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Pathology > Unit 2 - Hematology, Dermatology > Flashcards

Unit 2 - Hematology, Dermatology Flashcards

1
Q

What is primary hemostasis?

A

Formation of weak platelet plug

Mediated by interaction between platelet and vessel wall

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2
Q

What is secondary hemostasis?

A

Stabilization of platelet plug

Mediated by coagulation cascade

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3
Q

Steps in Primary Hemostasis

A

Transient vasoconstriction of damaged vessel
Platelet adhesion to surface of disrupted vessel - vWF and GPIb
Platelet degranulation - ADP and TXA2 released
Platelet aggregation - fibrinogen and GPIIb/IIIa

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4
Q

What are the clinical signs of disorders of primary hemostasis?

A

Mucosal Bleeding - epistaxis, hemoptysis, GI bleeding, hematuria, menorrhagia

Skin Bleeding - petechiae, purpura, ecchymoses, easy bruising

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5
Q

Disorder of primary hemostasis that involves autoimmune production of IgG against platelet antigens

A

Immune Thrombocytopenic Purpura (ITP)

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6
Q

Most common cause of thrombocytopenia in children and adults

A

Immune Thrombocytopenic Purpura (ITP)

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7
Q

Laboratory findings in Immune Thrombocytopenic Purpura

A

Low Platelet count
Normal PT/PTT
Increased megakaryocytes on bone marrow biopsy

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8
Q

Why would you remove the spleen in ITP?

A

Removes source of antibodies and site of platelet destruction

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9
Q

Treatment of ITP

A

Corticosteroids, sometimes IVIG (short lived effects), splenectomy in refractory cases

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10
Q

Disease that involves pathologic formation of platelet microthrombi in small vessels

A

Microangiopathic Hemolytic Anemia

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11
Q

In which 2 diseases do you see microangiopathic hemolytic anemia?

A

Thrombotic Thrombocytopenic Purpura (TTP)

Hemolytic Uremic Syndrome (HUS)

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12
Q

Thrombotic Thrombocytopenic Purpura is due to decreased ______

A

ADAMTS13 - normally cleaves vWF, in disease uncleaved vWF leads to abnormal platelet adhesion

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13
Q

What causes Hemolytic Uremic Syndrome?

A

Endothelial damage due to drugs or infection

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14
Q

Clinical findings in HUS and TTP

A 
Skin and mucosal bleeding
Microangiopathic hemolytic anemia - schistocytes
Fever
Renal Insufficiency - more common in HUS
CNS abnormalities = more common in TTP
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15
Q

Lab findings in TTP and HUS

A

Thrombocytopenia with increased bleeding time
Normal PT/PTT
Anemia with schistocytes
Increased megakaryocytes on marrow biopsy

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16
Q

Treatment of TTP and HUS

A

Plasmapheresis and corticosteroids

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17
Q

What is Bernard-Soulier syndrome?

A

Genetic GPIb deficiency - impaired platelet adhesion

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18
Q

What is Glanzmann Thrombasthenia?

A

Genetic GPIIb/IIIa deficiency - impaired platelet aggregation

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19
Q

How does aspirin impair primary hemostasis?

A

Irreversibly inactivates cyclooxygenase - lack of TXA2 impairs aggregation

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20
Q

How are the factors in the coagulation cascade activated?

A

Exposure to activating substance - tissue thromboplastin activates Factor VII in extrinsic, subendothelial collagen activates Factor XII in intrinsic

Phospholipid surface of platelets
Calcium

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21
Q

Clinical features of secondary hemostasis disorders

A

Deep tissue bleeding, rebleeding after surgical procedures

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22
Q

What do PT and PTT measure in coagulation cascade?

A

PT - extrinsic (factor VII) and common (Factors II, V, X, and fibrinogen) pathways

PTT - intrinsic (factors XII, XI, IX, VIII) and common pathways

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23
Q

What is Hemophilia A?

A

Genetic factor VIII deficiency - x linked recessive

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24
Q

Lab findings in Hemophilia A

A

Increased PTT, normal PT
PTT does correct if mix plasma with normal plasma
Decreased Factor VIII
Normal platelet count and bleeding time

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25
Q

What is Hemophilia B?

A

Genetic Factor IX deficiency - similar to Hemophilia A

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26
Q

Disease involving acquired antibody against a coagulation factor resulting in impaired factor function

A

Coagulation Factor Inhibitor

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27
Q

Lab findings of Coagulation Factor Inhibitor

A

Increased PTT, normal PT
PTT does not correct if mix plasma with normal plasma
Normal platelet count and bleeding time

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28
Q

Most common inherited coagulation disorder

A

Von Willebrand Disease

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29
Q

Lab findings in Von Willebrand Disease

A

Increased bleeding time
Increased PTT, normal PT
Decreased factor VIII half-life
Abnormal ristocetin test (test platelet agglutination)

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30
Q

Treatment for Von Willebrand Disease

A

Desmopressin (ADH analog) - increases vWF release from Weibel-Palade bodies of endothelial cells

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31
Q

What does Vitamin K deficiency lead to?

A

Interruption of coagulation factors - needed to carboxylate certain factors (II, VII, IX, X, proteins C and S)

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32
Q

Where would you see Vitamin K Deficiency?

A

Newborns - lack of GI colonization
Long term antibiotic therapy - disrupts bacteria in GI
Malabsorption

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33
Q

What is one consequence of heparin induced thrombocytopenia?

A

Fragments of destroyed platelets may activate remaining platelets - thrombosis

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34
Q

Disease involving pathological activation of coagulation cascade

A

Disseminated Intravascular Coagulation (DIC) - almost always secondary to another disease process

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35
Q

Pathogenesis of DIC

A

Widespread microthrombi - ischemia and infarction

Consumption of platelets and factors results in bleeding

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36
Q

Lab findings in DIC

A 
Low platelet count
Increased PT/PTT
Decreased fibrinogen
Microangiopathic hemolytic anemia
Elevated fibrin split products - D-Dimer (best screening test)
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37
Q

What are disorders of fibrinolysis due to?

A

Overactivity of plasmin - excessive cleavage of serum fibrinogen

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38
Q

Lab findings in disorders of fibrinolysis

A

Increased PT/PTT - plasmin destroys coag factors
Increased bleeding time with normal platelet count
Increased fibrinogen split products without D-Dimers

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39
Q

What distinguishes a thrombus from a postmortem clot?

A

Lines of Zahn

Attachment to vessel wall

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40
Q

3 major risk factors for thrombus formation (AKA Virchow Triad)

A

Disruption in blood flow
Endothelial Cell Damage
Hypercoagulable state

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41
Q

How do endothelial cells prevent thrombosis?

A

Block exposure to subendothelial collagen and tissue factor
Produce prostacyclin and NO - vasodilation
Secrete heparin-like molecules
Secrete tissue plasminogen activator (tPA)
Secrete thrombomodulin - redirects thrombin to activate Protein C, which inactivates factors V and VIII

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42
Q

Causes of endothelial cell damage

A

Atherosclerosis, vasculitis, high levels of homocysteine

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43
Q

Classic presentation of hypercoagulable state

A

Recurrent DVTs or DVT at a young age

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44
Q

How does Protein C and S deficiency cause a hypercoagulable state?

A

Decreased negative feedback on coagulation cascade - normally inactivate factors V and VIII

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45
Q

In which hypercoagulable state disease do you have increased risk for warfarin skin necrosis?

A

Protein C and S deficiency

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46
Q

Most common inherited cause of hypercoagulable state

A

Factor V Leiden - mutated form of Factor V that lacks cleavage site for deactivation by protein C and S

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47
Q

What is Prothrombin 20210A and how does it cause a hypercoagulable state?

A

Inherited point mutation in prothrombin, results in increased gene expression of prothrombin –> increased thrombin –> risk for thrombosis

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48
Q

How does ATIII deficiency lead to a hypercoagulable state?

A

Decreases protective effect of heparin-like molecules produced by endothelium (normally they activate ATIII which inactivates thrombin and coagulation factors)

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49
Q

Definition of anemia

A

Reduction in circulating RBC mass

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50
Q

Clinical signs and symptoms of anemia

A

Hypoxia - weakness, fatigue, dyspnea, pale conjunctiva and skin, headache, lightheadedness, angina

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51
Q

What causes microcytic anemias?

A

Decreased production of hemoglobin

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52
Q

Most common type of anemia

A

Iron Deficiency Anemia

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53
Q

Where does iron absorption occur?

A

Duodenum

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54
Q

Transporters for iron in GI, blood, and intracellular

A

GI - ferroportin
Blood - transferrin
Intracellular - ferritin

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55
Q

What is iron deficiency usually caused by?

A

Dietary lack of iron

Blood loss

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56
Q

Stages of Iron Deficiency Anemia

A
  1. ) Storage iron depleted - decreased ferritin, increased TIBC
  2. ) Serum iron depleted - decreased serum iron, decreased saturation
  3. ) Normocytic Anemia
  4. ) Microcytic, hypochromic anemia
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57
Q

Clinical features of Iron Deficiency Anemia

A

Anemia
Koilonychia (spoon shaped nails)
Pica (chewing on abnormal things like dirt)

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58
Q

Lab findings in Iron Deficiency Anemia

A

Microcyctic, hypochromic RBCs with increased red cell distribution width

Decreased ferritin, increased TIBC, decreased serum iron, decreased saturation
Increased free erythrocyte protoporphyrin

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59
Q

What is Plummer-Vinson Syndrome?

A

Iron deficiency anemia with esophageal web and atrophic glossitis

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60
Q

Most common type of anemia in hospitalized patients

A

Anemia of chronic disease

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61
Q

How does Hepcidin play a role in anemia of chronic disease?

A

Produced by liver as acute phase reactant

Sequesters iron in storage sites, making less available for hemoglobin production

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62
Q

Lab findings in anemia of chronic disease

A

Increased ferritin
Decreased TIBC
Decreased serum iron, decreased saturation
Increased free erythrocyte protoporphyrin

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63
Q

Anemia due to defective protoporphyrin synthesis

A

Sideroblastic Anemia

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64
Q

Where does iron end up if protoporphyrin is deficient?

A

Remains trapped in mitochondria - forms ringed sideroblasts

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65
Q

Congenital and acquired causes of Sideroblastic Anemia

A

Congenital - defect in ALAS
Acquired - Alcoholism (poisons mitochondria), Lead Poisoning (inhibits ALAD and ferrochelatase), Vitamin B6 deficiency (required cofactor for ALAS)

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66
Q

Lab findings in Sideroblastic Anemia

A

Increased ferritin
Decreased TIBC
Increased serum iron, increased saturation (iron overloaded state)

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67
Q

Anemia due to decreased synthesis of globin chains of hemoglobin

A

Thalassemia

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68
Q

Alpha-Thalassemia is usually due to which genetic defects and what are the phenotypes?

A

Gene deletion on Chromosome 16

1 deleted - asymptomatic
2 deleted - mild anemia with increased RBC count
3 deleted - severe anemia, HbH formed that damage RBCs
4 deleted - lethal in utero (hydrops fetalis), Hb Barts formed

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69
Q

Beta-Thalassemia is usually due to which genetic defects?

A

Gene mutations on chromosome 11

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70
Q

Mildest form of Beta-Thalassemia and how is it diagnosed?

A

Beta-Thalassemia Minor

Blood smear - microcytic, hypochromic RBCs and target cells
Electrophoresis - slightly decreased HbA with increased HbA2 and HbF

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71
Q

Most severe form of Beta-Thalassemia

A

Beta-Thalassemia Major

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72
Q

Clinical features of Beta-Thalassemia Major

A

Ineffective erythropoiesis and extravascular hemolysis (removal of RBCs by spleen) causes:

Expansion of hematopoiesis into skull (crewcut appearance) and facial bones (chipmunk facies)
Extramedullary hematopoiesis with hepatosplenomegaly

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73
Q

Diagnostic features of Beta Thalassemia Major

A

Blood smear - microcytic, hypochromic RBCs with target cells and nucleated RBCs
Electrophoresis - HbA2 and HbF with little or no HbA

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74
Q

Major and minor causes of Macrocytic Anemia

A

Major - Folate or Vitamin B12 deficiency (megaloblastic)

Minor - Alcoholism, liver disease, certain drugs (non-megaloblastic)

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75
Q

Where is folate absorbed in GI?

A

Jejunum

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76
Q

Causes of folate deficiency

A

Poor diet
Increased demand - cancer, pregnancy, hemolytic anemia
Folate antagonists - methotrexate

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77
Q

Clinical and Lab findings of folate deficiency

A 
Macrocytic RBCs and hypersegmented neutrophils
Glossitis
Decreased serum folate
Increased serum homocysteine
Normal methylmalonic acid
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78
Q

What does Vitamin B12 bind to in small bowel and where is it absorbed?

A

Binds to intrinsic factor, absorbed in ileum

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79
Q

How long does folate deficiency take to develop vs. Vitamin B12 deficiency?

A

Months vs. years

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80
Q

Most common cause of Vitamin B12 deficiency and minor causes

A

Major: Pernicious Anemia - autoimmune destruction of parietal cells leads to intrinsic factor deficiency

Minor: Pancreatic insufficiency, damage to terminal ileum

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81
Q

Clinical and lab findings in Vitamin B12 deficiency

A

Macrocytic RBCs with hypersegmented neutrophils
Glossitis
Subacute combined degeneration of spinal cord
Decreased serum Vitamin B12
Increased serum homocysteine
Increased methylmalonic acid

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82
Q

What are the 2 major causes of normocytic anemia and how do you differentiate between the two?

A

Increased peripheral destruction of RBCs or underproduction of RBCs

Reticulocyte count differentiates

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83
Q

Corrected reticulocyte count of >3% indicates ______ while corrected reticulocyte count of

A

Good marrow response, peripheral destruction; poor marrow response, underproduction

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84
Q

Clinical and lab findings of extravascular hemolysis of RBCs (peripheral destruction)

A

Anemia with splenomegaly, jaundice due to unconjugated bilirubin, and increased risk for bilirubin gallstones

Marrow hyperplasia with corrected reticulocyte count of >3%

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85
Q

Clinical and lab findings of intravascular hemolysis of RBCs (peripheral destruction)

A

Hemoglobinemia
Hemoglobinuria
Hemosiderinuria
Decreased serum free haptoglobin (binds to Hb in blood)

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86
Q

Normocytic anemias with predominately extravascular hemolysis

A

Hereditary Spherocytosis
Sickle Cell Anemia
Hemoglobin C

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87
Q

Anemia caused by inherited defect of RBC cytoskeleton-membrane tethering proteins

A

Hereditary Spherocytosis

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88
Q

Pathogenesis of Hereditary Spherocytosis

A

Membrane blebs formed and lost over time - loss of membrane causes round RBCs, which are less able to maneuver through sphenoid sinuses causing macrophages to consume them

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89
Q

Clinical and lab findings of Hereditary Spherocytosis

A

Spherocytes with loss of central pallor
Increased RDW and mean corpuscular hemoglobin concentration
Splenomegaly, jaundice, increased risk for bilirubin gallstones
Increased risk for aplastic crisis with parvovirus B19 infection of erythroid precursors

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90
Q

What are Howell-Jolly bodies?

A

Howell-Jolly bodies are fragments of nuclear material in RBCs, can see when spleen is removed

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91
Q

What genetic mutation causes Sickle Cell Anemia?

A

Autosomal recessive mutation of Beta chain of hemoglobin

Glutamic acid –> valine change

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92
Q

What increases risk of RBCs sickling in Sickle Cell anemia?

A

Hypoxemia, dehydration, acidosis

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93
Q

Complications in Sickle Cell Anemia due to RBC membrane damage

A

Extravascular hemolysis
Intravascular hemolysis
Massive erythroid hyperplasia resulting in expansion of hematopoiesis into skull, facial bones & extramedullary hematopoiesis

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94
Q

Complications of vaso-occlusion in Sickle Cell Anemia

A

Dactylitis - common presenting sign in infants
Autosplenectomy
Acute Chest Syndrome - most common cause of death in adult patients
Pain Crisis
Renal Papillary Necrosis

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95
Q

In patients with Sickle Cell trait, where does the sickling of RBCs occur?

A

Renal Medulla

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96
Q

Lab findings in Sickle Cell Disease

A

Blood smear - sickle cells and target cells
Positive metabisulfite screen
Hb electrophoresis for HbS

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97
Q

What is Hemoglobin C?

A

Hemoglobin caused by glutamin acid –> lysine mutation

Mild anemia

98
Q

Normocytic Anemias with predominant intravascular hemolysis

A 
Paroxysmla Nocturnal Hemoglobinuria (PNH)
G6PD Deficiency
Immune Hemolytic Anemia
Microangiopathic Hemolytic Anemia
Malaria
99
Q

Anemia defined by acquired defect in myeloid stem cells resulting in absent GPI - renders cells susceptible to destruction by complement

A

Paroxysmal Nocturnal Hemoglobinuria

100
Q

What does GPI do on blood cells and why does a deficiency cause anemia?

A

GPI anchors DAF to blood cells
DAF protects cells against complement
No GPI - No DAF - destruction by complement

101
Q

Why does intravascular hemolysis occur predominately at night in Paroxysmal Nocturnal Hemoglobinuria?

A

Shallow breathing causes mild respiratory acidosis, which activates complement

102
Q

Screening and confirmatory test for Paroxysmal Nocturnal Hemoglobinuria

A

Sucrose test - screening

Acidified serum test or flow cytometry - confirmatory test

103
Q

Complications of Paroxysmal Nocturnal Hemoglobinuria

A

Iron deficiencyanemia, acute myeloid leukemia (10% of patients)

104
Q

What is the pathogenesis of G6PD deficiency?

A

Reduced glutathione, which results in oxidative damage to RBCs
Leads to intravacular hemolysis

105
Q

Two major variants of G6PD deficiency

A

African Variant - mild form

Mediterranean Variant - severe form

106
Q

What is the term for precipitated Hb due to oxidative stress in G6PD deficiency?

A

Heinz Body

107
Q

Screening and confirmatory test for G6PD Deficiency

A

Screening - Heinz body stain

Confirm - enzyme studies

108
Q

Antibody mediated (IgG or IgM) destruction of RBCs

A

Immune Hemolytic Anemia

109
Q

IgG mediated destruction of RBCs usually involves ___ hemolysis, while IgM mediated destruction of RBCs usually involves ___ hemolysis

A

Extravascular; intravascular

110
Q

IgG binds RBCs in the ____ area of the body while IgM binds RBCs in the ____ area of the body

A

central body (warm temperature); extremities (cooler temperature)

111
Q

IgG mediated destruction of RBCs is associated with what?

A

SLE - most common cause

CLL, certain drugs

112
Q

IgM mediated destruction of RBCs is associated with what?

A

Mycoplasma pneumonia and infectious mononucleosis

113
Q

What test is used to diagnose Immune Hemolytic Anemia?

A

Coombs test
Direct - confirms presence of antibody or complemented-coated RBCs
Indirect - confirms presence of antibodies in patients serum

114
Q

How does malaria cause anemia?

A

Plasmodium lifecycle causes rupture of RBCs

Spleen also consumes some infected RBCs

115
Q

Anemias due to underproduction of RBCs

A

Parvovirus B19
Aplastic Anemia
Myelophthisic Process

116
Q

How does Parvovirus B19 cause anemia?

A

Infects progenitor red cells and temporarily halts erythropoiesis - leads to anemia in setting of preexisting marrow stress

117
Q

Anemia caused by damage to hematopoietic stem cells, results in pancytopenia with low reticulocyte count

A

Aplastic Anemia

118
Q

Causes of Aplastic Anemia

A

Drugs, chemicals, viral infections, autoimmune damage

119
Q

What do you see on biopsy of bone marrow in Aplastic Anemia?

A

Empty, fatty marrow

120
Q

What is a myelophthisis process?

A

Pathological process that replaces bone marrow

Results in pancytopenia

121
Q

Pruritic, erythematous, oozing rash with vesicles and edema, often involves face and flexor surfaces

A

Atopic (eczematous) Dermatitis

122
Q

What type of reaction is Atopic Dermatitis?

A

Type I Hypersensitivity reaction

123
Q

What is Contact Dermatitis?

A

Pruritic, erythematous, oozing rash with vesicles and edema that arises upon exposure to allergens

124
Q

What is Acne Vulgaris and what is it due to?

A

Comedones, pustules, and nodules common in adolescents

Caused by chronic inflammation of hair follicles and associated sebaceous glands

125
Q

Treatment for Acne Vulgaris

A

Benzoyl peroxide and Vitamin A derivatives

126
Q

Characteristic skin lesions associated with Psoriasis

A

Well-circumscribed, salmon-colored plaques with silvery scale
Usually on extensor surfaces and scalp
Pitting of nails can also be present

127
Q

What is Psoriasis due to?

A

Excessive keratinocyte proliferation

128
Q

Histology of Psoriasis lesion will show what?

A

Acanthosis (epidermal hyperplasia)
Parakeratosis (hyperkeratosis with retention of nuclei in stratum corneum)
Collection of neutrophils in stratum corneum
Thinning of epidermis above elongated dermal papillae

129
Q

Disease associated with pruritic, planar, polygonal, purple papules on wrists, elbows, and oral mucosa (can also have reticular white lines on surface)

A

Lichen Planus

130
Q

What does histology of a Lichen Planus skin lesion show?

A

Inflammation of dermal-epidermal junction with saw-tooth appearance

131
Q

Disease defined by autoimmune destruction of desmosome between keratinocytes

A

Pemphigus Vulgaris

132
Q

Clinical and histological characteristics of Pemphis Vulgaris

A

Skin and oral mucosa bullae (blisters)
Basal layer remains attached (desmosomes in stratum spinosum)
Rupture easily - leads to shallow erosions with dried crust
Immunofluorescence shows IgG in fishnet pattern

133
Q

Disease defined by autoimmune destruction of hemidesmosomes between basal cells and underlying basement membrane

A

Bullous Pemphigoid

134
Q

Differences between Pemphigus Vulgaris and Bullous Pemphigoid

A

Bullous Pemphigoid - no oral mucosa involvement, basal layer comes off, tense bullae do not rupture easily, linear pattern of IgG under immunofluorescence

135
Q

What is Dermatitis Herpetiforms?

A

Autoimmune deposition of IgA at tips of dermal papillae

Results in pruritic vesicles and bullae that are grouped

136
Q

Disease defined as hypersensitivity reaction characterized by targetoid rash and bullae

A

Erythema Multiforme

137
Q

Common and less common conditions associated with Erythema Multiforme

A

Most common - HSV infection

Others - Mycoplasma infection, drugs, autoimmune disease, malignancy

138
Q

What is Steven-Johnson Syndrome?

A

Erythema Multiforme + oral mucosa/lip involvement + fever

139
Q

What is Seborrheic Keratosis?

A

Benign squamous proliferation

Raised, discolored plaques with “stuck on” appearance

140
Q

Characteristic finding of Seborrheic Keratosis on histology

A

Keratin pseudocysts

141
Q

What is the Leser-Trelat sign and what does it suggest?

A

Sudden onset of multiple Seborrheic Keratoses

Suggests underlying carcinoma of GI tract

142
Q

What is Acanthosis Nigricans and what is it associated with?

A

Epidermal hyperplasia with darkening of skin

Associated with insulin resistance or malignancy

143
Q

Most common cutaneous malignancy

A

Basal cell carcinoma

144
Q

Risk factors for Basal Cell Carcinoma & Squamous Cell Carcinoma

A

UVB-induced DNA damage from sunlight, albinism, zeroderma pigmentosum

Additional for Squamous Cell - immunosuppressive therapy, arsenic exposure, chronic inflammation

145
Q

Classic location and presentation of Basal Cell Carcinoma

A

Upper lip

Elevated nodule with central, ulcerated crated surrounded by dilated vessels

146
Q

Malignant proliferation of squamous cells characterized by formation of keratin pearls

A

Squamous Cell Carcinoma

147
Q

Precursor lesion of squamous cell carcinoma that presents as hyperkeratotic, scaly plaque often on face, back, or neck

A

Actinic Keratosis

148
Q

What is vitiligo?

A

Localized loss of skin pigmentation due to autoimmune destruction of melanocytes

149
Q

Congenital lack of pigmentation due to enzyme defect that impairs melanin production

150
Q

What is a freckle due to?

A

Increased number of melanosomes (not melanocytes)

151
Q

Mask-like hyperpigmentation of cheeks associated with pregnancy or oral contraceptive use

152
Q

Most common mole in children

A

Junctional nevus

153
Q

Most common mole in adults

A

Intradermal nevus

154
Q

What is a nevus (mole)?

A

Benign neoplasm of melanocytes

155
Q

Most common cause of death from skin cancer

156
Q

Two growth phases of Melanoma

A

Radial Growth - along epidermis and superficial dermis, low risk for metastasis
Vertical Growth - into deep dermis, increased risk of metastasis

157
Q

Variants of Melanoma

A

Superficial Spreading - dominant radical growth, most common subtype, good prognosis
Lentigo Maligna Melanoma - radial growth, good prognosis
Nodular - early vertical growth, poor prognosis
Acral Lentiginous - arises on palms or soles, not associated with UV light exposure

158
Q

What is Impetigo and what are the main causes?

A

Superficial bacterial skin infection

S. Aureus or S. pyogenes

159
Q

How does Impetigo present?

A

Erythematous macules that progress to pustules, which can rupture and crust

160
Q

Dermal and subcutaneous infection most commonly due to S. Aureus of S. Pyogenes

A

Cellulitis

161
Q

How does Cellulitis present and what are the risk factors?

A

Red, tender, swollen rash with fever

Risk Factors - recent surgery, trauma, insect bite

162
Q

Sloughing of skin with erythematous rash and fever due to S. aureus infection

A

Staphylococcal Scalded Skin Syndrome

163
Q

What is a Verruca and what is it caused by?

A

Wart (flesh colored papules with rough surface)

Caused by HPV infection of keratinocytes

164
Q

What is Molluscum Contagiosum?

A

Firm, pink, umbilicated papules due to Poxvirus

165
Q

Two common causes of neutropenia

A

Drug toxicity - ex: chemotherapy with alkylating agents

Severe Infection - ex: gram negative sepsis

166
Q

4 causes of lymphopenia

A
  1. ) Immunodeficiency
  2. ) High cortisol state - induces apoptosis of lymphocytes
  3. ) Autoimmune destruction
  4. ) Whole body radiation - earliest change to emerge
167
Q

Two causes of Neutrophilic leukocytosis

A
  1. ) Bacterial infection or tissue necrosis - induces release of marginated pool and bone marrow neutrophils (immature forms too)
  2. ) High cortisol state - impairs leukocyte adhesion
168
Q

2 common causes of Monocytosis

A

Chronic inflammatory states

Malignancy

169
Q

3 common causes of Eosinophilia

A

Allergic reactions (Type I Hypersensitivity)
Parasitic infections
Hodgkins Lymphoma

170
Q

Common cause of Basophilia

A

Chronic Myeloid Leukemia

171
Q

2 common causes of Lymphocytic Leukocytosis

A

Viral infections

Bordella pertussis infection

172
Q

Disease defined as infection that results in lymphocytic leukocytosis comprised of reactive CD8+ cells

A

Infectious Mononucleosis - EBV or less commonly CMV

173
Q

EBV infection primarily infects ____, _____, and _____

A

Oropharynx; liver; B cells

174
Q

CD8+ T Cell response in Infectious Mononucleosis leads to ______, _______, and ______

A

Generalized lymphadenopathy - T Cell hyperplasia
Splenomegaly - T Cell hyperplasia
High WBC count with atypical lymphocytes

175
Q

Which test is used for screening for Infectious Mononucleosis?

A

Monospot test

176
Q

Complications of Infectious Mononucleosis

A

Increased risk for splenic rupture
Rash if exposed to ampicillin
Increased risk for recurrence/B Cell Lymphoma

177
Q

Disease defined by accumulation of >20% blasts in the bone marrow

A

Acute Leukemia

178
Q

Acute clinical presentation of Acute Leukemia (both types)

A

Anemia (fatigue)
Thrombocytopenia (bleeding)
Neutropenia (infection)
High WBC Count - blasts enter bloodstream

179
Q

Acute Lymphoblastic Leukemia cells are characterized by positive nuclear staining for _____

A

TdT (a DNA polymerase)

180
Q

Acute Lymphoblastic Leukemia is associated with which condition and at what age does it normally arise?

A

Down Syndrome, after age of 5

181
Q

Most common type of ALL

182
Q

Surface markers expressed in B-ALL vs. T-ALL

A

B-ALL: CD10, CD19, CD20

T-ALL: CD2 - CD8

183
Q

Which age population would you normally see T-ALL in and how would it present?

A

Teenagers - thymic mass

184
Q

Acute Myeloblastic Leukemia cells are characterized by positive nuclear staining for _____

A

Myeloperoxidase (MPO)

185
Q

In which age population is AML usually seen?

A

Older adults, 50-60 years old

186
Q

3 subtypes of AML and which ones lack MPO staining?

A

Acute Promyelocytic Leukemia (APL) - t(15;17) translocation

Acute Monocytic Leukemia - lacks MPO, characteristically infiltrates gums

Acute Megakaryoblastic Leukemia - lacks MPO, associated with Downs Syndrome before age of 5

187
Q

Group of diseases defined by neoplastic proliferation of mature circulating lymphocytes

A

Chronic Leukemia

188
Q

Most common leukemia overall

A

Chronic Lymphocytic Leukemia (CLL)

189
Q

Disease defined by neoplastic proliferation of naive B cells that co-express CD5 and CD20

A

Chronic Lymphocytic Leukemia

190
Q

Most common cause of death in CLL

191
Q

Complications of CLL

A

Hypogammaglobinemia
Autoimmune hemolytic anemia
Transformation to diffuse large B-Cell lymphoma

192
Q

What is Hairy Cell Leukemia?

A

Neoplastic proliferation of mature B cells characterized by hairy cytoplasmic processes

193
Q

Cells in Hairy Cell Leukemia are positive for _____

A

TRAP - tartrate resistant acid phosphatase

194
Q

Clinical features of Hairy Cell Leukemia

A

Splenomegaly - cells trapped in red pulp

Dry tap on bone marrow aspiration - bone marrow fibrosis

195
Q

Disease defined by neoplastic proliferation of CD4+ T Cells; associated with HTLV-1

A

Adult T Cell Leukemia/Lymphoma

196
Q

Clinical features of Adult T Cell Leukemia/Lymphoma

A

Rash, generalized lymphadenopathy with hepatosplenomegaly, lytic bone lesions with hypercalcemia

197
Q

Disease defined by neoplastic proliferation of CD4+ T Cells that infiltrate the skin; Pautrier microabscesses

A

Mycosis Fungoides

198
Q

What is Sezary Syndrome?

A

Mycosis Fungoides that has spread to the blood

199
Q

What is Chronic Myeloid Leukemia?

A

Neoplastic proliferation of mature myeloid cells, especially granulocytes and precursors
Basophils characteristically increased

200
Q

Which mutation is associated with CML?

A

t(9;22) –> Philadelphia Chromosome

201
Q

What does splenomegaly in CML suggest?

A

Progression to accelerated phase of disease - transformation to acute leukemia usually follows shortly

202
Q

How can you distinguish CML from a reactive neutrophilic leukocytosis?

A

Negative leukocyte alkaline phosphatase stain (LAP)
Increased basophils
t(9;22)
—> These are signs of CML

203
Q

Disease defined by neoplastic proliferation of mature myeloid cells, especially RBCs

A

Polycythemia Vera

204
Q

What mutation is associated with Polycythemia Vera and Essential Thrombocythemia?

A

JAK2 Kinase Mutation

205
Q

Clinical symptoms of Polycythemia Vera and what are they due to?

A 
Due to hyperviscosity of blood
Blurry vision/headache
Increased risk for venous thrombosis
Flushed face due to congestion
Itching
206
Q

How can you distinguish Polycythemia Vera from Reactive Polycythemia?

A

In polycythemia vera….
EPO level decreased, SaO2 is normal
(In reactive EPO is increased)

207
Q

Disease defined by neoplastic proliferation of mature myeloid cells, especially platelets

A

Essential Thrombocythemia

208
Q

What is Myelofibrosis?

A

Neoplastic proliferation of mature myeloid cells, especially megakaryocytes

209
Q

Clinical features of Myelofibrosis

A

Splenomegaly due to extramedullary hematopoiesis
Leukoerythroblastic smear
Increased risk of infection, thrombosis, bleeding

210
Q

What do megakaryocytes produce in Myelofibrosis and what does it cause?

A

Produce excess PDGF –> causes marrow fibrosis

211
Q

Painful lymphadenopathy can be seen with ____ while painless lymphadenopathy can be seen with ____, ____, and _____

A

Acute infection

Chronic inflammation; metastatic carcinoma; lymphoma

212
Q

Regions of lymph node that can undergo hyperplasia during inflammation and conditions associated with each

A

Follicular Hyperplasia - rheumatoid arthritis, early HIV
Paracortex Hyperplasia - viral infections
Hyperplasia of Sinus Histiocytes - cancer

213
Q

In which type of lymphoma does the leukemic phase occur?

A

Non-Hodgkins Lymphoma

214
Q

Types of Non-Hodgkins Lymphomas that involve small B Cells

A

Follicular Lymphoma - expansion of follicular zone
Mantle Cell Lymphoma - expansion of mantle zone
Marginal Zone Lymphoma - expansion of marginal zone

215
Q

Which translocation is seen in Follicular Lymphoma?

216
Q

Important complication of Follicular Lymphoma

A

Progression to diffuse large B-Cell lymphoma

217
Q

How can you distinguish Follicular Lymphoma from reactive follicular hyperplasia?

A

In Follicular Lymphoma….
Normal lymph node architecture is interrupted
Lack of tingible body macrophages in germinal centers
Bcl2 expressed in follicles
Monoclonality

218
Q

What is Marginal Zone Lymphoma associated with?

A

Chronic inflammatory states

219
Q

Which translocation is seen in Mantle Cell Lymphoma?

220
Q

Neoplastic proliferation of intermediate-sized B cells

A

Burkitt Lymphoma

221
Q

What translocation is seen in Burkitt Lymphoma?

A

Translocation of c-myc (chromosome 8)

Most commonly t(8;14)

222
Q

Neoplastic proliferation of large B Cells that grow diffusely in sheets

A

Diffuse Large B Cell Lymphoma

223
Q

Most common form of Non Hodgkins Lymphoma

A

Diffuse Large B Cell Lymphoma

224
Q

How does Diffuse Large B Cell Lymphoma arise?

A

Sporadically or from transformation of a low-grade lymphoma

225
Q

What are the malignant cells in Hodgkins Lymphoma and which surface markers are they characteristically positive for?

A

Reed-Sternberg Cells (large B cells with multilobed nuclei and prominent nucleoli)
CD15 & CD30

226
Q

Which type of cells make up the bulk of the tumor in Hodgkins Lymphoma?

A

Reactive inflammatory cells

227
Q

Most common subtype of Hodgkins Lymphoma

A

Nodular Sclerosis

228
Q

Subtype of Hodgkins Lymphoma with the best prognosis

A

Lymphocyte-rich

229
Q

Subtype of Hodgkins Lymphoma associated with abundant eosinophils

A

Mixed Cellularity

230
Q

Most aggressive subtype of Hodgkins Lymphoma

A

Lymphocyte-depleted

231
Q

Malignant proliferation of plasma cells in the bone marrow

A

Multiple Myeloma

232
Q

Most common primary malignancy of the bone

A

Multiple Myeloma

233
Q

Clinical features of Multiple Myeloma

A

Bone pain with hypercalcemia - lytic lesions
Elevated serum protein - M spike
Increased risk of infection - most common cause of death in MM
Rouleaux formation of RBCs on blood smear
Primary AL amyloidosis
Proteinuria

234
Q

Disease defined by increased serum protein with M spike on SPEP - other features of multiple myeloma absent

A

Monoclonal Gammopathy of undetermined significance

235
Q

Disease defined as B Cell lymphoma with monoclonal IgM production

A

Waldenstrom Macroglobulinemia

236
Q

Clinical features of Waldenstrom Macroglobulinemia

A

Generalized lymphadenopathy
Increased serum protein with M Spike
Visual and neurological deficits
Bleeding

237
Q

Characteristic feature of Langerhans Cell Histiocytosis seen on electron microscopy

A

Birbeck (tennis racket) granules

238
Q

Malignant proliferation of Langerhan Cells which presents as skin rash and cystic skeletal defects in an infant

A

Letterer-Siwe Disease

239
Q

Malignant proliferation of Langerhan Cells which presents as scalp rash, lytic skull defects, diabetes insipidus, and exophthalamos in a child

A

Hand-Schuller-Christian Disease

240
Q

Benign proliferation of Langerhans cells in bone

A

Eosinophilic Granuloma

Pathology (4 decks)

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