Cellular Adaptation Midterm Exam

Exam Information

• The midterm covers material from weeks 1-6.
• 2.5 hours are allotted to complete the exam.
• Preparation resources include Lecturio Videos & the Textbook.
• Review the Exam Essentials in the Exam instructions.
• The exam allows ONE attempt.
• Notes, books, or other resources are NOT permitted during the exam.
• The exam consists of 100 multiple-choice questions.
• Some questions will involve short patient cases.
• Questions are sourced from a test bank.
• Do NOT click "Take the Quiz" without readiness.
• Some topics may not be covered in this review.
• Students are responsible for covering all required material.
• Review the recommended materials.
• For technical issues, contact Tech support.

Cellular Adaptation

• Adaptation is a reversible cellular response to accommodate physiological and pathological conditions.
• For example, a uterus with pregnancy adapts by increasing in cell size and number to accommodate a growing fetus.
• Cellular injury occurs when factors disrupt cellular structures or deprive cells of oxygen and essential nutrients.
• Cellular injury can be sublethal (reversible) or lethal (irreversible).
• Causes of cellular injury include ischemic-hypoxic conditions, ischemia-reperfusion, free radical damage, immunological factors, infections, and both intentional and unintentional injuries.
• Stress from metabolic derangements can lead to intracellular excessive accumulations of carbohydrate, protein, and lipids.
• Cell death can be triggered by calcium accumulation, leading to pathologic calcification

Necrosis & Apoptosis

• Necrosis and apoptosis are two main types of cell death
• Autophagy occurs during cellular stress, typically triggered by nutrient deficiency.
  • During autophagy, cytoplasmic vesicles engulf cytoplasm and organelles, recycling the factory.
  • It is responsible for normal cell turnover, metabolism, and tissue atrophy but not for protein synthesis.
• Necrosis is a common type of cell death characterized by severe cell swelling and breakdown of organelles, considered an accidental cellular death.
• Apoptosis is cellular self-destruction, eliminating unwanted cell populations through programmed cell death.
• Necroptosis is genetically controlled necrosis through a defined molecular pathway, independent of apoptotic pathway inhibition; it acts as a fail-safe if apoptosis fails.
• Pyroptosis is suicide by inflammation, such as cell death seen in patients with sepsis.

Cellular Organelles

• Mitochondria is a cellular organelle primarily responsible for generating energy for cellular functions.
• Injury to the mitochondria leads to mitochondrial permeability transition (pore), resulting in the loss of the proton gradient and ATP.
• Cytochrome C drives the formation of the apoptosome and activates apoptosis-causing enzymes.
• The rough endoplasmic reticulum in a plasma cell is responsible for synthesizing immunoglobulins.

Cellular Adaptation Details

• Atrophy involves a decrease in cell size.
  • Brain atrophy in Alzheimer's disease serves as an example
• Atrophy secondary to chronic malnutrition is associated with autophagy, leading to the creation of self-destructive autophagic vacuoles within the cell.
• Hypertrophy involves an increase in cell size.
  • It occurs in response to mechanical load or stress, resulting in increased affected organ size.
• Hyperplasia involves an increase in cell number.
  • It results from an increased rate of cellular division
  • It can be results from severe or prolonged damage which causes cell death
  • Compensatory hyperplasia enables organ regeneration. For example, Liver regeneration, Hormonal effects (uterus during pregnancy), or BPH in men.
• Metaplasia is the reversible replacement of one differentiated cell type by another.
• Dysplasia is deranged cellular growth and is not considered a true cellular adaptation but rather atypical hyperplasia.

Atrophy Examples

• Atrophy involves a decrease or shrinkage of cell size.
• Physiologic atrophy occurs during early development in thymus glands
• Pathologic atrophy happens when there is decreased workload, lack of use, pressure, blood supply issues, poor nutrition, hormonal stimulation or nervous system stimulation.
• Disuse atrophy results from prolonged immobilization, leading to skeletal muscle atrophy, characterized by fewer mitochondria, endoplasmic reticulum, and myofilaments.
• Alzheimer disease displays shrinkage of the brain or atrophic organ through significant loss of neuronal network.
• Nerve loss, oxygen consumption, and amino acid uptake are rapidly reduced.
• Protein synthesis decreases, protein catabolism, or both may be present.
• Activity in the up-regulation of proteasome (protein degradation complex) is characteristic of atrophic muscle changes.
• In the Ubiquitin-proteasome pathway which is a primary pathway of protein catabolism
• Proteins that are degraded with this pathway use conjugation to ubiquitin and then degraded by proteasomes.

Hypertrophy in cells

• The size of cells, and consequently the size of the affected organ is increased during hypertrophy.
• The heart and kidneys are particularly responsive to enlargement
• Hypertrophy is an adaptive response.
• Mechanical (stretch) & Trophic (growth factors & vasoactive agents) trigger Hypertrophy.
• An example of hypertrophy is what occurs in the kidney when the Kidney adapts to and increased demand with increases with size and cell number.
• Heart hypertrophy begins with dilation of cardiac chambers, and is then follows up with increased synthesis of cardiac muscle proteins, allowing muscle fibers to do more work.
• There is an increased accumulation of protein in the cellular components
• Extracellular matrix remodeling & increase growth of adult myocytes when reaching the limits that hypertrophy can occur.

Hyperplasia Explained

• Hyperplasia occurs with an increase in the NUMBER cells where rates of cellular division increase.
• Severe injury response leads to hyperplasia as the injury is prolonged.
• Hypertrophy often accompanies hyperplasia.
• Compensatory hyperplasia enables certain organs to regenerate as an adaptive response.
  • Liver regrowth for example with the missing liver cells.
• Estrogen affects organs dependent estrogen and affects the uterus and breasts.
  • Pregnancy for example is a hormonal hyperplasia, as well as hypertrophy, enabling uterus to enlarge.
• Abnormal proliferation of normal cells lead to Pathologic hyperplasia when responses to excessive hormonal stimulation or the effects of growth factors target cells.
  • Endometrial hyperplasia causes excessive bleeding with pathologic conditions.
  • Under the influence of regular growth inhibition controls will fail, because of hyperplastic endometrial cells that can undergo malignant transformation.

Dysplasia Detailed

• Dysplasia is displayed with abnormalities of size, shape, and organization of mature cells.
• Dysplasia is associated with hyperplasia (atypical hyperplasia)
• Epithelial tissue of cervix & respiratory tracts are involved.
• Dysplasia has a strong association with common neoplastic growths & often are found adjacent to cancerous cells
• Dysplasia, does not mean cancer, indicate cancer.
• Dysplasia can be classified as mild, moderate, or severe
• Atypical hyperplasia is a strong predictor of breast cancer development.

Metaplasia Explained

• Metaplasia, is a reversible replacement of one mature cell to another, sometimes to undifferentiated, cell types.
• An example of this would be a replacement of normal columnar with ciliated epithelial cells of the bronchial (airway) lining with stratified squamous.
• Newly formed epithelial cells that are squamous do not secrete mucus or have cilia and cause a loss of vita protective mechanisms.
• Bronchial metaplasia can be reversed if exposure or inducing stimulus (usually cigarette smoking) is removed.
• There is potential and risk for long term exposure causing cancerous transformation.

Chemical or Toxic Injury

• The following toxic gases are common: smoke, ammonia, hydrogen chloride, sulfur dioxide, chlorine
• Toxins can damage airway epithelium and promote mucus secretion, inflammation, mucosal edema, ciliary damage, pulmonary edema, & surfactant inactivation.
• Acute toxic inhalation cases can frequently be complex and be ARDS and pneumonia.
• Coal, Dusts of silica, cement, talc, fiberglass, metals can cause pneumoconiosis, which restricts the lungs in ways such as silicon damage, asbestos, hypersensitivity pneumonitis can result.
• Also asbestos, some exposures can cause cancer which are mesothelioma, bronchogenic lung cancer.
• Acetaminophen metabolizes into a toxin and can cause permanent Liver damage.
• Mercury cellular component is primarily affected and damages the plasma membrane Sulfhydryl groups because there is leading to sodium-potassium inhibiting the ATPase function.

Hypersensitivity Reactions Described

• A Biphasic Reaction has been observed. It can improve in Allergen exposure, but can be worse 12-24 hours after first reaction.
• Type 1 hypersensitivity is IgE mediated: Anaphylaxis
  • Initial exposure, is the result production an antigen-specific IgE,
• Which can produce antigen specific IgE, binds to mast cell, subsequent exposure and mast cell degranulation.
• Foods, legumes, shellfish, dairy, eggs, berries, tree nuts, meds are environmental items that affect type 1.
• Treatment involves IM epinephrine, Antihistamines, Systemic corticosteroids, and Albuterol for wheezing.
• In severe cases: intubation, epinephrine drip is needed.
• In a Type II hypersensitivity IgG or IgM binds to an antigen on a target cell and causes Rheumatic Fever
• In a Type III hypersensitivity: there is a Circulating antigen/antibody complex such as Serum Sickness
• In a Type IV hypersensitivity: there is a T cell-mediated response and is observed after Poison Ivy

Type I Allergic Reactions

• Type I allergic reactions can result in Urticaria
• Urticaria is considered a Classic type I reaction
• IgE is most likely involved
• Hives are involved
• The reactions are profoundly itchy
• Urticaria reactions are stimulated by skin contact
• And it will come and go on its own
• May be associated with angioedema
• Can be acute and short lived.
• It there are Chronic Urticaria: lasting longer than 6 weeks
• Treatment may be oral antihistamines, H2 Antagonists. But likely steroids won't help.

Cardiac Anatomy & Physiology Simplified

• The L Coronary Artery (LCA) comes from a single ostium behind the aortic semilunar valve cusp.
• The LCA divides into the L anterior descending (LAD) which carries blood to portions of the L/R ventricles and much of the interventricular septum.
• Also the right circumflex artery which carries blood to the L atrium and the lateral wall of the L ventricle.
• RCA originates from one ostium behind the R aortic cusp.
• The RCA branch into the conus (carries blood to the upper R ventricle).
• Then also branches to the R marginal branch (carries blood to the R ventricle of the apex.
• There is also the posterior descending branch supplies small branches to both ventricles.
• The Coronary Sinus drains the great cardiac vein.

Cardiac Pathology

• Pump failure is a cardiac issue.
  • In ischemic heart disease, Thrombosis to coronary artery, MI, myocarditis one might observe when using an echo that there might be decreased LV motion & EF, but normal valve function
• A Flow Obstruction can be a cardiac issue.
  • Stenotic valves are a form of flow obstruction
• When there is Backwards reguritant flows it can impact cardiac pathology.
• Shunted flow can also be a big cardiac issue and leads to overload
  • An Example: Ventricular Septal Defect can increase damage due to heart overload
• Also there can cardiac conduction that are disorders.
  • such Afib, and Vfib
• The heart and vessels can rupture especially with Dissecting aneurysm issues.

Hypertension Explained

• There is a consistent elevation of systemic ARTERIAL blood pressure
• If sustained SBP is 130 and DBP is over 80 it is considered hypertension.
• Genetic, the environment, and neurohormonal effects may also influence the environment which can lead to primary factors with vascular volume and PVR.
• Secondary causes are generally attributed to (renal disease or endocrine disorder)
  • Hyperaldosteronism, renal artery stenosis, renin-secreting tumors, pheochromocytoma, polyarteritis nodosa
• Angiotensin II is a cause of HTN and has a role in it
• Upregulation of sympathetic nervous and enhancement of antidiuretic hormone secretion

Atherosclerosis Explained

• Atherosclerosis is thickening & the hardening the walls of vessels
• Lipid-laden macrophages are accumulated within the arterial wall and leading to the creation of a plaque
• This is known as CAD, PAD, and Cerebrovascular disease.
• There is a thickening of endothelial layer on Fibrofatty plagues.
• Scar tissues developing and a necrotic core will have dead cells can have lipid crystals.
• The severity of Atherosclerosis can be Mild, Moderate, and Severe
• Physical Injury to the endothelium increases the permeability.

Dysrhythmias Explained

• Dysrhythmias are the disturbance and issues with heart rhythms
• SA Nodes may generate normal heart rhythms
• Disorders affecting conduction, inherited abnormalities, ischemia, infection, underlying diseases, medications, and iatrogenic injury are all factors
• And changes in the pulse rate, cardiac output, & Blood pressure can ensue in dysrhythmias.
• Atrial Fibrillation,is a common one:
  • has these Risks: HTN, ischemia, cardiomyopathy, valve disease, hyperthyroidism, meds, alcohol/drugs, and inherited conduction abnormalities.
  • The Symptoms would be palpitations, lightheadedness, anxiety, dyspnea, chest pain, syncope
  • Main Complication being stroke caused by thrombus or emboli from Left Atrium
• Thrombin is needed Anticoagulation therapy and affects thrombin-induced platelet activation and aggregation

Myocardial Infarction Explained:

• A Myocardial Infarction (MI) has localized area of necrotic tissue.
• MIs are are caused by occlusion that cuts off supplies of oxygenated blood to the heart muscle.
• Time is Tissue can be restored and the faster blood flow can be restored, it is better minimize irreversible death cells within the heart.
• Tissue begins to infarct roughly 20 minutes if an artery is in blockage.
• Tissue can be salvaged within 4 hours of blockage.
• MIs can affect these area:
  • Left Circumflex that causes Lateral or posterior MI. -Left Anterior Descending (LAD) which is an anterior wall damage "Widow maker”. Which is rated a the most highest for morality and feeds the Left ventricle. -Right Coronary Artery (RCA) causing Inferior wall damage.

NSTEMI vs. STEMI explained

• NSTEMI: (NON-ST elevation MI) is a ST segment depression and is shown on an EKG.
• If segment is depressed the segment depression can and may be reversed for reversible myocardial ischemia
• NSTEMI is in fact a type of MI that involves a minor artery
• STEMI: (Transmural MI) the (ST elevation MI) shown on an EKG, shows how the heart is experiences more damage, and there is a condition in the heart worse progress than in a NSTEMI
  • in a STEMI mainly ventricles is the affected area.

Aortic Dissection

• Aortic Dissections are displayed when the media is weak. And the Ruptured and the separation of the media.
• These can be a Surgical Emergency
• Etiology is the most common cause of Hypertension (70% of affected individuals)
• Other causes: are Atherosclerosis, connective tissue disorders, and Inflammatory (vasculitis), anatomic abnormalities, as well as Trauma, Cardiac catherization, Drugs (amphetamines, cocaine)
• Rapid deceleration trauma like being involved in a vehicle collision will most likely cause dissection to occur and is most likely to affect the thoracic aorta adjacent to the ligamentum arteriosum (distal related to the vessels)

Aortic Stenosis

• Aortic Stenosis is most commonly diagnosed and a form of valvular heart disease
• 3 common examples: Congenital bicuspid valve, degeneration with aging, inflammatory damage due to Rheumatic heart disease
• Causing Calcific aortic stenosis will cause pressure gradient across and this affects the amount aortic valve calcifies to become more.

Frank Starling Law of the Heart

• When there is increase in initial length of cardiac muscle fiber [within physiological limits], there will be increased force of contraction. OR
• When there is increased end- diastolic volume [EDV], there is increased stroke volume [SV].
• This is INTRINSIC as relationship is between EDV and SV, the heart itself’ when contracting has a Law of the Heart.

Ischemic Heart Disease Explained

• With Ischemic Heart Diease the symptoms includeDyspnea, palpitations, dizziness, and restlessness, anxiety
• There is also Autonomic symptoms can cause Diaphoresis, N/V, Posterior wall which activates theis vagal nerve, , syncope, Bradycardia
• If you observe a Glagov Phenomenon of Vascular remodeling will have a Lumen where the size doesn't change, and the blood flow remains the same even event eventhough there is there s no changes the the flow of of of the heart. And it is is becaus ause of a the remodelin odelin of the vessel.
• With 70% the the the the Sten stenosis the the wall ll expand to to ability to keep up May have ay ve symptoms oms.

Infective Endocarditis explained

• Pathogenesis occurs whenever dental procedure are and even trivial breaks are in IV drug cause.
• Microorganisms can enter the vales and even cause.
• Is bacteria and Platelets and platelets as well as vegetations, due to odgement on valves

Asthma explained

• Asthma is a Chronic, reversible and obtrusive disease with it can be obtrusive
• Normal test and usually between asthma attacks Normal
• If early asthma occurs that is an an antigen response to inflammatory mediators for and response for and asthma.
• It can cause an response to increase for what for work of

Obstructive pulmonary diseases

• COPD is when Airways are limited from normal capacity for the for
• Chronic bronchitis is can result
• Airway obstructed even what what can have been expected
• Also what what what what what what can
• COPD can results
• Normal size also can damage

COPD explained

• That is be of and which is to

.

Key Study points from the respiratory system

• Diffusing capacity of oxygen
• If decreased that is the area between