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Pathology > Blood Disorders 1 > Flashcards

Blood Disorders 1 Flashcards

1
Q

cells of hematopoietic system

A

red blood cells
platelets
white blood cells
plasma

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2
Q

functions of hematopoietic system

A

distribute O2 nutrients, salts and hormones to cells
removes wastes from cellular metabolism
first line of defense against infection, toxic substance, and foreign antigens

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3
Q

hematopoiesis

A

produces red and white blood cells
birth to age 4
4+ red marrow replaced with yellow marrow

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4
Q

signs that could indicate systemic condition

A

excessive or uncontrolled gingival bleeding
spontaneous gingival bleeding
unexplained petechiae, ecchymoses, or tendency to bruise easily
pale mucosal tissue
glossitis and/or glossodynia
nonhealing mucosal ulcers, recurrent fungal infections
exaggerate gingival response to local irritants such as dental biofilm

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5
Q

3 major groups of blood diseases

A

disease of erythrocytes
diseases of leukocytes
disease of platelets

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6
Q

how are erythrocytes developed

A

in red bone marrow by erythropoiesis
production regulated by the kidney by release of erythropoeitin
start as pluripotential stem cells

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7
Q

jaundice

A

when there is a liver dysfunction or a condition causing excessive destruction of RBCs a buildup of yellow substances happens in skin and mucous membranes

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8
Q

disease of RBCs can be broken into two categories

A

anemia
polycythemia

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9
Q

anemia

A

inadequate number of erythrocytes or issues with hemoglobin (inadequate amount, defective structure, inadequate or defective function)

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10
Q

anemia symptoms common to all forms

A

tachycardia and palpitations
dyspnea
dizziness
weakness
fatigue
glossitis

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11
Q

hypochromic anemia

A

inadequate dietary intake of iron, chronic blood loss
formation of small pale RBCs unable to carry normal amount of O2

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12
Q

hypochromic anemia extraoral characteristics

A

classic symptoms of hypoxia
skin and conjunctiva are pale
brittle hair, brittle, ridged, concave or spoon-shaped nails
low hematocrit

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13
Q

hypochromic anemia perioral/intraoral characteristics

A

pale mucosal membranes
glossitis
angular cheilitis
ulcers
burning sensations
dysphagia

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14
Q

hypochromic anemia dental implications

A

vital signs
review medical history for indication of cause
appointment modifications
Plummer-Vinson syndrome
refer for evaluation

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15
Q

thalassemia

A

genetically determined defect in hemoglobin formation
alpha and beta defects in polypeptide chain

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16
Q

a-thalassemia

A

O2 not released from hemoglobin

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17
Q

B-thalassemia

A

inadequate production of hemoglobin, early destruction of RBCs

18
Q

thalassemia extraoral characteristics

A

vary according to number of genes affected

19
Q

thalassemia perioral/oral characteristics

A

B-thalassemia minor and intermedia, and lesser forms of a-thalassemia: mucosal pallor possible, usually no other abnormalities
B-thalassemia major: radiographic bone changes, bone growth abnormalities, dental abnormalities

20
Q

thalassemia radiographic bone changes

A

jaw bones: more radiolucent, honeycomb trabecular pattern
skull: hair-on-end trabecular pattern

21
Q

thalassemia bone growth abnormalities

A

prominent maxilla and zygoma
bossing of the frontal bone

22
Q

thalassemia dental abnormalities

A

abnormal spacing and flaring of maxillary incisors
lamina dura is thin or missing

23
Q

thalassemia dental implications

A

potential need for prophylactic antibiotic coverage
determine coagulation status
orthodontic evaluations during childhood: overjet, spacing, delayed eruption of both primary and permanent dentition possible

24
Q

thalassemia treatment

A

minor forms of both require little if any treatment
Beta-thalassemia major requires routine transfusions

25
Q

megaloblastic anemia and its causes

A

abnormally large RBCs
two major causes
1. Vitamin B12 deficiency: lack of intrinsic factor, inadequate dietary intake, malabsorption syndromes, alcoholism, pancreatic disorders
2. folic acid deficiency: inadequate intake or increased demand, malabsorption syndromes, alcoholism, neoplastic disease

26
Q

megaloblastic anemia pathogenesis

A

defective DNA and RNA synthesis
causes delayed maturation of nucleus of RBC
cytoplasm matures normally producing large cells
have thinner cell membranes (increased chance of rupture)
cells have short life span (weeks)

27
Q

megaloblastic anemia extraoral characteristics

A

classic signs of anemia
blotchy skin pigmentation (dark skin)
lemon yellow or jaundice (light skin)
chronic vitamin B12 deficiency can cause neurologic symptoms: paresthesia, loss of proprioception, ataxia

28
Q

megaloblastic anemia perioral/intraoral characteristics

A

pale ulcerated mucosa
glossitis
folic acid deficiency possible link to cleft lip and/or palate

29
Q

megaloblastic anemia dental implications

A

abnormal vital signs
refer for medical evaluation
discuss folic acid deficiency with female patients of childbearing age
rule out burning mouth syndrome or oral candidiasis

30
Q

megaloblastic anemia treatment

A

folic acid
Vitamin B12

31
Q

sickle cell disease etiology

A

genetic abnormality causing the substitution of valine for glutamic acid in the B hemoglobin chain
considered hemolytic disease
autosomal recessive inheritance pattern: heterozygous (sickle cell trait), homozygous (sickle cell disease)

32
Q

sickle cell disease pathogenesis

A

defective hemoglobin S molecules in RBC combine into solid mass when exposed to stress
stretches into long sickle shape
cells easily destroyed
occlusion of blood vessels because they get trapped due to shape
tissue infarcts, pain, necrosis
sickle cell crisis

33
Q

extraoral characteristics sickle cell disease

A

classic symptoms of anemia
jaundice from RBC hemolysis
damage to multiple organs
chronic pain
depression
complications due to organ damage

34
Q

perioral/intraoral characteristics sickle cell disease

A

bone trabecular changes: skull (hair-on-end), periapical (step-ladder) trabecular pattern between posterior teeth

35
Q

dental implications sickle cell disease

A

prevent oral infections that may trigger crisis
education
appointment modification
plain local anesthetic
prophylactic antibiotic coverage during surgical procedures
supplemental oxygen may be needed

36
Q

sickle cell disease treatment

A

no cure or definitive treatment
management: pain control, maintain hydration and oxygenation, manage complications of disease, avoid crisis triggers, transfusions

37
Q

aplastic anemia etiology

A

the bone marrow fails to produce any of the blood cells usually due to destruction of pluripotential stem cells
80% acquired: chemical, microbial, or environmental agents
20% congenital or inherited

38
Q

aplastic anemia pathogenesis

A

bone marrow stops producing cells
bone marrow replaced with fatty tissue

39
Q

aplastic anemia extraoral characteristics

A

classic symptoms of anemia
bleeding tendencies
infections
severe periodontal infections
spontaneous gingival bleeding
mucosal petechiae and ecchymoses
epistaxis

40
Q

aplastic anemia treatment

A

identify and remove the cause
bone marrow transplants
immunosuppressive therapy
untreated aplastic anemia is fatal

41
Q

polychythemia

A

excess RBCs in relationship to plasma
increases viscosity of blood
can impair blood flow to extremities and increase tendency for thrombi
three forms: relative, primary, secondary

Pathology (12 decks)

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