NUR 3031 PATHO FINAL EXAM 2023-2024 ACTUAL EXAM 100 QUESTIONS AND CORRECT DETAILED ANSWERS|AGRADE

NUR 3031 PATHO FINAL EXAM 2023-2024 ACTUAL EXAM
100 QUESTIONS AND CORRECT DETAILED
ANSWERS|AGRADE

1. Dysplasia , hyperplasia , metaplasia (6questions)

• Dysplasia – deranged cell growth of a specified tissue, results in cells that vary in size, shape and
  organs.
• Metaplasia- reversible change in which one adult cell type replaces another adult cell type.
• Hyperplasia- increase in the number of cells in an organ or tissue- responds to a stimulus and
  stops when the stimulus is removed.
• Atrophy- the decrease in cell size. Disuse, denervation, loss of endocrine stimulation, inadequate
  nutrition and ischemia and decreased blood flow can cause atrophy.
• Physiological atrophy- for example when you don’t use your muscles they get smaller and this is
  usually reversible.
• Pathological atrophy- has to do with diseases that cause cell size to shrink- for exampledenervation atrophy is a form of disuse atrophy in paralyzed limbs. This can be from polio
  syndrome or people who have ALS (a neurodegenerative disease that affects nerves in the brain
  and spinal cord- no muscle nourishment).
• Hypertrophy- an increase in cell size and with an increase in tissue mass.
• Physiological hypertrophy- the increase muscle mass relating to exercise.
• Pathological hypertrophy- disease conditions and maybe adaptive (thickening urinary bladder
  from long-continued obstruction of urinary flow), and compensatory (one liver is removed the
  other remaining one enlarges to compensate the loss).

1. Patho of CAD, The process of Atherosclerosis
   CAD- atherosclerotic plaque deposits lining walls of coronary arteries and narrowing these
   vessels, causing decreased oxygen supply to myocardium.

• Injury to the lining of the artery occurs, resulting in increased permeability of endothelial
  cells, allowing components of plasma to enter.
• An inflammatory response occurs bringing macrophages and platelets to the area of
  injury
• Hemorrhage into plaque causes thrombi. Thrombus formation within arterial lumen is
  started by platelet aggregation.
• Embolization of a thrombus or plaque can occur.
• Two types of CAD;
• 1. Acute Coronary Syndrome represents a spectrum of acute ischemic heart disease
  ranging from unstable to MI resulting in disruption of atherosclerosis plaque.
• 2. Chronic Ischemic heart disease is characterized by recurrent and transient episodes of
  myocardial ischemia and stable angina that result from narrowing of a coronary artery
  lumen due to atherosclerosis and/or vasospasm.

1. ATHEROSCLEROSIS (KNOW ABOUT PLAQUE) 5 QUESTIONS
   Atherosclerosis is the most common cause of CAD, it is slow and progressive.
   There are two types of atherosclerotic lesions;
2. Fixed or stable plaque- which obstructs blood flow
3. Unstable/vulnerable plaque or high risk plaque – which can rupture and cause platelet
   adhesion and thrombus formation.
4. The body response to stress

• Stress – Seyle’s definition- a state manifested by a specific syndrome of the body developed in
  response to any stimuli that made an intense systemic demand on it. The body adapts to stress by
  GAS (general adaptation syndrome).
• General – the effect was a general systemic reaction
• Adaptive – the response was in reaction to a stressor
• Syndrome- the physical manifestations were coordinated and dependent on each other.
• Three stages to GAS: the alarm stage – stimulation of SNS and HPA (hypothalamic- pituitaryadrenal) this in turn releases catecholamine and cortisol.
• Resistance stage- the body selects the best defense. Cortisol levels drop because they are no
  longer needed.
• The exhaustion phase- prolonged stressor overwhelms the body, wear and tear or systemic
  damage appears.
• Eustress – means moderate or normal stress that is beneficial to the experiencer makes you push
  harder to achieve, it may be seen as a challenge to overcome.
• Distress- negative stress, disruptive to health.

1. Metastasis and Cancer
   Process of metastasis: the development of a SECONDARY tumor in a location distant from the PRIMARY
   tumor; cancer can spread through blood or lymph
   Development/Etiology of Cancer- both molecular & external:
   -Molecular/Genetic: originate from genetic damage or mutation with resultant changes in cell physiology
   that transform a normally functioning cell into a cancer cell
   -External: more likely, cancers develop because of interactions among host factors & repeated exposure
   to chemical carcinogens, radiation, & microorganisms in the environment
   Risk factors: factorsthat have been linked to cancer are heredity, hormonal factors, obesity, &
   immunologic mechanisms
   Complications/Clinical Manifestations: the initial manifestations of cancer usually reflect the function
   of the primary site of involvement; as the tumor metastasizes, other body structures become affected;
   also produces generalized manifestations such as anorexia & cachexia, fatigue & sleep disorders; in its
   late stages, cancer compresses blood vessels, obstructs lymph flow, disrupts tissue integrity, invades
   serous cavities, & compresses visceral organs
   Diagnostics: methods used is determined largely by the location & type of cancersuspected; procedures
   used for diagnosis of cancer include blood tests for tumor markers, cytologic studies & tissue biopsy,
   endoscopic examinations, ultrasound, x-ray studies, magnetic resonance imaging (MRI), computed
   tomography (CT), & positron emission tomography (PET) scans
2. Patho of Cancer

Cell Well differentiated cells that resemble tissue Undifferentiated and often bear little
of origin resemblance to tissue of origin
Mode of growth By expansion, usually encapsulated Invasive, infiltrates surrounding tissue
Cancerous tumors are malignant; they spread into or invade nearby tissues. as these
tumors grow some cancer cells break off and travel to distant places in the body
through the blood or lymph system and form new tumors far from the original
tumor.
Tumor suppressor genes;

• Retinoblast- prevent cell division
• TP53- becomes activated in DNA damage cell to start apoptosis
• TP53 has become a reliable prognostic indicator.

1. Benign and Malignant Tumors
   Benign vs Metastatic
   Benign tumors are:

• WELL DIFFERENTIATED (cells get replaced) but have lost ability to control proliferation
  (cell division)
• produce the same hormones as their “normal” counterparts
• generally ENCAPSULATED
  We should remove benign tumors bc it can grow and compress other organs.
  Ex: papilloma are benign
  Metastatic (Malignant) tumors:
  Malignant neoplasms tend to grow rapidly, invade and infiltrate nearby tissue, and spread to other parts of
  the body.
• Are NOT ENCAPSULATED.
• Because of rapid growth malignant tumors can cause ischemia and tissue injury.
• less differentiated and have lost control over proliferation and differentiation
• very invasive to surrounding tissues
  The better the differentiation the slower the rate of growth that is why malignant tumors replicate quickly
  due to the less-differentiation.
  Characteristics Benign Metastatic
  Rate of growth Progressive and slow- may stop or regress Variable- more undifferentiated the faster
  the growth