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MHD 1 > L68-72 > Flashcards

L68-72 Flashcards

1
Q

Compliance = ?

A

Change in V/Change in P

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2
Q

When is compliance increased?

A

Loss of elastic recoil (emphysema)

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3
Q

When is compliance decreased?

A

Increased elastic recoil (pulmonary fibrosis)

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4
Q

Why is there no blood flow through zone 1 of the lungs normally?

A

Alveolar pressure&raquo_space; arteriole and venous pressures

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5
Q

What happens to minute ventilation and PaCO2 during exercise?

A

Minute ventilation increases

PaCO2 is normal

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6
Q

What happens to minute ventilation and PaCO2 during a panic attack?

A

Minute ventilation increases

PaCO2 decreases

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7
Q

What happens to minute ventilation and PaCO2 with increased dead space and intact CNS?

A

Minute ventilation increases

PaCO2 is normal

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8
Q

What happens to minute ventilation and PaCO2 with increased dead space but without an intact CNS?

A

Minute ventilation is normal

PaCO2 is increased

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9
Q

What happens to minute ventilation and PaCO2 with PE?

A

Minute ventilation is increased

PaCO2 is decreased

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10
Q

What is PaO2?

A

Partial pressure of oxygen in the veins

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11
Q

What is SaO2?

A

Saturation of Hgb - how much of your available Hb sites around bound to oxygen?

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12
Q

What is CaO2?

A

Content of O2 in the blood - how much oxygen is contained per dL of blood?

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13
Q

What is DaO2?

A

Delivery of O2 - how much O2 is delivered to the periphery?

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14
Q

What is saturation at PO2 of 40? 60?

A

75%

90%

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15
Q

What happens to PaO2, SpO2, CaO2, and DaO2 in lung disease?

A

All are low

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16
Q

What happens to PaO2, SpO2, CaO2, and DaO2 at altitude?

A

All are low

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17
Q

What happens to PaO2, SpO2, CaO2, and DaO2 in CO poisoning?

A

All BUT PaO2 are low

SpO2 is normal by pulse ox

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18
Q

What happens to PaO2, SpO2, CaO2, and DaO2 in anemia?

A

PaO2 and SpO2 are normal; CaO2 and DaO2 are low

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19
Q

What happens to PaO2, SpO2, CaO2, and DaO2 in cardiomyopathy?

A

All but DaO2 (low) are normal

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20
Q

A-a gradient = ?

A

P(alv)O2 - PaO2

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21
Q

P(alv)O2 = ?

A

[(P(B) - P(H2O)) x FiO2] - (PaCO2/RQ)

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22
Q

What is a normal PmvCO2 and PmvO2?

A

PmvCO2: 45 mmHg
PmvO2: 40 mmHg

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23
Q

What is a normal PaCO2 and PaO2?

A

PaCO2: 40 mmHg
PaO2: 95 mmHg

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24
Q

What is a normal A-a gradient?

A

(Age/4) + 4

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25
Q

What happens to A-a gradient in most diseases?

A

Increases (but not with altitude, decreased FiO2, or hypercapnea)

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26
Q

What is the barometric pressure at 15,000 feet?

A

450 mmHg

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27
Q

What causes the Oxy-Hgb dissociation curve to shift right?

A

Increased temperature
Increased 2-3 DPG
Decreased pH

(Decreases affinity)

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28
Q

What is VQ mismatch?

A

Decreased V relative to Q

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29
Q

What is Shunt?

A

No O2 reaches capillaries

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30
Q

Diffusion-perfusion impairment is occasionally seen in ___.

A

Cirrhosis

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31
Q

What is the first stage of RBC released from the marrow into peripheral blood?

A

Reticulocyte

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32
Q

What is the normal life-span of RBCs?

A

120 days

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33
Q

What is the unique structure of the RBC membrane and what are its components?

A

Membrane skeleton; spectrin fibers + ankyrin

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34
Q

Heme consists of four ___ groups joined into a large ring with a ___ ion incorporated into the center.

A

Pyrrole; ferrous

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35
Q

Two ___ dimers form hemoglobin.

A

Globin

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36
Q

How are RBCs catabolized?

A

Removed by mononuclear phagocytic engulfment in the spleen

Heme is divided into iron (recycled) and porphyrin (bilirubin) and globin is dismantled into amino acids

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37
Q

What are 3 ways to categorize anemia (according to lecture)?

A
  1. Blood loss (acute vs. chronic)
  2. Increased rate of destruction (hemolytic anemias)
  3. Impaired red cell production (diminished erythropoiesis)
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38
Q

How are hemolytic anemias further categorized?

A

Intrinsic vs. extrinsic abnormalities of RBCs

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39
Q

How can intrinsic abnormalities of RBCs be further categorized?

A

Hereditary vs. acquired

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40
Q

How can hereditary intrinsic abnormalities of RBCs in hemolytic anemia be further categorized?

A
  1. Red cell membrane disorders
  2. Red cell enzyme deficiencies
  3. Disorders of hemoglobin synthesis (structural abnormality vs. deficient globin synthesis)
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41
Q

What are the extrinsic abnormalities of RBCs in hemolytic anemia?

A
  1. Ab mediated
  2. Mechanical trauma
  3. Infections
  4. Chemical injury
  5. Sequestration
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42
Q

What is an example of a red cell membrane disorder?

A

Hereditary spherocytosis

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43
Q

What is an example of a red cell enzyme deficiency?

A

G-6-PD deficiency

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44
Q

What is an example of abnormal globin production?

A

Sickle cell anemia

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45
Q

What is an example of deficient globin production?

A

Thalassemias

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46
Q

What is an example of an acquired intrinsic abnormality of RBCs?

A

Paroxysmal noctural hemolysis

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47
Q

What is an example of a mechanical trauma-related extrinsic abnormality?

A

Microangiopathic hemolytic anemia

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48
Q

What are two ways to categorize impaired red cell production anemia?

A
  1. Disturbances of proliferation/differentiation of erythroblasts
  2. Disturbances of proliferation/differentiation of stem cels
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49
Q

What are three ways to categorize disturbances of proliferation/differentiation of erythroblasts?

A
  1. Deficient heme synthesis
  2. Deficient DNA synthesis
  3. Multiple mechanisms
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50
Q

What is an example of deficient heme synthesis?

A

Iron deficiency anemia

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51
Q

What is an example of deficient DNA synthesis?

A

Megaloblastic anemia/B12/folate deficiency

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52
Q

What is an example of disturbances of proliferation/differentiation of erythroblasts caused by multiple mechanisms?

A

Anemia of chronic disease

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53
Q

What is an example of disturbances of proliferation/maturation of stem cells?

A

Aplastic anemia

54
Q

What is MCV?

A

Mean cell volume - volume of the red cell

55
Q

What is MCH?

A

Mean cell hemoglobin - amount of Hgb/red cell

56
Q

What is MCHC?

A

Mean cell hemoglobin concentration - amount of Hgb/volume of red cell

57
Q

What is RDW?

A

RBC distribution width (variation of red cell volume or shape)

58
Q

What is a large variation in red cell volume?

A

Anisocytosis

59
Q

How are anemias classified by MCV?

A
  1. Microcytic (<80 fL)
  2. Macrocytic (>100 fL)
  3. Normocytic (80-100 fL)
60
Q

When is sideroblastic anemia seen?

A
  1. Lead poisoning
  2. Vitamin B6 deficiency
  3. Drugs
  4. Chronic alcoholism
  5. Myelodysplastic syndrome (malignant)
61
Q

What is the difference between intra/extravascular hemolysis?

A

Intravascular: RBCs destroyed within vascular compartment

Extravascular: RBCs destroyed by tissue macrophages

62
Q

What is the most common abnormality in hereditary spherocytosis?

A

Deficiency of spectrin

63
Q

What is the most frequent mutation in the AD form of hereditary spherocytosis?

A

Mutation in ankyrin gene; leads to reduced synthesis of ankyrin and a secondary reduction in spectrin assembly

64
Q

What is mutated in the AR form of hereditary spherocytosis?

A

Alpha-spectrin gene

65
Q

What are the clinical features of hereditary spherocytosis?

A

Anemia
Splenomegaly
Jaundice

66
Q

What is the inheritance pattern of G6PD deficiency?

67
Q

What is G6PD used for?

A

Reforming NADPH, which is used to reduce glutathione to prevent damage from oxidative stress

68
Q

What happens in G6PD deficiency?

A

H2O2 accumulates and oxidizes sulfhydryl groups of globin chains. Hgb denatures, forming precipitates known as Heinz bodies. These attach to the RBC membrane, causing damage. RBCs with Heinz bodies pass through splenic cords. Macrophages bite out Heinz bodies. Spherocytes form.

69
Q

What is the mutation in sickle cell disease?

A

Point mutation leading to substitution of Valine for Glutamic Acid at the 6th position of the beta-globin gene - results in HgbS

70
Q

What are a group of genetic disorders characterized by the lack, or decreased synthesis, of either alpha or beta-globin chains of HgbA?

A

Thalassemias

71
Q

What are the hematologic consequences of thalassemias?

A

Low intracellular Hgb (hypochromia)

Relative excess of other chain

72
Q

What codes for alpha-globin chains?

A

2 alpha-genes on each chromosome 16

73
Q

What are the 4 types of alpha-thalassemias?

A
  1. Silent carrier (1 deletion)
  2. Alpha-thalassemia trait (2 deletions)
  3. HbH disease (3 deletions)
  4. Hydrops fetalis (4 deletions)
74
Q

What codes for beta-globin chains?

A

1 beta-globin gene on each chromosome 11

75
Q

What is beta degree thalassemia?

A

Lack of beta-globin expression

76
Q

What is beta + thalassemia?

A

Decreased beta-globin expression

77
Q

What happens in beta-thalassemia major?

A

Expanded marrow space, skeletal deformities, hepatosplenomegaly

78
Q

What happens in PNH?

A

Mutation in PIGA gene leads to deficiency of GPI anchor and lack of GPI-linked protein expression

79
Q

What are 3 important GPI-linked proteins and what are they involved in?

A

CD55, CD59, C8 binding protein

Inactivating complement

80
Q

What happens to TIBC in iron deficiency anemia?

81
Q

What are symptoms of iron deficiency anemia?

A

Spoon-shaped nails, smooth tongue, intestinal malabsorption, esophageal webs (rare)

82
Q

What is nuclear-cytoplasmic asynchrony and where is it seen?

A

Cellular nuclei are immature and cytoplasm is fully mature

Megaloblastic anemia

83
Q

What are causes of B12 deficient megaloblastic anemia?

A
  1. IF deficiency
  2. Pancreatitis
  3. Gastrectomy
  4. Ileal resection
  5. Regional enteritis
  6. Parasites (fish tapeworm)
84
Q

___ applies to Vitamin B12 deficiency secondary to atrophic gastritis with failure of IF production.

A

Pernicious anemia

85
Q

Vitamin B12 is an essential cofactor for 5-methyltetrahydrofolate homocystein methyltransferase, aka ___. Deficiency leads to decreased availability of ___.

A

Methionine synthase; THF

86
Q

Vitamin B12 is involved in isomerization of ___ to succinyl CoA. Deficiency leads to increased ___.

A

Methylmalonyl CoA; methylmalonate

87
Q

What are clinical findings of megaloblastic anemia - Vitamin B12 deficiency?

A

Alimentary tract: atrophic glossitis, chronic gastritis
Blood and bone marrow: megaloblastic anemia, leukopenia with hypersegmented granulocytes, mild to moderate thrombocytopenia
CNS: subacute comined degeneration

88
Q

What clinical finding of Folate deficiency/megaloblastic anemia is unique?

A

No CNS abnormalities

89
Q

Anemia of chronic disease is caused by high levels of plasma hepcidin - what does this do?

A

Blocks transfer of iron from macrophages to erythroid precurosrs

90
Q

In ___ anemia, there is failure or suppression of stem cells leading to hypocellular marrow. What are the peripheral blood findings?

A

Aplastic

Pancytopenia

91
Q

What does the reticulocyte count measure?

A

Hypo vs. hyperproliferative

92
Q

Where does the name reticulocyte originate from?

A

From the mesh-like/reticular ribosomal RNA visible under the microscope

93
Q

What does a high reticulocyte count reflect?

A

Adequate response of the bone marrow

94
Q

What does a low reticulocyte count reflect?

A

Inadequate response of the bone marrow

95
Q

What is the RI?

A

Corrected reticulocyte count - % of reticulocytes x (Hct/45)

96
Q

What is a normal RI?

97
Q

What is a normal absolute reticulocyte count?

A

25,000-75,000 microL

98
Q

What is a virus which replicates in erythroid precursor cells and kills them, leading to aplastic anemia in persons with chronic hemolytic anemias?

A

Parvovirus B19

99
Q

What are physical exam findings of anemia?

A
  1. Conjunctival pallor
  2. Koilonychia
  3. Papillary atrophy
  4. Angular stomatitis
  5. Slapped cheek rash (Parvovirus)
  6. Scleral icterus
  7. Jaundice
100
Q

MCH = ?

A

(Hgb x 10)/RBC

101
Q

MCHC = ?

102
Q

What happens to MCH and MCHC in hypochromic anemias?

A

Both decrease

103
Q

What happens to MCHC in hyperchromic anemias?

104
Q

Patients with ___ are at risk for infections with encapsulated bacteria.

A

Sickle cell anemia

105
Q

Patients with malaria may develop symptoms of ___ upon treatment.

A

G6PD deficiency

106
Q

What represents the amount of iron stored in the body?

107
Q

What is the protein that transports iron through the blood?

A

Transferrin

108
Q

What measures the body’s ability to bind iron to transferrin?

A

TIBC

High - little iron in the blood, so transferrin is very available

Low - production of transferrin is decreased

109
Q

What indicates how much of the transferrin that is available in the blood is actually boudn to iron?

A

Serum iron to TIBC ratio

Low - low levels of iron, high levels of transferrin

High - low levels of iron and very low levels of transferrin

110
Q

What are the two most common blood types?

111
Q

What is the difference between the A and B Ags?

A

A has an extra GALNAC

112
Q

What are RBC isoagglutinins?

A

Ab against the dominant polysaccharide, naturally occurring

113
Q

RBC isoagglutinins are typically ___ (which Ab). Do they activate complement? What type of hemolysis do they cause?

A

IgM

Yes

Fast intravascular

114
Q

List the Ab found in plasma and the Ag on the RBC for each blood type.

A

Group A: anti-B, A Ag
Group B: anti-A, B Ag
Group AB: no Ab, A and B Ag
Group O: anti-A and anti-B, no Ag

115
Q

What is the universal RBC?

116
Q

What is the universal plasma?

117
Q

What are alloantibodies and how do we get them?

A

Ab against Ag we lack; exposure to Ag on RBCs through pregnancy, transfusion, transplantation

118
Q

Alloantibodies are typically ___ (which Ab). Do they activate complement? What type of hemolysis do they cause?

A

IgG

Most do not

Slow extravascular

119
Q

Compare and contrast autoantibodies (temperature, Ig type)

A

Warm: react at 37 C, IgG
Cold: IgM, activate complement

Both have positive DAT/IAT

120
Q

What happens in type and screen?

A

Determination of ABO and Rh type

121
Q

What happens in forward typing?

A

Mix patient’s RBCs with Antibodies (against A, B, D)

122
Q

What happens in reverse typing?

A

Mix patient serum with A and B cells

123
Q

What happens in an IAT?

A

Patient serum + donor blood - look for anti-RBC Ab in serum

124
Q

What happens in a DAT?

A

Patient RBC + anti-human Ab - look for Ab on RBCs

125
Q

What are possible causes of a positive DAT?

A

Acute and delayed hemolytic transfusion reactions
Autoimmune hemolytic anemia
Hemolytic diseases of the newborn

126
Q

What are the pre-requisites to develop HDN?

A
  1. Mom lacks Ag and is exposed by pregnancy/transfusion
  2. Baby possess Ag
  3. Mom produces IgG Ab
127
Q

What are clinical findings of HDN?

A
  1. Hemolysis (anemia, jaundice)
  2. Accelerated red cell destruction, followed by compensation (hepatomegaly)
  3. Edema (hydrops fetalis)
  4. Fetal death
128
Q

When is RhIg administered?

A

At 28 weeks + within 72 hours postpartum

129
Q

What is autoimmune hemolytic anemia (AIHA)?

A

AutoAb against RBC Ags

130
Q

What is TRALI?

A

Transfusion related acute lung injury

Acute onset of respiratory distress during or within 6 hours of transfusion caused by donor HLA Ab against recipient WBCs

131
Q

What is TACO?

A

Transfusion related circulatory overload

MHD 1 (58 decks)

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