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Systemic Disease (Wolfe) > Hematologic Disorders > Flashcards

Hematologic Disorders Flashcards

1
Q

DDx of clinical findings commonly seen in diabetic retinopathy

A

anemia/leukemia, vascular occlusive disease, radiation retinopathy, ocular ischemic syndrome, purtcher’s ret etc

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2
Q

totipotent

A

directed just to blood

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3
Q

pluripotent

A

directed toward anything in the body

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4
Q

Stem cells differentiate into…

A

lymphoid or myeloid stem cells

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5
Q

Lymphoid stem cells produce

A

lymphocytes

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6
Q

Myeloid stem cells produce

A

Monocytes, RBCs, platelets, neutrophil, eosinophil, basophil

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7
Q

Where are RBCs generated?

A

red bone marrow in large bones

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8
Q

How long do mature RBCs live?

A

120 days, then they are recycled by macrophages in the liver and spleen via phagocytosis

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9
Q

What is a heme broken down into?

A

iron + globulin

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10
Q

What is globulin broken down into?

A

essential amino acids

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11
Q

What is heme broken down into?

A

bilirubin, then secreted into gallbladder through liber through digestion then excreted

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12
Q

What releases erythropoietin?

A

Kidney

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13
Q

What are causes of anemia?

A

blood loss, hypo-proliferation, hemolytic

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14
Q

What is morphologic anemia?

A

macrocytic vs normocytic vs microcytic

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15
Q

What are hemoglobin content colors?

A

red is normochromic and pale is hypochromic

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16
Q

Symptoms of anemia

A

fatigue/weakness, dizziness, HA, SOB, numbness or coldness in fingers and toes

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17
Q

Signs of anemia

A

pallor of skin and nails, brittle nails, fast heartbeat, cutaneous hemorrhages, epithelial abnormalities (vascular), lymphadenopathy, bone tenderness, hepatosplenomegaly

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18
Q

Elderly patient have a higher chance of being anemic primarily through

A

poor nutrition

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19
Q

What is the most common anemia in the US?

A

iron-deficiency

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20
Q

How is iron deficiency anemia categorized?

A

microcytic and hypochromic aka inadequate levels of essential compounds causes RBCs to be smaller and pale

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21
Q

Define iron deficiency anemia

A

inadequate iron levels from chronic recurrent hemorrhage from GI tract and GU tract secondary to dietary deprivation or malabsorption from small intestine

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22
Q

Is iron deficiency anemia more common in men or women

A

women

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23
Q

Systemic signs and symptoms of iron deficient anemia

A

HA, light headedness, pica, glossitis, koilonychia, dysphagia

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24
Q

What is koilonychia?

A

spooning brittle nails

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25
Q

What is dysphagia?

A

trouble swallowing

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26
Q

Ocular manifestations of iron deficient anemia

A

conjunctival findings of pallor and hemorrhage; hemorrhage, CWS, exudates, dilated tortuous veins, CRVO with or without macular edema, cranial nerve palsies

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27
Q

Define aplastic anemia

A

reduction in all cell types from bone marrow

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28
Q

How is aplastic anemia characterized?

A

normocytic and normochromic

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29
Q

What is the cause of aplastic anemia?

A

bone marrow dysfunction from unknown origin in >50% of cases or secondary to external chemical or physical agent

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30
Q

What drugs can cause aplastic anemia?

A

chloramphenicol, acetazolamide and methazolamide

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31
Q

What is acetazolamide used to treat?

A

angle closure glaucoma and IIH

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32
Q

What is the mortality associated with aplastic anemia?

A

80%

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33
Q

What is the treatment for aplastic anemia?

A

bone marrow transplant

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34
Q

Systemic signs and symptoms of aplastic anemia?

A

aplastic anemia, easy bruisability, epistaxis (nosebleed), increased menstrual flow, bacterial infections of mouth and perirectal area

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35
Q

Ocular signs and symptoms of aplastic anemia?

A

conjunctival pallor, subconjunctival hemorrhage (recurrent subconj hemes is a sign of anemia), hyphema, retinal findings (hemes, CWS, pallor of ON)

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36
Q

How is pernicious anemia categorized?

A

macrocytic and normochromic

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37
Q

What is the definition of pernicious anemia?

A

hereditary autoimmune disorder of the gastric mucosa which leads to absence of intrinsic factor and can’t absorb B12

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38
Q

What is B12 critical for?

A

synthesis of nucleic acids which are involved in forming blood precursors (RBCs grow without dividing)

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39
Q

Who gets pernicious anemia?

A

elderly people of northern european ancestry, african americans and latino americans

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40
Q

What is the treatment of pernicious anemia?

A

vitamin b12 injections

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41
Q

Systemic signs and symptoms of pernicious anemia

A

glossitis, GI disturbances like atrophic gastritis, anorexia, diarrhea, neurogenic disturbances, autoimmune diseases

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42
Q

Ocular manifestations of pernicious anemia

A

conjunctival pallor, retinal findings (dilated veins, hemorrhages, pallor of fundus, retinal edema), optic nerve pallor

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43
Q

Treatment of anemias

A

iron deficient: 200 mg elemental iron (3 tabs daily); aplastic anemia: remove causative agent and receive bone marrow transplant; pernicious anemia 1000 mg IM injection of vit B12 monthly for life

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44
Q

Define thrombocytopenia

A

destruction of platelets leads to platelet thrombi and tissue hypoxia

45
Q

What are the types of thrombocytopenia?

A

TPP and ITP

46
Q

What is TPP?

A

thrombocytopenia purpura: hemolytic anemia, non-immune mediated, inherited

47
Q

What is ITP?

A

idiopathic thrombocytopenia purpora; hemolytic anemia, antiplatelet antibodies, following viral infections in children and drug exposures in adults

48
Q

What drugs may cause thrombocytopenia?

A

quinine, quinidine, sulfonamides, heparin, phenytoin, diazepam, and acetaminophen

49
Q

Define sickle hemoglobinopathies

A

inherited disorder with abnormal erythrocyte function; abnormal hemoglobin structure due to substitution of single amino acid

50
Q

What amino acid may be substituted in sickle cell?

A

either lysine or glutamate

51
Q

What is the result of distorted Hb?

A

decreases RBC O2 transport capability

52
Q

What is the evolutionary reason for sickle cell?

A

protects against infection; 10% of AA and 20% of africans

53
Q

What type of hemoglobin exists after birth?

A

HbA, tetramer protein with two alpha chains and two beta chains

54
Q

HbF

A

normal fetal hemoglobin

55
Q

HbS

A

valine for glutamate

56
Q

HbC

A

lysine for glutamate

57
Q

Beta thalassemia

A

abnormal Hb chain synthesis prevalent in mediterranean countries

58
Q

HbS + HbS

A

sickle cell anemia SS, most severe systemic

59
Q

HbS + HbC

A

sickle cell C, moderate severity with more severe ophthalmic presentations

60
Q

HbS + betathal

A

sickle cell thalassemia, moderate severity and more severe ophthalmic

61
Q

HbA + HbC

A

hemoglobin C trait AC

62
Q

HbA + HbS

A

sickle cell trait AS; most common

63
Q

Which sickle cell form is most common?

A

trait AS, asymptomatic with no anemia

64
Q

SC and Sthal produce more hyper-viscosity in the blood =

A

higher prevalence of sickle cell retinopathy

65
Q

What causes sickling?

A

stress, viral illness, dehydration, hypoxia, exertion

66
Q

What are effects of sickling?

A

obstructive occlusions, microvascular occlusions, hemolysis

67
Q

What are systemic complications of SCD?

A

Acute chest syndrome and splenic sequestration crisis

68
Q

What is acute chest syndrome?

A

chest pain, coughing, difficulty breathing, fever

69
Q

What is splenic sequestration crisis?

A

due to RBCs being trapped within the spleen, leads to hypoxia, thrombosis, infarction and fibrosis; usually manifests between 3 months and 5 years of age, symptoms: abdominal fullness, weakness, pallor, tachycardia, and tachypnea

70
Q

What systemic manifestations from SCD?

A

acute sickle-cell crisis, chronic organ damage, non-vaso occlusive

71
Q

Acute sickle cell crisis

A

due to vaso-occlusion of microvasculature; extreme pain of back/chest/extremities; complications of CVA, hepatic crisis and renal failure

72
Q

Chronic organ damage from SCD

A

skin ulcer, microinfarct of renal medulla (can’t concentrate urine), autospenectomy

73
Q

Non-vaso occlusions in SCD

A

increases infections, gallstones, abnormal growth and development

74
Q

Proliferative sick cell retinopathy

A

10% of SS and 32% of SC

75
Q

T/F High VEGF levels in SS are counterbalanced by high level of thrombospondin whereas elevated levels of VEGF in HbSc are unaffected because of low THBS levels

A

true, THBS counter-acts the VEGF response

76
Q

Ocular manifestations of SCD

A

conjunctival sickling, focal iris atrophy, hyphema, increase in IOP, rubeosis irides, optic disc sign, choroidal vascular occlusion

77
Q

T/F first line of treatment of elevated IOP in sickle cell is CAI

A

false, contraindicated because CAIs induce a sickling event due to CO2 changing the pH to be more acidic which increases the viscosity of the blood

78
Q

Is elevated IOP a concern in patients with a hyphema and SCD?

A

yes

79
Q

When is IOP concerning for SCD?

A

> 24 mmHg, ocular emergency, may require anterior chamber washout if hyphema present

80
Q

Non proliferative SCR

A

venous tortuosity, black sunbursts, refractile deposits, silver wire arterioles, salmon patch hemorrhages, angiod streaks, CRAO or CRVO, enlarged FAZ

81
Q

Stage 1 and 2 sickle cell retinopathy

A

peripheral occlusions, anastomoses between artery and veins in periphery

82
Q

Stage 3, 4, 5

A

anastomoses between sea fan neo, hemorrhaging and fibrosis, and tractional detachment

83
Q

Lab tests for SCD

A

sickledex tests for HbS; (+) test= turbid blood after shaking in solutions// electrophoresis

84
Q

Systemic SCD treatment

A

oxygen supplementation, good nutrition and folic acid supplements, genetic counseling, blood transfusions, bone marrow transplants, hydroxyurea

85
Q

What is hydroxyurea for?

A

increases amount of HgF

86
Q

Treatment for SCD neo

A

focal ablation, feeder vessel treatment, pan-retinal scatter, anti-VEGF, vitrectomy

87
Q

Define chronic myeloproliferative disorders

A

overproduction of any of the formed elements of blood increasing blood viscosity

88
Q

What is polycythemia vera?

A

most common myeloproliferative disorder; over production of RBCs

89
Q

What is Waldenstom’s macroglobulinemia?

A

myeloproliferative disorder, overproduction of globulin

90
Q

What are anticardiolipin antibodies?

A

auto-antibodies against protein-phospholipid complexes; often seen in lupus or RA

91
Q

What’s a hyper-coagulable state?

A

causes arterial and venous thrombosis, coronary artery disease, pulmonary HTN

92
Q

When should you consider antiphospholipid syndrome?

A

if you see vascular occlusion in young patient

93
Q

Define leukemia

A

neoplastic disease of bone marrow; abnormal proliferation of lymphocytes and their precursors

94
Q

Leukemia is linked to exposure to what medications

A

benzene, cigarettes, and chemotherapy drugs

95
Q

Acute lymphocytic leukemia

A

mostly children under 10, M>F, highly treatable and typically detected early

96
Q

Acute myeloblastic leukemia

A

mid aged and elderly, M>F, whites, malignancy of granulocytes, radiation/chemical/hereditary factors, 8 subtypes depending on stage of development of myeloblasts

97
Q

Chronic lymphocytic leukemia

A

middle-aged and elderly, 75% of cases after 60 years, WBCs have extended lifespan

98
Q

Treatment for CLL

A

suppression of humoral immunity

99
Q

Treatment of CML

A

bone marrow transplant

100
Q

Chronic myeloblastic leukemia

A

adults > 50, caused by philadelphia chromosome in bone marrow

101
Q

Systemic manifestations of acute leukemia

A

failure of normal hematopoiesis, infection, CNS involvement, joint and bone pain

102
Q

Systemic manifestations of chronic leukemia

A

asymptomatic early, insidious onset of vague symptoms, disease progression

103
Q

Ocular manifestations of leukemia

A

adnexa, lacrimal gland infiltration, EOM infiltration, swelling or subconj heme, exophthalmos, sterile peripheral ulcers with pannus, episcleritis, infiltrates of perivascular regions, secondary angle closure glaucoma, iris color change, pseudohypopyon

104
Q

What is leukemic retinopathy?

A

dilated and tortous venules, yellowing of vascular reflex, hemorrhages, retinal infiltrates, roth spots, CWS, micro-As

105
Q

Opportunistic infection

A

cytomegalovirus, herpes simplex, herpes zoster ophthalmicus, mumps, toxoplasmosis, bacterial infection, fungal infection

106
Q

Systemic leukemia management

A

chemotherapy, radiation, bone marrow transplantation

107
Q

Ocular management of leukemia

A

systemic chemotherapy, irradiation and intrathecal chemotherapy, bone marrow transplantation

108
Q

Ocular side effects to leukemia cytotoxic drug tx

A

Cataracts, cranial nerve palsy, optic atrophy, intraocular inflammation

109
Q

Ocular side effects to leukemia bone marrow transplants with chemo

A

graft vs host; sjogren like dry eye, conjunctival keratinization, ectropion, uveitis

Systemic Disease (Wolfe) (10 decks)

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