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Pathophysiology 1 > Chapter 2 > Flashcards

Chapter 2 Flashcards

1
Q

ADAPTION

A
  • reversible, structural or functional response to normal, physiologic conditions and adverse/pathologic conditions
  • long term stressors can overwhelm and cause cellular injury/death
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2
Q

CELL DEATH

A
  • two main types: necrosis and apoptosis

* nutrient deprivation can cause autophagy = cell death

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3
Q

TYPES OF CELLULAR CHANGE

A
  • 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
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4
Q

ATROPHY

A
  • most common in skeletal muscle, heart, sex organs and brain
  • Physiologic atrophy: natural
  • Pathologic atrophy: decrease in use, blood supply, hormones, etc.
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5
Q

HYPERTROPHY

A
  • heart and kidneys most common
  • Physiologic: increased demand/stimulation/hormones
  • Pathologic: chronic hemodynamic overload
  • mechanical (stretch) or trophic signals (growth or vasoactive)
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6
Q

HYPERPLASIA

A
  • 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
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7
Q

DYSPLASIA or ATYPICAL HYPERPLASIA

A
  • abnormal changes in size, shape and organization of mature cells
  • NOT cancer, but can progress
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8
Q

METAPLASIA

A

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

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9
Q

FREE RADICAL

A
  • 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
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10
Q

ISCHEMIA REPERFUSION INJURY

A
  • 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
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11
Q

REACTIVE OXYGEN SPECIES

A
  • 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
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12
Q

METH

A

*CNS stimulant causing irritability, violence, anxiety, excitement, hallucinations, paranoia, euphoria, alertness and percieved increased energy

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13
Q

COCAINE AND CRACK

A
  • 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
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14
Q

LIPEDEMIA

A

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.

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15
Q

DIVING RESPONSE

A
  • 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
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16
Q

HYPOTHERMIC INJURIES

A
  • 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
17
Q

HYPERTHERMIC INJURIES

A
  • 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
18
Q

MALIGNANT HYPERTHERMIA

A
  • 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
19
Q

NEUROLEPTIC MALIGNANT SYNDROME

A
  • caused by administration of neuroleptic drugs (antipsychotics, haloperidol, metocloprimide) or withdrawl of dopaminergic drugs
  • muscle rigidity, autonomic dysregulation
20
Q

HIGH ALTITUDE ILLNESS (HAPE, AMS, HACE)

A

*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
*

21
Q

BILIRUBIN

A
  • 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
22
Q

CALCIUM DISORDERS

A
  • 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
23
Q

URATE

A
  • major end product of catabolism
  • high levels can deposit sodium urate crystals in tissues causing gout and nephritis
  • named chronic hyperuricemia

Pathophysiology 1 (2 decks)

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