Brainscape's Knowledge GenomeTM

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


See full index

Tropical Medicine > Hematology > Flashcards

Hematology Flashcards

1
Q

What vaccines are recommended for asplenic patients or functionally asplenic patients (e.g. sickle cell disease)?

A

pneumococcal, H. flu type B (Hib), meningococcus, influenza.

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

Sickle cell anemia: how much protection against malaria and how?

A
  • carriers have up to 10 times better protection against severe malaria than those with normal hgb, in part due to accelerated immunity
  • up to 30% of births are HbAS in parts of Africa, also east Saudi Arabia, east central India
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Sickle cell anemia: clinical complications

A
  • increased thrombosis
  • stroke
  • MI
  • gall stones
  • leg ulcers
  • priapism
  • pulmonary hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What complications affect sickle carriers?

A
  • normally ok, BUT
    • increased renal problems
      • hematuria
      • urine concentrating probs
      • rarely renal medullary carcinoma
      • rarely exercise-induced sudden death
      • caution with anesthesia, deep sea diving, high altitude activities
      • may combine with other Hgbinopathies to cause conditions similar to sickle cell anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the clinical features and complications of sickle cell anemia?

A
  • chronic hemolysis, hgb steady state 60-80 g/L
  • pronounced bone marrow expansion: frontal bossing, maxillary overgrowth
  • stunting, bony deformities, pain and swelling small bones hands and feet (dactylitis)
  • acute sequestration of red cells in spleen
  • aplastic crises
  • strokes
  • older kids painful sickle crises, sickle chest syndrome
  • splenic microthrombi lead to splenic atrophy, dysfunction
  • social effects: diff schooling, employment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sickle cell anemia: how do you confirm diagnosis (lab)?

A
  • during acute crisis, sickle slide or solubility test
  • hgb electrophoresis to distinguish HbAS, HbSS, HbSC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What treatment should be offered to sickle cell patients in their steady state (non-crisis)?

A
    • multidisciplinary treatment ideal
    • folic acid 5 mg/day because of high hematopoiesis
  • -prophylactic oral penicillin 250 mg bid
  • -aim to increase HbF (fetal hemoglobin) via hydroxycarbamide 500 mg daily (adult dose)
    • where possible regular transfusions to reduce HbS to <30%
    • iron chelators rarely used for iron overload because hard to use and expensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Sickle Cell tx: Acute care

A
  • -iv hydration
  • -analgesia
    • treat precipitating infection
    • because of increased risk thrombosis, preserve blood transfusions for sequestration, aplastic crises, NOT to increase hgb above steady state
  • -exchange transfusion to drop HbS to <30% only for spec indications eg rds or incipient stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sickle Cell Hemoglobinopathy? What is the defect?

A
  • -glutamic acid to valine switch on gene encoding beta globin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Sickle cell trait relation to malaria?

A
  • Sickle cell trait provides 90% risk reduction against severe malaria
  • 30% against uncomplicated malaria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of raised MCV, low hgb

A
  • folate or b12 deficiency
  • reticulocytosis
  • myelodysplasia
  • alcohol misuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Sickle Solubility Test

A
  • Screen for Sickle Cell
  • Sodium dithionite is added to lyse red cells, releasing Hb into solutino
  • reduced solubility of HbS causes cloudiness if HbS is present, more if SS disease, less if carrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do you distinguish neutrophilia from chronic granulocytic leukemia on a slide?

A
  • neutrophilia has toxic granules and vacuolation
  • CGL/CML has many early myeloid cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  • What causes pancytopenia?
  • If diagnosed on slide, how would you proceed to distinguish them?
A
  • low folate
  • TB
  • marrow infiltration with TB or cancer
  • aplastic anemia
  • marrow exam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name some possible complication of CLL.

A
  • hemolytic anemia
  • thrombocytopenia
  • infections
  • high-grade transformation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What kind of Hemoglobin do sickle cell patients and carriers have?

A
  • 80-95% of Hgb is HbS, rest HgF
  • in carriers, only 30% HbS, rest mainly HbA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What was the mortality rate from Sickle Cell anemia in children prior to widespread screening and treatment?

A
  • before early detection and systematic care, mortality under 5 >95%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
  • Describe the physical characteristics of Neutrophils on a slide.
  • What is their role?
A
  • multi-lobed nuclei
  • chromatin threads
  • granules in cytoplasm
  • defending against bacterial and fungal infections
  • phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
  • Describe the characteristics of Eosinophils on a slide.
  • What is their role?
A
  • bilobed nucleus or “spectacle cells”
  • pink staining granules in cytoplasm
  • allergic and parasitic responses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
  • Describe the characteristics of Basoophils on a slide.
  • What is their role?
A
  • Blue staining granules in cytoplasm
  • release of histamine to cause vasodilation in allergen and antigen responses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  • Describe the characteristics of Lymphocytes on a slide.
  • What is their role?
A
  • large nucleus to cytoplasm ratio
  • no lobulated nuclei
  • small ranging in size from 7-15 microns; most are 7-10 microns
  • B-cells produce antibodies
  • T-cells co-ordinate immune response against bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the characteristics of Monocytes on a slide.

A
  • large nucleus to cytoplasm ratio
  • kidney shaped nucleus
  • no lobulated nuclei
  • size 15-30 microns
  • phagocytosis, but longer lived than neutrophils
  • present pathogens to T-lymphocytes for recognition and immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What size is an RBC?

A

7 microns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is anisocytosis and in what conditions does it occur?

A
  • a variation in size of RBC’s
    • thalassemia
    • fe deficiency
    • megaloblastic anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Name 4 causes of macrocytosis.

A
  1. hemolysis
  2. b12 deficiency
  3. folate deficiency
  4. liver disease esp alcholism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q
  • What is poikilocytosis?
  • Name variations and the diseases associated with them.
A
  • sickle cells in Sickle cell anemia
  • pencil cells in fe deficiency anemia & thallasemia, also anemia of chronic disease.
27
Q

What is a spherocyte and what does it indicate?

A

Overly round or spheroid red cell the usually indicate hemolysis.

28
Q

What is a schistocyte and what do they indicate?

A
  • RBC fragments that result from membrane damage encountered during passage through vessels.
  • hemolytic anemia
29
Q

Teardrop red cells?

A
  • myelofibrosis
  • metastatic marrow infiltration
  • myelodysplastic syndrome
30
Q
  • What are target cells and in what conditions do they occur?
A
  • sickle cell
  • HgbC (benign ß-chain variant common in Africans)
  • thalassemia
31
Q

What is a crenated red cell?

A

RBC with many blunt spicules resulting from faulty drying of blood smear or exposure to hyperosmotic solutions. Differ from acanthocytes in that crenations are regularly spaced.

32
Q

What is a Howell-Jolly body and what does it usually indicated?

A
  • Spherical blue-black inclusions in red cells consisting of nuclear fragments of condensed DNA. They would normally be removed by the spleen so indicate a malfunctioning or absent spleen.
33
Q

What is a right shift and what does it indicate?

A
  • The presence of hypersegmented neutrophils (>5 lobes)
  • seen in
    • liver disease
    • uremia
    • megaloblastic anemia
34
Q

What is a left shift and what does it indicate?

A
  • an increase in band forms, immature wbc’s released from marrow, typically due to infection
35
Q

What is a smear cell and what does it indicate?

A
  • Lymphocytes where cell membranes have been ruptured in preparation of blood film. May be seen in CLL.
36
Q

What does CML look like on a slide? How different from AML.

A
  • increased
    • basophils
    • eosinophils
    • bands
    • immature myeloid cells
  • not many blasts, which are found in AML
37
Q

What size are normal WBC’s?

Neutrophils?

Eosinophils?

Basophils?

Lymphocytes?

Monocytes?

A
  • Neutrophils and Eosinophils 10-18 µm
  • Basophils 10-15 µm
  • Lymphocytes 7-10µm small, large 10-15 µm
  • Monocytes 15-30 µm
38
Q

What is Sarcocystis?

A
  • Sarcocystis species are intracellular protozoan parasites with an intermediate-definitive host life cycle based on a prey-predator relationship. Asexual stages develop in intermediate hosts after they ingest the oocyst stage from definitive-host feces and terminate with the formation of intramuscular cysts (sarcocysts). Sarcocysts in meat eaten by a definitive host initiate sexual stages in the intestine that terminate in oocysts excreted in the feces.
  • Man is the definitive host for Sarcocystis hominis and S. suis, with cattle and pigs being intermediate hosts
  • May cause intestinal symptoms, diarrhea, abd pain
  • dx by finding oocysts in feces
  • rarely man can be accidental intermediate host for other species (as with cysticercosis)
  • Rare, pred Asia, but widespread
39
Q

What are the general categories to consider in Eosinophilia?

A
  1. Allergy associated eosinophilia
  2. Drugs
  3. Parasitic Infections
  4. Auto-immune, conn tissue and rheumatological
  5. Primary Eosinophilias/Lymphoproliferative Eosinophilia
  6. Malignancy-associated eosinophilia
  7. Other
40
Q

What are the main Infectious causes of eosinophilia?

A
  • Protozoan: Not many: Isospora belli, Dientameba fragilis, Sarcocystis
  • Nematodes/Roundworms:
    • Ascariasis, Hookworm, Enterobiasis, Srongyloidiasis, Trichinellosis (note Trichuriasis does not usually cause eosinophilia, and if present may indicate co-existing toxocara infection), Cysticercosis, Echinococcosis
    • other: Angiostrongyliasis costaricensis or cantonensis, Visceral larva migrans (toxocara), Gnathostomiasis
  • Trematodes/Flukes
    • Schistosomiasis, Fascioliasis, Clonorchiasis, Paragonimiasis, Fasciolopsiasis
  • Filiariases
    • Tropical pulmonary eosinophilia (W. bancrofti and B. malayi)
    • Loaisis
    • Onchocerciasis
  • Cestodes
    • non-invasive tapeworms usually don’t cause Eosinophilia, but may do so, esp Hymenolipsis nana
    • Echinococcus/Hydatid cysts should be considered
  • Fungi: histo, aspergillus, cocciodoidomycosis, blasto,
41
Q

What is gnathostomiasis?

A
  • larva migrans profundus (cutaneous, ocular, visceral, neurological)
  • caused by roundworm Gnathostoma spp.
  • primarily South East Asia, but reported cases in Central and South America
  • People become infected primarily by eating undercooked or raw freshwater fish, eels, frogs, birds, and reptiles
  • Man is accidental host
  • Definitive hosts are pigs, pelicans etc
  • Intermediate hosts, several stages copepods, fish, frogs
42
Q

What is angiostrongyliasis?

A
  • caused by rat lungworm
    • Angiostrongylus cantonensis causes eosinophilic meningitis in Asia, Pacific Islands, parts of Africa
    • A. costaricensis causes eosinophilic enteritis in Central and South America
  • Humans accidental host
  • Rats definitive host
  • Snail intermediate host
43
Q

What is Tropical Pulmonary Eosinophilia?

A
  • Tropical (pulmonary) eosinophilia, or TPE, is characterized by coughing, asthmatic attacks, and an enlarged spleen, and is caused by Wuchereria bancrofti, a filarial infection. It occurs most frequently in India and Southeast Asia. Tropical eosinophilia is considered a manifestation of a species of microfilaria. This disease can be confused with tuberculosis,[1] asthma, or coughs related to roundworms.
  • hyperimmune response
  • dx by high filarial ab titres and response to tx
  • responds to treatment with Diethylcarbamazine (DEC)
    • albendazole in refreactory cases or doxycyline followed by ivermectin
44
Q

What is probably the most useful way to measure hemoglobin in the tropics?

A
  • The HemoCue® system is based on wavelength analysis of as little as 10 μL of blood from any source (capillary, arterial, venous). The microcuvette is placed into a portable analyser and results are read in about 10 seconds. There is no calibration necessary and allowance is made for turbidity, lipids and white blood cells.

The HemoCue® 301 system is optimized for primary care and is ideal for areas of high temperatures and high humidity. A video of its use can be seen on the Internet. The reader need hardly be reminded about the intrinsic inaccuracies in the other methods listed above. For example the direct visual matching of the colour of a drop of blood on filter paper colours against standard colours has an acknowledged error of 20–50% (Talliquist scale).

45
Q

What are Heinz bodies?

A
  • Heinz bodies are oxidised, denatured bits of haemoglobin found in G-6-PD deficiency for example. Special stains are required to see Heinz bodies.
46
Q

What are the common Causes of anaemia in 381 Malawian children with Hb <5g/dl

What are not common?

A
  • Common (odds ratio 2.2-5.3)
    • •Bacteraemia
    • •Malaria
    • •Hookworm
    • •HIV
    • •G6PD deficiency
    • •Vitamin A or B12 deficiency
  • Uncommon
    • Folate deficiency, sickle cell disease, iron deficiency
  • serum ferritin not appropriate to use as it is generally elevated. Using bone marrow iron as gold standard, ferritin cut-off for iron deficiency should change from 30ug/l to 273ug/l
47
Q
A
48
Q

What are the common causes of Anemia?

However note study on Malawian children which did not find high rates of Fe Deficiency.

A
  • Common causes of anaemia

(often multi-factorial)*

  • Infections
  • Nutritional anaemias (iron, folate)
  • Anaemia of chronic disease (renal failure, TB, cancer)
  • Blood loss
  • Haemoglobinopathies (sickle cell, thalassaemia)
  • Haemolysis (G6PD deficiency, immune, transfusion reactions)
  • Malignancies and bone marrow failure
49
Q

Ojukwu JU, Okebe JU, Yahav D, Paul M. Oral iron supplementation for preventing or treating anaemia among children in malaria-endemic areas. Cochrane Database of Systematic Reviews 2009, Issue 3. Art. No.: CD006589.

*Spottiswoode. Front Pharmacol. 2014; 5: 125.

A
  • •Iron supplementation – no increase* in malaria, other infections or mortality
  • Iron supplementation significantly improves haemoglobin and reduces the prevalence of anaemia
  • Where iron deficiency and anaemia are common (e.g. sub-Saharan Africa) iron supplementation should not be restricted for fear of infections or death
  • Prevention and treatment of malaria should be offered to children regardless of iron supplementation, since these interventions reduce malaria, mortality and anaemia
50
Q

Managing anemia a practical approach

A
  • Chronic anaemia (if no tests available)
  • Dietary advice
  • Give iron, folate and de-worm
  • Continue iron for 3 months after Hb normal

Anticipated response:

•Hb should rise by 0.5-1g/dl each week. Refer if no response

51
Q

Clinical diagnosis of hemolysis

A
  • Clinical diagnosis
  • •Worsening anaemia
  • •Jaundice (don’t assume hepatitis)
  • •Dark urine (Coca-Cola)
  • Laboratory diagnosis
  • •Falling haemoglobin
  • •Raised unconjugated bilirubin
  • •Polychromasia/reticulocytes
52
Q

G6PD deficiency

A

•Protects red cells from oxidant damage (e.g. from infection, drugs, fava beans)

•Early red cells have higher levels than older cells so haemolysis is self-limiting

•Occurs especially in malarious areas (gives protection)

•X-linked

  • Prevalence: Africa 25%, Mediterranean basin 35-40%
  • Many different genetic defects
  • Clinically important because it causes acute haemolysis

e.g. G6PD deficiency in Vietnam is strongly associated with haemoglobinuria (OR=15, P<0.0001). 7 genetic variants*

53
Q

What are Hereditary Spherocytosis and Elliptocytosis?

A
  • •Structural abnormalities of proteins in red cell membrane result in loss of lipid from bilayer ® abnormal shape

•

•Many varieties; usually autosomal dominant inheritance

•

•Common in malarious areas

HE - 6:1000 in Africa

HS - 1:5000 in Europe

54
Q

Hereditary Spherocytosis and Elliptocytosis

Clinical Aspects and Management

A
  • Clinical features
    • •Generally asymptomatic, gallstones
    • •Features of haemolysis (jaundice, macrocytosis, polychromasia, reticulocytosis) +/- anaemia
  • Management
    • •Supportive (extended matching of blood for repeated transfusions)
    • •Folate only if severe or pregnant (5mg/week)
    • •Splenectomy if persistently severely anaemic (284 x risk of pneumococcal sepsis). Greater risk if done <3yrs age
    • •+/- cholecystectomy (check for gallstones every 3-5 years)
55
Q
A
56
Q
A
57
Q

Management of Sickle Cell Anemia

A
  • Anaemia
    • Do not transfuse unless Hb drops below baseline
    • Lifelong folate supplements?
  • Pain
    • Analgesia (opioids, NSAIDs,) – control pain within 60-90 minutes of admission
    • Fluids, oxygen, treat underlying infections
    • Infections
    • Advise to seek medical help early; prophylactic penicillin 250mg 2/day (lifelong?), immunisations
58
Q

Exchange Transfusions in Sickle Cell Anemia

A
  • Aim to reduce Hb S% to <30-50% for:
    • Incipient stroke (reduced blood flow)
    • Previous stroke
    • Multi-organ failure
    • Recurrent severe crises
    • Chest syndrome – chest pain, fever, reduced oxygen saturation
  • When to stop?
59
Q

Pregnancy in Sickle Cell Anemia

A
  • Increased pain crises, hypertension, still births, preterm, small for gestational age
  • 45% need Tx in pregnancy
  • Ante-natal and neo-natal screening programmes
  • 42% reduction in mortality in children 0-3 years in US between 1995-1998 and 1999-2002*
  • No evidence for increased thrombosis with oral contraceptives
  • *Yanni E. et al. Journal of Pediatrics. 154(4):541-5, 2009
60
Q

Hydroxycarbamide in SC disease

A
  • Rationale: increased HbF associated with less severe disease
  • Hydroxycarbamide increases Hb F (hNO, reduced WBC and platelets, end organ protection)
  • Results: less crises, transfusions, chest syndromes and hospital stay. No effect on death, stroke or sequestration.
  • No evidence of increased malignancies*
  • HU upregulates cerebral receptors for MPs so may increase malaria risk
  • New therapeutics: reviewed in Ataga and Stocker, Brit J Haem, 2015, 170. 768-780
    • *Castro O et al. BJH 2014,167,687-691. Hankins and Aygun. BJH 2009:145;296-308
61
Q

In 1973 in US the average life span of a patient with sickle cell disease was 14 years: now it is 50 years.
Why?

A

Therapeutic advances: prophylactic antibiotics, red cell exchange, hydroxycarbamide, ACE inhibitors for renal disease

Multi-organ screening

Better transfusion practice

Stem cell transplantation

62
Q
A
63
Q

Sickle Cell Anemia

Clinical Features

A
  • Very variable phenotype
  • Chronic, haemolytic anaemia – Hb 6-9g/dl, jaundice, marrow expansion
  • Painful crises – organ damage, bony deformities, hospitalisations
  • Intercurrent infections – hyposplenism, high mortality <5 years, pneumococcal prophylaxis (penicillin + vaccination)
  • Strokes/TIAs – peak 2-3y, 11% in <20y, annual Doppler screening till 16y, Rx chronic transfusion
  • Acute splenic sequestration – age 1-2y, 67% recur, 37% need splenectomy (Europe)

Tropical Medicine (17 decks)

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