Patho Exam 1 Flashcards
What happens to a stressed cell
It adapts It heals- reversible injury It dies-irreversible injury Apoptosis Necrosis Autolysis
Know
____ is programmed, internal or external triggers. It kills cell off.
Apoptosis
___ is sudden death, due to severe injury- cell explodes or dissolves
Necrosis
____ is self eating, cell cannibalizes itself for the nutrients
Autolysis
___ response to pathological (normal) and pathologic (adverse) changes
Adaptive changes: Atrophy Hypertrophy Hyperplasia Dysplasia Metaplasia
Reversible
____ - cells get smaller
If you don’t use it you lose it
Atrophy
___ cells get bigger
Ex: hypertrophic cardiomyopathy
Hypertrophy
___ is more cells.
Example: endometrial hyperplasia & benign prostatic hyperplasia
Hyperplasia
___ is abnormal type of growth of cells
Dysplasia
____ is chronic irritation that leads to change in cell type to less functional, less mature type:
Example: bronchial cell type changes
Metaplasia
Pathogenesis
Normal-Barrett’s esophagus-dysplasia-cancer
The progression: metaplasia, then goes to dysplasia, and then cancer.
Know
____ (not really adaptive) cells irregular sizes and shapes. Another name is atypical hyperplasia, pre-cancerous
Dysplasia
___ ___ in infants due to respiratory distress requiring increased oxygen flow, tissue gets thicker, with poor gas exchange.
Bronchopulmonary dysplasia
Mechanisms of cellular injury. How is cell actually hurt?
Cell membrane damage- cell explodes or can’t transport over the membrane anymore
Mitochondrial damage, no ATP, so no energy, can’t maintain cell membrane
Unstable calcium- may accumulate in cells (calcification of cancer cells or instance)
Oncotic pressure changes- water drawn into cell, it blows up.
Know
4 types of cellular injury
___ is lack of oxygen in cells common reason is ischemia. The single most common cause of cellular injury
Hypoxic
4 main types of cellular injury
___ is return of oxygen to hypoxic cells
Reperfusion
___ ___- formation of ROS (reactive oxygen species)
Oxidative stress
___ ___ many chemicals toxic to cells
Chemical injury
Cellular response to hypoxia- cell swells up.
ATP production is decreased.
Sodium and water move into cell. Potassium moves out of cell.
Osmotic pressure increases
More water moves into cell
Cisternae of endoplasmic reticulum distention, rupture and form vacuoles
Extensive vacuolation
Hypertropic degeneration
Know
____ ___:
Additional injury is caused by restoration of blood flow and oxygen.
4 mechanisms** Oxidative dress** Increased intracellular calcium Inflammation Complement activation
Ischemia reperfusion
Cellular injury: free radicals and reactive oxygen species (ROS)
These do damage to cells.
Know
Chemical or toxic injury
Environmental toxins especially air pollution is the main one.
Heavy metals will cause toxic injury to cells
Alcohol exposure will lead to cellular death
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Blunt force injuries
Contusions
Lacerations
Fractures
Sharp force injury: Incised wound Stab wounds Puncture wound Chopping wound
Gunshot wounds
Asphyxial injuries Suffocation Strangulation Chemical asphyxiants Drowning
Know
___ injury is disease producing potential
Invasion and destruction
Toxin production.
Production of hypersensitivity reactions
Infectious
___/___ injury
From substances generated during inflammatory response
Phagocytes
Biochemical substances
Membrane alterations
Immunologic/inflammatory
Other types of injury:
Excessive or deficient cell nutrients- sugar
Environmental factors- temperature, radiation, noise
Genetic abnormalities
Asphyxia
Know
Manifestations of cellular injury
Abnormal metabolism can cause fatty liver
Lack of enzyme can cause lysosomal storage disease: accumulation of endogenous materials
Defect in protein folding transport can cause accumulation of abnormal proteins
Ingestion of indigestible materials can cause accumulation of exogenous materials
Know
Manifestations of cellular injury: accumulations of endogenous materials.
Bruising> extravasated red cells> phagocytosis of red cells by macrophages> hemosiderin and iron free pigments
Know
Example of manifestations of injury
___ ___ water blows up cell
Oncotic damage
Example of manifestations of injury
___ ___ seen in cancer
Calcium accumulation
Example of manifestations of injury
___ Uric acid crystals accumulate
Gout
Example of manifestations of injury
___ is bruises, bilirubin
Pigmentation
Systemic (whole body) manifestations of cell injury
Fever Malaise (sore tired sick) Fatigue Pain Stress response- heart rate up Enzymes in the blood (blood tests for tissue damage, like heart and liver enzymes) Increased wbc Much due to the inflammatory response How you know your sick
Know
Cellular death:
Due to necrosis or apoptosis
Know
___ is rapid loss of plasma membrane organelle swelling, mitochondrial dysfunction, lacks typical features of apoptosis
May be regulated or programmed
Autolysis (auto digestion) one type
Necrosis
___ necrosis is from protein denaturation
Albumin is transformed from a gelatinous, transparent state to a FIRM OPAQUE substance
Example is infarct
Most common
Coagulative necrosis
___ necrosis
Example: neurons and glial cells of the brain
Cells digested by own enzymes
Tissues become soft and liquefied
Triggered by bacterial infection.
Staphylococci, streptococci, and E. coli.
Liquefactive necrosis
___ necrosis- from tuberculosis infection.
Combination of coagulative and liquefactive necrosis
Caseous
___ necrosis affects the breast and abdominal organs.
Action of lipases (fat digesting enzymes)
Fatty acids combine with elements to create soaps
Tissue appears opaque and chalky white
Fatty necrosis
Gangrenous necrosis
___ is worse and spreads fast
Wet
Gangrenous necrosis ___ is slow and red rim
Dry
___ is a programmed death, active processed cells targeted.
Physiologic vs pathologic- no inflammation & normal part of aging
Apoptosis
___ is self destructive & a survival mechanism
Cytoplasmic contents degraded by lysosomes
May be die to lack of nutrients
Autophagy
___ ___ is death of an entire person.
Somatic death
___ ___ is pale skin
Pallor Mortis
___ ___ is cold
Algor mortis
___ ___ is stiffness
Rigor mortis
___ ___ blood sinks to low areas
Livor mortis
___ is dissolving tissue
Putrefaction
___ absorb into environment
Decomposition
Total body water= 60% of body weight in adults.
Know
___ ___ pushes water out of capillaries (filtration)
Hydrostatic pressure
___ ___ pulls water into capillaries (reabsorption)
Osmotic/oncotic pressure
Water movement- balance of push and pull
Know
Capillary fluid movement by net filtration pressures
Cell- fluid movement by passive and active forces
Know
___ is fluid movement OUT of the capillary and into the interstitial space
Filtration
___ is fluid movement INTO the capillary from the interstitial space.
Reabsorption
What causes edema??
Excessive accumulation of fluid that’s within the interstitial spaces
(Renal failure generalized edema)
(Congestive HF lower extremity edema)
Know
Albumin is a protein that attracts and holds water in the blood vessels
If albumin is low then your edema will be worse
What causes this? Kidney disease Open wounds Hemorrhage Burns
Know
Severe generalized edema
Anasarca
___ ___ gravity dependent edema; will see in legs and feet with standing and sacrum and buttocks when supine
Dependent edema
___ is fluid gathered in body cavity or space (pulmonary and cardiac is common)
Effusion
___ edema is edema more widespread
Generalized
___ edema is limited to a single body region, maybe with trauma (sprained ankle) or could be organ related (cerebral pulmonary or laryngeal)
Localized edema
___ ___ is an area where edematous fluid gathers/process of edema formation
This fluid is NOT available for perfusion (trapped)
Third spacing
Antidiuretic hormone secretion ADH
Made in posterior pituitary.
Increases water reabsorption into the blood from urine; in the kidney.
Secreted if blood volume of patient decreases or drop in BP
Thirst perception- (osmoreceptors cause thirst)
Two types:
volume sensitive receptors- right and left atria of heart and found in thoracic vessels of chest
Baroreceptors- pressure sensitive receptors. Found in aorta, pulmonary arteries, and carotid sinus
Know
Sodium and chloride travel together.
Sodium- accounts for 90% of positive charged ions.
Primary extra cellular fluid cation +
Regulates osmotic forces, thus regulates water
Roles: nerve impulse conduction, acid base balance and cellular biochemistry, and membrane transport
Chloride:
Primary ECF anion -
Provides electroneutrality (keeping the pulses and minuses equal)
Levels vary inversely (opposite) with those of biocarbonate
Know
Renin angiotensin aldosterone system (RAAS)- keep water IN.
When the blood pressure drops the kidney will secrete renin and released if there is low sodium or potassium.
Renin stimulates the formation of angiotensin 1. Made from angiotensinogen (secreted by liver)
Angiotensin converting enzyme (ACE) converts angiotensin 1 to angiotensin 2.
Angiotensin 2 narrows vessels to rise blood pressure and get kidney perfusion restored and you won’t need renin anymore. It also stimulates secretion of aldosterone which helps the body reabsorption of sodium and water and secrete potassium.
Know
RAAS keeps water IN.
Balanced with
Natriuretic peptides keeps water OUT.
BNP shows patient is in HF.
ANH produced by atria.
Natriuretic peptide go against RAAS and makes BP lower.
Know
Total body water volume changes, with proportional electrolyte and water change (no change in concentration)
Isotonic fluid loss: hypovolemia
Isotonic fluid excess- hypervolemia
Isotonic
___ is increased osmolality (concentration)
Hypernatremia
Water deficit in extra cellular fluid (dehydration)
Hypertonic
___ is decreased osmolality
Hyponatremia
Water excess in ECF (water intoxication)
Hypotonic
