Cell Biology Quiz

Protein Synthesis

• Protein synthesis involves transcription, translation, and transportation.
• Transcription copies a gene's DNA sequence into mRNA. mRNA carries instructions.
• Translation: mRNA binds to ribosomes on the rough ER; tRNA brings amino acids to build the protein. mRNA detaches once the protein is complete.
• Transportation: The Golgi apparatus modifies the finished protein, packaged into secretory vesicles for release.

Waste Removal

• Lysosomes and peroxisomes are responsible for cellular cleanup.
• Peroxisomes detoxify molecules using catalase and oxidases; they contain free radicals like hydrogen peroxide.
• Lysosomes digest larger components (organelles, bacteria, dead cells) using digestive enzymes in a low-pH environment.

Cellular Transport

• Passive mediated transport doesn't require energy; it moves substances with a concentration gradient.
  • Simple diffusion: movement across a membrane without protein channels.
  • Facilitated diffusion: movement across a membrane using protein channels.
• Active transport requires energy; it moves substances against a concentration gradient.
  • The Na-K ATPase pump maintains low intracellular sodium and high potassium, opposite of extracellular concentrations.
• Pinocytosis (fluid endocytosis) and phagocytosis are also methods of cellular transport.

Cellular Adaptation and Injury

• Reversible adaptations:
  • Atrophy: cell shrinkage without cell death.
  • Hypertrophy: cell enlargement.
  • Hyperplasia: increase in cell number.
  • Metaplasia: change in cell type.
• Dysplasia: irreversible adaptation, a precursor to disease.
• Cellular injury causes: ischemia, hypoxia, chemical agents, physical agents, infections, stressors, genetic defects, nutritional deficiencies, aging.
• Biochemical responses to injury: Free radicals, unstable molecules that react with others, can be beneficial in moderation but cause damage in excess.
• Apoptosis/Necrosis:
  • Necrosis: messy cell death with swelling and bursting; usually pathological; does not require energy.
  • Apoptosis: programmed cell death; tidy and controlled; requires energy.

Neoplasia (Cancer)

• General hallmarks of cancer: self-sufficient growth pathways (often due to oncogene mutations or tumor suppressor gene inactivation).
• Benign vs. Malignant:
  • Benign: slow-growing, resemble normal tissue, don't invade or metastasize (often end in "-oma").
  • Malignant: variable growth rate, invade surrounding tissue, metastasize; cells are poorly differentiated.
• Cancer spread:
  • Initiation phase: carcinogen exposure causing DNA damage.
  • Promotion phase: proliferation of cells with altered DNA, potentially leading to a neoplasm.

Fluid Regulation

• Electrolyte Imbalances:
  • Sodium imbalances:
    • Hypernatremia (high blood sodium): "fried salts" (flushed skin, restlessness, increased BP/fluid retention, edema, decreased urine output, dry skin, agitation, low fever, thirst, seizures).
    • Hyponatremia (low blood sodium): "salt loss" (stupor, anorexia, lethargy, tachycardia, limp muscles, orthostatic hypotension, seizures/coma, stomach cramps).
  • Potassium imbalances:
    • Hypokalemia (low blood potassium): "Ned has many strange symptoms" (nausea, EKG changes/arrhythmias, decreased reflexes/fatigue, hypotension, muscle weakness/paralysis, shallow breathing, slow GI tract).
    • Hyperkalemia (high blood potassium): "murder" (muscle weakness, urine abnormalities, respiratory distress, decreased cardiac contractility, decreased BP and HR, decreased reflexes).
  • Calcium imbalances:
    • Hypocalcemia (low blood calcium): "cahbs go numb" (cramps, anxiety/irritability, heart failure, bronchospasm/stridor, numbness/tingling/paralysis).
    • Hypercalcemia (high blood calcium): "back me" (bone pain, arrhythmias, cardiac arrest, kidney stones, muscle weakness, excessive urine output).
• Starling's forces: govern fluid movement between capillaries and interstitial space. Interstitial hydrostatic pressure, interstitial oncotic pressure, capillary oncotic pressure, and capillary hydrostatic pressure all contribute.
• Edema formation: Imbalances in Starling's forces (e.g., increased capillary hydrostatic pressure due to hypertension from RAAS overactivation) lead to fluid filtration exceeding reabsorption.
• RAAS (Renin-Angiotensin-Aldosterone System): regulates blood pressure and volume; renin release leads to angiotensin II production, causing vasoconstriction and aldosterone release (sodium and water retention).
• ADH (Antidiuretic Hormone): produced by the pituitary gland; promotes water reabsorption by the kidneys, increasing blood volume and decreasing plasma osmolarity; deficiency causes diabetes insipidus.

Hemoglobin and Oxygen Transport

• SPO2: Percentage of hemoglobin carrying oxygen.
• Hemoglobin synthesis requires: Vitamin C (keeps iron in 2+ state), copper (transports iron), B6 and pantothenic acid (heme ring synthesis), folate, B12, and B2 (hemoglobin transport).
• Hemoglobin recycling: Senescent RBCs are phagocytosed by macrophages in the spleen. Heme is broken down into iron and bilirubin. Bilirubin is processed by the liver and excreted. Iron is transported by transferrin to the bone marrow for erythropoiesis and stored in the spleen.

Oxygen-Hemoglobin Dissociation Curve

• Left shift (increased hemoglobin affinity for oxygen): Alkalosis, low temperature, low partial pressure of CO2.
• Right shift (decreased hemoglobin affinity for oxygen): Acidosis, high temperature, high partial pressure of CO2.

Anemia Classifications

• Normocytic normochromic: Normal cell size and color. Caused by low RBC production (bone marrow defects, crowding, leukemia, chronic disease) or increased RBC destruction (hemorrhage, hemolysis, malignancy).
• Microcytic hypochromic: Small, pale cells. Caused by insufficient heme synthesis (chronic blood loss, iron deficiency, hemoglobin defects).
• Macrocytic normochromic: Large cells, normal color. Caused by folate or B12 deficiency.

Anemia CBC Findings

• Decreased hemoglobin and hematocrit.
• Altered RBC size and shape.
• Hemoglobin below 13.5 g/dL (men) or 12.0 g/dL (women).
• Hematocrit below 35-47% (women) or 40-52% (men).

Sickle Cell Anemia

• Autosomal recessive disorder causing defective hemoglobin (HbS).
• HbS polymerization leads to sickled, rigid RBCs.
• Sickled RBCs obstruct blood flow, causing pain crises, organ damage (acute chest syndrome, glomerular disease) and increased susceptibility to infections.
• Low oxygen levels trigger sickling.

Blood Components

• Plasma: Liquid portion of blood (anticoagulated); contains water, proteins (albumin, globulins, clotting factors), and other solutes. Albumin maintains oncotic pressure; globulins contribute to immune defense.
• Serum: Liquid remaining after blood clotting; lacks clotting factors.

Hematopoiesis

• Myeloid cell line: Produces erythrocytes (RBCs), granulocytes (neutrophils, eosinophils, basophils), monocytes, and platelets.
• Lymphoid cell line: Produces lymphocytes (B cells and T cells).

Erythropoietin (EPO)

• Hormone produced by the kidneys that stimulates erythrocyte production.
• Low blood oxygen levels trigger EPO release, increasing RBC production and hemoglobin levels.
• Increased oxygen levels suppress EPO production.

Hemoglobin Function and Production

• Iron-containing protein in RBCs that transports oxygen and carbon dioxide.
• Iron is essential for hemoglobin synthesis.
• Hemoglobin is produced in bone marrow.
• Recycling involves breakdown in the spleen and liver, with iron re-use.

Anemia Classifications

• Normocytic normochromic anemia: Normal cell size and color; caused by low RBC production (bone marrow defects, crowding, leukemia, chronic disease) or high RBC consumption (hemorrhage, hemolysis, malignancy).
• Microcytic hypochromic anemia: Small, pale cells; due to insufficient heme and hemoglobin synthesis (iron deficiency, chronic blood loss, hemoglobin defects).
• Macrocytic normochromic anemia: Large cells, normal color; typically caused by folate or B12 deficiency.

Anemia Complete Blood Count (CBC) Findings

• Decreased hemoglobin and hematocrit.
• Altered RBC size and shape.
• Hemoglobin <13.5 g/dL for men, <12.0 g/dL for women.
• Hematocrit 35-47% for women, 40-52% for men.

Sickle Cell Anemia

• Autosomal recessive disorder; defective hemoglobin (HbS) leads to fragile, sickle-shaped RBCs.
• Symptoms: Pain crises, edema, acute chest syndrome, glomerular disease, infections.
• Low oxygen causes RBC sickling, clumping, and vaso-occlusion.
• HbS is less efficient at carrying oxygen.

Acid-Base Imbalances

• Metabolic acidosis: Low pH, low bicarbonate; excess acid or bicarbonate loss. Anion gap helps differentiate causes (normal vs. elevated).
• Metabolic alkalosis: High pH, high bicarbonate; loss of acid.
• Respiratory acidosis: Low pH, high carbon dioxide; hypoventilation.
• Respiratory alkalosis: High pH, low carbon dioxide; hyperventilation.

Acid-Base Interpretation

• Consider patient history.
• Assess pH (acidosis/alkalosis).
• Evaluate bicarbonate (high, low, normal).
• Evaluate carbon dioxide (high, low, normal).
• Determine if pH and abnormal values move in the same (metabolic) or opposite (respiratory) directions.
• Anion gap (normal 12 mmol/L): Helps in diagnosing metabolic acidosis (low bicarbonate vs. high acid).

Blood Components: Plasma vs. Serum

• Plasma: Liquid portion of blood with anticoagulants; contains water, proteins (albumin, globulins, clotting factors), and other solutes.
• Serum: Liquid remaining after blood clotting; lacks clotting factors.

Myeloid vs. Lymphoid Cell Lines

• Myeloid: Produces RBCs, WBCs (neutrophils, lymphocytes, monocytes, eosinophils, basophils), and platelets.
• Lymphoid: Produces B and T lymphocytes.

Erythropoietin (EPO)

• Hormone produced by the kidneys; stimulates RBC production.
• Low blood oxygen triggers EPO release, increasing RBCs and hemoglobin levels to improve oxygen-carrying capacity.
• EPO production decreases when blood oxygen levels are adequate.

Hemoglobin

• Iron-containing protein in RBCs; carries oxygen and returns carbon dioxide.
• Iron, vitamin C, copper, B6, pantothenic acid, folate, B12, and B2 are necessary for its synthesis.
• RBCs are recycled in the spleen; macrophages break down heme into iron and bilirubin.
• Iron is transported by transferrin; bilirubin is processed by the liver.
• SpO2 reflects the percentage of hemoglobin carrying oxygen.

Oxygen-Hemoglobin Dissociation Curve: Shifts

• Left shift (increased affinity of hemoglobin for oxygen): Alkalosis, low temperature, low partial pressure of CO2.
• Right shift (decreased affinity; oxygen release to tissues): Acidosis, high temperature.

Hemophilia

• Hemophilia A: Factor VIII deficiency (produced in endothelium).
• Hemophilia B (Christmas disease): Factor IX deficiency.
• von Willebrand factor (vWF) carries factor VIII and promotes platelet adhesion and aggregation.

Blood Clotting: Platelets

• Regulate blood flow to injured vessels.
• Form platelet plugs.
• Activate clotting cascade.
• Initiate tissue repair.
• Participate in clot breakdown.

Blood Clotting: Counteractions

• Endothelial surfaces release prostaglandins (inhibit platelet aggregation) and nitric oxide (inhibits platelet adhesion and aggregation).
• Proteins C and S (vitamin K-dependent) inactivate clotting factors.
• Tissue factor inhibitor and antithrombin III inhibit thrombin activity.

Vitamin K

• Essential for the synthesis of functional clotting factors II, VII, IX, X, and proteins C and S.
• Obtained from diet (plants) and intestinal bacteria.

Lab Tests

• D-dimers: Indicate fibrinolysis (clot breakdown).
• Prothrombin time (PT): Measures time for blood to clot.