lumen of the effected vessel which restricts the flow of blood through the body.

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3
Q

How can artherosclerosis lead to Coronary artery disease??

A

Artherosclerosis narrows the arteries close to your heart with plaque creating blood clots and it can end up into the heart which may develop coronary disease which can cause chest pain (angina).

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4
Q

What is ischemia?

A

Inadequate blood supply (circulation) to a local area due to blockage of the blood vessels supplying the area. Ischemic means that the heart is not getting enough blood and oxygen.

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5
Q

What is Myocardial infarction (MI)

A

When blood flow to the heart muscle is completely blocked, the myocardial tissue die due to anoxia, result in necrosis of myocardial cells (permanent damage)

  • tissue ischemia to point of injury/necrosis
  • Damage is irreversible
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6
Q

What is angina pectoris?

A

A condition marked by severe pain in the chest; often also spreading to the shoulders,arms and neck, caused by an inadequate blood supply to the heart.

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7
Q

What is the difference between angina pectoris and MI??

A

Angina occurs when the heart muscle is not receiving enough blood to the myocardium decreasing oxygen to the heart causing a chest pain
As for an MI is more of a medical emergency an outcome of destruction or death of myocardial cells a prolonged ischemia causing thrombus formation

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8
Q

What are the three zones of damage seen in an MI?

A
  • zone of ischemia: oxygen deprived; functioning erratically, source of arrhythmias causing ST segment depression w/ or w/out T wave inversion —> altered repolarization
  • zone of injury: injured but not necrotic; nonfunctional but hopefully salvageable with treatment; causes ST segment elevation w/ or w/out Loss of R wave
  • Zone of infarction: causes deep Q waves as a result of a sense of depolarization current from necrotic tissue and receding current from opposite side of heart
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9
Q

What causes an MI?

A

70-75% clot formation on an artherosclerotic plaque

Occlusion of a coronary artery by an embolus(valve damage)

Rupture of an atherosclerotic plaque on a coronary artery

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10
Q

Which part of the heart are infarctions likely to occur??

A

They are likely to occur in the coronary arteries which they supply oxygenated blood and when there’s a blockage and not enough oxygen the myocardial cells start dying.

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11
Q

How does the body try to compensate for coronary ischemia??

A

The body’s hormone and nervous system try to make up for this by increasing BP, retaining salt, and water and increasing heart rate

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12
Q

How is an MI initially treated and then how it is treated after the patient has been stabilized?

A

An immediate treatment is Mona ( morphine,oxygen, nitroglycerine, and ASA). Once stabilize they can do a balloon angioplasty, stent angioplasty and a coronary artery bypass graft (CABG)

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13
Q

PVC arrhythmia

A

PVC are extra heartbeats that start in one of the ventricles. Ischemia makes ventricles irritable increases automaticity. It is a wasted beat no effective output …usually bigger and wiser than normal QRS, more than one shape, couplet pvc occurs in pairs

Treatment: O2, beta blockers , ca2+

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14
Q

Vtach arrhythmia

A

3 or more consecutive pvc’s or may be continuous

Patient will often loose consciousness:
No effective output
CPR and defibrillation

Treatment: O2, anti-arrhythmic (lidocaine, procainamide, amiodorone)

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15
Q

VFIB arrhythmia

A 
Multiple irritable foco in the ventricles 
Results in a chaotic electrical activity
Ventricle quivers does not contract 
No effective cardiac output
Form of cardiac arrest 
CPR and rapid defibrillation
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16
Q

How does CHF develop after an MI?

A

Failure to the heart to pump adequate amount of blood to the tissues post an MI the cardiovascular tries to maintain adequate blood flow by:

  • increase in heart rate
  • increase in systemic vascular resistance
  • fluid retention (done by the kidney) this is the problem and develops CHF
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17
Q

CHF Fluid retention

A

Decreases blood flow to kidney causes:

  • release of renin
  • renin converted to angiotensin (1,then 2)
  • angiotensin 2 causes the adrenals to secrete aldosterone which causes the retention of na+—> water follows na+
  • k+ gets release —> fluid volume increases
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18
Q

What are the CHF manifestations?

A 
Manifestations:
-ventricular hypertrophy 
-edema 
   •systemic-> swollen feet & ankles
   •pulmonary-> wet lung sounds & gurgling
-SOB with exertion or at rest
-hypoxia & Cyanosis
-hypernatremia & hypokalemia
19
Q

What are some treatments for CHF?

A
  • oxygen-> NPPV for respiratory distress
  • Diuretics
  • ACE inhibitor
  • Beta-blocker
  • Inotropic drugs
  • lifestyles
20
Q

What is cardiogenic shock and what are it’s manifestations??

A

Is when the heart can not maintain cardiac put out for tissue perfusion…can’t sustain life

manifestations:
- severely low BP
- severe SOB, rapid breathing
- sudden tachypnea
- weak pulse
- sweating

21
Q

What are some of the treatments for cardiogenic shock??

A
  • oxygen (ventilator)
  • medication
  • surgical repair (chambers,valves,vessels)
  • intra-aortic ballon pump
  • ventricular assist device
  • heart transplant
22
Q

Atrial Septal Defect (ASD)

A

It is cause by an embryonic anomaly. The lesion is a hole in the septum between the right and left atria. The manifestation is a murmur and heart failure( late)

Patent foramen ovale

Treatment: surgery

23
Q

Ventricular septal defect (VSD)

A

Cause by an embryonic anomaly. Lesión in a hole in the septum between right and left ventricles
Manifestations will be a murmur and heart failure

24
Q

Patent Ductus Arteriosus (PDA)

A

Is persistent opening between the two major blood vessels leading from the heart. The opening called the ductus arteriosus is a normal part of a baby’s circulatory system before birth that usually closes shortly after birth. Failure to do so higher BP in aorta , lower blood pressure in pulmonary artery -blood flows backward into pulmonary artery . Treatment O2, anti-inflammatories, surgery

25
Q

Tetralogy of fallout

A

Cause by embryonic anomaly, lesions are overriding aorta pulmonary stenosis ventricular septal defect and right ventricular hypertrophy and the manifestations include murmurs cyanosis retarded body growth and heart failure

26
Q

Coarctation of the aorta

A

Cause by embryonic anomaly and lesion is by stenosis of descending thoracic aorta and the manifestations are decreased femoral pulse, hypertension in upper extremity, murmur, and heart failure (late)

27
Q

Rheumatic heart disease

A

Causative organism strep infection. chronic rheumatic heart disease, patients develop mitral valve stenosis with varying degrees of regurgitation, atrial dilation, arrhythmias, and ventricular dysfunction.

28
Q

Which heart valves are commonly affected in rheumatic heart disease?

A

Vegetation’s form on valves ( mitral 1) which lies between two chambers of the left side of the heart. The damage can cause valve stenosis reducing or blocking blood flow from heart into main artery. Valve regurgitation leaking heart valves (valves don’t close tightly)slowing blood flow backward into the atrium during systole and cause damage to the muscle. Left Atrial hypertrophy

29
Q

Which valves are commonly affected in endocarditis?

A

Can damage or destroy valves it leads to vegetation forming on valves mitral and aortic which stenosis insufficiency can be cause. It can extend to the atrial wall and chord tindinae. Emboli petechiae due to rupture of capillaries, hematuria

30
Q

How are endocarditis and rheumatic heart disease treated??

A

Endocarditis immediate and extensive antimicrobial treatment of extensive damage surgical intervention may occur.

Rheumatic will need daily antibiotics

31
Q

What are the two general types of anemia??

A

Iron deficiency-> not enough iron in the body

vitamin deficiency-> low levels of vitamin B12 or folic acid

32
Q

What are the general signs and symptoms of anemia??

A

Symptoms are fatigued decrease tolerance for exercise, dyspnea & palpitations one major sign is pallor

33
Q

Describe the pathology of pernicious anemia and it’s treatment??

A

Is a condition in which vitamin B12 can not be absorbed in the GI tract or deficiency in a protein called intrinsic factor which is produce in the stomach and is essential for absorption of B12 in the intestine without both membranes immature RBC rupture easily within the blood.

Treatments: b12 injections

Positive schilling test

34
Q

What are the causes of iron deficiency anemia??

A

Excessive blood loss, menstruation, pregnancy and rapid growth during adolescences, and poor dietary intake

35
Q

List example of hemolytic anemia’s?

A

Is a reduction in circulating RBC that is caused by accelerated destruction of RBC. Some examples of hemolytic anemia are thalassemia,, low levels of enzymes such as glucose-6 phosphate dehydrogenase deficiency

36
Q

List signs and symptoms associated with hemolytic anemia’s

A

SOB, early fatigue, pallor, enlarge spleen, increase of bilirubin levels , increase reticulocytes, organ dysfunction

37
Q

What is primary polycythemia

A

A genetic Abnormality of the cells in the bone marrow which makes an overproduction of RBC. ( RBC will be high -but will have low level of erythropoietin)

Treatments: analgesics, medications to decrease viscosity, and antihistamines

38
Q

What is secondary polycythemia?

A

Is an elevated absolute red blood cell mass caused by enhanced stimulation of RBC production (excess of hormone erythropoietin) causing blood to thicken and increasing the risk of a stroke. Other condition is causing your body to produce to many RBC ex: sleep apnea heart disease enhancement drugs, high altitude
(Increase RBC + increase of Erythropoietin)
Treatment: low dose aspirin, phlebotomy or venesection

39
Q

What is the primary abnormality in hemophilia and what are the manifestations and treatments??

A

Is an inherited x linked recessive disorder transmitted form mother to son. It is cause by missing or defective factor 8 a clotting protein.

Manifest: mild-severe bleeding(GI tract, joints, under the skin) inflammation, intracranial hemorrhage, platelets usually ok

Treatments: administer missing clotting factor, chronic replacement of factor eight, synthetic hormone (desmopressin)

40
Q

What is the primary abnormality in thrombocytopenia púrpura?manifestations and treatments??

A

An abnormally small number of circulating platelet count less than 60,000 and púrpura will appear and when markedly depresses pallets count is associate with spontaneous bleeding small petechiae also appear.
-prolonged bleeding from minor and major trauma, spontaneous bleeding from mucous membranes of mouth and internal organs, excessive menstrual bleeding.
Treatments: corticosteroid(decrease destruction) splenectomy, packed RBC w platelets.

41
Q

Describe leukemia??

A

-several types of malignant neoplasms of WBC which differentiate &spread diffusely in the bone marrow. (Acute myelogenous, acute lymphoblastic, chronic lymphoblastic, chronic myelogenous)
acute: cells poorly differentiated and rapid course
Chronic: well differentiated cells and a slow course
Abnormal cells: myelogenous if abnormal WBC are PMN, lymphocytic if abnormal WBC are lymphocytes
Increase production of useless WBC and decrease production of RBC and platelets

42
Q

What are leukemia’s manifestations and treatments??

A

Chemotherapy and radiation and bone marrow transplant

Systemic: weight loss, fever and frequent infections
Skin: night sweats, easy bleeding, purplish patches or spots

43
Q

What is the abnormal cell seen in Hoskins lymphoma and how is it treated??

A

Is a large malignant B cell, multi lines nucleus prominent nuclei reed ste berg cell( has owl nuclei eyes)

Treatment will be aggressive radiation and or chemotherapy

44
Q

What does mycrocytic and hypochromic mean??

A

Microcytic- small RBC
Hypochromic- pale

They both can indicate it’s a case of iron deficiency anemia

Cardiovascular Diseases (1 decks)

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