Chapter 2, 3, and 48

Question 1

Coagulative necrosis

Answer 1

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

Question 2

Gangrenous necrosis

Answer 2

tissue necrosis caused by hypoxia and subsequent bacterial invasion

Question 3

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

HYPOXIA

Answer 3

• 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

Question 3

Name the 3 most common causes of cellular injury

Answer 3

• Hypoxia
• Free Radicals
• Chemical

Question 3

What hormones regulate salt and water balance?

Answer 3

• 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

Question 4

How does a decrease in capillary oncotic pressure cause edema?

Answer 4

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

Question 5

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

ATROPHY

Answer 5

• 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

Question 5

Define and contrast necrosis and apoptosis

Answer 5

• 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

Question 5

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

Answer 5

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

Question 6

Hypokalemia

Answer 6

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

Question 8

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

Answer 8

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

Question 9

What causes isotonic imbalance?

Answer 9

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

Question 9

How do alterations in CO2 influence acid-base states?

Answer 9

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

Question 10

Manifestations of Cellular Injury

Answer 10

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

Question 12

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

Answer 12

• 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

Question 12

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

Answer 12

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

Question 13

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

2nd degree

Answer 13

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

Question 14

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

3rd degree

Answer 14

• 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

Question 15

Liquefactive necrosis

Answer 15

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

Question 16

Caseous necrosis

Answer 16

Caused by tuberculosis pulmonary infection

Question 17

Fat necrosis

Answer 17

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

Question 18

What forces promote net filtration?

Answer 18

• 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

Question 19

Hyperkalemia

Answer 19

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

Question 20

How does an increase in capillary hydrostatic pressure cause edema?

Answer 20

• 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

Question 21

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

Answer 21

* 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)

Question 23

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

Answer 23

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

Question 24

How do cells become markedly swollen with hypoxic injury?

Answer 24

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

Question 25

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

Answer 25

* 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

Question 26

Diagram the common sequence of events in cell death

Answer 26

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

Question 27

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

Answer 27

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

Question 29

Name the common biochemical derangements of cellular injury and death

Answer 29

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

Question 30

Describe postmortem changes and approximate temporality of the physiologic transitions

Answer 30

* 1. Algor mortis (↓ body temperature); * 2. Livor mortis (blood gravity-dependent, purplish discoloration) * 3. Rigor mortis (muscle stiffening) * 4. Postmortem autolysis (putrefaction, flaccidity, greenish discoloration, bloating)

Question 32

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

Answer 32

* 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

Question 34

4 types of necrosis

Answer 34

* coagulative * liquefactive * caseous * fat

Question 35

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

Answer 35

H+ ion and HCO3 ions

Question 36

Discuss how intracellular calcium levels affect the cell

Answer 36

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

Question 37

Diagram the mechanisms of reperfusion injury and discuss its treatment

Answer 37

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

Question 38

What is a hypotonic imbalance? Give 2 examples

Answer 38

* 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

Question 39

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

Answer 39

* 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

Question 40

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

Answer 40

* 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

Question 41

Why is an increase in intracellular calcium injurious?

Answer 41

* 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

Question 42

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

Answer 42

* 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

Question 43

What role does potassium play in the body?

Answer 43

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