Final Exam

Hypoxia

lack of oxygen in cell or tissue

Asphyxiation

injury due to failure of cells to receive or use oxygen

Suffocation

lack of oxygen in the environment or blockage of airways

Strangulation

compression and closure of the blood vessels and air passages of the neck

Chemical

carbon monoxide, cyanide

Drowning

breathing in of fluid instead of O2

Carbon Monoxide Poisoning

higher affinity to heme than oxygen; binds to hemoglobin and prevents the transportation of oxygen around the body

Free radicals

molecules which have lost an electron. Due to the loss of an electron, they are highly reactive and will bind to anything. This initiates a chain reaction and causes damage to the cell

Reactive oxygen species (ROS)

naturally formed during mitochondrial respiration. They have important roles in chemical signaling but can lead to pathology when in excess

Air pollution

the world's largest environmental health risk. Increases risk of strokes, heart disease, lung cancer, chronic, and acute respiratory diseases

6 air pollutants

Carbon monoxide, particle pollution, ozone, sulfur dioxide, nitrogen dioxide, and lead

Heavy metal toxicity

lead, mercury, arsenic, cadmium

Lead poisoning

exposure in children can result in learning/behavior problems, speech/hearing problems, brain/nervous system injury, slowed growth and development. Most common source is paint in older homes, the environment, and at work. Toxicity affects central and peripheral nervous systems. Prevention is key. Treatment may include chelation therapy. Need to have a high index of suspicion, especially in children with behavioral disorders

Ethanol

results in major nutritional deficiencies. Metabolism occurs primarily in the liver. Acute alcoholism affects the central nervous system. Chronic alcoholism also affects the liver and stomach. Consumption of alcohol during pregnancy can result in fetal alcohol spectrum disorders

Street drugs

methamphetamine, marijuana, opioids

Infectious agents

viruses, bacteria, and parasites can cause injury to cell within the human body

Virulence of an organism depends on its ability to

invade and destroy cells, produce toxins, produce damaging hypersensitivity reactions

Immune-mediated hypersensitivity reactions

abnormal immune system response to a perceived foreign substance

Autoimmune disorders

antibody formation against normal cell receptors; interfere with intercellular communication and cell membrane function

Hypothermic injuries

chilling or freezing of cells. Occurs at body temperatures of

In response to heat, your body will

produce sweat, vasodilate peripheral blood vessels

Hyperthermic injuries

injury caused to the cell due to excessive heat.

Heat cramps

cramping of muscles due to loss of salt and water.

Heat exhaustion

hemoconcentration from salt and water loss

Heat stroke

body temperature \>106°F or 41°C; life-threatening vasodilation and hypotension; loss of compensatory thermoregulation

Barometric

sudden increases or decreases in pressure causing tissue injury

Ionizing radiation

capable of removing orbital electrons from atoms; production of free radicals that damage DNA.

Noise

acoustic trauma and noise-induced hearing loss

Genetic factors

inherited genetic disorders may alter a cell's nucleus or plasma membrane structure, shape, receptors, or transport mechanisms

Micronutrients

vitamins, minerals, trace elements, phytochemicals, antioxidants

Macronutrients

carbohydrates, fats, protein

Nutritional imbalances

Pathology can occur when there is excessive nutrient intake, deficient nutrient intake, or the body is unable to process the nutrients.

Necrosis

cellular changes after local cell death and lysis

Coagulative necrosis

occurs primarily in the kidneys, heart, and adrenal glands, commonly results from hypoxia caused by severe ischemia or hypoxia caused by chemical injury

liquefactive necrosis

commonly results from ischemic injury to neurons and glial cells in the brain

caseous necrosis

commonly results from tuberculous pulmonary infection. Tissues appear soft and granular and resemble clumped cheese.

Fat necrosis

occurs in the breast, pancreas, and other abdominal structures. Tissue appears opaque and chalk white.

Gangrenous necrosis

death of tissue and results from severe hypoxic injury, commonly occurring because of arteriosclerosis, or blockage, of major arteries

Hypernatremia

high sodium level, water moves from ICF to ECF; intracellular dehydration and shrinkage

Risk factors hypernatremia

advanced age, impaired mental state, fever, diarrhea, vomiting, uncontrolled diabetes mellitus, tube feedings, and use of diuretics

Clinical manifestations hypernatremia

more severe hypernatremia can affect central nervous system by causing injury to the neurons - lethargy, muscle twitching, confusion, coma, seizures

Hyponatremia

low sodium level, water moves from ECF to ICF; intracellular edema

Cause hyponatremia

loss of sodium, inadequate intake of sodium, or dilution of sodium by excess water intake

clinical manifestations hyponatremia

more severe hyponatremia can affect the central nervous system by causing injury to the neurons (cerebral edema) - lethargy, confusion, coma, seizures

Hyperkalemia

high potassium level

Cause hyperkalemia

kidney impairment due to inability to excrete potassium, insulin deficiency, increased dietary intake, excessive cell breakdown, certain medications

Clinical manifestations hyperkalemia

Moderate: tingling of lips and fingers, intestinal cramping/diarrhea, peaked T waves on EKG Severe: muscle weakness, paralysis, further EKG changes, cardiac arrest

Hypokalemia

low potassium level

causes hypokalemia

insufficient dietary intake, increase potassium loss (diarrhea, vomiting, some diuretics), intake of potassium into the cell (insulin overdose)

clinical manifestation hypokalemia

decreased neuromuscular excitability, muscle weakness, cardiac arrythmias, EKG changes (U waves), cardiac arrest

hypercalcemia

high calcium levels

cause hypercalcemia

hyperparathyroidism, bone metastasis, excessive vitamin D intake, immobilization, acidosis

clinical manifestations hypercalcemia

decreased neuromuscular excitability, weakness, kidney stones, constipations, nausea, vomiting, bradycardia, and heart block

Hypocalcemia

low calcium levels

cause hypocalcemia

inadequate intake or absorption, decreases in parathyroid hormone (thyroidectomy), decreases in vitamin D, blood transfusions, pancreatitis

clinical manifestations hypocalcemia

increased neuromuscular excitability, muscle spasms and stiffness (tetany), convulsions, Chvostek and Trousseau signs

Hypophosphatemia

low phosphate levels

causes hypophosphatemia

malabsorption syndromes, poor nutrition, refeeding syndromes

Clinical manifestations hypophosphatemia

symptoms of hypercalcemia, low ATP, hypoxia, bradycardia, coma

Hyperphosphatemia

high phosphate levels

causes hyperphosphatemia

cell breakdown (chemotherapy), inability to excrete (renal failure)

clinical manifestations hyperphosphatemia

symptoms of hypocalcemia, calcifications

Hypomagnesemia

low magnesium levels

causes hypomagenesemia

malabsorption, poor nutrition, associates with hypocalcemia and hypokalemia

clinical manifestations hypomagnesemia

Depression, confusion, irritability, increased reflexes, muscle weakness

Hypermagnesemia

high magnesium levels

causes hypermagnesemia

renal failure, associated with hypercalcemia

clinical manifestations hypermagnesemia

Nausea, vomiting, muscle weakness, hypotension, bradycardia, and respiratory depression

Respiratory acidosis

pH is less than 7.35 and PaCO2 is greater than 45 mmHg. Body will attempt to compensate by increasing renal bicarbonate reabsorption and eliminating H+ in urine

clinical manifestations Respiratory acidosis

Headache, restlessness, blurred vision, apprehension, lethargy, muscle twitching, convulsions, coma

Respiratory alkalosis

pH is greater than 7.45 and PaCO2 is less than 35 mmHg. Body will attempt to compensate by increasing H+ reabsorption and eliminating bicarbonate in urine

clinical manifestations Respiratory alkalosis

Dizziness, confusion, tingling sensations, convulsions, coma, symptoms of hypocalcemia (uncontrolled movement

Metabolic acidosis

pH is less than 7.35 and bicarbonate is less than 22 mEq/L. Body will attempt to compensate by excretion of H+ and reabsorption of bicarbonate and through hyperventilation and kussmaul respirations.

clinical manifestations Metabolic acidosis

Headache, lethargy, confusion, nausea, vomiting, diarrhea, arrythmias, and kussmaul respirations

Metabolic alkalosis

pH is greater than 7.45 and bicarbonate is greater than 26 mEq/L. Body will attempt to compensate by excreting bicarbonate and reabsorbing H+ and slowing down respirations and retain CO2.

clinical manifestations Metabolic alkalosis

Depends on underlying causes, symptoms of hypocalcemia, muscle weakness, muscle cramps, convulsions, confusion, and slow shallow breathing.

normal pH

7.35-7.45

normal PaCO2

35-45 mmHg

normal HCO3

22-26 mEq/L

cause Respiratory acidosis

impaired alveolar ventilation and resultant of hypercapnia

cause Respiratory alkalosis

hyperventilation and resultant of hypocapnia

cause Metabolic acidosis

either loss of bicarbonate or an increase in non-carbonic acids

cause Metabolic alkalosis

either loss of non-carbonic acids or an increase in bicarbonate

Transcription

RNA is synthesized from DNA template via RNA polymerase and continues until a termination sequence is reached. To continue the process of gene expression, the mRNA is removed from the nucleus. Once removed from the nucleus RNA matures through the removal of introns. Extrons are combined to form functional mRNA

Translation

functional mRNA is converted into polypeptides with the assistance of ribosomes and transfer RNA. tRNA contain a sequence of nucleotides complementary to the triad of nucleotides on the mRNA strand. The termination signal on the mRNA sequence ends translation

Autosomal dominant

expressed equally in males and females, no generational skipping, transmission is about 50%

X-linked dominant

incredibly rare, females are more likely to be affected.

Autosomal recessive

rare, more common to be a carrier, expressed equally in both sexes.

X-linked recessive

more significant in males, generational skips may occur

Turner syndrome

females who have only 1 x chromosome

Clinical manifestation turner syndrome

absence of ovaries, infertility, short stature, webbing of the neck, widely spaced nipples, high rates of fetal mortality

Treatment of Turner Syndrome

estrogen replacement therapy to promote secondary sexual characteristics

Klinefelter syndrome

at least one Y and 2 or more X chromosomes

clinical manifestation klinefelter syndrome

overall male appearance, gynecomastia, small testes, sparse body hair

benefits of inflammation

* Allowing influx of fluid to the site, influx and activation of plasma proteins, influx of WBCs to destroy potential pathogens.
* Plasma protein systems prevent inflammatory response from spreading to healthy tissue.
* Interacting with adaptive immunity to elicit a more specific response.
* Allowing for the initiation of wound healing

process of phagocytosis

1. Recognition: Phagocyte must recognize the foreign body through the process of opsonization
2. Engulfment: The foreign body is surrounded by the phagocyte
3. Fusion: Phagocyte fuses the foreign body with lysosome to form phagolysosome
4. Destruction: Lysosome causes destruction of foreign body

phases of wound healing

1. Inflammation
2. Reconstruction
3. Remodeling and Maturation

Active immunity

antibodies or T-cells that are produced after natural exposure to an antigen or after immunization (typically long lived)

Passive immunity

pre-formed antibodies or T-cells that are transferred from a donor to a recipient (typically temporary).

IgG

most abundant type (80%-85% of immunoglobulins); account for most of the protective activity against infections; transported across the placenta for fetal passive immunity.