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Haematology Flashcards

1
Q

Define anaemia

A
  1. Decrease of Hb in blood
  2. Below reference level for age and sex of individual
  3. Can be caused by low red cell mass (RCM) or increased plasma volume
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2
Q

Diagnosis to determine cause of anaemia

A
  1. Cause = reduced production from bone marrow
    • Reticulocyte (immature RBC’s in bone marrow) count LOW
  2. Cause = increased removal
    • Reticulocyte count HIGH
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3
Q

How are the types of anaemia classified?

A

Mean Corpuscular Volume (MCV) = avg volume of RBC’s

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4
Q

What are the 3 major types of anaemia?

A
  1. Hypochromic microcytic - LOW MCV
  2. Normochromic microcytic - NORMAL MCV
  3. Macrocytic - HIGH MCV
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5
Q

Consequences of anaemia

A
  1. Reduced O2 transport
  2. Tissue hypoxia
  3. Compensatory changes
    • Increased tissue perfusion
    • Increased O2 transfer to tissues
    • Increased RBC production
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6
Q

Pathological consequences of anaemia

A
  1. Myocardial fatty change
  2. Fatty change in liver
  3. Aggravates angina and claudication
  4. CNS cell death
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7
Q

Generic clinical features of anaemia

A
  1. Fatigue
  2. Dyspnoea
  3. Angina (if pre existing coronary disease)
  4. Anorexia
  5. Palpitations
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8
Q

Generic signs of anaemia

A
  1. Pallor
  2. Tachycardia
  3. Systolic flow murmur
  4. Cardiac failure
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9
Q

Aetiology of microcytic anaemia

A
  1. Low MCV
  2. Iron deficiency (most common cause)
  3. Anaemia of chronic disease (anaemia caused by chronic disease)
  4. Thalassaemia (decreased Hb production)
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10
Q

Aetiology of iron deficiency anaemia

A
  1. Blood loss
    • Menorrhagia (menstruation)
    • GI bleed
    • Hookworm
  2. Poor diet
  3. Increased demand during growth and pregnancy
  4. Malabsorption
    • Poor intake
    • Coeliac disease
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11
Q

Pathophysiology of iron deficient anaemia

A
  1. Less Fe available for haem synthesis
  2. Leads to reduction in Hb
  3. .˙. Smaller RBC’s -> microcytic anaemia
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12
Q

Clinical presentations for iron deficient anaemia

A
  1. Brittle nails + hair
  2. Spoon shaped nails
  3. Atrophy of the papillae of tongue
  4. Angular stomatitis (ulceration of corners of mouth)
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13
Q

Differential diagnosis of iron deficient anaemia

A
  1. Thalassaemia
  2. Sideroblastic anaemia
  3. Anaemia of chronic disease
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14
Q

Diagnosis of iron deficient anaemia

A
  1. Hb M < 130g/L
  2. Hb F < 120g/L
  3. Hb Fp < 110g/L
  4. MCV < 80fL
  5. Serum ferrite = decreased
  6. Blood film
    • Micro + hypochrom (pale)
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15
Q

Treatment of iron deficient anaemia

A
  1. Oral iron - Ferrous sulphate
    • Side effects: nausea, diarrhoea/constipation, black stool
  2. Ferrous gluconate if side effects bad
  3. IV/ deep IM iron
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16
Q

Define anaemia of chronic disease

A
  1. Secondary to chronic disease
  2. Essentially, body is sick .˙. bone marrow sick -> anaemia
  3. RBC’s often normocytic
  4. Microcytic in rheumatoid arthritis and Chron’s
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17
Q

Aetiology of anaemia of chronic disease

A

Chronic infections such as
- TB
- Crohn’s
- Rheumatoid arthritis
- Systemic Lupus Erythematosus (SLE)
- Malignant disease

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18
Q

Pathophysiology of anaemia of chronic disease

A
  1. Decreased release of Fe from bone marrow to developing erythroblasts
  2. Inadequate erythropoietin (cytokine which increase RBC production) response to anaemia
  3. Decreased RBC survival
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19
Q

Diagnosis of anaemia of chronic disease

A
  1. Serum iron and TIBC = low
  2. Serum ferritin = normal/raised
  3. Serum soluble transferrin receptor level = normal
  4. Blood count & film
    • Normocytic or microcytic
    • Hypochromic
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20
Q

Treatment of anaemia of chronic disease

A

Erythropoietin injection = effective in raising Hb level

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21
Q

Aetiology of normocytic anaemia

A
  1. Acute blood loss
  2. Anaemia of chronic disease
  3. Endocrine disorders
  4. Renal failure
  5. Pregnancy
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22
Q

Diagnosis of normocytic anaemia

A
  1. Normal B12 and folate
  2. Raised reticulocytes
  3. Low Hb
  4. Blood count & film - RBCs = normocytic
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23
Q

Treatment of normocytic anaemia

A
  1. Improve diet + vitamins
  2. Erythropoietin injection
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24
Q

Define macrocytic anaemia

A
  1. High MCV
  2. Megaloblastic
  3. Non-megaloblastic
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25
Q

Define megaloblastic macrocytic anaemia

A
  1. Erythroblasts with delayed nuclear maturation because of delayed DNA synthesis
    • Megaloblasts: high MCV and no nuclei
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26
Q

Define non-megaloblastic macrocytic anaemia

A

Erythroblasts = normal

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27
Q

Aetiology of macrocytic anaemia

A
  1. Megaloblastic
    • B12 deficiency
    • Folate deficiency
  2. Non-megaloblastic
    • Alcohol
    • Liver disease
    • Hypothyroidism
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28
Q

Pathophysiology of pernicious anaemia

A
  1. Autoimmune disorder + megaloblastic
  2. Parietal cells of stomach attacked ->atrophic gastritis + loss of intrinsic factor production .˙. B12 malabsorption
  3. Intrinsic factor antibodies = specific for diagnosis
  4. Autoimmune gastritis -> parietal and chief cells replaced by mucin-secreting cells
  5. Leads to achlorhydria (reduced HCl)
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29
Q

Clinical presentation of pernicious anaemia

A
  1. Progressively increasing symptoms of anaemia
  2. Lemon-yellow skin colour (pallor + mild jaundice)
  3. Glossitis (red sore tongue)
  4. Neurological features
    • Symmetrical paresthesia (tingling fingers and toes)
    • Progressive weakness
    • Paraplegia
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30
Q

Differential diagnosis of pernicious anaemia

A
  1. Folate deficiency
  2. Disease of terminal ileum
  3. Bacterial overgrowth in small bowel
  4. Gastrectomy
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31
Q

Diagnosis of pernicious anaemia

A
  1. Blood count & film
    • Megaloblastic anaemia characteristics
    • Macrocytic RBCs
    • Peripheral film = oval macrocytes + hypersegmented neutrophil polymorphs
  2. Serum bilirubin = raised
  3. Serum B12 = low
  4. Hb = low
  5. Reticulocyte = low
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32
Q

Treatment of pernicious anaemia

A
  1. If cause malabsorption -> B12 injection
  2. Dietary = oral B12
  3. Replenish B12 stores with IM hydroxocobalamin
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33
Q

Pathophysiology of folate deficiency

A
  1. Megaloblastic anaemia
  2. Absorbed by duodenum/proximal jejunum
  3. Essential for DNA synthesis .˙. impairment of DNA synthesis + delayed nuclear maturation -> large RBCs + decreased RBC production in bone marrow
  4. Deficiency can lead to fetal neural tube defects
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34
Q

Aetiology of folate deficiency

A
  1. Poor intake
  2. Increased demand
  3. Malabsorption - Crohn’s , Coeliac
  4. Antifolate drugs - Methotrexate, Trimethoprim
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35
Q

Clinical presentation of folate deficiency

A
  1. Symptoms of anaemia
  2. Glossitis
  3. No neuropathy like B12 deficiency (way to differentiate)
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36
Q

Diagnosis of folate deficiency

A
  1. Blood count & film
    • Megaloblastic anaemia characteristics
    • Macrocytic RBCs
    • Oval macrocytes, hypersegmented neutrophil polymorphs
  2. Serum red cell folate = low
  3. GI investigation = small bowel biopsy to exclude occult GI disease
  4. Serum bilirubin = raised
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37
Q

Treatment of folate deficiency

A

Folic acid tablets daily for 4 months WITH B12 ALWAYS unless confirmed normal B12

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38
Q

Define haemolytic anaemia

A
  1. Destruction of RBCs&raquo_space; Production of RBCs
  2. RBCs = normocytic or macrocytic if many young RBCs
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39
Q

Consequences of haemolytic anaemia

A
  1. Shortening red cell survival -> compensatory RBC production by bone marrow
  2. If loss close enough to compensatory production -> compensated haemolytic disease
  3. Compensatory production -> reticulocytes released prematurely .˙. cells larger than mature cells -> macrocytic
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40
Q

Aetiology of haemolytic anaemia

A
  1. RBC membrane defect
    • Hereditary spherocytosis
  2. Enzyme defects
    • G6PD deficiency
  3. Haemoglobinopathies
    • B Thalassaemia
    • A Thalassaemia
    • Sickle cell disease
  4. Autoimmune haemolytic anaemia
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41
Q

Clinical presentation + diagnosis of haemolytic anaemia

A
  1. Pallor
  2. Jaundice
  3. Serum unconjugated bilirubin - HIGH
  4. Urinary urobilinogen - HIGH
  5. Faecal stercobilinogen - HIGH
    DIAGNOSIS
  6. Hb = LOW
  7. Reticulocytosis (increased reticulocytes)
  8. MCHC = INCREASED
42
Q

Define sickle cell anaemia

A

Disorder of quality of RBCs

43
Q

Pathophysiology of sickle cell anaemia

A
  1. Sickle cell haemoglobin (HbS) = insoluble and polymerise when deoxygenated
  2. Flexibility of cells decreased -> rigid and sickle appearance
  3. Initially reversible but repeated sickling -> membrane flexibility lost .˙. irreversibly sickled
  4. Sickling -> shortened RBC survival
  5. Impaired passage through microcirculation -> tissue infarct
44
Q

Clinical presentation of heterozygous sickle cell trait

A
  1. Symptom free except in hypoxia
  2. Carriage offer protection against Falciparum malaria
45
Q

Clinical presentation of homozygous sickle cell anaemia

A
  1. Vaso-occlusive crises
    • acute pain in hand and feet
  2. Acute chest syndrome
    • Vaso-occlusive crisis of pulmonary vasculature
  3. Pulmonary hypertension
    • Mean pulmonary artery pressure > 25mmHg
  4. Long term presentations
    • Delayed sexual maturation
    • osteomyelitis
    • Infection in bones, lungs and kidneys
    • MI
    • Retinopathy
46
Q

Diagnosis of sickle cell anaemia

A
  1. Blood count
    • Hb = 60-80 g/L
    • Reticulocyte = raised
  2. Blood films
    • Sickled erythrocytes
  3. Sickle solubility test = positive
  4. Hb electrophoresis - 80-95% HbS and absent HbA
47
Q

Treatment of sickle cell anaemia

A
  1. Treat precipitating factors (infection, dehydration) first
  2. Folic acid
  3. Acute painful attacks
    • IV fluids
    • Analgesia
    • Oxygen
  4. Anaemia
    • Blood transfusion (increased risk of iron overload)
    • Oral hydroxycarbamide
    • Stem cell transplant
48
Q

Define Thalassaemia

A
  1. Disorder of quantity (reduced production)
  2. Genetic disease -> unbalanced Hb synthesis with under production of one globin chain
  3. Precipitation of imbalance globin chains in matured red cells -> haemolysis
  4. Alpha thalassaemia = reduced alpha chain synthesis
  5. Beta thalassaemia = reduced beta chain synthesis
49
Q

Define beta thalassaemia

A
  1. Little/no B chain production -> excess A chains
  2. Excess A combines with D and G chains
  3. Results in increased HbA2 and HbF
50
Q

What are the different types of Haemoglobin?

A
  1. Normal Hb (HbA) = Haem + 2 alpha chains + 2 beta chains (97% of Hb in adults)
  2. Foetal Hb (HbF) = Haem + 2 alpha chains + 2 gamma chains (1% of Hb in adults)
  3. Hb delata (HbA2) = Haem + 2 alpha chains + 2 delta chains (2% of Hb in adults)
51
Q

Pathophysiology of B thalassaemia

A
  1. Defect caused by point mutation
  2. Mutation -> highly unstable B-globin which cannot be utilised
  3. Heterozygous B-thalassaemia = asymptomatic microcytosis with or without mild anaemia
52
Q

Clinical presentation of B thalassaemia minor

A
  • Trait carrier
    • Heterozygous B-thalassaemia
    • Asymptomatic
    • Anaemia = mild/absent
    • RBCs = hypochromic, microcytic, low MCV
    • Differential diagnosis confusion of Fe deficiency; checked by serum ferritin = normal
    • Hb electrophoresis = raised HbA2
53
Q

Clinical presentation of B Thalassaemia intermedia

A
  • Symptomatic with moderate anaemia and do not require regular transfusion
    • Splenomegaly
    • Bone deformities
    • Recurrent leg ulcers
    • Gallstones
    • Infections
54
Q

Clinical presentation of B thalassaemia major

A
  • Homozygous B-thalassaemia in first year of life
    • Recurrent bacterial infections
    • Severe anaemia from 3-6 months
    • Extramedullary haematopoiesis (infective RBC prod. outside marrow) -> hepatosplenomegaly + bone expansion
    • Life long transfusion dependency
55
Q

Diagnosis of B-thalassaemia

A
  • Homozygous = blood count + film
    • Hypochromic. microcytic anaemia
    • Raised reticulocyte count
    • Nucleated RBC in peripheral circulation
    • Hb electrophoresis: Increased HbF, absent/normal HbA
56
Q

Treatment of B Thalassaemia

A
  1. Regular (every 2-4w) lifelong transfusion too keep Hb > 90g/L
  2. Iron chelating agents to prevent iron overload
    • Oral DEFERIPRONE and sc DESDERRIOXAMINE
    • Side effects: deafness, cataracts, retinal damage
  3. Ascorbic acid -> increase urinary excretion of iron
  4. Splenectomy if hypersplenism persists
  5. Bone marrow transplant
57
Q

State side effects of regular blood transfusions

A
  1. Increase in body iron load
  2. Deposits in liver and spleen -> liver fibrosis + cirrhosis
  3. Deposits in endocrine glands and heart -> hormonal conditions
58
Q

Pathophysiology of A-thalassaemia

A
  1. Gene deletions
  2. No A chain synthesis
  3. Only Hb Barts (4 gamma chains) present
  4. Hb Barts = unable to carry O2 -> incompatible with life
59
Q

Clinical presentation of alpha thalassaemia

A

Infants = stillborn or die soon after birth

60
Q

What are the 4 main subtypes of leukaemia?

A
  1. Acute Lymphoblastic Leukaemia (ALL)
  2. Acute myeloid leukaemia (AML)
  3. Chronic myeloid leukaemia (CML)
  4. Chronic lymphocytic leukaemia (CLL)
61
Q

Define leukaemia

A

Presence of rapidly proliferating immature blast blood cells in the bone marrow that are non functional
- Rapidly dividing cells with no function = wasted energy
- Rapid replication = excess space occupied by non functional cells
- COMBINED = limited resources for healthy cells -> limited production of healthy cells

62
Q

Aetiology of ALL

A
  1. Most common age 2-4
  2. Malignancy of immature lymphoid cells -> rise to T and B cells
  3. Ionisation radiation during pregnancy
  4. Down’s syndrome
63
Q

clinical presentation of ALL

A
  1. Marrow failure
    • Anaemia - low Hb
    • Infection - low WCC
    • Bleeding - low platelets
  2. Bone infiltration -> bone pain
  3. Liver/spleen infiltration ->hepatosplenomegaly
  4. Node infiltration -> lymphadenopathy
  5. CNS infiltration -> cranial nerve palsies
64
Q

Diagnosis of ALL

A
  1. FBC & blood film
    • WCC high
    • Blast cells on film and in bone marrow
    • Normocytic
    • Normochromic
    • Reticulocyte decreased
65
Q

Treatment of ALL

A
  1. Blood & platelet transfusion
  2. Neutropenia -> deadly infections; antivirals etc
  3. ALLOPURINOL -> prevent tumor lysis syndrome
  4. IV fluids - Hickman line (permanent cannula into main vessel under sub-cut fat to prevent infection)
  5. Chemo
  6. Marrow transplantation
66
Q

Aetiology of AML

A
  1. Neoplastic proliferation of blast cells from marrow myeloid elements
  2. Rapid progression with death in 2 months
  3. Radiation
  4. Down’s
67
Q

Clinical presentation of AML

A
  1. Marrow failure
    • Anaemia - low Hb
    • Infection - low WCC
    • Bleeding - low platelets
  2. Hepatomegaly and splenomegaly
  3. Gum hypertrophy
68
Q

Diagnosis of AML

A
  1. WCC often raised but can be normal or low
  2. Few blast cells in peripheral blood so need bone marrow biopsy
  3. Differential from ALL based on microscopy, immunophenotyping and molecular methods
69
Q

Treatment of AML

A
  1. Blood and platelet transfusions
  2. Neutropenia
  3. ALLOPURINOL
  4. IV fluids + hickman line
  5. Chemo
  6. Marrow transplant
69
Q

Aetiology of CML

A
  1. Exclusively adult
  2. Uncontrolled clonal proliferation of myeloid cells
  3. 49-60 yrs
70
Q

Clinical presentation of CML

A
  1. Symptomatic anaemia
  2. Splenomegaly -> Abdominal discomfort
  3. Weight loss
  4. Fatigue
  5. Pallor
71
Q

Diagnosis of CML

A
  1. Blood count
    • V. high WCC
    • Low Hb (normochromic & normocytic)
    • Low or normal or raised platelets
  2. Bone marrow aspirate -> hypercellular
72
Q

Treatment of CML

A
  1. Oral Imatinib
  2. Stem cell transplant
73
Q

Aetiology of CLL

A
  1. Most common leukaemia
  2. Accumulation of mature B cells that. escape apoptosis and undergo cell cycle arrest
  3. Mutations & deletions
  4. Trisomies
  5. Pneumonia may be a trigger event
74
Q

Clinical presentation of CLL

A
  1. Often no symptoms; surprise diagnosis through routine FBC
  2. Anaemic
  3. Weight loss
  4. Hepatosplenomegaly
  5. Enlarged rubbery non tender nodes
75
Q

Diagnosis of CLL

A

Blood count
- Normal/low Hb
- Raised WCC with v high lymphocytes
- Blood film - smudge cells in vitro

76
Q

Treatment of CLL

A
  1. Blood transfusions
  2. Human IV immunoglobulins
  3. Chemo or radiotherapy
  4. Stem cell transplant
  5. PROGNOSIS (Rule of 3’s)
    • 1/3 = never progress
    • 1/3 = progress slowly
    • 1/3 = progress actively
77
Q

What are the 2 types of lymphomas

A
  1. Hodgkin
  2. Non-hodgkin
78
Q

Define lymphoma

A
  1. Malignant proliferations of lymphocytes
  2. Accumulate in lymph nodes -> lymphadenopathy
79
Q

How are the lymphomas be distinguished histologically?

A
  1. Hodgkins
    • Characteristic cells with mirror-image nuclei: Reed-Sternberg cells
  2. Non-hodgkins
    • No characteristic cells
    • Low grade: follicular lymphoma
    • high grade: diffuse large B cell lymphoma
    • V high grade: Burkitt’s lymphoma
80
Q

Aetiology of lymphoma

A
  1. Primary immunodeficiency
  2. Secondary immunodeficiency
    • HIV
    • Transplant recipients
  3. Infection
    • Epstein-Barr Virus (EBV)
    • Human T-lymphotropic virus
    • Helicobacter pylori
  4. Autoimmune disorders
81
Q

Risk factors of Hodgkin’s

A
  1. Affected sibling
  2. EBV
  3. SLE
  4. Obese
  5. Post-transplantation
82
Q

Clinical presentation of Hodgkin’s

A
  1. Painless cervical lymphadenopathy
  2. Hepatosplenomegaly
  3. Infection
  4. Superior vena cava obstruction with increased jugular venous pressure (JVP)
  5. Sensation of fullness in head
83
Q

Diagnosis of Hodgkin’s

A
  1. CT/MRI - chest, abdomen and pelvis for STAGING
  2. Lymph node excision or bone marrow biopsy
  3. Bloods
    • High ESR or low Hb
    • High serum lactate dehydrogenase
  4. Immunophenotyping
  5. Cytogenetics
  6. PET scan
84
Q

What is Staging in Hodgkin’s lymphoma diagnosis?

A
  1. 4 stages of classification
  2. STAGE I
    • confined to single lymph node region
  3. STAGE II
    • 2 or more nodal areas on SAME SIDE of diaphragm
  4. STAGE III
    • Nodes on both sides of diaphragm
  5. STAGE IV
    • Spread beyond lymph nodes
  6. ALL STAGES HAVE ATTACHMENT OF A OR B
    • A = no systemic symptoms other than pruritus (itchy skin)
    • B = presence of B symptoms such as fever, weight loss and night sweats
85
Q

Treatment of Hodgkin’s syndrome

A
  1. Combination chemotherapy ABVD
    • A = Adriamycin
    • B = Bleomycin
    • V = Vinblastine
    • D = Dacarbazine
86
Q

Aetiology of Non-Hodgkin’s lymphoma

A
  1. All lymphomas without Reed-Sternberg cells
  2. More varied in presentation, treatment, etc
  3. Strong link with EBV and Burkitt’s
87
Q

Clinical presentation of Non-Hodgkin’s lymphoma

A
  1. Nodal disease - superficial lymphadenopathy
  2. Extranodal disease
    • Skin
    • Oropharynx, gut, small bowel, bone, CNS, lungs
  3. B SYMPTOMS
    • Fever
    • Night sweats
    • Weight loss
88
Q

How are the clinical presentations of Non-Hodgkin’s lymphoma classified?

A
  1. Low/indolent grade
    • E.g - Follicular lymphoma
    • Slow growing
    • Advanced in presentation
    • Incurable
  2. High grade
    • E.g. - Diffuse Large B-cell lymphoma
    • Nodal presentation
89
Q

Diagnosis of Non-Hodgkin’s lymphoma

A
  1. Raised lactose dehydrogenase = worse prognosis
  2. Lymph node excision or bone marrow biopsy = NON REED STERNBERG OR PPCORN CELLS PRESENT
  3. CT/MRI of chest abdomen and pelvis for staging
  4. Immunophenotyping
  5. Cytogenetics
90
Q

Treatment of Non-Hodgkin’s lymphoma

A

R-CHOP
1. R = RITUXIMAB
2. C = CYCLOPHOSPHAMIDE
3. H = HYDROXY-DAUNORUBICIN
4. O = VINCRISTINE (Oncovin = brand name)
5. P = PREDNISOLONE

91
Q

Define myeloma

A

Cancer of differentiated B lymphocytes (plasma cells)

92
Q

Aetiology of myeloma

A
  1. Accumulation of malignant plasma cells in bone marrow -> progressive bone marrow failure
  2. Malignant plasma cells produce excess of one type of immunoglobulin (monoclonal paraprotein)
    • IgG (55%)
    • IgA (20%)
    • Other are suppressed -> immunoparesis
93
Q

Clinical presentation of myeloma

A

OLD CRAB
1. OLD age
2. C - Calcium elevated
3. R - Renal failure - nephrotic syndrome due to high immunoglobulin (protein) deposit in kidneys
4. A - Anaemia
5. B - Bone lytic lesions -> back pain

94
Q

Diagnosis oof myeloma

A
  1. Blood
    • Normocytic normochromic anaemia
    • Raised ESR
    • Rouoleaux formation on blood film
  2. U&E’s
    • High Ca
    • High alkaline phosphatase
  3. Bence-jones protein in urine
  4. X-Ray
    • Lytic ‘punched out’ lesions
    • Pepper pot skull
    • Vertebral collapse
      ESSENTIALS FOR DIAGNOSIS
  5. MONOCLONAL PROTEIN BAND IN SERUM + URINE
  6. INCREASED PLASMA CELLS ON BONE MARROW BIOPSY
  7. HYPERCALCAEMIA/RENAL FAILURE/ANAEMIA
  8. BONE LESIONS ON SKELETAL SURVEY
95
Q

Treatment of myeloma

A
  1. Bone pain -> analgesia AVOID NSAIDS RENAL IMPAIRMENT
  2. Fracture risk -> BISPHOSPHONATE (ZOLENDRONATE)
  3. Anaemia -> RBCs transfusion; eryhtropoietin
  4. Renal failure -> rehydrate, renal dialysis
  5. Infection -> broad spectrum antibiotics
  6. Chemotherapy LESS FIT
96
Q

Treatment of HIV/AIDS

A
  1. Highly Active Antiretroviral Therapy (HAART)
    • Start before CD4<200
    • More than 3 drugs to minimise replication and cross-resistance
    • 2 NRTI + 1 NNRTI
    • 2 NRTI + 1 PI
    • Requires strict adherence
97
Q

What is NRTI (HIV/AIDS)

A
  1. Nuceloside Reverse Transcriptase Therapy
  2. Inhibit synthesis of DNA by reverse transcription
  3. Abacavir
  4. Didanosine
  5. Emtricitabine
98
Q

What is NNRTI (HIV/AIDS)

A
  1. Non-Nuceloside Reverse Transcriptase Inhibitors
  2. Binds directly to inhibit reverse transcriptase
  3. Efavirenz
  4. Etravirine
  5. Nevirapine
99
Q

What is PI

A
  1. Protease Inhibitors
  2. Acts competitively on HIV enzymes that make viral proteins
  3. Atazanavir
  4. Darunavir
  5. Indinavir

SJ Phase 2a (13 decks)

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