UCF FERDOWSI PATHO 1 FINAL

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104 Terms

1
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What is pathophysiology?

The study of abnormalities in physiologic functioning of living beings.

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Etiology 

the study of causal factors provoking a disease

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What is pathogenesis?

describes how these factors alter physiologic function and lead to clinical manifestations.

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What is an example of a clinical manifestation known as a sign?

Bruise

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What is the time during which early signs/symptoms begin to appear called?

Prodromal period

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What reflects the fluctuation of serum levels of cortisol over a 24-hour period?

both

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How are reversible and irreversible cellular injuries differentiated?

By the cell's ability to adapt or repair.

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reversible injuries

hydropic swelling and intracellular accumulation typically resolve when the causative factors are removed


cell adaptation:
atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia

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irreversible cellular injuries

occur when the injury is too severe or prolonged to allow cellular adaptation or repair

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What is necrosis?

Pathologic cell death usually due to ischemia, resulting in inflammation and loss of function.

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What is apoptosis?

Cell suicide resulting from activation of intracellular signaling cascades, not usually associated with inflammation.

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How is pedigree analysis used to determine inheritance patterns?

It helps identify if a trait is autosomal dominant, autosomal recessive, or X-linked.

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What describes autosomal dominant traits?

Expressed in heterozygous condition, typically present in every generation. (at least one parent is affected)

ex: Marfan syndrome, Huntington disease 

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What describes autosomal recessive traits?

Expressed only in homozygous condition; unaffected parents can have affected offspring. (two affected parents)

ex: albinism, phenylketonuria, cystic fibrosis

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What is a characteristic of X-linked traits?

Generally only males are affected.

16
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How might abnormal meiosis lead to alterations in chromosome number?

Through nondisjunction and anaphase lag, leading to aneuploidy or altered structure.

17
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What are benign tumors characterized by?

Resembling their tissue of origin, growing slowly, and having little vascularityrarely have necrotic areas, and often retain functions similar to those of the tissue of origin.

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What are malignant tumors characterized by?

Growing rapidly, spreading to distant sites, and often having necrotic tissue, initiate
vessel growth in the tumor, and are dysfunctional.

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How do overexpression of proto-oncogenes affect cellular proliferation?

abnormal cellular proliferation through increased coding for components of the

cellular growth-activating pathways: growth factors, receptors, cytoplasmic signaling

molecules and nuclear transcription factors

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How does under-expression of tumor suppressor genes affect cellular proliferation?

less regulation of cellular proliferation, or uninhibited cellular proliferation.

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What is tumor grading used for?

To determine the malignancy potential: tumors with a higher malignancy potential are

treated more aggressively

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What is tumor staging used for?

To identify the location and pattern of spread to determine treatment modality: surgical removal, radiation therapy, chemotherapy, or a combination of these.

23
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Which type of cell injury initiates an inflammatory response?

Necrosis

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What are the steps leading to coagulative necrosis?

Ischemic cell injury, loss of plasma membrane integrity, degradation of nuclear structures.

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What describes a trait influenced by multiple genes and the environment?

Multifactorial

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What best describes a malignant tumor?

Has a greater degree of anaplasia.

27
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What is a mutation caused by the substitution of one DNA nucleotide for another called?

Point mutation.

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What is the multi-step nature of carcinogenesis?

Initiation, promotion, and progression.

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Which chromosomal disease is categorized as monosomy?

Turner syndrome

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What is the term for the process of a tumor forming new blood vessels?

Angiogenesis

31
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What are the major organs of the body's defense against foreign antigens?

Skin and mucous membranes= monocytes and macrophages

bone marrow= B lymphocytes and leukocytes

thymus= T lymphocytes

tonsils, spleen, and lymph nodes= B and T lymphocytes

Peyer patches= mainly B lymphocytes

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How does innate immune mechanisms work?

do not require any previous exposure to mount an effective response against an antigen, and a wide variety of different antigens are recognized.

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How does adaptive immune mechanisms work?

respond more effectively on second exposure to an antigen, and are highly restricted in the ability to recognize antigens.

34
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What characterizes Type I hypersensitivity reactions?

• an immediate allergic or anaphylactic type of reaction mediated primarily by sensitized mast cells.

• symptoms of anaphylaxis, including vascular permeability, vasodilation, hypotension, urticaria, and bronchoconstriction.

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What characterizes Type II hypersensitivity reactions?

antibodies are formed against antigens on cell surfaces (cytotoxic) resulting in lysis of target cells: mediated by activated complement fragments or by phagocytic cells

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What characterizes Type III hypersensitivity reactions?

antigen-antibody complexes are deposited in tissues .

• Antigen-antibody complexes activate the complement cascade and subsequently attract phagocytic cells to the tissue.

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What characterizes Type IV hypersensitivity reactions?

T-cell–mediated and do not require antibody production. Sensitized T cells react with altered or foreign cells and initiate inflammation

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What is the first line of defense in the immune system?

Innate def. require no previous exposure to respond to Ag

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Which statements are correct regarding inflammation?

Inflammation is an innate defense

40
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What complicates organ/tissue transplants?

Genetic polymorphism of MHC genes

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What substance is primarily responsible for pain during inflammation?

Bradykinin

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Which genetic aspect is associated with autoimmune diseases?

MHC genes

43
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How is oxygen primarily transported in blood?

Bound to hemoglobin within red cells, with only 3% dissolved in plasma

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How is carbon dioxide transported in the blood?

As dissolved gas, bicarbonate ion, and in association with hemoglobin

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What are the general effects of anemia on body systems?

Reduction in oxygen-carrying capacity, tissue hypoxia and compensatory mechanisms to restore oxygenation.

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Compensatory mechanisms of Anemia

47
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What triggers the release of erythropoietin?

A patient with lung disease and chronic hypoxia

48
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What shifts the O2-Hb dissociation curve to the right and ↓he oxygen affinity to Hb

Fever, exercise, anemia

49
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What is secondary polycythemia associated with?

Chronic hypoxemia associated with chronic bronchitis

50
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What is not seen in a patient with aplastic anemia?

Leukocytosis

51
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What is the relationship between blood pressure, cardiac output, and systemic vascular resistance?

BP = cardiac output (CO) × systemic vascular resistance (SVR)

change in either will result in change of BP

52
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How is blood pressure regulated short-term?

carotid and aortic baroreceptors, the vasomotor center in the brainstem, and the

activations of the SNS and inhibition of the PSN

53
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How is blood pressure regulated long-term?

nervous system, release of hormones, and responses of the kidneys to pressure

changes.

54
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What occurs during diastole in the cardiac cycle?

Ventricles are relaxed and blood flows in from the atria through open AV

Toward the end of ventricular diastole, the atrial pressure rises, leading to atrial

contraction, which squeezes more blood through the AV valves into the ventricles.

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What occurs during systole in the cardiac cycle?

Ventricular pressure rises and blood is ejected into the aorta

isovolumic contraction, causing intraventricular pressure to rise and AV valves to

close; the rise in ventricular pressure exceeds aortic pressure and the valves are

forced open, leading to ventricular ejection.

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How do heart rate, preload, afterload, and contractility affect cardiac output?

CO= SV * HR
Increase in any of these factors increases cardiac output

Increased afterload

• decrease stroke volume: decreased cardiac output

57
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Angina

Partial blockage of CAV

Occur with trigger

Tightness/pressure in the chest and radiated to Jaw or neck

Usually not fatal

No permanent damage

Less than 5 min.

relieved by rest/Nitrate

Cardiac Marker Not present

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MI

Complete blockage of CAV

Occur at any time

Substernal and crushing severe chest pain

May be fatal

Serious and permanent

Persist after 15 min.

relieved by rest/Nitrate

Cardiac Marker Present

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Myocarditis

inflammatory disorder characterized by scattered necrotic and dead heart muscle cells

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Cardiomyopathies

non-inflammatory disorders characterized by dilation, hypertrophy, or fibrotic ventricles

• abnormal ventricular function.

The major complication associated with myocarditis is left ventricular dysfunction and dilation of the heart chambers (dilated cardiomyopathy), with reduced contractility.

61
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What is the difference between systolic and diastolic heart failure?

• Heart failure with primarily systolic dysfunction (Lt- sided)

• characterized by reduced myocardial contractility resulting in a low ejection fraction and reduced inotropy during ventricular systole.

• Heart failure with primarily diastolic dysfunction (Rt -sided)

• characterized by reduced ventricular compliance during diastole resulting in a ventricle that does not fill effectively; however, the ejection fraction remains normal.

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What is the ejection fraction?

Stroke volume divided by end diastolic volume

63
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What are the clinical manifestations of forward heart failure?

low cardiac output (confusion, fatigue, tachycardia), reduced urine output, and poor peripheral circulation

64
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What are the clinical manifestations of backward heart failure?

• Lt – sided: pulmonary congestion (dyspnea, orthopnea, crackles, cough,

pulmonary edema, and hypoxemia)

• Rt – sided: systemic venous congestion and edema formation (jugular vein

distension, hepatomegaly, splenomegaly, and peripheral edema)

65
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Jay jumps up quickly from bed to answer the phone and feels a bit lightheaded. what has happened?

Stimulation of the baroreceptors

66
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What is the blood pressure classification for 120/79?

Elevated

67
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What is the blood pressure for Stage 2?

≥ 140/≥90

68
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What is the blood pressure for Stage 1?

130-139/80-89

69
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Betty suddenly develops a BP of 210/130 with ischemic stroke. What is this situation?


Hypertensive emergency

70
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What diagnostic test records a patient's heart rate for 48 hours?

Holter monitor

71
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How do the structures involved in gas exchange in the lungs differ from conducting structures?

The trachea, bronchi, and bronchioles serve as conducting passageways for air and do not engage in gas exchange.

Exchange of respiratory gases occurs in the alveoli that have a grapelike structure providing a huge surface area for gas exchange.

72
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What factors determine the work of breathing?

Lung compliance, airway resistance, and opposing lung forces.

73
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How does body position affect the distribution of ventilation in the lungs?

Ventilation is higher in the bottom of the lung and decreases toward the apices when in an upright position.

74
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What affects the distribution of blood flow in the lungs?

Distribution of blood flow is affected by gravity: perfusion is greatest in dependent

lung fields (in the bases)

75
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What are common clinical manifestations of acute airway obstruction?

Wheezing, feelings of tightness in the chest, dyspnea, cough, and increased sputum production.

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What are common causes of acute airway obstruction?

Exposure to allergens, exercise, stress, and exposure to pulmonary irritants.

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What is the rationale for using drugs like β2 agonists and corticosteroids in obstructive pulmonary disorders?

They decrease inflammation

B2 agonists and corticosteroids= inhibit bronchial smooth muscle cell contraction, mucosal edema, and mucus secretion.

acetylcholine antagonists= decrease parasympathetic nervous system stimulation of

mast cells

leukotriene inhibitors= lock the release of histamine, leukotrienes

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What pulmonary function test abnormalities are characteristic of obstructive pulmonary disorders?

Decreased FEV1, low FEV1/FVC ratio (<70%), improvement in FEV1 after bronchodilator use, increased residual volume, and increased functional residual capacity.

79
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What neuromuscular disorders are associated with reduced lung compliance?

Poliomyelitis, amyotrophic lateral sclerosis, muscular dystrophies, Guillain-Barré syndrome, and myasthenia gravis.

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What pulmonary function test abnormalities are characteristic of restrictive pulmonary disorders?

Decreased vital capacity, total lung capacity, and diffusing capacity.

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Which information is correct regarding the respiratory system?

The blood in the pulmonary artery is unoxygenated.

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What lab findings are expected in a patient with acute respiratory failure?

Hypoxemia and hypercapnia

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Which disease has increased airway responsiveness to various stimuli?

Asthma.

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What stimulates the chemoreceptors in the medulla?

An increase in arterial CO2.

85
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What is a common cause of both Adult and Infant Respiratory Distress Syndrome?

Pulmonary compliance is decreased

86
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What distinguishes bacterial from viral pneumonia?

A cough productive of purulent sputum

87
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What is a characteristic outcome of Amyotrophic Lateral Sclerosis (ALS)?

Leads to death by respiratory failure.

88
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Are fibrotic lung disorders characterized by reduced lung compliance and increased tidal volumes?

True.

89
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What regulates water and electrolyte movement between plasma and interstitial fluids?

Filtration due to opposing hydrostatic and colloid osmotic pressures.

90
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What conditions lead to extracellular volume deficit?

• removal of a sodium-containing fluid from the body:

    • excessive gastrointestinal or renal excretion, or other losses such as hemorrhage.

• Clinical findings of ECV deficit include:

    • sudden weight loss, postural blood pressure with increased heart rate, flat neck              veins, and oliguria

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What are the clinical findings of extracellular volume deficit?

Sudden weight loss, postural blood pressure changes, increased heart rate, flat neck veins, and oliguria.

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What conditions lead to extracellular volume excess?

Excessive intravenous infusion of sodium-containing isotonic fluids and renal retention of sodium and water.

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What are the clinical findings of extracellular volume excess?

Sudden weight gain, edema, and manifestations of circulatory overload.

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What causes hyponatremia?

Excessive antidiuretic hormone secretion or hypotonic fluid intake.

95
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What are the clinical findings of hyponatremia?

Confusion, lethargy, seizure, and coma due to cell swelling.

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What causes hypernatremia?

Inadequate water intake or excessive water excretion.

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What are the clinical findings of hypernatremia?

Confusion, lethargy, seizure, and coma due to cell shriveling.

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How do the lungs compensate for acid-base imbalances caused by altered levels of metabolic acids?

Increased rate and depth of inspiration to excrete carbonic acid.

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How do the kidneys compensate for acid-base imbalances from carbonic acid?

Adjusting the excretion of metabolic acids.

100
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What could cause edema in a patient?

Increased interstitial fluid osmotic pressure.