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805 > Lecture 4 (Cut off for Exam 1) > Flashcards

Lecture 4 (Cut off for Exam 1) Flashcards

Hypoxia & Anemia

1
Q

Hypoxia

A

Lack of available oxygen. Ex: fire, increases in altitude

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2
Q

Hypoxemia

A

Lack of oxygen in the body. Ex: impairments of the lungs diffusion or ventilation, heart’s contracting ability, blood’s capacity to carry oxygen

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3
Q

Blood Gases (2)

A
  1. Oxygen - carried dissolved in the blood and chemically combined to heme portion of hemoglobin
  2. Carbon Dioxide - waste product that is transported by being dissolve, bound to proteins (carbamino compounds), or as bicarbonate (most common)
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4
Q

Reasons for Reduced Lung Ventilatory Drive (5)

A
  1. Lack of chemical receptor development or response
  2. Brain injury
  3. CNS depressants
  4. Respiratory irritants
  5. Alkylosis
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5
Q

Receptors Connected to Ventilatory Drive (2)

A
  1. Chemoreceptors - detect H+ in response to CO2 levels (more sensitive)
  2. Peripheral chemoreceptors - found in the periphery like the carotid body and detect oxygen levels
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6
Q

2 Examples of CNS Depressants

A

Alcohol and barbiturates

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7
Q

3 Examples of Respiratory Irritants

A

Ozone, hydrochloride, and capsaicin

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8
Q

Alkylosis

A

Caused by hyperoxia (decreased tissue metabolism) that increases blood pH and decreases CO2 levels.

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9
Q

Lung Gas Diffusion Equation & Coefficient Meaning (4)

A
  1. A = area
  2. D = diffusion coefficient
  3. T = thickness of barrier
  4. P = differential pressure

Vgas = [(A * D * (P1-P2)) / T]

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10
Q

Conditions Affecting the Diffusion Equation (2)

A
  1. Acute alveolar edema - increases T. Increases distance oxygen needs to diffuse from alveolar to capillaries
  2. Remodeling from chronic cigarette use - decreases A as septal is destroyed and the air sacks become large and “floppy.” Leads to emphysema (Blue bloaters)
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11
Q

Lung Ventilation Measurements (4)

A
  1. Tidal volume - amount you normally breathe in and out
  2. Vital Capacity - total volume you can fully inhale down to fully exhale
  3. Residual Volume - amount between completely exhaling and a volume of zero (non-measurable)
  4. Total Lung Capacity = Vital Capacity + Residual Volume (non-measurable). Drops with age, faster if you smoke
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12
Q

Condition Affecting Ventilation Measurements

A

Fibrosis (pink puffers) make all the ventilation measurements decrease (IRV, TV, ERV, & RV). Restrictive disease that tries to push air back out as quickly as possible and resist expansion.

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13
Q

Heart’s Part in Oxygen Transport

A

Pumps blood and regulates fluid volume via atrial natriuretic peptides.

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14
Q

Heart Pathologies + Side Effects

A
  • Hypoperfusion - pumping ability/contractility
  • Cardiomyopathy - growth/hypertrophy
  • Arrhythmia - electrical conductivity
  • Ischemia/infarctions - coronary vasculature
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15
Q

Blood’s Role in Oxygen Transport

A
  • RBCs carry oxygen from lungs to tissues

- contain hemoglobin (HGB) which was a high affinity for oxygen

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16
Q

Hemoglobin (HGB)

A
  • binds with oxygen in RBCs
  • made up of 4 globin chains (2 alpha, 2 beta)
  • each chain has a heme, made with an iron molecule (Fe^+2) which is the site of oxygen binding
  • carbon dioxide binds to the globins
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17
Q

Myoglobin

A
  • Myoglobin has a higher affinity (stronger grip) on oxygen and assists in transfer of oxygen from hemoglobin to myoglobin
  • myoglobin is a transfer component found in most cells outside of the blood
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18
Q

pH/CO2 Affects on HGB Saturation Curve

A

As CO2 partial pressure increases the blood becomes more acidic and the pH drops - curve shifts right (let’s go of oxygen soon)
As CO2 partial pressure decreases the blood becomes less acidic and the pH increases - curve shifts left (holds onto oxygen longer)

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19
Q

Carbon Monoxide

A

CO takes up the same place as oxygen, so amount of HGB-O2 compounds decrease as the concentration of CO rises. Kind of anemia since it decreases the oxygen-carrying capacity of blood.

20
Q

Fetal Isoforms of HGB

A

Tighter bond than HGB but less than myoglobin. Assists in the extra step of transporting oxygen from mother to baby to baby’s tissues. Has 2 gamma chains instead of beta.

21
Q

DPG

A
  • made by RBCs during glycolysis
  • binds to HGB and decreases its affinity for oxygen
  • In hypoxic conditions, RBCs make more DPG and release oxygen sooner to the tissues
22
Q

Other HGB Modifiers (3)

A
  1. Oxidation states of iron (Fe^+3 = methemoglobin and doesn’t bind to oxygen)
  2. Nitrate poisoning - can lead to methemoglobinemia which can occur when exposed to amyl nitrate, nitroglycerin, and nitroprusside for example. Can occur when using nitrate fertilizers
  3. Cyanide - can lead to cyanosis
23
Q

Bicarbonate <=> Carbon Dioxide Equation

A

CO2 + H2O <=> H2CO3 (carbonic acid) <=> H+ + HCO3- (bicarbonate)

  • The conversion of CO2 into carbonic acid and its dissociation is what increases blood pH when CO2 concentrations increase.
  • Bicarbonate = important blood buffer
24
Q

Carbamino Compounds

A

RNH2 + CO2 <=> RNHCO2- + H+

Also increases blood pH as CO2 concentrations increase since its formation releases hydrogen ions.

25
Q

Anemia

A

Reduction in the oxygen carrying capacity of the blood. Commonly a decrease of RBCs circulating

26
Q

Anemia Diagnostic Tests

A
  1. Hematocrit - cells/volume
  2. HGB - finding its amount directly
  3. Mean RBC - cell volume, cell HGB, and mean corpuscular [HGB}
  4. Iron and total iron blood capacity
  5. WBC count/differential platelet count
  6. EPO concentrations
27
Q

Hematopoiesis

A

GEMM : Granulocyte, Erythrocyte (most made cell), Monocyte, and Megakaryocyte (makes platelets)
GM: Macrocyte and granulocyte

28
Q

Anemia Classifications (3)

A
  1. Microcytic - (<80 fL), iron deficiency, sickle cell anemia, heavy metal poisoning, chronic disease, thalassemia
  2. Normocytic - (80-95 fL), blood loss, aplastic anemia (not making blood), marrow failure, chronic disease, renal failure, endocrine disorders, acute infection
  3. Macrocytic - (>95 fL), B12 deficiency, folic acid deficiency, alcoholism
29
Q

Erythrocyte Lifespan

A

120 days with very little deviation

30
Q

Erythrocyte Destruction Methods (2)

A
  1. Extravascular ingestion (normal) by macrophage in spleen & liver
  2. Intravascular destruction (bad) occurs at low frequency except in ABO-incompatible transfusions and hemolytic anemias
31
Q

Hemolytic Anemias Causes (4)

A
  1. Chemically - induced
  2. Physical damages
  3. Infection
  4. Autoimmunity (mother and fetus)
32
Q

Chemically - Induced Anemias (6)

A 
Intravascular Destroyed
1. Hypotonic solution (irrigation in surgery)
2. Pore-forming animal toxins
3. Heat/damage to proteins
Extravascular Ingestion
1. Hyperoxia (100% oxygen levels)
2. Arsenic hydride
3. Chlorates
33
Q

Bone-Marrow Failure Causes (3)

A
  1. Toxicity from radiation or drugs (chemotherapy, antimalarials, benzos, etc)
  2. Malignancies
  3. Red cell aplastic syndromes (can be idiopathic, infectious, autoimmune, or acquired (Fanconi))
34
Q

Macrocytic Anemias

A

Deficiency in cofactors essential for DNA synthesis (like B12 or folate). Can stem from alcoholism, strict vegetarians, or infants

35
Q

Hemoglobinopathies

A

Inherited defects in the genes coding for HGB. Ex: Sickle cell, thalassemia

36
Q

Sickle Cell Anemia

A

Genetic mutation in the production of HGB that makes RBCs rigid and sticky. This can cause the RBCs to get stuck, rupture, can lead to dehydration, membrane damages, and potassium loss long term.

37
Q

Clinical Outcomes of Sickle Cell Anemia (4)

A
  1. Mild to moderate basal anemia
  2. Recurring pain in focal regions (fingers, feet, toes)
  3. Crises - vasoocclusive painful crises, aplastic, sequestration, hemolytic
  4. Mean lifespan = 42-48 years
38
Q

Thalassemia

A

Seen in Arabia, South + SE Asia, Mediterranean, central & parts of north Africa. Causes you to make fetal HGB your whole life which doesn’t deliver oxygen as well to the tissues (hypoxia).

39
Q

Thalassemia Clinical Manifestations (2)

A
  1. Longer lifespan than sickle cell anemia patients

2. Bones get bigger and deform due to increases EPO, iron overloading, and growing marrow

40
Q

Thalassemia Treatment Options

A
  1. Blood transfusions - can lead to iron overload main treatment
  2. Iron chelation - deferoxamine
  3. Stem cell transplatation
41
Q

Hypoproliferation

A

Not making enough RBCs. NOT the same as aplastic (not making ANY RBCs)

42
Q

Hypoproliferation Causes (4)

A
  1. Inadequate generation or response to EPO
  2. Protein deprivation
  3. Endocrine disorders (hypothyroidism)
  4. Chronic diseases (AIDS, kidney disease, rheumatoid arthritis)
43
Q

EPO

A

Present in blood and stimulates RBC production over other cells. Peptide hormone that is made by the kidney in response to hypoxia and transcribed by HIF-1alpha. As HGB concentrations rise, EPO concentration drop. EPO agents given to people with many ailments like cancer, renal failure, and AIDS.

44
Q

HIF-1alpha

A

Transcription factor that enables all cells to respond to a lack of oxygen. Degraded in normoxic conditions. As oxygen levels drop, degradation drops, and HIF-1alpha increases and allows for greater nuclear transport and transcriptional activity to make things like EPO (BUT not just EPO).

45
Q

Iron for Heme

A

Added to porphyrin ring by ferrochelatase enzyme to make heme. Iron is efficiently conserved within healthy individuals though women due lose more due to periods and pregnancy.

46
Q

Polycythemia

A

Too much RBC production. Can occur naturally from hypoxic conditions through high altitudes, cigarette smoking, sleep apnea, and pulmonary disease. Can occur unnaturally via mutations like Chuvash and Von Hippel Lindau

47
Q

Polycythemia Clinical Manifestations (3)

A
  1. Increased blood viscosity
  2. Slows blood flow
  3. Regions of ischemia and coagulation

805 (18 decks)

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