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Pathophysiology Exam 2 > Exam 2 Checklist > Flashcards

Exam 2 Checklist Flashcards

1
Q

What is the pathophysiology of Atherosclerosis?

A

*Fibrous plaques form over fatty deposits protruding into the lumen causing hypercholesterolemia, inflammation, and impairing blood flow.
* Develops over time as arteries grow thick and harden losing elasticity and causing hypertension.
*Forms in intimate (most inner layer)
*This is the cause of hypertension.
*Begins in early adulthood and usually effects larger vessels like coronary artery bed, aorta, carotids, vertebral, renal, and femoral arteries.

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2
Q

Types of plaque:

A

*Stable plaque
*Unstable plaque

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3
Q

Which type of plaque is more dangerous and why?

A

*Unstable plaque is more dangerous because exposed underlying tissue can cause platelet adhesion and fast thrombus formation resulting in sudden blockage of the artery leading to ischemia (inadequate blood supply) or infarction (tissue death due to inadequate blood flow).

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4
Q

Mechanism of BP regulation?

A

RAAS (Renin Angiotensin Aldosterone System) System

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5
Q

RAAS from activation to end result:

A
  1. Juxtaglomerular cells in the kidney produce the hormone renin in response to hypotension or reduced sodium levels in the kidney
  2. Renin acts on circulating angiotensin and converts it to angiotensin I.
  3. Angiotensin Converting Enzyme (ACE - produced in lungs) converts angiotensin I to angiotensin II. This takes place in the filtration system of kidneys.
    *Angiotensin II Long Term Regulation: If BP is high then kidneys excrete more sodium and water (less aldosterone secreted) and if BP is low then kidneys retain more sodium and water (more aldosterone secreted)
    *Angiotensin II Short Term Regulation: Vasoconstriction of arterioles increases arterial BP
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6
Q

Risk Factors of Hypertension:

A

*Family History
*Race (Elevated for African Americans)
*Advanced Age
*Insulin Resistance
*High Sodium Intake
*Obesity
*Stress
*Smoking
*Excess Alcohol Consumption
*Diet High in Saturated Fats

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7
Q

Differences between Peripheral Arterial Disease and Peripheral Venous Disease:

A

PAD:
Pathology: Develops when atherosclerosis narrows arteries in legs and feet decreasing blood flow. The obstruction cuts off blood flow to body’s peripheral structures.
CM: Claudication pain (thigh, calf, buttocks), thinning skin that’s cool to touch, weak pulse, dependent rumor (flush), standing helps perfusion, pale dry ulcers in distal extremities (toes) with round punched out look.

PVD
Pathology: Valves in veins become damaged, allowing blood to collect in legs instead of flowing to the heart.
CM: Pulse present with warm skin, standing increases edema, ulcers with copious serous exudate and irregular margins.

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8
Q

What is cardiac output?

A

It’s the quantity of blood pumped by the heart every beat - heart rate x stroke volume

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9
Q

What are the different types of angina?

A

*Chronic Stable Angina
*Unstable Angina

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10
Q

Which type of angina is more serious?

A

Unstable Angina

  • Worse because it is the warning sign of a heart attack and comes with more severe symptoms that do not subside with rest.
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11
Q

Chronic Stable Angina:

A

*Characterized by the intermittent imbalance of coronary blood flow and metabolic demands of the myocardium
*CM: Chest pain and SOA that is relieved by rest and nitro tabs
*Brought on by physical exertion, exposure to cold, and emotional stress

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12
Q

Unstable Angina:

A

*Can be symptom of myocardial infarction but mostly caused by ischemia significant enough to cause symptoms
*CM: Severe chest pain, SOA, and other symptoms of myocardial infarction - symptoms not relieved by rest

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13
Q

Pathology of Left-Sided Heart Failure:

A

Pathology: Left ventricle dysfunction leaves left ventricle impaired leading to diminished cardiac output, decreased ejection fraction, and accumulation of blood in left ventricle and left atrium which increases pressure and leads to pulmonary congestion.
*Blood back flows into lungs from accumulation in LV and LA and then back flows into lungs via pulmonary veins

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14
Q

Clinical Manifestations of Left-Sided Heart Failure:

A

DROWNIN: Dyspnea, Rales (crackling due to fluid in lungs), Orthopnea (SOB while lying flat), Weakness/Fatigue, Nocturnal Dyspnea, Impaired Gas Exchange, Nagging Cough (pink/frothy)
*Decreased CO
*Activity Intolerance
*Cyanosis and hypoxia due to pulmonary congestion (impaired gas exchange)
*Pulmonary edema

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15
Q

Pathology of Right-Sided Heart Failure:

A

Pathology: Usually precipitated by left-side dysfunction - right ventricle impairment leads to reduced blood flow into pulmonary circulation and left side of heart as well as decreased cardiac output. Pressure in right ventricle, right atrium, and systemic venous system increase and peripheral tissues and organs become congested.
*Pressure from lung backs into pulmonary artery and into right ventricle, right atrium and then inferior vena cava due to gravity.

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16
Q

Clinical Manifestations of Right-Sided Heart Failure:

A

SWELLING: Swelling of legs/liver/GI, weight gain (rapid) due to fluid, edema, large neck vein, lethargy, irregular heart rate, nocturia, girth
*Congestion of peripheral tissues and organs causing peripheral edema with fluid weight gain of 2 lbs per day or 5 lbs per week
*Liver congestion
*GI congestion

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17
Q

Stages of heart failure (ABCD):

A

*A: High risk for developing heart failure but no identified structural abnormalities
*B: Presence of structural heart disease but no history of signs and symptoms of heart failure
*C: Current or prior symptoms of heart failure with structural heart disease
*D: Advanced structural heart disease and symptoms of heart failure at rest on maximum medical therapy

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18
Q

Risk Factors for Left-Sided Heart Failure:

A

*Acute myocardial infarction
*Aortic Stenosis (Narrowing of aortic valve)
*Hypertension
*Hypertrophic Cardiomyopathy (Walls of ventricle become stiff and have trouble pumping blood out)

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19
Q

Risk Factors for Right-Sided Heart Failure:

A

*Left Ventricle Dysfunction
*COPD
*Cor Pulmonale (Alteration in structure/function of right ventricle)
*Pulmonary Hypertension
*valve Dysfunction

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20
Q

What is Congestive Heart Failure?

A

Pathology: Combination of left and right heart failure - the backup of fluid into the lungs and/or peripheral tissues secondary to heart failure.

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21
Q

How does a murmur happen in Endocarditis?

A

Bacteria invade the heart valves, damaging them with the formation of vegetations and making it so that they can’t full close. The swishing sound of a valve not fully closing is a heart murmur.

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22
Q

What is Aortic Stenosis?

A

Incomplete closing of the aortic valve increasing the resistance to the ejection of blood from the left ventricle into the aorta. The valve maintains ejection fraction until it is 1/4 of its normal size.

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23
Q

What is the complication of Aortic Stenosis?

A

Left Ventricular Heart Failure

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24
Q

What is Mitral Valve Regurgitation?

A

Incomplete closing of the mitral valve resulting in blood regurgitation back into the atrium during systole.

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25
Q

What should be included in heart failure education?

A
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26
Q

What is the cause of Rheumatoid Heart Disease?

A

Caused by valvular damage due to an abnormal immune response to Streptococcal throat infection.

27
Q

Pathology of Endocarditis:

A

Infection of the inner heart surface. S. aureus invades the heart valves and busy friable vegetations form destroying cardiac tissue.

*CM: High fever, chills, new heart murmur, emboli

28
Q

Pathology of Pericarditis:

A

Inflammation of the pericardium (outside of the heart) due to a viral infection, bacterial infection, or connective tissue disease.

*CM: Chest pain (sharp with abrupt onset) that worsens with deep breath, pericardial friction rub (Leathery sound) - relief found when sitting up.

29
Q

Pathology of Atrial Fibrillation:

A

Most common chronic arrhythmia. Rapid disorganized atrial activation causing uncoordinated atrial contraction and valve response.

*Irregular pulse for 1 min. can point to atrial fibrillation

30
Q

Where does gas exchange take place?

A

In the alveoli in the lungs

31
Q

What is Ventilation-Perfusion Mismatching (V/Q)?

A

When blood goes to parts of the lung that do not have oxygen and doesn’t go to parts of lungs that do have oxygen.

Examples: Asthma, COPD, Cystic Fibrosis, Pulmonary Hypertension

32
Q

What are the clinical manifestations of Hypoxemia?

A

Early Stage:
*Increased respiratory rate
*Tachycardia
*Increased CO
*Vasoconstriction
*Increased BP
Late Stage:
*Decreased respiratory effort
*Bradycardia
*Hypotension
*Cyanosis
*Arrhythmias
*Metabolic Acidosis
*Death
Neurological Response:
*Agitation
*Euphoria
*Stupor
*Impaired judgement
*Convulsions
*Coma
*Death

33
Q

What is the pathology of Atelectasis?

A

The blockage of air passages or pressure on the lung resulting in collapse of all or part of the lung. Caused by incomplete lung expansion.

34
Q

Types of Atelectasis and their risk factors?

A

*Compression: Tumor, pleural effusion, pneumothorax
*Absorption: Hypoventilation, anesthesia
*Surfactant Impairment: Mechanical ventilation

35
Q

Clinical Manifestations of Atelectasis?

A

*Signs and symptoms of Hypoxemia
*Absence of breath sounds
*Tachycardia
*Tachypnea
*Dyspnea
*Cyanosis

36
Q

What is latent TB infection?

A

TB infection is in your body but is not active and can’t spread to people.

*Only sign is positive TB test

37
Q

What are the risk factors for pneumonia?

A

*Tobacco/drug use
*Exposure
*Atelectasis
*Immune Status/Age
*Mechanical Ventilation
*Chronic Lung Disease
*Aspiration Risk

38
Q

What is pleural effusion?

A

Occurs when there’s an abnormal collection of fluid in the pleural cavity which collapses the lung. Various fluids can collect in the pleural cavity so effusion can have multiple causes.

39
Q

What is pneumothorax?

A

Cause by a collection of air in the pleural space and the resulting increase in pressure collapses the lung. Two types: Primary and Secondary.

40
Q

What is the primary type of pneumothorax?

A

Spontaneous: Rupture of lung bleb (young male or smoker)

41
Q

What are the secondary types of pneumothorax?

A

*Closed: Air from lung escapes into pleural space (rib fracture)

*Open: Air from atmosphere enters pleural space (penetrating chest wound)

*Tension Pneumothorax: Air is trapped in pleural space which may be result of open or closed pneumothorax

42
Q

What is the pathology of asthma?

A

Chronic inflammatory disorder of the airways. IgE activation causes inflammatory response in airways resulting in mucus production, mucosal edema, and bronchoconstriction. This creates intermittent and recurrent airway obstruction.

43
Q

What is the pathology of COPD?

A

Inflammation and destruction of the lung parenchyma and central airways causing irreversible expiratory airflow limitation.

*Chronic Bronchitis: Inflammatory response causes excess mucus production and hyper secretion resulting in a mucus plug .

*Emphysema: Loss of elastic recoil can cause lung collapse during expiration due to air trapping.

44
Q

What are the complications of COPD?

A

Hypercapnia and hypoxemia cause pulmonary vascular shunting and vasoconstriction. Vasoconstriction results in increase in vascular resistance, pulmonary arterial hypertension, right side of heart pushes against high pressure in pulmonary arteries, right ventricle hypertrophies, right sided heart failure or cor pulmonale.

45
Q

What are the clinical manifestations of cystic fibrosis?

A

*Airway Obstruction: 100% of patients - thick mucus in bronchi causing impaired mucociliary clearance - causes chronic inflammation.
*Exocrine Pancreatic Insufficiency: 90% of patients - decreased fluid and HCO3 secretion in acinary cells - thickened secretions clog ducts and trigger auto digestion of pancreatic cells.

46
Q

What is a pathologic fracture?

A

Occurs in bone already weakened by diseases or tumors. May happen spontaneously with little to no stress and can be associated with local or generalized disease conditions.

47
Q

What are the different types of fractures?

A
  1. Closed
  2. Open
  3. Complete
  4. Incomplete
  5. Comminuted
  6. Impacted
  7. Compression
  8. Transverse
48
Q

What is a closed fracture?

A

Inside the body

49
Q

What is an open fracture?

A

Compound with latter involving bone breaking through skin

50
Q

What is a complete fracture?

A

Bone completely broken through

51
Q

What is an incomplete fracture?

A

Greenstick - partially broken with part of the bone remaining unbroken

52
Q

What is an comminuted fracture?

A

Bone broken into more than two pieces

53
Q

What is an impacted fracture?

A

Two bones wedged together

54
Q

What is a compression fracture?

A

Two bones crushed together

55
Q

What is a transverse fracture?

A

Fracture occurring across the bone at a right angle to its long axis

56
Q

What are the categories of fractures?

A
  1. Sudden Injury Fractures
  2. Stress Fracture
  3. Pathologic Fracture
57
Q

What is acute compartment syndrome?

A

A reduction in size of the fascial envelope that encloses muscles and nerves in an extremity.

Occurs due to constrictive casts or dressings in combination with increased compartment volume due to bleeding, inflammation, or swelling.

58
Q

How is osteomyelitis treated?

A

*Long term antibiotics
*Surgical removal of damaged areas
*Hyperbaric oxygen therapy
*Measures to prevent limb loss

59
Q

What are the clinical manifestations of acute compartment syndrome?

A

*The 6 P’s
1. Pain
2. Poikilothermia (cool feeling limbs)
3. Paresthesia
4. Paralysis
5. Pulselessness
6. Pallor

60
Q

What is the pathology of gout?

A

Elevated uric acid leads to the formation of irate crystals which are deposited in the joints initiating local inflammatory response.

61
Q

What are the risk factors for gout?

A
  • Males over age 40
  • Food and beverages rich in purine (alcohol, fish, shellfish, seafood, bacon, turkey, and venison)
62
Q

Rheumatoid Arthritis Vs. Osteoarthritis

A
  • RA is an autoimmune disease
  • Osteoarthritis is wear and tear on the joints from prolonged mechanical stress
63
Q

What is the pathology of Systemic Lupus Erythematosus (SLE)?

A

An autoimmune rheumatic disorder characterized by the immune system attacking the body’s own tissues leading to widespread inflammation and organ damage.

  • Primarily affects females in childbearing years
64
Q

Clinical manifestations of SLE?

A
  • Arthralgia
    *Arthritis
    *Skin Symptoms (red butterfly rash)
    *Photosensitivity
    *Fatigue
    *Weight Loss
    *Renal Issues
    *Cardiac Problems

Pathophysiology Exam 2 (2 decks)

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