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Uncategorized > Chapter 2, 3, and 48 > Flashcards

Chapter 2, 3, and 48 Flashcards

1
Q

Coagulative necrosis

A
  • Caused by protein denaturation as a result of hypoxia
  • Occurs in kidney, heart, adrenal glands
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2
Q

Gangrenous necrosis

A

tissue necrosis caused by hypoxia and subsequent bacterial invasion

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3
Q

Compare and contrast the pathophysiologic mechanisms of the three most common causes of cellular injury and their clinical manifestations

HYPOXIA

A
  • Lack of oxygen, usually caused by ischemia (cessation of blood flow into vessels that supply the cell with oxygen/nutrients) ex: ateriosclerosis, thrombus
  • Mechanisms: Decrease ATP –> anaerobic metabolism Na-K pump failure –> Inc Na and Ca, Dec K in cell Cellular swelling from sodium influx
  • Clincal manisfestations: increased heart rate, skin turns blue
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3
Q

Name the 3 most common causes of cellular injury

A
  • Hypoxia
  • Free Radicals
  • Chemical
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3
Q

What hormones regulate salt and water balance?

A
  • Antidiuretic hormone (ADH) - released by posterior pituitary gland, causes h20 to be reabsorbed into the blood from distal tubules/collecting ducts of kidneys
  • Aldosterone - from adrenal cortex. causes kidneys to reabsorb both sodium and h20 when ECF level or Na level is low
  • Natriuretic hormones - responds to increase BP/BV –> increase sodium and water excretion
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4
Q

How does a decrease in capillary oncotic pressure cause edema?

A

Lost or diminished plasma albumin production contributes to decreased plasma oncotic pressure. The decreased oncotic attraction of fluid within the capillaries causes capillary fluid to move into the interstitial space = edema

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5
Q

Differentiate mechanisms of cellular adaptation and provide examples of physiologic and pathologic cellular adaptation, as appropriate

ATROPHY

A
  • Decrease in cell size caused by decreased protein synthesis, increased protein catabolism, or both
  • Physiologic: the thymus gland involutes and atrophies; aging of brain cells
  • Pathologic: atrophy occurs as a result of decreases in workload, use, pressure, blood supply, nutrition, hormonal stimulation, and nervous stimulation
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5
Q

Define and contrast necrosis and apoptosis

A
  • Necrosis - sum of cellular changes after local cell death and process of cellular autodigestion; widespread, pathologic, irreversible injury, dense clumping
    • Causes: prolonged hypoxia, infection, cell membrane damage
  • Apoptosis - programmed cell death, scattered single cell; normal or pathologic
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5
Q

What is the most prominent ECG changes associated with hyperkalemia? With hypokalemia?

A
  • Hyperkalemia: decreased cardiac conduction, more rapid repolarization of heart muscle.
  • Hypokalema: delays ventricular repolarization
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6
Q

Hypokalemia

A
  • < 3.5 mEq/L
    1. Carbohydrate metabolism is affected b/c insulin secretion is depressed, muscle/liver glycogen synthesis is reduced
    1. Metabolic ALKALOSIS can occur b/c K moved from ECF to ICF, H+ ions move out of cells to maintain cation balance
    1. Polyria & volume depletion can occur b/c low K impairs renal function = decreased ability of kidneys to respond to ADH or concentrate urine
    1. skeletal, smooth, cardiac muscle weakness and cardiac dysrhythmias occur b/c low K levels = decrease neuromuscular and cardiac excitability
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8
Q

Distinguish the pathophysiology, clinical manifestations, and treatment among 1st, 2nd, and 3rd degree burns 1st degree

A

Partial thickness, epidermal injury, no scarring Mani: local pain, redness, blisters; severe: chills, HA, localized edema, N&V Rx: IV hydration, ASA/NSAID, H20 soluble lotion

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9
Q

What causes isotonic imbalance?

A

Gain/Loss of ECF or sodium that changes the normal 0.9% salt soltuion of the body fluids

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9
Q

How do alterations in CO2 influence acid-base states?

A

CO2 levels are controlled by lungs. Hyperventilation reduces CO2 levels (& H+ concentration) of the blood = respiratory alkalosis. Hypoventilation increases CO2 cocentration = respiratory acidosis

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10
Q

Manifestations of Cellular Injury

A

Fever Increase heart rate Increase WBC Pain Elevated enzyme Fatigue, malaise, anorexia

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12
Q

Differentiate the various types of hematoma formation and their etiologies and clinical manifestations

A
  • Definition: collection of blood in soft tissue vs enclosed space
  • Subdural: blood between brain surface & dura venous blood, slow manifestation fall, blow, sudden acceleration/deceleration
  • Epidural: blood between dura & skull arterial blood, faster manifestation skull fracture
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12
Q

Give 2 examples of hypertonic alterations, and explain the mechanisms of action for each

A
  • Def: Elevated solute concentration in the blood
    1. Increased Na, secondary to hyperaldosteronism. Kidneys reabsorbed too much sodium
    1. Water loss. ex: severe diarrhea
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13
Q

Distinguish the pathophysiology, clinical manifestations, and treatment among 1st, 2nd, and 3rd degree burns

2nd degree

A
  • Partial thickness, skin loses barrier and vapor functions.
    1. Superficial (epidermal/dermal)
    1. Deep (epidermal/dermal, scarring, requires skin graft)
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14
Q

Distinguish the pathophysiology, clinical manifestations, and treatment among 1st, 2nd, and 3rd degree burns

3rd degree

A
  • Full thickness, epiderma/dermal/subq injury. Skin loses barrier & vapor functions. Nerve endings destroyed.
  • Manifestation: Dry/leathery wound, marked edema, hypovolemia, burn shock Rx: escharotomy, graft
15
Q

Liquefactive necrosis

A

Caused by ischemic injury to neurons and glial cells in the brain. Can also be caused by bacterial infections

16
Q

Caseous necrosis

A

Caused by tuberculosis pulmonary infection

17
Q

Fat necrosis

A

Caused by lipases Occurs in breast, pancreas, other abdominal structures

18
Q

What forces promote net filtration?

A
  • Net filtration = movement of water back and forth across capillary membrane
  • Controlled by capillary and interstitial hydrostatic and oncotic pressures (starling forces)
  • Forces for H20 moving from capillary to interstitium: capillary hydrostatic pressure, interstitial oncotic pressure
  • Forces for H20 moving from interstitium to vascular compartment: capillary oncotic pressure, interstitial hydrostatic pressure
19
Q

Hyperkalemia

A
  • > 5.0 mEq/L
    1. skeletal/smooth/cardiac muscle excitability increased
    1. cardiac dysrhythmias (heartblock, cardiac arrest) can occur
    1. metabolic ACIDOSIS occur b/c K moves from ICF to ECF, H+ moves into of cell
    1. Renal function affected –> fluid retention, oliguria
20
Q

How does an increase in capillary hydrostatic pressure cause edema?

A
  • Hydrostatic pressure increases as a result of venous obstruction or salt and water retention.
  • Venous obstruction causes hydrostatic pressure to increase behind the obstruction, pushing fluid out of the capillaries and into the interstitial space = edema
21
Q

How can you note have a deficiency in total body potassium and still have hypokalemia?

A
  • ECF hypokalemia can develop w/o loss of total body K
  • K can shift into the cells during respiratory or metabolic acidosis (plasma acid-base balance) or after administration of insulin (promotes cellular uptake of K, causing ECF K deficit)
23
Q

Differentiate mechanisms of cellular adaptation and provide examples of physiologic and pathologic cellular adaptation, as appropriate

DYSPLASIA

A

Change in size, shape, organization of mature cell tissues Physiologic: Pathologic:

24
Q

How do cells become markedly swollen with hypoxic injury?

A

Lack of O2 to the cells reduces production of ATP (necessary to maintain Na-K pump). Sodium can now enter cells freely, water follows sodium into cells = edema

25
Q

Compare and contrast the pathophysiologic mechanisms of the three most common causes of cellular injury and their clinical manifestations

CHEMICAL

A
  • From damage or destruction of the plasma membrane by chemical agents
  • Cellular response: Membrane defects –> cellular swelling Decreased ATP, Ca++ influx into mitochondria (dec oxidative metabolism) DNA degradation Lysosomal membrane injury –> enzyme leak into cytoplasm –> digests all cell organelles –> DNA synthesis stopped
  • Causes: lead, carbon monoxide, ethanol, mercury, and social or street drugs
26
Q

Diagram the common sequence of events in cell death

A
  1. Decreased ATP production
  2. Sodium-potassium pump failure
  3. Cellular swelling
  4. Ribosome detaches from ER
  5. Decreased protein synthesis
  6. Calcium enters cell –> mitochondrial swelling
  7. Vacuolation
  8. Lysozyme leakage of digestive enzymes
  9. Autodigestion of intracellular structures
  10. Plasma membrane lysis
27
Q

Describe the concept and process of oncosis and its relation to cellular injury and death

A
  1. Hypoxia
  2. ATP production decreases
  3. Na and H20 move out of cell, K moves in
  4. Osmotic pressure increases
  5. more H20 moves into cell
  6. cisternae of endoplasmic reticulum distend, rupture, form vacules
  7. extensive vacuolation
  8. hydropic degeneration
29
Q

Name the common biochemical derangements of cellular injury and death

A
  1. Depletion of ATP
  2. Decreased levels of oxygen and increase of oxygen-derived free radicals
  3. Increased concentration of Ca++ in cells
  4. Defects in membrane permeability
30
Q

Describe postmortem changes and approximate temporality of the physiologic transitions

A
    1. Algor mortis (↓ body temperature);
    1. Livor mortis (blood gravity-dependent, purplish discoloration)
    1. Rigor mortis (muscle stiffening)
    1. Postmortem autolysis (putrefaction, flaccidity, greenish discoloration, bloating)
32
Q

Differentiate mechanisms of cellular adaptation and provide examples of physiologic and pathologic cellular adaptation, as appropriate HYPERPLASIA

A
  • Increase in # of cells caused by increased rate of cellular division
  • Physiologic: compensatory (organ regeneration), hormonal (pregnancy)
  • Pathologic: excessive hormonal stimulation of growth factors on target cells -> abnormal proliferation of normal cells
34
Q

4 types of necrosis

A
  • coagulative
  • liquefactive
  • caseous
  • fat
35
Q

Metabolic acid-base disturbances are caused by alterations in what 2 chemicals?

A

H+ ion and HCO3 ions

36
Q

Discuss how intracellular calcium levels affect the cell

A

Increased amounts of Ca++ in cell = intracellular damage from enzyme activation

37
Q

Diagram the mechanisms of reperfusion injury and discuss its treatment

A

Increased ATP consumption during ischemia –> catabolites –> Increased ROS with reperfusion –> cell membrane damage, ATP loss, apoptosis Calcium overload, Neutrophil adhesion to endothelium Rx: antioxidants, anti-inflammatories

38
Q

What is a hypotonic imbalance? Give 2 examples

A
  • Def: Decrease in serum Na levels
  • Ex: Diuresis (too much Na excreted by kidneys), sweating (Na lost through skin)
  • Excessive oral/IV h2o intake or decreased water excretion (renal failure) can also cause hypotonic imbalance
39
Q

Differentiate mechanisms of cellular adaptation and provide examples of physiologic and pathologic cellular adaptation, as appropriate

METAPLASIA

A
  • Reversible replacement of mature cells types
  • Thought to be caused by reprogramming of stem cells in most epithelia or of undifferentiated mesenchymal cells in connective tissue
40
Q

Differentiate mechanisms of cellular adaptation and provide examples of physiologic and pathologic cellular adaptation, as appropriate

HYPERTROPHY

A
  • Increase in cell size caused by increased work demands or hormonal stimulation. Results in an increased amounts of protein in the plasma membrane, endoplasmic reticulum, microfilaments, and mitochondria
  • Physiologic: pregnancy
  • Pathologic: thickening of the muscle
41
Q

Why is an increase in intracellular calcium injurious?

A
  • Intracellular Ca damages cellular components like the mitochondria –> causing it to swell –> stops ATP production = cell death
  • Dystrophic calcification occurs in dying tissues as cells become deprived of their oxygen supply and cell membrane becomes permeable to calcium
42
Q

Compare and contrast the pathophysiologic mechanisms of the three most common causes of cellular injury and their clinical manifestations

FREE RADICALS

A
  • Electrically unstable molecules that can disrupt chemical bonds of cell memranes
  • Result: Lipid peroxidation, destroy unsaturated fatty acids Alterations of proteins and DNA High levels - apoptosis and necrosis
43
Q

What role does potassium play in the body?

A

Potassium facilitates glycogen deposition in the liver and skeletal muscles. Maintains resting membrane potentials of cells

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