Chapter 2 Flashcards
ADAPTION
- reversible, structural or functional response to normal, physiologic conditions and adverse/pathologic conditions
- long term stressors can overwhelm and cause cellular injury/death
CELL DEATH
- two main types: necrosis and apoptosis
* nutrient deprivation can cause autophagy = cell death
TYPES OF CELLULAR CHANGE
- Atrophy: decrease in cell size
- Hyperplasia: increase in cell number
- Metaplasia: reversible replacement of one mature cell with a less mature cell
- Dysplasia: atypical hyperplasia
ATROPHY
- most common in skeletal muscle, heart, sex organs and brain
- Physiologic atrophy: natural
- Pathologic atrophy: decrease in use, blood supply, hormones, etc.
HYPERTROPHY
- heart and kidneys most common
- Physiologic: increased demand/stimulation/hormones
- Pathologic: chronic hemodynamic overload
- mechanical (stretch) or trophic signals (growth or vasoactive)
HYPERPLASIA
- response to severe or prolonged injury
- Compensatory: adaptave mechanism that enables regeneration; occurs in intestinal epithelia, bone marrow, fibroblasts. IE a callus
- Hormonal: estrogen dependent organs
- Pathologic: abnormal growth of normal cells from hormonal stimulation or growth factors
DYSPLASIA or ATYPICAL HYPERPLASIA
- abnormal changes in size, shape and organization of mature cells
- NOT cancer, but can progress
METAPLASIA
replacement of cells due to change of environment
IE: replacing squamous epithelium cells in esophagus with glandular epithelium when increased acid present. Glandular cells are more tolerant of acidic environment
FREE RADICAL
- Any molecular species capable of independant existance that contain a single unpaired electron in an outer orbit ring
- Having 1 unpaired electron = unstable, becomes stabalized by donating or accepting
- When molecule loses the electron, it becomes a free radical
- Can cause injury to DNA, RNA, proteins, lipids, and carbs
- Initiate chain reactions
ISCHEMIA REPERFUSION INJURY
- results from generation of highly reactive oxygen intermediates
- radicals can cause membrane damage and calcium overload
- during ischemia, excessive ATP consumption leads to accumuation of free radicals which are then metabolized by influx of O2 and converted into peroxides
- influx of O2 causes pH/osmotic/gap junction changes, inflammatory signaling and calcium overload
REACTIVE OXYGEN SPECIES
- chemically reactive molecules from molecular oxygen formed as a natural oxidant species in cells during mitochondrial respiration and energy generation
- Mitochondira utilize O2 to generate ATP, byproduct is ROS
- can cause significant damage in cells and promote cell death
METH
*CNS stimulant causing irritability, violence, anxiety, excitement, hallucinations, paranoia, euphoria, alertness and percieved increased energy
COCAINE AND CRACK
- crack more potent than cocaine
- CNS stimulant, blocks reuptake of norepi, dopamine, serotonin with increased synthesis of each
- HTN, tachycardia, vasocontriction, dysrhythmias, sudden death, cardiomyopathy, MI
LIPEDEMIA
Hypo: low serum lipids, body mobilizes fatty acids from adipose tissue. Causes an increase productio and circulation of ketone bodies (byproducts of lipid metabolism). Causes loss of water and electrolytes
Hyper: increase levels of lipoproteins in blood result in deposits of fat in heart, liver and muscle.
DIVING RESPONSE
- promotes a parasympathetic mediated bradycardia
- combined with cold shock response (tachycardia and SNS response) can cause “autonomic conflict”
- Can cause sudden death depending on patient history
HYPOTHERMIC INJURIES
- increases intracellular CA++ by slowing Na+K+ pump activity, leading to Na+ accumulation in cell
- abrupt drop in temp causes vasocontriction and increasted viscosity = ischemic injury/necrosis
- prolonged causes vasodilation producing severe swelling
HYPERTHERMIC INJURIES
- Heat exhaustion: hypotension due to fluid loss, weakness, nauea and sudden collapse. Collapse results from cardiovascular system failure due to hypovalemia
- Heat stroke: core body temp above 41C
MALIGNANT HYPERTHERMIA
- inherited disorder of skeletal muscle sarcoplasmic reticulum in response to inhaled asesthetics or succinylcholine
- elevated temp, increased muscle metabolism, muscle rigidity, rhabdo, acidosis and cardiovascular collapse
NEUROLEPTIC MALIGNANT SYNDROME
- caused by administration of neuroleptic drugs (antipsychotics, haloperidol, metocloprimide) or withdrawl of dopaminergic drugs
- muscle rigidity, autonomic dysregulation
HIGH ALTITUDE ILLNESS (HAPE, AMS, HACE)
*high altitude pulmonary edema: non cardiogenic edema associated with pulmonary HTN
*cerebral edema: AMS symptoms with neurologic disfunction (ataxia, ALOC) and severe lassitude (weakness)
*less severe is acute mountain syndrome (AMS): headache, loss of appetite, nausea, weakness, dizziness and insomnia
*rate of ascent from altitude, sleeping altitude and final altitude are all factors
*
BILIRUBIN
- product of structural hemoglobin
- bilirubin extrected via liver
- elevated levels due to disease of RBCs, metabolism of bilirubin via the liver, or obstruction of CBD (common bile duct)
- albumin binds to unconjugated bilirubin in plasma to protect plasma membranes
CALCIUM DISORDERS
- calcification due to influx of injured cells releasing intracellular calcium
- dystrophic calcification: occurs in dying tissues, present in chronic TB of lungs of lymph nodes and arteries with advanced atherosclerosis
- present in tumors; center of tissue deprived of O2 and becomes calcified
- metastic calcification: deposits in normal undamaged tissue; related to cancers/diseases
URATE
- major end product of catabolism
- high levels can deposit sodium urate crystals in tissues causing gout and nephritis
- named chronic hyperuricemia
