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Generic Clinical Skills > The Hemotological Exam > Flashcards

The Hemotological Exam Flashcards

1
Q

What are we looking for when doing a hematological examination?

A

1-Red blood cells Abnormalities (Anaemia, Polycythaemia, Microcytosis, Macrocytosis) 2-Platelets Changes (Thrombocytosis/peania, medication related) 3-Clotting Factors Abnormalities (Factor Deficiency, Factor V Leiden Mutation) 4-White Blood Cells Abnormalities (Leukaemias) 5-Reduction in Bone Marrow cell production (MDS, myelofibrosis, BM infiltration, drug/ immune induced aplasia) 6-Immunoglobulin- producing cells (Multiple Myeloma, deficiencies) 7-Cancers of Lymph Nodes (HL, NHL)

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2
Q

10 stages of the hematological exam?

A
  1. General Exam 2. Hands and Arms 3. Eyes 4. Oral Cavity 5. Body tenderness 6. Legs 7. Lymph Nodes 8. Abdominal exam 9. tests 10. Imaging
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3
Q

What are some general signs that could indicate a patient has a hematological disease?

A

-Pallor (Anaemia) -Racial Origin (Thalassemia/ Sickle Cell Disease, –Pernicious Anaemia in Northern Europeans) -Bruising (Distribution/Extent) -Cyanosis (Polycythaemia) -Jaundice (Haemolytic Anaemia) -Scratch Marks (Pruritis – lymphoma, myeloproliferative disease) In northern Europeans the combination of prematurely grey hair and blue eyes may indicate a predisposition to the autoimmune disease pernicious anaemia , where there is a vitamin B 12 deficiency due to lack of intrinsic factor secretion by an atrophic gastric mucosa.

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4
Q

What is Koilonychia? what does it indicate?

A

Dry, brittle, ridged, spoon shaped- rare finding- severe iron deficiency - anaemia

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5
Q

What are some other hand/arm indications of anemia?

A

Digital Infarction, Pallor of nail beds, Pulse (Tachycardia), Koilonychia

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6
Q

What is Purpura & Ecchymoses? and what are some causes of their presentation?

A

Purpura: is a condition of red or purple discolored spots on the skin that do not blanch on applying pressure Ecchymoses: a discoloration of the skin resulting from bleeding underneath, typically caused by bruising. -Trauma - PLT Dysfunction - Coagulation Disorders ( Vit K def, Liver diseases, Anticoagulants, DIS) - Congenital (with haemorrhage- Factor VII, IX def, Von Willebrand’s) - Senile Ecchymoses (Loss of skin elasticity, chronic corticosteroids)

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7
Q

What is Petechiae and what causes it?

A

Petechiae are pinpoint, round spots that appear on the skin as a result of bleeding. The bleeding causes the petechiae to appear red, brown or purple. Do not blanch. -Thrombocytopenia (ITP, SLE, Drugs; Marrow aplasia/ Malignancy -Platelet Dysfunction (CKD, Antiplatelets, Myeloproliferative disease) -Small Vessel Diseases (Infections, Steroids, Vasculitis, Dysproteinaemia) . Raised Petechiae – systemic vasculitis, not thrombocytopenia

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8
Q

What can eyes indicate about hematological disease?

A

sclera - jaundice Conjunctival Pallor (Severe anemia- more reliable than nail bed exam)

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9
Q

Signs of hematological disease in the oral cavity?

A

Gingival Hypertrophy (Monocytic Leukaemia) Ulceration, Infections, Haemorrhage buccal/ pharyngeal mucosa (Marrow Aplasia) Atrophic Glossitis, Angular Stomatitis (Iron/ Vit Deficiency) Tonsillar or Adenoid Enlargement (Waldeyer’s Ring) – NHL

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10
Q

What causes bony tenderness?

A

Spinal, Sternum, Clavicular, Shoulders (MM, Lymphoma)

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11
Q

What signs of hematological disease can we see on the legs?

A

Bruising (joints), pigmentation, ulcerations (haemoglobinopathies), neuropathies (Vit b 12 deficiency), Popliteal N Leg Ulcers: thalassaemia, macroglobulinemia, thrombotic thrombocytopenic purpura and polycythaemia, Hydroxyurea medication The legs should also be examined for evidence of the neurological abnormalities caused by vitamin B 12 deficiency: peripheral neuropathy and subacute combined degeneration of the spinal cord. Vitamin B 12 is an essential cofactor in the conversion of homocysteine to methionine; in B 12 deficiency, the lack of methionine impairs methylation of myelin basic protein. Deficiency of vitamin B 12 can also result in optic atrophy and mental changes.

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12
Q

Causes of Lymphadenopathy ?

A

Causes of Lymphadenopathy: 1. Inguinal nodes: infection of lower limb, sexually transmitted disease, abdominal or pelvic malignancy, immunisations 2. Axillary nodes: infections of the upper limb, carcinoma of the breast, disseminated malignancy, immunisations 3. Epitrochlear nodes: infection of the arm, lymphoma, sarcoidosis 4. Left supraclavicular nodes: metastatic malignancy from the chest, abdomen (especially stomach—Troisier’s sign) or pelvis 5. Right supraclavicular nodes: malignancy from the chest or oesophagus 6. Cervical nodes: cancers of the oropharynx and head and neck

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13
Q

What do we test when looking at lymph nodes?

A

-Site (Localised (Local infection vs Generalised (Late Lymphoma) -Size: > 1cm (abnormal) -Consistency (Firm – Carcinoma, Soft – normal, -Rubbery – lymphoma) -Tenderness (Acute inflammation) -Fixation (Carcinoma) -Overlying Skin (Tethering – carcinoma, inflammation- infection)

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14
Q

What do we look for when checking the abdomin?

A
  • Splenomegaly & Hepatomegaly (Multiple leukemias, myeloproliferative conditions)
  • Para-aortic adenopathy (Lymphomas)
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15
Q

Percussion by Castell Method?

A

Percussion by Castell Method:

  • Lay supine
  • Palpate the lower left intercostal space, in anterior axillary line
  • With in full inspiration and expiration
  • Splenomegaly- dull note
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16
Q

An examination of the patient’s blood film can?

A

(1) assess whether the morphology of RBCs, white blood cells (WBCs) and platelets is normal
(2) help characterise the type of anaemia,
(3) detect the presence of abnormal cells and provide clues about quantitative changes in plasma proteins (e.g. paraproteinemia), and
(4) help make the diagnosis of an underlying infection, malignant infiltration of the bone marrow or primary proliferative haematological disorder.

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17
Q

What blood panels can we do to check hemotological status of a patient?

A
  • FBC (Types of Anaemia, Leukemia, Thrombocytopenia, Thrombocytosis)
  • Peripheral Blood Film (Cellular morphology> dx, abnormal cells, malignant bone marrow infiltration)
  • Reticulocyte Count (Low: RBC production defects, High: RBC with short survival)
  • Bleeding Tests - PT/ INR, APTT
  • Clotting Tests – Thrombophilia, Factor V Leiden Mutation, Protein S/ C deficiency
  • Other Tests: JAK2 (Polycythaemia Ruba Vera)
18
Q

What imagine can support examination?

A

­CT & Ultrasound – Splenomegaly/lymphadenopathy

­PET : Staging of Lymphoma

­X- Ray: Osteolytic lesions (Pepper pot Skull) – Multiple Myeloma

19
Q

Coagulation screen types?

A
  1. INR (International Normalised Ratio) & PT (Prothrombin Time):
    - Measures Extrinsic Pathway
    - Factors II, V, VII, X
    - PT: 12-15 seconds, INR is ratio of PT of test sample, against normal PT.
    - INR > 1 (longer coagulation time)
    - INR 2-3: Therapeutic range for anticoagulants
    - INR >3.5: Prosthetic Heart Valve patients
    - Increased in liver disease, Vit K deficiency or Warfarin
  2. APTT (Activated Partial Thromboplastin Time)
    - 25+/ 10 seconds
    - Measures intrinsic pathway, Factors V, VIII, IX, X, XI
    - Prolonged in haemophilia, Heparin Therapy, DIC
20
Q

What is anemia?

A

A condition in which the blood doesn’t have enough healthy red blood cells.

Anaemia results from a lack of red blood cells or dysfunctional red blood cells in the body. This leads to reduced oxygen flow to the body’s organs.

Signs:

  • Pallor, Tiredness, Tachycardia, wide pulse pressures, systolic ejection murmurs
  • Increased Cardiac Output, CF in reduced cardiac reserve
21
Q

What is Pancytopenia?

A

Pancytopenia is a condition that occurs when a person has low counts for all three types of blood cells: red blood cells, white blood cells, and platelets. Pancytopenia is usually due to a problem with the bone marrow that produces the blood cells.

PANCYTOPENIA CAUSES

  • Aplastic anaemia: severe hypoplasia of the erythroid, myeloid and platelet precursor cell lines in the bone marrow, resulting in a bone marrow that is fatty and empty of cells. The causes are listed in List 22.1 ; 50% have no cause identified.
  • Marrow infiltration by MDS, leukaemia, lymphoma, carcinoma, multiple myeloma, myelofibrosis or granulomata.
  • Other: pernicious anaemia, hypersplenism, systemic lupus erythematosus, folate deficiency, paroxysmal nocturnal haemoglobinuria (PNH).
22
Q

What are the issues with anemia/pancytopenia for us?

A

Increased risk of bleeding and infection post surgical procedure

Management:

  • Syncope
  • Infection/ Sepsis
  • Reduce Procedure Time?
  • Risk of Cardiac Arrest
23
Q

Acute Leukemic Patients?

A

Acute Signs: Pallor, Fever (neutropenia), Petechia (thrombocytopenia), weight loss, muscle wasting, localised infections (Neutropenia)

Other: Bony tenderness, lymphadenopathy, Splenomegaly, Hepatomegaly

Oral Signs:

  • Gingival hyperplasia & bleeding
  • Ecchymoses, petechiae
  • Tonsillar enlargement (ALL)
  • Bacterial, Viral, Fungal superinfections due to immunosuppressive medication (Esp. post transplant1-6 months)
  • Oral GVHD (Transplant Cases)

Medical Management: Chemotherapy, HCT (leukopenia, nephrotoxicity, diabetes)

Peri-operative Surgical Management:

  • Pre-Transplant Screening from Dental Officer – Aggressive mx
  • Immunosuppressive Medications? (Corticosteroids, Antimetabolites (Azathioprine), Calcineurin Inhibitors (CNI’s, Cyclosporin), mTOR inhibitors (Sirolimus)
  • Current Blood Test Results (WBC, PLT)?
  • Consultation with Haematologist regarding surgery and possible pre-op AB’s/ post op?
24
Q

Lymphoma types?

A

HL

  • Lymph node enlargement (Discrete, rubbery, superficial node) in 1 side, group
  • Splenomegaly, hepatomegaly
  • Pleural Effusion, bone pain

NHL:

  • Lymph Node enlargement in > 1site/ group
  • Waldeyer’s Ring enlargement
  • Profuse night sweats, weight loss, fevers
25
Q

What is the most common oral lymphoma?

A

Most common lymphomas of oral origin- Diffuse Large B Cell Lymphoma (NHL).

Most common complaint is pain in the maxilla (55%) and swelling accompanied by paraesthesia or numbness (20%); symptoms of lower frequency include poor dentition, tooth mobility, continuous pain and swelling after exocytosis, and even pathologic fracture

Lymphoma Types:

DLBCL is the most common type of NHL.

  • Centroblastic, anaplastic, and immunoblastic types.
  • DLBCL can also be further subdivided by gene expression profiles: B cell-like, activated B cell-like, or type 3 gene expressing profile
  • Each type has a different clinical outcome, genetic alterations, and underlying oncogenic mechanisms.
  • Most maxillary lymph gland tumours are highly malignant DLBCL.
  • Tx: Chemotherapy and Rituximab (Reduce BP, increase infection risk)
26
Q

What is myeloproliferative Disease?

A

ØProliferation of abnormal cells in the bone marrow

­-Chronic Myeloid Leukemia: Tiredness, Anaemia, Gout

­-Polycythaemia Vera:

  • ­Ruddy, plethoric appearance, injected conjunctiva
  • ­Hypertension, Gout, Pruritis, Cyanosis

­-Primary Myelofibrosis: Pallor, Petechiae

­-Thrombocythemia: Spontaneous bleed, thrombosis

Ø Splenomegaly, common haematopoietic sign

Surgical Challenges: Risk of infection and bleeding due to platelet dysfunction

27
Q

What patients have an increased risk of infection?

A

Leukemic, Lymphoma, Myeloproliferative Disorder Patients

  • Chemotherapy
  • Haemopoietic Stem Cell Transplant
  • Immunosuppressive Medications
28
Q

Risk of infection and management?

A

Ø Management:

  • Treat patients prior to chemotherapy (At least 3 weeks prior to start of chemo)
  • AB Prophylaxis (< 6 months post chemotherapy- Neutrophil count < 1.5 *10^9/L)
  • Consult with Haematologist

•Timing of Chemotherapy (Exodontia during chemo- MRONJ, life threating bacteraemia (Koulocheris P et al, 2009)

­Grade of Chemotherapy > Severity of myelosuppression

­Platelet Infusion?

­

Akashi M et al, 2018, PCS: Age, type of malignancy(commonly AML), shorter time between extraction and chemotherapy, low haemoglobin and PLT levels, absorbable haemostatic agents – increased risk of complications

Medical Emergency: Bacteraemia > Septic Shock

­

29
Q

How do platelets effect extraction healing?

A

Platelet-derived growth factor and endothelial growth factor have pivotal roles in the natural healing of extraction sockets

Platelet-rich plasma improves soft tissue healing of extraction sockets and decreases the incidence of alveolar osteitis and postoperative pain

Platelets contain α-granules that at degranulation release cytokines that stimulate cell migration and enhance cellular-level events to expedite wound healing.

In addition, platelet-rich fibrin allows the slow release of cytokines, contributing to the formation and stabilization of blood clots after dental extraction

Platelet quantity and quality are critical because some patients’ immune systems sequester and destroy platelets shortly after platelet administration.

Anaemia affects wound healing and haemoglobin decrease correlates with deterioration and progression of wounds.27 Haemoglobin is an essential oxygen transporter to wounds and probably has an important role in socket healing after dental extraction.

30
Q

What hematological patients have a higher risk of bleeding?

A

­Inherited Bleeding Disorders (Factor Deficiencies)

­Platelet Destruction/ Dysfunction (Hypersplenism, Autoimmune, ITP, TTP, DIC)

­Bone Marrow Conditions (Aplastic Anaemia, Iron/ folate Deficiency, Leukemia, chemotherapy, cirrhosis)

31
Q

Management of patients with bleeding risk?

A

Management:

  • Inherited Bleeding Disorder Patients (Factor Deficiencies) (Hsieh JT et al, 2017)
  • Poorly researched and no current standardised guidelines to follow
  • Variability in definition of ‘high risk procedure’, type/ severity of bleeding disorder, use of factor replacement/ antifibrinolytic therapy, local agents used.
  • Factor Replacement or Desmopressin Infusion or local haemostatic measures – risk of antibodies
  • Consultation with Haematologist
  • Appropriate patient post-operative care and information
32
Q

What are the 4 types of leukemia?

A
  1. Acute myeloid (or myelogenous) leukemia (AML) - usally seen in kids
  2. Chronic myeloid (or myelogenous) leukemia (CML) - we may pick up
  3. Acute lymphocytic (or lymphoblastic) leukemia (ALL)
  4. Chronic lymphocytic leukemia (CLL)
33
Q

What are NOACs?

(breigur 2014)

A

Noval Oral Anticoagulants

The NOACs currently approved in Australia are dabigatran, rivaroxaban and apixaban. Direct thrombin inhibitors (dap) and the factor Xa inhibitors (Riv,Api).

Pradaxa (dabi), Xeralto (riveroxaban), Eliquis (apixoban)

  • careful in renal failure
  • not continously monitored.
34
Q

What is the minimal platlet count for treatment?

A

do not touch under 50 (will not stop bleeding), 100 safe limit, normal count 140-300.

35
Q

What is mean cell volume

verse

Pack cell volume?

A

The mean corpuscular volume, or mean cell volume (MCV), is a measure of the average volume of a red blood corpuscle (or red blood cell). The measure is attained by multiplying a volume of blood by the proportion of blood that is cellular (the hematocrit), and dividing that product by the number of erythrocytes (red blood cells) in that volume. The mean corpuscular volume is a part of a standard complete blood count.

The hematocrit, also known by several other names, is the volume percentage of red blood cells in blood, measured as part of a blood test. The measurement depends on the number and size of red blood cells. It is normally 40.7%–50.3% for men and 36.1%–44.3% for women

  • in anemia it decreases
36
Q

How does a platelet plug form?

A
  1. von Willebrand’s Factor (vWF) adheres to the vascular injury.
  2. vWF then binds to GpIb receptors on surrounding platelets.
  3. After binding, the ADP (P2Y12) receptor on the platelet may then become activated and will lead to increased expression of GpIIb/IIIa.
  4. These newly expressed receptors then finally bind to fibrinogen, which leads to further platelet aggregation.
37
Q

What does low lymphacytes indicate?

A

Low lymphacytes = lymphacytopenia

Indicates an infection

B cells make antibodies and signaling proteins that help to flag or attack invading bacteria, viruses, and toxins.

T cells seek and destroy the cells that have become infected or are cancerous, and they also communicate with B cells.

Natural killer (NK) cells contain compounds that can kill cancer tumor cells and cells infected with a virus.

Low levels of T cells or too few NK cells can lead to uncontrolled viral, fungal, and parasitic infections. B-cell lymphocytopenia can lead to an increase in harmful and different types of infections.

38
Q

What causes low T or low B cell counts?

A

Your bone marrow constantly produces cells that will become lymphocytes. Some will enter your bloodstream, but most will move through your lymphatic system. The lymphatic system is the group of tissues and organs, like the spleen, tonsils, and lymph nodes, that protect your body from infection (1).

About 25 percent of the new lymphocytes remain in the bone marrow and become B cells. The other 75 percent travel to your thymus and become T cells

39
Q

What can cause low hemoglobin?

A

Anemia

cancers, systemic immune issues, syndromes eg HPT.

Can be due to:

Your body produces fewer red blood cells than usual

Your body destroys red blood cells faster than they can be produced

You have blood loss

Risks: High levels = stroke/Clots/HA

Low levels = infection risk and desaturation risk

40
Q

What is the intrinsic clotting pathway?

A

Factor XII → Factor XI → Factor IX (+ Factor VIII + vWF) → Common pathway

41
Q

What is the extrinsic clotting pathway?

A

Factor VII → Common pathway

42
Q

What is the common clotting pathway?

A

Factor X (+ Factor V) → Factor II → Factor I (+ Factor XIII → Fibrin mesh)

Generic Clinical Skills (10 decks)

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