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Therapeutics 1 > Anemia and Drug-Induced Hemolysis > Flashcards

Anemia and Drug-Induced Hemolysis Flashcards

1
Q

Outline the cycle of production of RBCs, starting with a stimulus for increased production.

A

(1) Kidneys release erythropoietin.
(2) Erythropoietin stimulates RBC production in red bone marrow.
(3) Increased RBCs means increased O2 carrying capacity.

These RBCs will remain in circulation for about 120 days.

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2
Q

Define anemia.

A

a functional inability of blood to properly deliver oxygen to organs to meet metabolic needs

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3
Q

True or False: Anemia is an expression of an underlying disease, not a disease itself.

A

True

For this reason, treatment of anemia involves acute symptom suppression while searching for the underlying cause to treat.

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4
Q

What are examples of acute anemia symptoms that must be treated immediately?

A

tachycardia
tachypnea
angina (acute chest syndrome)

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5
Q

Describe the etiology of anemia (3 main sets of causes).

A

(1) RBC loss (bleeding)
(2) decreased RBC production (kidney dx, iron/b12/folic acid deficiencies)
(3) increased RBC destruction (hemolysis: can be genetic or acquired)

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6
Q

Which demographics are at the highest risk for anemia?

A

elderly, teenager, female, alcohol abusers, those in poverty, those with poor dentition/GI disease

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7
Q

normal male and female hemoglobin values

A

male: 13.5-17.5 g/dL
female: 12-16 g/dL

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8
Q

normal hematocrit for males and females

A

male: 41-53%
female: 36-46%

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9
Q

normal RBC count for males and females

A

male: 5.2 +/- 0.7 million/mcL
female: 4.6 +/- 0.5 million/mcL

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10
Q

Knowing normal anemia-related values is important, but what must also be considered when a patient’s bloodwork suggests anemia?

A

their baseline values

Some patients are generally lower in some areas, but may not necessarily be anemic.

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11
Q

normal MCV and RDW values

A

MCV: 80-100
RDW: 11-15%

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12
Q

Recall and explain 3 special considerations in a patients anemia workup.

A

(1) acute blood loss: patient’s Hgb or Hct may not drop until 36-48 hours after acute bleed
(2) pregnancy: RBC production increases by 25%, but volume is expanded by 50%, creating a false diluting effect
(3) severe volume depletion: may mask anemia before rehydration

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13
Q

How does smoking affect Hct, and therefore an anemia workup?

A

Smoking can increase Hct, masking an underlying anemia.

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14
Q

What 3 conditions would likely cause a normocytic anemia?

A

(1) mixed anemia due to multiple nutrient deficiency
(2) acute bleed
(3) erythropoietin deficiency

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15
Q

Iron deficiency is the most common cause of what kind of anemia?

A

microcytic (MCV < 80 fL)

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16
Q

clinical manifestations of iron deficiency anemia

A

(1) pica
(2) angular stomatitis
(3) glossitis
(4) koilonychia

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17
Q

If iron levels are low, TIBC will be ______, and if iron levels are high, TIBC will be _____.

A

high, low

TIBC is indicative of how much iron your body “wants”. That is why it is high when iron levels are low, and vice versa.

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18
Q

goal for elemental iron daily consumption in IDA

A

200 mg elemental iron/day

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19
Q

amount of elemental iron in: ferrous sulfate, polysaccharide iron complex, ferrous fumarate, carbonyl iron, ferrous gluconate

A 
ferrous sulfate: 65 mg
polysaccharide: 150 mg
ferrous fumarate: 99 mg
carbonyl iron: 50 mg
ferrous gluconate: 35 mg
20
Q

common SE of PO iron therapy

A 
GI discomfort
N/V
dark, discolored feces
abd cramping
constipation (sometimes diarrhea)
21
Q

What kinds of drugs will interact with PO iron and decrease efficacy? In contrast, what things will increase iron absorption?

A

(1) anything that affects acid status (PPIs, H2 receptor antagonists), tea, wine, coffee

Vitamin C will increase absorption.

22
Q

PO Iron patient education

A

(1) best absorbed on an empty stomach (can eat something small if GI upset, such as a few crackers)
(2) take with glass of OJ to keep environment acidic
(3) add stool softener if constipation becomes a problem
(4) separate from antacids by 2 hours before or 4 hours after

23
Q

Though oral iron is first-line therapy when possible, what conditions warrant use of IV iron?

A

(1) severe malabsorption
(2) severe intolerance with oral
(3) dialysis patients (erythropoietin deficiency)
(4) noncompliance with oral therapy
(5) chronic uncorrectable bleeding

24
Q

True or False: Oral iron resolves anemia slower than IV iron.

A

false

25
Q

monitor TSAT and ferritin every ________

A

3 months

26
Q

We should expect to see an increase in Hgb by _____ every ______ of therapy.

A

1 g/dL

2-3 weeks

27
Q

What are some signs to watch for regarding iron overload/toxicity?

A

GI ulcer, metabolic acidosis, internal organ damage

28
Q

Transfusions are not first-line therapy for anemia patients, but what conditions are appropriate for transfusion?

A

If the patient is symptomatic or their hemoglobin has dropped below 8 g/dL.

29
Q

One unit of PRBCs should increase Hgb by _____ and Hct by _____.

A

1 g/dL

3%

30
Q

What are some of the complications associated with transfusions?

A

(1) infections (less prevalent now)
(2) transfusion related reactions
(3) volume overload
(4) hyperviscosity (stroke risk)
(5) iron overload

31
Q

What are the most common causes of macrocytic anemia?

A

(1) folic acid deficiency and vitamin B12 deficiency
(2) hemolysis
(3) EtOH abuse
(4) liver disease
(5) hyperthyroidism
(6) drugs (namely chemo)

32
Q

The macrocytic anemia previously known as “pernicious” anemia is caused by ___________.

A

vitamin B12 deficiency

33
Q

Describe the absorption of vitamin B12 and the significance of this specific process with other drugs/surgical procedures.

A

HCl released in the stomach releases B12 bound to protein in food. Then, it combines with intrinsic factor in the stomach before absorption. Because it is dependent on HCl production, patients with altered acid status in the stomach (gastric bypass surgery, H2 blockers/PPI/metformin) can slowly cause a deficiency.

34
Q

What are some of the symptoms of B12 deficiency, besides possible anemia?

A

psychiatric sx, dysphagia, neurologic sx, glossitis, muscle weakness, anorexia

35
Q

Why are patients that require B12 supplements usually on them for the rest of their life?

A

It takes several years to develop a deficiency (2 mcg RDA, but 2-5 mg stored in the liver). Because the supplemental dose is 1000-2000 mcg per day, it takes a lifetime of supplementation to completely replenish this store.

36
Q

How is folic acid deficiency treated?

A

oral supplementation, dietary intake

37
Q

Anemias not caused by nutritional deficiencies could be caused by __________.

A

chronic disease

38
Q

What is sickle cell anemia and what are its consequences?

A

SCA is an inherited genetic disorder involving a mutation that affects the structure of hemoglobin. This causes formation of long, rigid RBCs that more easily lodge in small blood vessels. In addition, poor oxygenation results from structurally deficient Hgb and causes aggregation of Hgb molecules.

39
Q

Name some clinical manifestations of SCA.

A

enlarged liver/spleen, arthralgia, anorexia, chronic anemia, fever, pallor, scleral icterus, abd px, fatigue

40
Q

Which acute complication is the most common cause of death in SCA patients?

A

acute chest syndrome

41
Q

How does acute chest syndrome (ACS) manifest?

A

(1) new pulmonary infiltrate
(2) respiratory symptoms
(3) fever
(4) unclear response to antibiotics

42
Q

What is the treatment for SCA?

A

(1) broad spectrum antibiotics
(2) pain management
(3) supportive care (O2, fluids)
- with caution to avoid pulmonary edema
(4) steroids

43
Q

What are two other complications associated with SCA?

A

sickle cell crises and priapism

44
Q

What are two medications used to increase production of fetal hemoglobin in anemia patients?

A

hydroxyurea and butyrate

45
Q

What are the 5 steps for evaluating an anemia patient?

A

(1) check Hgb/Hct
(2) PMH that suggests possibility of anemia
(3) are they bleeding?
(4) are other cell lines also low?
(5) any jaundice, elevated bilirubin, hemolysis?

46
Q

Which problems in a patient’s PMH would suggest the possibility of anemia?

A

sickle cell dx, thalassemia, hereditary spherocytosis, renal dx (epo deficiency)

Therapeutics 1 (24 decks)

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