Video Lecture Flashcards: Cell Injury, Adaptation, Neoplasia, Genetics, ECG & Electrolytes

A comprehensive set of vocabulary flashcards covering: cellular transport, cell injury and death, adaptation and metaplasia, intracellular accumulations and calcifications, hypoxic/ischemic injury, necrosis types, apoptosis, neoplasia and genetics, major inherited disorders, teratogens, fetal alcohol syndrome features, and essential ECG/electrolyte concepts.

Osmosis

Passive diffusion of water across a semipermeable membrane driven by osmotic pressure.

Osmotic pressure

Pressure exerted by solutes that drives water movement across membranes.

Active transport

Movement of substances against a concentration gradient that requires energy.

Endocytosis

Cellular intake of material from the exterior via vesicle formation; includes phagocytosis and pinocytosis.

Phagocytosis

Endocytosis of large particles by cells (e.g., macrophages).

Pinocytosis

Endocytosis of fluids (cell drinking).

Exocytosis

Release of materials from the cell through vesicle fusion with the plasma membrane.

Adaptation

Cellular adjustment to changes in the internal environment or work demands.

Atrophy

Decrease in cell size and tissue mass.

Hypertrophy

Increase in cell size; increase in tissue mass.

Hyperplasia

Increase in the number of cells in a tissue.

Metaplasia

Replacement of one mature cell type by another; usually reversible.

Physiological hyperplasia

Normal proliferation, such as breast and uterine enlargement.

Compensatory hyperplasia

Regeneration or growth after tissue loss (e.g., liver regeneration).

Nonphysiologic hyperplasia

Hyperplasia due to abnormal stimulation (e.g., endometrial hyperplasia from estrogen).

Dysplasia

Disordered cellular growth; a precursor to cancer; may be reversible if stimulus is removed.

Intracellular accumulations

Buildup of substances cells cannot immediately use or eliminate.

Fatty liver

Intracellular accumulation of fat within hepatocytes.

Tay-Sachs disease

Genetic GM2 ganglioside accumulation due to hexosaminidase A deficiency.

Icterus (jaundice)

Pigment accumulation from bilirubin leading to yellowing of tissues.

Metastatic calcification

Calcium salts deposited in normal tissues due to hypercalcemia.

Dystrophic calcification

Calcium deposits in damaged tissue with normal serum calcium.

Hyperparathyroidism

Endocrine disorder causing elevated calcium mobilization and phosphate changes.

Calcification in damaged tissues (locations)

Common sites include lungs and kidneys in calcification disorders.

Ischemia

Reduced blood flow to tissue leading to hypoxia.

Hypoxia

Tissue oxygen deprivation.

Infarction

Necrosis of tissue due to prolonged ischemia.

Necrosis

Pathologic cell death with loss of membrane integrity; several morphological types.

Coagulative necrosis

Protein denaturation preserves tissue architecture; typical of ischemic organs (heart, kidney).

Liquefactive necrosis

Enzymatic digestion of tissue leading to liquefaction; common in brain and abscesses.

Caseous necrosis

Cheese-like necrosis seen in tuberculosis granulomas.

Fat necrosis

Necrosis of adipose tissue often due to enzymatic destruction.

Gangrene

Necrosis with tissue decay; dry (slow spread) or wet (infected, rapidly spreading).

Free radicals

Unstable molecules that can damage cells; generated by many injuries.

Apoptosis

Programmed, controlled cell death with minimal inflammation.

Necrosis vs apoptosis

Necrosis is uncontrolled cell death from injury; apoptosis is orderly, programmed cell death.

Hypoxic cell injury

Cell injury caused by inadequate oxygen supply; affects brain, heart, kidneys severely.

Ischemia vs hypoxia

Ischemia is reduced blood flow; hypoxia is reduced oxygen, which can result from ischemia.

Fibrodegeneration-free radicals injury (general concept)

Injury from reactive oxygen species and other radicals leading to cellular damage.

Neurodegenerative diseases (Alzheimer’s, Parkinson’s, ALS)

Disorders where abnormal apoptosis or cell death contributes to neuron loss.

Carcinogenesis

Process of cancer development: initiation, promotion, progression.

Neoplasm

New and abnormal tissue growth; can be benign or malignant.

Benign neoplasm

Slow-growing, localized tumor that resembles tissue of origin.

Malignant neoplasm

Rapid, invasive, metastatic cancer with poor differentiation.

Staging

Assessment of cancer spread (extent of disease).

Grading

Assessment of cancer differentiation and aggressiveness.

Remission

Cancer considered under control; symptoms reduced or disappear.

Metastasis

Spread of cancer from its primary site to distant locations.

Oncogenesis

Process of tumor formation and progression.

Autosomal dominant

Inheritance pattern where one mutated allele on an autosome can cause disease.

Autosomal recessive

Inheritance pattern requiring two mutated alleles for disease expression.

Homozygous

Two identical alleles for a gene.

Heterozygous

Two different alleles for a gene.

Genotype

The genetic constitution of an individual.

Phenotype

Observable traits resulting from genotype and environment.

Allele

Alternative form of a gene.

Gene mutation

Permanent alteration in the DNA sequence.

Marfan syndrome

Autosomal dominant connective tissue disorder due to FBN1 mutation.

Adult polycystic kidney disease

Autosomal dominant disorder with kidney cysts and progressive renal failure.

Familial hypercholesterolemia

Autosomal dominant condition with high LDL cholesterol and premature atherosclerosis.

Neurofibromatosis type 1 (NF1)

Autosomal dominant disorder with neurofibromas and skin findings.

Neurofibromatosis type 2 (NF2)

Autosomal dominant disorder with vestibular schwannomas.

Phenylketonuria (PKU)

Autosomal recessive disorder (PAH mutation) causing phenylalanine buildup; dietary treatment.

Tay-Sachs disease

Autosomal recessive GM2 gangliosidosis due to HEXA deficiency; neurodegeneration in infancy.

Hexosaminidase A

Enzyme deficient in Tay-Sachs disease.

Albinism

Autosomal recessive hypopigmentation disorder.

Cystic fibrosis

Autosomal recessive CFTR mutation causing thick mucus secretions.

Sickle cell disease

Autosomal recessive hemoglobinopathy with sickle-shaped cells and hemolytic anemia.

Down syndrome (Trisomy 21)

Chromosomal disorder with Trisomy 21; characteristic facial features and risk of congenital defects and early Alzheimer’s.

Turner syndrome (Monosomy X)

Sex chromosome monosomy (45,X) with gonadal dysgenesis and other features.

Klinefelter syndrome (XXY)

Sex chromosome polysomy with testosterone deficiency and infertility.

Teratogenic agents

Agents that cause fetal malformations (radiation, chemicals, drugs, infections, alcohol).

Fetal alcohol syndrome

Prenatal exposure to alcohol causing microcephaly, facial features, growth retardation.

Infectious teratogens (measles, mumps, herpes simplex)

Infections during pregnancy that can harm fetal development.

Trisomy 21 manifestations

Upward slanted palpebral fissures, developmental delay, congenital anomalies.

Turner syndrome manifestations

Gonadal streaks, short stature, webbed neck, cardiovascular anomalies.

Klinefelter syndrome manifestations

Small testes, infertility, gynecomastia, tall stature.

Down syndrome (Trisomy 21) manifestations

Characteristic facial features, hypotonia, and risk of congenital heart disease.

ST segment

Section of the ECG between the end of S and start of the T wave; ventricular repolarization.

PR interval

Time from atrial depolarization to onset of ventricular depolarization; normally 0.12–0.20 s.

QRS complex

Ventricular depolarization; usually 0.06–0.12 s in duration.

P wave

Atrial depolarization on ECG.

R wave

First positive deflection after the P wave within the QRS complex.

S wave

Downward deflection following the R wave in the QRS complex.

Wenckebach (Mobitz I) block

Type I AV block with progressively lengthening PR interval and dropped beat.

Mobitz II block

Type II AV block with intermittent non-conducted P waves and constant PR interval.

Third-degree AV block

Complete dissociation between atrial and ventricular activity; no impulses reach the ventricles.

Sinus rhythm

Normal heartbeat rhythm initiated by the sinus (SA) node.

Premature atrial complex (PAC)

Early atrial beat with preceding P wave before the QRS.

Premature ventricular complex (PVC)

Early ventricular beat with wide, bizarre QRS; often with absent or distorted P wave.

Atrial/ventricular tachycardia terminology

Rapid heart rhythms originating above (SVT) or within ventricles; advised to monitor.

Dominant ranges of electrolyte sodium

Sodium (Na+): major extracellular cation; controls fluid balance and nerve/muscle function.

Hypernatremia

Sodium >145 mEq/L; dehydration, dry mucous membranes, thirst.

Hyponatremia

Sodium <135 mEq/L; due to excess water or sodium loss; confusion, seizures possible.

Potassium (K+)

Major intracellular cation; essential for muscle and nerve function; tight regulation.

Hyperkalemia

Elevated potassium; can cause paresthesias, muscle weakness, arrhythmias.

Hypokalemia

Low potassium; can cause cramps, weakness, arrhythmias.

Calcium (Ca2+)

Important for bones, clotting, nerve transmission, and muscle contraction.

Hypercalcemia

Calcium > about 10.5 mg/dL; symptoms include dysrhythmias, lethargy, weakness.

Hypocalcemia

Low calcium; signs include Trousseau’s and Chvostek’s signs; due to losses or deficiency.