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MSII Pathology > Chapter 1. Cell Injury - Tissue Hypoxia > Flashcards

Chapter 1. Cell Injury - Tissue Hypoxia Flashcards

1
Q

what are clinical findings of hypoxia?

A

cyanosis, confusion, cognitive impairment, lethargy

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2
Q

what are causes of tissue hypoxia?

A
  1. ischemia
  2. hypoxemia
  3. Hb-related abnormalities
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3
Q

describe ischemia

  • what are examples?
  • what are consequences?
A

decreased arterial blood flow or venous outflow of blood

  • ex: coronary artery atherosclerosis, decreased CO, thrombosis of splenic vein
  • causes atrophy, infarction, and organ dysfunction
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4
Q

why does a pulse oximeter sometives calculate falsely high SaO2?

A

it cannot identify dyshemoglobins like metHb and carboxyHb when they are present, thus causing a falsely high SaO2

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5
Q

what is the definition of hypoxemia?

A

decrease in PaO2 (<40 mmHg)

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6
Q

what is the definition of PaO2, contributing factors, and its significance?

A

pressure keeping O2 dissolved in plasma of arterial blood

  • % of O2 in inspired air, atomospheric pressure, normal O2 exchange in lungs, driving force for movement of O2 from capillaries into tissue by diffusion
  • reduced in hypoxemia
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7
Q

what is the definition of SaO2, contributing factors, and its significance?

A

average percentage of O2 bound to Hb

  • PaO2 and valence of heme ion in each of 4 heme groups (Fe2+ binds to O2, Fe3+ doesn’t)
  • SaO2 < 80% produces cyanosis of skin and mucus membranes
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8
Q

what is the definition of O2 content, contributing factors, and its significance?

A

total amount of O2 carried in blood

  • Hb concentration in RBCs (most important; determines total amount of O2 delivered to tissue), PaO2, SaO2
  • Hb is most important carrier of O2
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9
Q

what are causes of hypoxemia?

A
  1. decreased inspired PO2
  2. respiratory acidosis (hypoventilation)
  3. ventilation defect
  4. perfusion defect
  5. diffusion defect
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10
Q

if there is an increase in alveolar PCO2, there is a corresponding DECREASE in…

A

alveolar PO2 (PaO2), and SaO2

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11
Q

explain ventilation defects

-what’s an example?

A

impaired O2 delivery to alveoli, as in RDS

-no O2 exchange in lungs that are perfused but NOT ventilated (intrapulmonary shunt)

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12
Q

explain respiratory distress syndrome

A

ventilation defect with collapse of distal airways due to lack of surfactant
-pulmonary capillary blood has same PO2 and PCO2 as venous blood returning from tissue (much of pulmonary blood flow not arterialized) –> intrapulmonary shunting of blood

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13
Q

explain perfusion defects

A

absence of blood flow to aveoli (pulmonary embolus)

-no O2 exchange in lungs that are ventilated, but NOT perfused (increased dead space)

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14
Q

explain diffusion defects and examples

A

decreased O2 diffusion through alveolar-capillary interface

-interstitial fibrosis, pulmonary edema

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15
Q

what do ventilation, perfusion, and diffusion defects all affect?

A

increase difference in O2 concentration between alveolar PO2 (PAO2) and arterial PO2 (PaO2), AKA the alveolar-arterial gradient

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16
Q

what are 3 hemoglobin-related abnormalities?

A
  1. anemia
  2. methemoglobinemia
  3. CO poisoning
17
Q

what is the definition of anemia and the causes?

A

decreased Hb concentration (<7 g/dL) but normal PaO2 and SaO2

  • decreased Hb production (Fe deficiency)
  • decreased production of RBC (aplastic anemia)
  • increased destruction of RBCs (hereditary spherocytosis)
  • increased sequestration of RBCs (splenomegaly)
18
Q

what is methemoglobinemia, causes, pathogenesis, and treatment?

A

heme Fe3+, decreased SaO2 (but normal PaO2)

  • caused by oxidant stress and congenital deficiency of cytochrome b5 reductase
  • Fe3+ can’t bind O2
  • ferric heme groups impair unloading of O2 by oxygenated ferrous heme causing left-shifted o2 binding curve
  • causes chocolate-colored blood (increased [deoxyHb]) and cyanosis
  • -skin color doesn’t return to normal after administration of O2
  • treat with IV methylene blue (artificial e- carrier in pentose phosphate shunt)
19
Q

what is methemoglobin (metHb)? how is it reduced?

A

Hb with oxidized heme groups (Fe3+)

-converted to ferous state by reduced NADH reductase system in glycolytic pathway

20
Q

CO poisoning

  • pathogenesis
  • clinical findings
  • treatment
A

leading cause of death due to poisoning

  • CO competes with O2 for binding sites on Hb, which then inhibits cytochrome oxidase in ETC, causing left-shifted O2 binding curve
  • decreases CaO2 WITHOUT affecting PaO2
  • cherry red skin/blood, headache, dyspnea/dizziness, seizures/coma, lactic acidosis due to hypoxia
  • treat w/ O2 via nonbreather mask or endotracheal tube (100% O2)
21
Q

what factors cause left-shifted O2-binding curve?

A
  1. decreased 2,3-bisphosphoglycerate (BPG)
  2. CO, alkalosis, metHb, fetalHb, hypothermia
    all increase affinity of Hb for O2 with less release of o2 to tissue
22
Q

what happens at high altitudes?

A

atmospheric pressure is decreased, but percentage of O2 in atmosphere is the same

  • hypoxemia stimulates peripheral chemoreceptors causing respiratory alkalosis, which shifts the O2 binding curve to the left
  • alkalosis activates phosphofructokinase, increasing 1,3-BPG, which is converted to 2,3-BPG, shifting OBC to right, causing increased release of O2 to tissue
23
Q

what are mitochondrial causes of ATP depletion?

A

enzyme inhibition of oxidative phosphorylation or uncoupling of oxidative phsophorylation

24
Q

what are the causes of enzyme inhibition of oxidative phosphorylation? go into more detail about one of the culprits

A
  1. ATP synthesis decreases
  2. CO and cyanide inhibit cytochrome oxidase in ETC
    - CN poisoning from drugs, combustion of polyurethane products, producing initial CNS and CV stimulation followed by CNS depression and death, producing lactic acidosis from hypoxia and increased venous PO2 and saturation
    - -requires treatment with amyl nitrite (makes metHb that combines with CN to make cyanmetHb) then thiosulfate (CN converted to thiocynanate)
25
Q

what does uncoupling of oxidative phosphorylation do?

A

uncoupling proteins carry H+ in intermembranous space through IMM into matrix without damaging membrane

  • bypass of ATP syntahse causes decreased ATP synthesis
  • ex: thermogenin and dinitrophenol
  • heat normally used to make ATP raises core body temp
26
Q

what are thermogenin and dinitrophenol used for?

A

both are uncouplers of oxidative phosphorylation

  • thermogenin: natural uncoupler in brown fat, useful in stabilizing body temps
  • dinitrophenol: used in making nitroglycerin, but danger of developing hyperthermia
27
Q

what are examples of mitochondrial toxins? what is their mechanism?

A

alcohol and salicylates

  • damage IMM causing H+ to move into matrix
  • hyperthermia is common complication
28
Q

what tissues are susceptible to hypoxia?

A
  1. watershed areas between terminal branches of major arterial blood supplies
  2. subendocardial tissue
  3. renal cortex (esp. straight portion of PT) and medulla (esp. Na-K-Cl cotransport channel in TAL)
  4. neurons in CNS (most adversely affected)
  5. hepatocytes in central vein (esp. zone III)
29
Q

what does decreasing coronary artery blood flow cause?

A
  • subendocardial ischemia (angina and ST-segment depression)

- left ventricle hypertrophy in presence of increased myocardial demand for O2 can also cause subendocardial ischemia

30
Q

what are consequences of hypoxic cell injury?

A
  1. decreased ATP synthesis
  2. anaerobic glycolysis used for ATP (net gain of 2 ATP, lactic acidosis, impaired Na/K-ATPase pump)
  3. decreased PRO synthesis due to detachment of ribosomes (potentially reversible)
  4. irreversible cell changes (mostly caused by impaired Ca-ATPase pump causing increased cytosolic Ca++)
31
Q

why does increased cytosolic Ca++ have lethal effects?

A
  1. enzyme activation
    - phospholipase increases membrane permeability
    - proteases damage cytoskeleton
    - endonucleases cause fading of nuclear chromatin (karyolysis)
  2. reentry of Ca++ into mitochondria
    - increases mitochondrial membrane permeability
    - release of cyt c into cytosol activates apoptosis

MSII Pathology (11 decks)

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