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IHO Mike Rose > Diseases Exam 3 > Flashcards

Diseases Exam 3 Flashcards

1
Q

Leukemia vs. Lymphoma

A

Leukemia:

  • Malignancy of hematopoetic cells
  • Starts in bone marrow (can spread to blood, nodes)
  • Myeloid or lymphoid
  • Acute or chronic

Lymphoma:

  • Malignancy of hematopoetic cells
  • Starts in lymph nodes (can spread to blood, marrow)
  • lymphoid only
  • Hodgkin or non-hodgkin
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2
Q

Acute vs. Chronic Leukemia

A

Acute:

  • Sudden onset
  • Can occur in either adults or children
  • Rapidly fatal w/o treatment
  • Composed of immature cells (blasts)
  • Patient will present w/ bleeding problems, infx probs, anemia etc.

Chronic leukemia:

  • Slow onset
  • ONLY in adults (
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3
Q

Acute Leukemia

A

Definition: Malignant proliferation of immature myeloid or lymphoid cells in the bone marrow

Cause: clonal expansion, maturation failure

Problems caused:

  • Crowd out normal cells
  • Inhibit normal cell funcitons
  • Infiltrate other organs (i.e. brain) - not very common

Clinical findings:

  • Sudden onset (days)
  • Symptoms of bone marrow failure (fatigue, infx, bleeding)
  • Bone pain (expanding marrow
  • Organ infiltration (liver, spleen, brain)

Labs:

  • Blasts/immature cells in blood
  • Leukocytosis
  • Anemia
  • Thrombocytopenia
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4
Q

Acute Myeloid Leukemia

A

Things you must know:

  • Malignant proliferation of myeloid blasts in blood, bone marrow
  • 20% blast cells is cutoff for dx
  • many subtypes
  • bad prognosis

Old classification:
M0,1,2,3 - Involve neutrophilic series (myeloblasts, promyelocytes, etc.)
M4,5- involve monocytic series (monoblasts etc.)
M6 - involves erythroid series (erythroblasts)
M7 - involves megakaryocytic series (megakaryoblasts)

New clasification: AML w/:

  • genetic abnormalities
  • FLT-3 mutation
  • w/ multilineasge dysplasia
  • therapy related
  • not otherwise classified

Treatment:

  • Chemo
  • Bone marrow transplant

Prognosis:

  • Dismal
  • t(8;21), inv(16), t(15;17) better
  • FLT-3, therapy-related worse
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5
Q

AML - M0

A

Things you must know:

  • large increase in myeloblasts
  • Bland
  • Myeloperoxidase negative
  • Need markers (to run flow cytometry)

So early it’s hard to even tell they are myeloblasts.

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6
Q

AML - M1

A

Things you must know:

  • large increase in myeloblasts
  • no maturation
  • auer rods
  • Myeloperoxidase positive
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7
Q

AML-M2

A

Things you must know:

  • Increase in myeloblasts
  • Maturing neutrophils
  • t(8:21) in some cases
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8
Q

AML - M3

A

Things you must know:

  • Large increase in promyelocytes
  • Faggot cells (lots of auer rods)
  • DIC
  • t(15;17) in all cases

Mutated retinoic acid receptor –> treat with ATRA (all trans retinoic acid). This has high cure rate and prevents DIC

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9
Q

AML-M4

A
  • Significant increase in myeloblasts
  • Significant increase in monocytic cells
  • Extremedullary tumor masses
  • inv (16) in some cases
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10
Q

AML- M5

A

Significant increase of monocytic cells
NSE (non specific esterase) positive
M5A and M5B
Extramedullary tumor masses

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11
Q

AML - M6

A

Significant increase in erythroblasts and myeloblasts

Dyserythropoiesis

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12
Q

AML-M7

A

Significant megakaryoblasts
Bland blasts
MPO negative
Need markers (to run flow cytometry)

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13
Q

AML w/ genetic abnormalities

A

t(8;21) –> M2 = good prognosis
inv(16) –> M4 = good prognosis
t(15;17) –> M3 = good prognosis
11q23 –> therapy related often = bad

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14
Q

AML w/ FLT-3 mutation

A
  • Mutation of FLT-3 (a tyrosine kinase)
  • Present in 1/3 of cases of AML!
  • Monocytic cells
  • Poor prognosis
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15
Q

AML w/ multilineage dysplasia

A
  • ≥ 20% blasts + dysplasia in ≥ 2 cell lines
  • Elderly
  • Severe pancytopenia
  • Chromosome abnormalities (5, 7)
  • Poor prognosis
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16
Q

AML, Therapy-Related

A
  • Previous chemotherapy
  • Alkylating agents (Busulfan) or topoisomerase II inhibitors (Etoposide) (others too)
  • 2-5 years to onset
  • Chromosomal abnormalities sometimes (5, 7, 11q23)
  • Very hard to treat
17
Q

Meyelodysplastic Syndrome (MDS)

A
  • Problem: abnormal stem cells
  • Dysmyelopoiesis
  • Maybe increased blasts
  • May evolve into acute leukemia

Clinical and Lab findings:

  • older patients
  • Asymptomatic, or BM failure
  • Macrocytic anemia

Treatment:

  • Low grade: support, follow
  • High-grade: be aggressive –> treat like leukemia
18
Q

Red cell dysplasia looks like ?

A

megaloblastic nuclei, fragmentation

19
Q

Neutrophilic dysplasia looks like ?

A

hypogranulation, hyposegmentation

20
Q

Magakaryoctyic dysplasia looks like

A

small, non-lobulated cells

21
Q

Acute Lymphoblastic Leukemia

A

Things you must know:

  • Malignant proliferation of lymphoid blasts in blood, bone marrow
  • Classified by immunophenotypes (B vs. T)
  • More common in children
  • Prognosis is often good

T-lymphoblastic leukemia has worse prognosis

Prognosis:

  • Immunophenotype (T is bad)
  • Age (1-10 good)
  • WBC (
22
Q

T-Lymphoblastic Leukemia

A

= T-lymphoblastic lymphoma

-Teenage male with mediastinal mass
-WBC usually very high
Bad prognosis

23
Q

B lymphoblastic Leukemia

A

= B-cell lymphoblastic lymphoma

  • Several sub- and sub-subtypes
  • TdT +
  • Rarely, Philedelphia chromosome + ! (if so = bad)
24
Q

Malaria

A

1 child killer (1 per minute)

Epidemiology:

  • Most prevalent in Africa, Asia, Latin America
  • 216 million affected, 655,000 die each year (90% in SSA)

Vector: Anopheles Mosquito

Causative agent: Plasmodium vivax (common; more benign), P. falciparum (common ; most lethal), P. ovale, P. malariae

Life cycle: sporozoites transmitted from mosquito –> hepatic schizonts –> Merozoites –> ring form –> trophozoite –> schizont

Organ findings:

  • Splenomegaly (parasites in RBCs, super-active macrophages, if chronic: fibrosis, grayish color)
  • Hepatomegaly and liver becomes pigmented (gray)
  • Brain vessels get plugged (rosettes and binding of endothelium) causes hypoxia and eventual ischemia
  • Heart, lungs may also be involved.

Clinical presentation:
-Incubation = 1-2 weeks
-Prodrome: flu-like illness
-Paroxysms! Fever/chills, sweating, myalgia
Quotidian (daily) - P. falciparum
Tertian (every 48 hours) - P. vivax or ovale
Quartan (every 72 hours) P. malaria

Host resistance:

  • Inherited RBC alterations: Hemoglobinopathies (i.e. sickle cell), Thalassemias, G6PD, RBC antigens (ABO - O is best, Duffy)
  • Partial immune-mediated resistance: develops over time in patients in endemic areas, reduces severity of disease, and P. falciparum uses antigenic variation

Dx: Clinical sx + hx; identification of plasmodia in RBCs on regularly-stained blood smear (gold standard); and rapid immunochromatographic tests (quicker but less accurate)\

Rx: Depends on resistance, previous treatment, and area where they were infected (which species, and on sickness of person. 1.) protection/nets, 2.) prophylaxis, and 3.) treat malaria, and 4.) radical cure (primaquine) for latent forms? (debated)

25
Q

Plasmodium falciparum

A

Worst cause of malaria. Especially endemic to Africa.

Lots of ring forms and crescent shaped gametocytes

Able to infect RBCs of any age

Have P-Femps which cause agglutination (rosettes)

Causes red cell pathology:

  • rosettes (clumping of RBCs around infected cell)
  • abnormal binding to endothelium
  • blood flow is impeded
  • main cause of death in children is cerebral ischemia

Stimulates high production of cytokines –>Suppress RBC, cause fever, tissue damage, and RBC binding to endothelium.

Quotidian (daily) fever

Uses antigenic variation

Chloroquine resistance common

26
Q

Plasmodium malariae

A

Not super common or lethal. Low paraside burden, mild anemia.

Rosette arrangement of merozoites

Quartan (every 72 hours) fever

27
Q

Plasmodium vivax

A

Common but not super lethal

Low parasite burden, mild anemia

Relapses

Schuffner’s dots and enlarged red cells

Chloroquine resistance common

28
Q

Plasmodium ovale

A

Not super common or lethal. Low paraside burden, mild anemia.

Relapses

Schuffner’s dots and enlarged red cells

29
Q

Allergic rhinitis, sinusitis (hay fever)

A

localized allergic reaction (Type I hypersensitivity) that causes increased mucus secretion and inflammation

30
Q

Bronchial asthma (atopic forms)

A

Localized allergic reaction (Type I hypersensitivity) that causes airway obstruction due to bronchial smooth muscle hyperactivity; inflammation and tissue injury caused by late-phase reaction.

31
Q

Food allergies (allergic gastroenteritis)

A

Localized allergic reaction (Type I hypersensitivity) that causes increased peristalsis due to contration of intestinal mucosa.

32
Q

Urticaria (hives)

A

Often a manifestation of a systemic reaction (i.e. allergic drug reaction) often precedes anaphylaxis.

33
Q

Type I hypersensitivity

A

Seen in patients who make too much IgE to an environmental antigen, which is often innocuous like a pollen or food.

More than 10% of the population have allergenic sx

Usually a nuisance, but anaphylaxis can be fatal.

Genetic and environmental component.

Rx: avoid offending allergen if possibel; antihistamines, corticosteroids, agents that inhibit release of histamine from mast cells ,leukotriene modifiers, immunotherapy (desensitization therapy)

34
Q

Type II hypersensitivity

A

Autoimmunity due to antibodies which can react against self.

Can come about from a number of ways:

  1. ) foreign antigen happens to look like a self molecule, the response can cross-react.
  2. )Antigen sticks to certain cells in the body. Immune system destroys innocent bystanders.

Ex: Hemolytic disease of newborn, myasthenia gravis, Good pasture’s syndrome

35
Q

Type III hypersensitivity

A

Can occur whenever someone makes antibody against a soluble antigen.

Small immune complexes become trapped in basement membranes or capillaries and activate complement. The usual inflammatory response occurs, with the tissue damaged as an innocent bystander.

No matter where the antigen is the symptoms tend to be the same: arthritis, glomerulonephritis, pleurisy, rash.

Examples of foreign antigens that cause type III are: large dose penicillin, antiserum (aka serum sickness). Also can be reactions to self such as SLE and RA.

I.e. Lupus and RA.

36
Q

Type IV hypersensitivity

A

Cell-mediated hypersensitivity caused by activated CD$ T cells. Can be autoimmune or more commonly innocent bystander injury.

I.e. Tuberculosis and hepatitis most damage is done by T cells, not the bacteria or viruses.

Examples: Contact hypersensitivity, Tuberculin rxn, Granulomatous hypersensitivity (macrophages wall off TB or Crohn’s)

37
Q

Anaphylaxis

A

Immediate type I hypersensitivity

A life threatening systemic allergic reaction characterized by fall in BP w/ vascular shock, bronchospasm and laryngeal edema w/ difficulty breathing due to massive mast cell degranulation.

Inciting agents include drugs (beta-lactams, contrast), exposure to food products (peanuts, seafood), insect toxin (bees or wasps), and latex allergy.

Death can ensue in minutes if untreated due to asphyxiation from upper airway edema or acute respirator failure due to bronchial constriciton and obstruction, and/or shock w/ cardiovascular collapse.

Treatment: IM epinepherine. 0.01mg/kg (0.01ml/kg of 1:1000 –> be sure it’s not cardiac 1:10000 epi); supplemental oxygen, IV fluids, continuous monitoring/admisson, consider antihistamine (benadryl), albuterol neb, and wearable allergy id.

Use O.01mg/kg to a maximum dose of 0.5mg. Adult EpiPen is 0.3 mg. (kids is 0.15mg).

38
Q

Tumor lysis syndrome

A

Sudden rapid death of millions of cells (esp. leukemia/lymphoma). Causes electrolyte/metabolic disturbances. Can be life threatening.

Treat w/ allopurinol to help w/ hyperuricemia (must lower 6-mp dose 25%)

IHO Mike Rose (20 decks)

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