Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

D&T:1 > Anemias > Flashcards

Anemias Flashcards

1
Q

Anemia of Chronic Disease

A

Normocytic, normochromic

  • Occurs due to increased destruction of RBCs by factors released from damaged tissue; BM is suppressed by inflammatory cytokines
  • Defective reutilization of iron leads to an accumulation in phagocytes

Lab: Ferritin =» Increased
TIBC =» Decreased
% Saturation => Decreased

*Hepcidin released by the liver limits iron transfer and EPO to decrease the available iron for bacteria (logic behind this)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Megaloblastic Anemias

Folate or Vit-b12 deficiency

A
  • Pancytopenia
  • Megloblastic , hypercellular BM w/ giant bands and nuclear asynchrony
  • PB: Macroovalocytes, hypersegmented PMNS, and anisopoikolocytosis

Treatment: Give B12 injection and Folate supplements (folate will not treat neurological symptoms of B12 deficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Vitamin B12 deficiency

A

Commonly caused by pernicious anemia

  • Dietary deficiency only occurs in vegans, pregnancy, hyperthyroidism, tumorigenic states
  • Typically assoc. w/ AI disease, possibly gastritis =» parietal cell destruction

***Will see neurologic defects due to demyelination of nerves; also see glossitis and increased methlymalonic acid

-Can diagnose w/ the Schilling Test

Treat w/ B12 supplements; folate supplements sorta work but will not correct neurologic symptoms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Folate Deficiency

A
  • Typically due to diet lacking green, leafy vegetables or fish; increased demand during pregnancy
  • Glossitis, increased homocysteine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Schilling Test

A

Stage I: Give pt. oral radiolabeled B12 and inject B12 intramuscularly; if radiolabel seen in urine, there is no IF-deficiency and it is probably dietary

If no radiolabel in urine, then…

Stage II: Give oral radiolabeled B12 AND IF
=» If still not in urine, probably general malabsorption issue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Macrocytic Anemias (other than B12/Folate)

A

Caused by alcoholism, chemotherapy, liver disease, hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Aplastic Anemia

A

Damage to hematopoetic stem cells causing pancytopenia w/ NO resulting reticulocytosis; BM will be hypocellular resulting in a dry tap

Clinical: Anemia, weakness, pallor, prone to bleeding and infections, no spleen abnormalities

*Can be caused by CHLORAMPHENICOL, alcohol, benzene, radiation therapy

Treatment: Supportive G-CSF; if severe enough, BM transplant or immunosuppression if indicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Fanconi’s Anemia

A

AR defect in the DNA repair mechanism that is a potential cause of aplastic anemia

Clinical: Hypoplastic thumbs and organs

-Pre-malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diamond-Blackfan Syndrome

A

Pure red cell aplasia caused by AI mediated destruction of red cell precursors

  • Pure red cell aplasia also caused by parvovirus B19, chloramphenicols, thymomas, SLE
  • Chronic, severe anemia characterized by no reticulocytosis but normal myeloid and platelets

Treatment: Immunosuppresion, IVIG (parvovirus), thymic resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Sideroblastic Anemia

A

Failure to incorporate heme into protoporphyrin IX ring =» presence of ringed sideroblasts and basophilic stipling

-Mild, dimorphic anemia w/ ineffective erythropoesis

Labs: Increased Ferritin
Increased Transferrin
Decreased TIBC
Increased % saturation

*Hereditary = ALA-synthase deficiency
Acquired = **Isoniazid therapy, myelodysplasia, hemochromatosis, lead toxicity (painters)

Treatment: Pyridoxine (Vit B6); treatment of underlying problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ringed Sideroblasts

A

Iron-laden mitochondria w/ iron collections in erythroid precurors

-Seen in sideroblastic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hemolytic Anemias

A

Acute: Jaundice, SOB, fever, lower back pain

Chronic: Gallstones, fractures, abnormal bone growth

Labs: Increased LDH
Decreased haptoglobin
Increased unconj. bilirubin

PB: Spherocytes, schistocytes, polychromasia, reticulocytosis, Howell-Jolly bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Intravascular Hemolysis

A

Releases free Hgb =» Hemoglobinuria, hemoglobinemia, decreased serum haptoglobin

-Usually occurs in burn pts., immune disorders, microangiopathic conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Extravascular Hemolysis

A

Occurs in the spleen, liver, macrophages

-Usually due to inherited defect in Hgb prod., RBC membrane, enzymes

Lab: Increased unconj. bilirubin w/ no schistocytes, anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Beta-Thalassemia Major

A

Microcytic, hypochromic anemia w/ codocytes due to gene mutation on chromosome 11; common in people of Mediterranean descent

If B zero/B zero =» No B-globin produced=» MOST SEVERE

Clinical: Onset 6 months after birth after HbF levels normally decrease in favor of HbA
=»Ineffective erythropoesis causes hepatosplenomegaly, bone malformations, organ damage, Howell-Jolly bodies (ppt. of a-chains), basophilic stipling, NRBCs, iron overload, **CREWCUT appearance of skull

*Electrophoresis: Decreased HbA, Increased HbA2 and HbF

Treatment: Chronic transfusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Beta Thalassemia Minor

A

One normal and one abnormal gene on chromosome 11

*Must differentiate from iron deficiency anemia
=»B-thalassemia minor will not improve w/ iron supplementation

*PB will also have basophilic stipling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Alpha-Thalassemia

A

COMPLETE deletion of a-genes on chromosome 16

4 gene deletion: Hydrops fetalis =» tetramers of y-chains that have an increased affinity for Hgb

3 gene deletion: severe anemia assoc w/ Hemoglobin H (tetramer of B-chains); ppt. as Heinz bodies and can produce “Bite cells” after passing thru the spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Alpha-Thalassemia Trait (2 gene deletion)

A

Alpha-thal-1: cis deletion of genes on same chromosome
-Hb Bart at birth: Hb H during life

Alpha-thal-2: trans deletion of genes on opposite chromosomes
-Hb Bart at birth; No Hb-H during life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Sickle Cell Anemia

A

Valine=»Glutamic Acid on gene 6 of the B-globin chain causes the prod. of HbS

-Sickled cells form spectrin dimers that are dense and not easily deformable therefore posing a risk for small vessel occlusion and increasing the viscosity of blood

Clinical: Chronic hemolysis and vaso-occlusive crises
Autosplenectomy
Chronic leg ulcers
Organ infarction
Gallstone formation
Dactylitis (swelling of hands and feet)
Basophilic stippling/Howell-Jolly bodies

Labs: Increased HbF (~10%) 
          Sickling test (+) -Metabisulfate

⭐️⭐️Dehydration, acidosis, thalassemia all induce increased sickling

20
Q

Iron Deficiency Anemia

A

Hypochromic, microcytic anemia

*Most common nutritional deficiency worldwide; also very common cause of thrombocytosis

Caused by: menorrhagia in females and peptic ulcers in males; malabsorption (duodenal problem); nutritional deficiency; other forms of chronic blood loss
*Colonic adenocarcinoma

*Pts. appear w/ pallor, koilonychia, pica

Labs: Ferritin =» decreased
TIBC =» Increased
% saturation =» Decreased

Treatment: Give iron supplements; find source of bleeding

21
Q

Hereditary Spherocytosis

A

Microcytic, hyperchromic RBCs w/ decreased lifespan

Caused by mutations in ankyrin gene which anchors spectrin to the RBC membrane =» spherical, less deformable shape

Clinical: Slight anemia, jaundice, splenomegaly, anemic crises

Labs: Osmotic fragility test (+); Increased MCHC; reticulocytosis
-OF test will shift curve to the right although reticulocytes can persist; may also be necessary to incubate the cells for 24hrs to accentuate fragility

Treatment: Splenectomy; Howell-Jolly bodies will now emerge on smear

22
Q

G6PD deficiency

A

Lack of G6PD causes the denaturation of Hgb (and formation of Heinz bodies) during times of oxidative stress; induced by fava beans, drugs (***Dapsone, chloramphenicol, sulfonamides, antimalarials), and viral infecion

Clinical: Intravascular & Extravascular hemolytic symptoms (chills, fever, back pain, SOB, pallor)

Treatment: Attacks are self-limiting (only old RBCs affected) so therapy is supportive
*B/w attacks, PB is NORMAL

23
Q

Warm Autoimmune Hemolytic Anemia

A

Due to IgG abs reactive at warm temperature of the central body; spleen destroys ab-coated RBCs

-Assoc. w/ lymphatic malignancies and AI disorders

*Includes Drug-Induced WAHA which occurs due to:
Methyldopa (against Rh-ag)
Penicillin-hapten
Cephalosporins/Tetracyclines

Treatment: Immunosuppression, splenectomy, treat underlying disorder, blood transfusions

24
Q

Cold Autoimmune Hemolytic Anemia

A

IgM binds to RBCs and induces agglutination during exposure to cold temperature in the limbs; also causes opsonization by C3 and phagocytosis in the spleen BUT no splenomegaly

Acute: Due to Mycoplasma pneumoniae (I-Ag) or infectious mononucleosis (i-Ag)

Chronic: Lymphoid malignancy

Treatment: Keep warm; treat underlying illness

25
Q

Paroxysmal Cold Hemoglobinuria

A

Due to Donath-Landsteiner IgG that binds RBCs in cold temperatures (limbs) and binds complement in warm temperatures (torso) =» hemolysis

  • Assoc. w/ skiing or recovery from illness
  • Characterized by biphasic nature of the antibody

Labs: Chill antibody, heat it, check for lysis

Treatment: Keep pt. warm

26
Q

Microangiopathic Hemolytic Anemia

A

Due to abnormalities in vessel circulation resulting from DIC, HUS, TTP, Preeclampsia

Labs: Predominance of schistocytes on PB

27
Q

Alcoholic Liver Disease

A

Abnormal lipid structure of RBC membrane =» acanthocytes, spur cells, and target cells

28
Q

Paroxysmal Nocturnal Hemoglobinuria

A

Caused by mutations in the Phosphatidyl-inositol glycan class A gene (pig-A); codes for GPI anchor required for CD55 and CD59

*CD59-inhibits lysis by complement; CD55-DAF

=»Increased susceptibility to complement destruction

Screen: Sucrose lysis test (+)

Confirmatory Ham’s Test (+)/ Flow for CD55 (-)

Treatment: Iron supplements; prednisone; BM transplant

*Can progress to AML

29
Q

Secretion products of platelets

A

a-granules: Fibrinogen, P-selectin, PDGF, Factors V, VIII, Platelet Factor 4

delta granules: ADP, ATP, Ca2+, Serotonin, epinephrine

30
Q

Point at which primary hemostasis is reversible to

A

Until Thrombin binds to protease-activated receptor (PAR) on the platelet membrane w/ ADP and TXA2

(Aggregation)

31
Q

Last step in formation of platelet plug

A

Fibrinogen binding to GpIIIa/IIb receptors on platelet

32
Q

Anti-platelet properties of endothelial cells

A

ADPase

NO and PGI2 (vasodilators)

ATIII (II, X, XII, XI)

TFPI (inhibits VIIa and Xa)

t-PA (activates Plasminogen)

Thrombomodulin (activates Protein C)

33
Q

Virchow Triad

A
  1. Endothelial Injury (exposes vWF, releases TF)
  2. Abnormal Blood Flow (Increased coagulants)
  3. Hypercoaguability (Coag Factor deficiencies/mutations)
    - describes the cases in which thrombosis can occur
34
Q

Factor V Leiden

A

Arginine =» Glutamine substitution makes Factor V much more resistant to cleavage by Protein C

-Many pts. w/ recurrent DVTs have this

35
Q

Homocystinuria

A

Mutation in the MTHFR gene (motherfucker) causes a variation in a THF-reductase gene elevating homocysteine

Homocysteine inhibits ATIII and thrombomodulin

*Clinical: MR, thrombosis, long-slender fingers

36
Q

Antiphospholipid Antibody Syndrome

A

Abs bind to epitopes exposed by phospholipids; can be primary or secondary

-Causes recurrent DVTs, thrombocytopenia, prolonged PTT, cardiac vegetations

Treatment: Anticoagulants, immunosuppressants

37
Q

Arterial Thrombi

A

Usually occlusive, overlies an atherosclerotic plaque and grows retrograde to blood flow

38
Q

Venous thrombi

A

Always occlusive; typically in the lower extremities, and grows anterograde to blood flow

39
Q

Post-mortem clots

A

Usually not attached to the vessel wall and the dependent portion is dark red

-Yellow, gelatinous supernatant

40
Q

Superficial Venous Thrombi

A

Causes edema distal to the obstruction; predisposes overlying skin to injury

-Rarely embolizes

41
Q

Deep Venous Thrombi

A

Above the knee: Most likely will embolize

Below the knee: Make sure it doesn’t move above the knee

Treatment: Anticoagulants

42
Q

Pulmonary Thromboembolism

A

Greater than 60% go asymptomatic; obstruction of end arteries causes infarct

  • Hemorrhage can occur due to dual circulation of the lung
  • Saddle embolus=most serious
43
Q

Systemic thromboembolism

A

Typically from the left heart; sometimes the left if it bypasses pulmonary circulation

*Typically go down to the legs

44
Q

Fat embolism

A

Occurs 1-3 days after broken bone;

Clinical: Pulmonary insufficiency, anemia, thrombocytopenia, **neurological defects

45
Q

Air embolism

A

Often caused by thoracentesis, neck injury, obstetric procedures, AND decompression sickness

=»Air breathed in @ increased pressure has increased N2 content; bubbles out when rapidly surfacing causing pain around the joints

46
Q

Amniotic Fluid Embolism

A

Uncommon occurrence of infusion of amniotic fluid at delivery

Clinical: Severe dyspnea, hypotensive shock, pulmonary edema, DIC

-Very fatal, yes

D&T:1 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions