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Clinical Med I > Clin Med Final > Flashcards

Clin Med Final Flashcards

1
Q

What is defined as the concentration of Hb in whole blood?

A

Hemoglobin

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2
Q

What is defined as the volume of packed RBCs?

A

Hematocrit

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3
Q

What is a calculated value used to determine the average size/volume of RBCs

A

Mean corpuscular volume MCV

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4
Q

What is the average Hb concentration in a RBC?

A

Mean corpuscular Hb concentration MCHC

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5
Q

What measures the degree of variation in RBC size?

A

Red cell distribution width RDW

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6
Q

What is anisocytosis?

A

Variation in size of RBCs

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7
Q

What is poikilocytosis?

A

Variation in shape of RBCs

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8
Q

What are the three types of microcytic hypochromic anemias?

A

Iron deficiency
Thalassemia
Sideroblastic

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9
Q

What is the one normocytic normochromic anemia?

A

Anemia of chronic disease

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10
Q

What are the two macrocytic megaloblastic anemias?

A

Folate deficiency

Vitamin B12 deficiency

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11
Q

What are common signs of all anemias?

A

Pallor
Heme in stool
Orthostatic changes
Tachycardia

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12
Q

What are common symptoms of all anemias?

A 
Fatigue
Weakness
Headache
Dizziness
Dyspnea
Palpitations
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13
Q

What is the most common cause of anemia? What population is it most prevalent in?

A

Iron deficiency anemia

Women of childbearing age

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14
Q

What are the causes of iron deficiency anemia?

A

Blood loss*
Decreased dietary intake
Decreased iron absorption

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15
Q 
Labs show
↓ RBC
↓ Ferritin
↓ Serum Fe
↑ TIBC
↑ RDW

Smear shows
Microcytic, hypochromic RBCs
Anisocytosis
Poikilocytosis

What do you suspect?

A

Iron deficiency anemia

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16
Q

Clinical presentations include:

Atrophic glossitis
Angular cheilitis
Koilonychia
Pica
Dysphagia
Restless leg syndrome

What do you suspect?

A

Iron deficiency anemia

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17
Q

What is the treatment for iron deficiency anemia?

A

Treat underlying cause*
Replace iron stores

Oral Ferrous Sulfate 325mg TID
Should see an increase of Hb at a rate of 2-4g/dL every 3 weeks until return to baseline
Continue for 3-6 months

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18
Q

What type of anemia is an inherited hemoglobinopathy that results in a reduction in synthesis of globin chains?

A

Thalassemia

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19
Q

What type of anemia leads to bone changes, impaired growth, and iron overload?

A

Thalassemia

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20
Q 
Labs show
↑ RBC
RDW is normal
↑ Ferritin 
↑ Serum Iron
↓ TIBC

Smear shows
Microcytic, hypochromic RBCs
Target cells

What do you suspect?

A

Thalassemia

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21
Q

What can be used to help diagnose Thalassemia and can detect the type of Hb present?

A

Hemoglobin electrophoresis

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22
Q

A deletion of 1 of the 4 alpha globin chains results in what?

A

Silent carrier of Thalassemia

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23
Q

A deletion of 2 of the 4 alpha globin chains results in what?

A

a-thalassemia minor or mild microcytic anemia

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24
Q

A deletion of 3 of the 4 alpha globin chains results in what?

A

Hemoglobin H disease or moderate microcytic anemia

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25
Q

A deletion of 4 of the 4 alpha globin chains results in what?

A

Hydrops fetalis

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26
Q

A deletion/absence of 1 of the 2 beta globin chains results in what?

A

Thalassemia minor

Mild microcytic anemia

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27
Q

A deletion/absence of 2 of the 2 beta globin chains results in what?

A

Thalassemia Major

Severe hemolytic anemia

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28
Q

What is the treatment for Thalassemia?

A

Folic acid supplementation
AVOID iron supplementation
Regular transfusions (severe)
Hematopoietic cell transplant (severe b-Thalassemia)

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29
Q

What causes sideroblastic anemia?

A 
Acquired 
-Often a variant of MDS
-Chronic alcoholism
-Copper deficiency
Inherited
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30
Q

What will a bone marrow aspirate of a person with sideroblastic anemia show?

A

Ring sideroblasts

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31
Q

What will a blood smear of a person with sideroblastic anemia show?

A

Siderocytes with Pappenheimer bodies

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32
Q

Labs show
↑ RDW
↑ Ferritin
↑ Serum Iron

Smear shows
Microcytic, hypochromic RBCs
Pappenheimer bodies

What do you suspect?

A

Sideroblastic anemia

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33
Q

Systemic iron overload may be indistinguishable from what?

A

Hereditary hemochromatosis

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34
Q

What is the treatment of sideroblastic anemia?

A 
Patient education- refer to hematology
Treat underlying cause
Discontinue offending drug
Pyridoxine (vit B6)
Transfusion
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35
Q

What is the second most common cause of anemia and is due to a reduction of RBC production?

A

Anemia of chronic disease

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36
Q

What is a contributing factor to anemia of chronic disease?

A

Hepcidin-induced alteration in iron metabolism

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37
Q 
Labs show
Mild anemia (Hb 10-100 g/dL)
↑ Ferritin (acute phase)
↓ Serum Iron
↓TIBC

Smear shows
Normocytic and normochromic RBCs

What do you suspect?

A

Anemia of chronic disease

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38
Q

What is the treatment for anemia of chronic disease?

A

Treat underlying disease

Erythropoietin

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39
Q

How long does it take folate deficiency to develop into anemia?

A

Folate total body stores are small, and have a short half-life so, 4-5 months deprivation can result in anemia

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40
Q

What are some dietary sources of folate?

A

Fresh leafy vegetables
Citrus fruits
Meat
Fortified cereals, rice

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41
Q

Where is folate absorbed?

A

Jejunum

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42
Q

What are the clinical presentations of folate deficiency anemia?

A

Glossitis
Vague GI symptoms
NO neurologic abnormalitie

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43
Q

What can folate deficiency in pregnancy cause?

A

Neural tube defects

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44
Q

Labs show
↓ Serum folate
↑ Homocysteine
Serum methylmalonic acid is normal

Smear shows
Macro-ovalocytes, hypersegmented neutrophils

What do you suspect?

A

Folate deficiency anemia

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45
Q

What is the treatment for folate deficiency?

A

Treat underlying cause
Replacement therapy
-1mg PO daily

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46
Q

What must you always rule out when diagnosis folate deficiency anemia?

A

Coexisting B12 deficiency

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47
Q

Why must you always rule out a coexisting B12 deficiency when diagnosis folate deficiency anemia?

A

If b12 is not also replaced, pt may develop irreversible neurological damage called subacute combined degeneration of the spinal cord

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48
Q

What are sources of vitamin B12?

A

Only available from diet

Animal sources

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49
Q

What is the most common cause of a vitamin B12 deficiency?

A

Malabsoption

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50
Q

How long does it take a vitamin B12 deficiency to develop into anemia?

A

Body has large stores for B12 so anemia typically takes years to develop

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51
Q

Where is vitamin B12 absorbed? Where is it stored?

A

Absorbed in the ileum

Stored in the liver

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52
Q

What are common causes of vitamin B12 deficiency anemia?

A

Pernicious anemia
Decreased intake (vegan diet)
Medications

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53
Q

What is pernicious anemia?

A

Autoimmune disorder that causes impaired IF secretion

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54
Q

What are the clinical presentations of vitamin B12 deficiency anemia?

A

Glossitis
GI symptoms
Neurologic symptoms
-defective myelin synthesis in CNS

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55
Q

Labs show
↓ Serum vitamin B12
↑ Homocysteine
↑ Serum methylmalonic acid

Smear shows
Macro-ovalocytes, hypersegmented neutrophils
Ansiocytosis
Poikilocytosis

What do you suspect?

A

Vitamin B12 deficiency anemia

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56
Q

Labs show antibodies to IF, parietal cells, and ↑ gastrin. What do you suspect?

A

Pernicious anemia

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57
Q

What is the treatment for vitamin B12 deficiency anemia?

A

Parenteral Vitamin B12
Treat reversible causes
PO repletion for mild disease
Monitor potassium levels

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58
Q

What is the normal survival time for RBCs? What survival . time can the marrow not compensate for?

A

Normal= 120 days

Cannot compensate for survival less than 20 days

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59
Q

What are clinical presentations of hemolytic anemia?

A

Jaundice
Gallstones
Dark urine

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60
Q 
Labs show
↑ Reticulocytes, polychromasia
↑ Unconjugated bilirubin
↑ Serum lactate dehydrogenase
↓ Serum Haptoglobin (intravascular)

Smear shows
Immature RBCs
Nucleated RBCs
Schistocytes (fragmented RBCs)

What do you suspect?

A

Hemolytic anemia

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61
Q

In addition to labs and blood smear, what test can be done to help distinguish between hemolytic anemias?

A

Direct antiglobin (Coombs) test

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62
Q

What are the four types of extravascular hemolytic anemias?

A

G6PD deficiency
Hereditary spherocytosis
Sickle cell
Autoimmune

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63
Q

What are the two types of intravascular hemolytic anemias?

A

Hemolytic transfusion reaction

Paroxysmal nocturnal hemoglobinuria

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64
Q

What type of hemolysis causes destruction of RBCs in the reticuloendothelial system (spleen)

A

Extravascular hemolysis

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65
Q

What type of hemolysis causes destruction of RBCs within the blood stream?

A

Intravascular hemolysis

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66
Q

What do G6PD enzymes protect RBCs from?

A

Oxidative stress

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67
Q

What type of genetic inheritance does G6PD deficiency anemia follow?

A

X-linked recessive disorder

Female carries rarely affected

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68
Q

What are symptoms of G6PD deficiency anemia during a hemolytic episode?

A

Back or abdominal pain
Splenomegaly
Jaundice

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69
Q

Labs show
↑ Reticulocytes
↑ Indirect bilirubin
↓ G6PD

Smear shows
Bite cells
Heinz bodies

What do you suspect?

A

G6PD deficiency anemia

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70
Q

What is the treatment of G6PD deficiency anemia?

A

Hemolytic episodes usually self limited

Avoid oxidative drugs

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71
Q

What type of genetic inheritance does hereditary spherocytosis anemia follow?

A

Autosomal dominant disorder with mild hemolytic anemia

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72
Q

In hereditary spherocytosis anemia, why is the RBC life-span reduced in patients with a spleen?

A

RBCs are poorly deformable Get trapped in the splenic sinusoids
Phagocytized by splenic macrophages

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73
Q

What are the clinical presentations of hereditary spherocytosis anemia?

A

Often asymptomatic
Mild jaundice, scleral icterus
Pigmented black gallstones
Splenomegaly

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74
Q

What diagnostic tests can be used for hereditary spherocytosis anemia? What do they show?

A

Osmotic Fragility Test

Coombs (negative)

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75
Q

What is the treatment for hereditary spherocytosis anemia?

A

Folate supplement

Splenectomy tx of choice for chronic disease

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76
Q

What type of genetic inheritance does sickle cell anemia follow?

A 
Autosomal recessive 
Homozygous form
-Sickle cell disease: Symptoms
Heterozygous from
-Sickle cell trait: Carriers
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77
Q

What are the clinical presentations of sickle cell anemia?

A

Vaso-occlusive ischemic tissue injury
Pain crisis
Acute chest syndrome

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78
Q

What is the diagnostic test of choice for sickle cell anemia? What does it show?

A

Hgb electrophoresis reveals Hb S

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79
Q

Blood smear shows Normocytic, normochromic anemia
Howell- Jolly bodies

What do yo suspect?

A

Sickle cell anemia

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80
Q

What is the treatment for sickle cell anemia?

A

Avoid precipitating factors (hypoxia)
Analgesics, fluid, and oxygen during pain crisis
Hydroxyurea to decrease painful crises
Bone marrow transplant

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81
Q

What type of antibodies would produce “cold” autoimmune hemolytic anemia symptoms?

A

IgM

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82
Q

What type of antibodies would produce “warm” autoimmune hemolytic anemia symptoms?

A

IgG

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83
Q

Smear shows
Polychromasia
Spherocytosis

Positive Coombs

What do you suspect?

A

Autoimmune hemolytic anemia

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84
Q

What are the treatments for warm and cold autoimmune hemolytic anemia?

A

Cold- avoid cold

Warm- corticosteroids

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85
Q

Which anemia is caused by antibodies to RBCs being directed against ABO/Rh blood group antigens?

A

Hemolytic Transfusion Reaction

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86
Q

What are some symptoms of hemolytic transfusion reaction anemia?

A 
Fever
Severe hypotension
Severe flank pain
Pain at infusion site
Chest tightness
N/V/D
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87
Q

What type of anemia is a rare acquired stem cell mutation that may progress to myelodysplastic syndrome or acute myeloid leukemia?

A

Paroxysmal Nocturnal Hemoglobinuria

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88
Q

What tests can be used to diagnose paroxysmal nocturnal hemoglobinuria?

A

Flow cytometry
Osmotic fragility test
Coombs (negative)

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89
Q

What is the treatment of paroxysmal nocturnal hemoglobinuria?

A

Monoclonal antibody against complement C5
Steroids
Stem cell transplant
Folic acid supplementation

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90
Q

What type of anemia is an acquired abnormality of hematopoietic stem cells?

A

Aplastic anemia

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91
Q

What is treatment for aplastic anemia?

A

Bone marrow transplant (preferred treatment)
Treat underlying cause
Hematology referral
Transfusions
Immunosuppressants if no bone marrow transplant

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92
Q

What is considered a major risk factor for recurrent VTE?

A

Previous thrombotic event

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93
Q

What is Virchow’s triad?

A

Stasis
Vessel wall injury
Hypercoagulability

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94
Q

What are classic symptoms of a DVT?

A 
Larger calf diameter
Swelling
Pain
Warmth
Erythema
Palpable cord
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95
Q

What can be used to calculate a patients probability of a DVT before any diagnostic tests?

A

Wells Criteria

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96
Q

What are some of the Wells criteria?

A 
Bedridden
Surgery
Swelling
Pitting edema
Cancer
Alternative diagnosis more likely (-2 points)
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97
Q

If pt has a low or moderate probability for DVT according to Wells score, what should you do next?

A

D-dimer should be obtained

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98
Q

When is a D-dimer useful?

A

Sensitive, but not specific

Only useful when negative and low clinical suspicion

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99
Q

If pt has a low or moderate Wells score and negative D-dimer, what should you do next?

A

No further workup

100
Q

If pt has a high probability for DVT according to Wells score, what should you do next?

A

Skip D-dimer

Further workup indicated (compression ultrasound)

101
Q

What is the treatment for a DVT?

A

Initial anticoagulation for first 10 days to protect from recurrent thrombosis or embolization
Long term therapy for a minimum of 3 months
Early ambulation

102
Q

What is the most common cause of a PE?

103
Q

What are the four ways in which PEs are classified?

A

Hemodynamic stability
Temporal pattern
Anatomic location
Presence or absence of symptoms

104
Q

What defines hemodynamic instability (massive PE)?

A

Systolic BP less than 90mmHg

105
Q

What are signs and symptoms of a PE?

A 
Dyspnea
Pleuritic pain
Symptoms of DVT
Cough
Tachypnea/Tachycardia
106
Q

If you suspect a PE and pt is hemodynamically stable what should you do?

A

Combine clinical and pretest probability according to Wells criteria, D-dimer, and diagnostic imaging (CTPA)

107
Q

If you suspect a PE and pt is hemodynamically unstable what should you do?

A

Skip diagnostic imaging (may do bedside echocardiography)

108
Q

If you suspect a PE and pt has low probability (Wells criteria <2), what should you do?

A

Use PERC criteria
Pts who fulfill all 8 criteria (PERC negative), do not need additional testing
Pts who do not fulfill all 8 criteria, further testing with D-dimer is indicated

109
Q

If you suspect a PE and pt has intermediate probability (Wells criteria 2-6), what should you do?

A

D-dimer testing necessary
Negative D-dimer = no further workup
Positive D-dimer = imaging (CTPA)

110
Q

If you suspect a PE and pt has high probability (Wells criteria >6), what should you do?

A

Skip D-dimer, go directly to diagnostic imaging (CTPA)

111
Q

What is the definitive diagnostic test of choice for PE?

A

CT Pulmonary Angiography

CTPA

112
Q

If you suspect a PE and a CTPA cannot be obtained, what can be used instead?

A 
Ventilation perfusion (V/Q)
Not test of choice because poorly specific and diagnostic dilemma with intermediate probability result
113
Q

What is the treatment for PE?

A

Anticoagulant

Supplemental O2, mechanical ventilation, vasopressors

114
Q

What type of anticoagulant should be given to patients with severe renal failure, hemodynamic instability, or massive iliofemoral DVT and those more likely to require rapid reversal of anticoagulation?

A

IV Unfractionated heparin

115
Q

What anticoagulant preferred in pregnancy and in pts with active cancer?

A

Low molecular weight heparin (LMWH)

116
Q

What anticoagulants are used in most patients?

A

LMWH, Fondaparinux, Rivaroxaban, or Apixaban

117
Q

What can be used to reverse UFH?

118
Q

What can be used to reverse LMWH?

119
Q

What can be used to reverse warfarin?

A

Vitamin K and fresh frozen plasma

120
Q

What can be used to reverse factor Xa inhibitors?

A

Tranexamic acid and maybe andexanet alfa

121
Q

What can be used to reverse direct thrombin inhibitor (Dabigatran)?

A

Idarucizumab

122
Q

How long should anticoagulants be given for provoked cases?

123
Q

How long should anticoagulants be given for unprovoked cases?

A

Consider extending therapy, 6-12 months

124
Q

What can be used as in addition to anticoagulants in tx of DVT and PE?

A

Thrombolytics “clot buster”
-Used for unstable patients with PE
IVC Filter
Thrombectomy/embolectomy

125
Q

What are the four categories of the innate immune system?

A

Physical barriers
Complement system
White blood cells
Inflammation

126
Q 
What type of immune system is:
First line of defense
Rapid response
Non-specific defense
No memory defense
A

Innate immune system

127
Q

What are the five cells of the adaptive immune system?

A 
Lymphocytes
T Cells
B Cells
Antibodies
NK Cells
128
Q 
What type of immune system is:
Second line of defense
More sophisticated response
Long lasting response
Highly specific
Develops memory with each exposure
A

Acquired immune system

129
Q

What causes activation of the complement system?

A

Activated when C1 binds to an antigen antibody complex on a bacterial cell

130
Q

Activation of the complement system causes the formation of what enzyme?

A

C3 convertase

131
Q

In the complement system, C3 convertase converts C3 into C3a and C3b. What does C3b do?

A

C3b coats the microbe (opsonization) to “tag” it for phagocytosis

132
Q

What causes inflammation in the complement system?

A

Mast cells and basophils release cytoplasmic granules

133
Q

In the complement system,

what combines on the surface of an antigen, and causes to the cell to disintegrate and the cell to lyse?

A

Membrane Attack Complex (MAC)

134
Q

In the inflammatory system, tissue damage causes chemical signals to alter what kind of cells?

A

Endothelial cells

135
Q

In the inflammatory system, what sticks along the capillary walls?

A

Neutrophils

136
Q

In the inflammatory system, what releases histamine?

A

Mast cells

137
Q

In the inflammatory system, what causes vasodilation and openings between endothelial cells?

138
Q

What is the process of neutrophils squeezing through endothelial openings called?

A

Extravasation

139
Q

In the inflammatory system, what type of cells are attracted to the damaged site and ingest/destroy bacteria?

A

Neutrophils

140
Q

What type of cells are first responders and active against bacteria?

A

Neutrophils

141
Q

What does an increase in band neutrophils indicate?

A

Bone marrow has been signaled to release WBCs = Leukocytosis with left shift
>8% bands signifies a left shift

142
Q

What type of infection does neutrophillia indicate?

A

Bacterial infection

143
Q

What type of infection does neutropenia indicate?

A

Viral infection

144
Q

What type of cells target parasite and are numerous in mucous membranes?

A

Eosinophils

145
Q

What type of cells are active against an allergic response and release histamine and heparin?

146
Q

What are the largest type of WBC, often found in the blood and spleen, that migrate to tissues to become macrophages and dendritic cells?

147
Q

What type of cells are active against an anaphylaxis response and release histamine?

A

Mast cells

148
Q

Where do B-cells and T-cell mature?

A

B-cells: bone marrow

T-cells: thymus

149
Q

What type of immunity is antibody mediated and has primary defense against extracellular pathogens?

A

Humoral immunity

150
Q

How are mature naïve B-cells activated?

A

One step activation

Antigen binds to the mature B-cell

151
Q

What can B-cells differentiate into?

A 
Plasma cells (which make antibodies)
Memory B-cells
152
Q

Which antibody is the first responder, indicates acute or recent infection, and activates the complement system?

153
Q

Which antibody is the second responder, is good at opsonization, and is the most abundant?

154
Q

Which antibody eliminates pathogens through mucosa, is a weak opsonizer, and does not activate the complement system?

155
Q

Which antibody is produced in response to allergens, defends against parasites, and binds to mast cells to release histamine?

156
Q

What type of antibody activates B-cells?

157
Q

What type of immunity has direct contact and has primary defense against intracellular pathogens?

A

Cell-mediated immunity

158
Q

How are T-cells activated?

A

Two step activation
TCR binds to the MHC-antigen complex of antigen-presenting cell
T-cell surface receptor CD28 must bind with B7, located on the antigen-presenting cell

159
Q

What can T-cells differentiate into? (4)

A

Helper T cells
Cytotoxic T cells
Suppressor T cells
Memory T cells

160
Q

What type of cell has a CD4 receptor and binds to MCH II?

A

Helper T cells

161
Q

What type of cell has a CD8 receptor and binds to MCH I?

A

Cytotoxic T cells

162
Q

What MCH class is on the surface of all nucleated cells?

163
Q

What MCH class is only on the surface of B-cells, dendritic cells, and macrophages?

164
Q

What is the most common acute leukemia in adults?

A

Acute Myeloid Leukemia (AML)

165
Q

CBC with dif & Bone marrow aspiration = Myeloid blasts > 20%
Peripheral smear = Auer Rods
Elevated uric acid and lactate dehydrogenase (LDH)

What do you suspect?

A

Acute Myeloid Leukemia (AML)

166
Q

Myelodysplastic syndrome has a risk for progression to what?

A

Acute Myeloid Leukemia (AML)

167
Q

What treatment can offer a cure to patients with myelodysplastic syndrome?

A

Allogenic bone marrow transplant

168
Q

What can cause tumor lysis syndrome?

A

Initiation of cytotoxic therapy (12-24hr after chemo)

Spontaneous

169
Q

What are the manifestations of tumor lysis syndrome?

A

Hyperkalemia
Hyperphosphatemia
Hypocalcemia
Hyperuricemia

170
Q

What type of cancer has an accumulation of leukemic blast?

A

Acute Myeloid Leukemia (AML)

171
Q

What type of cancer has unregulated production and proliferation of granulocytes?

A

Chronic Myeloid Leukemia (CML)

172
Q

What gene is associated with Chronic Myeloid Leukemia?

173
Q

Patient presents with splenomegaly, bleeding,
pain over lower sternum, and
B Symptoms
You identify a Philadelphia chromosome.

What do you suspect?

A

Chronic Myeloid Leukemia (CML)

174
Q

What treatment could offer a cure for Chronic Myeloid Leukemia?

A

Allogenic stem cell transplant

175
Q

What are possible complications of Chronic Myeloid Leukemia?

A

Tumor lysis syndrome
Hyperleukocytosis (emergency)
Hyperviscosity syndrome

176
Q

What is the most common cancer in children and teens with a peak incidence at 2-5 years old?

A

Acute Lymphoblastic Leukemia (ALL)

177
Q

Patient presents with lymphadenopathy, hepatosplenomegaly, pallor/brushing, MSK pain, bone pain, and fever.
You identify 20% lymphoblasts on a peripheral blood smear

What do you suspect?

A

Acute Lymphoblastic Leukemia (ALL)

178
Q

What is the most common type of Acute Lymphoblastic Leukemia? Favorable or unfavorable prognosis?

A

Precursor B-cell ALL

Favorable prognosis

179
Q

What type of Acute Lymphoblastic Leukemia has

bulky extramedually disease and CNS symptoms? Favorable or unfavorable prognosis?

A

Mature B-cell ALL
Favorable prognosis

**Also called Burkitt cell leukemia/lymphoma

180
Q

What is Mature B-cell ALL also called?

A

Burkitt cell leukemia/lymphoma

181
Q

What type of Acute Lymphoblastic Leukemia has hyperleukocytosis at dx and is found in older patients? Favorable or unfavorable prognosis?

A

T-cell ALL

Less favorable prognosis

182
Q

What type of cancer has progressive accumulation of functionally incompetent monoclonal B-cells?

A

Chronic Lymphocytic Leukemia (CLL)

183
Q

Is Chronic Lymphocytic Leukemia found in children or adults?

A

Adult leukemia (70 years old)

184
Q

Patient presents wit bone marrow failure, organomegaly, and leukemia cutis.

Labs show
B Lymphocytes > 30%

What do you suspect?

A

Chronic Lymphocytic Leukemia (CLL)

185
Q

What is the treatment for early stage 1 Chronic Lymphocytic Leukemia?

A

Observation

186
Q

Which type of lymphoma is less common and most prevent between ages 15 and 34?

A

Hodgkin Lymphoma (HL)

187
Q

What is a risk factor for Hodgkin Lymphoma?

A

Epstein-Barr virus

188
Q

Patient presents with painless cervical lymphadenopathy,
mediastinal mass, severe pain after alcohol, B Symptoms, and
pruritus w/o rash.

What do you suspect?

A

Hodgkin Lymphoma (HL)

189
Q

What blood smear finding is associated with Hodgkin Lymphoma?

A

Reed-Sternberg cells

Multinucleated B-cells “popcorn cells”

190
Q

What treatment is usually curative for Hodgkin Lymphoma?

A

Chemotherapy

191
Q

What type of cells are majority of Non-Hodgkin Lymphoma cells derived from?

A

Can be derived from B or T cells, but 90% are derived from B-cells

192
Q

Patient presents with painless lymphadenopathy, mediastinal mass, extra lymphatic sites, and
B symptoms.

What do you suspect?

A

Non-Hodgkin Lymphoma

193
Q

What is used for dx of Non-Hodgkin Lymphoma?

A

Lymph node biospy

194
Q

What is the treatment of indolent Non-Hodgkin Lymphoma?

A

Radiation alone

195
Q

What is the treatment of aggressive Non-Hodgkin Lymphoma?

A

Chemotherapy
Immunotherapy
Autologous stem cell transplant

196
Q

Which type of cancer is more common in African Americans and is a malignancy of plasma cells?

A

Multiple myeloma

197
Q

In multiple myeloma, what do plasma cells secrete?

A

Paraproteins

198
Q

What do paraproteins in the blood lead to?

A

Hyperviscosity

199
Q

What do paraproteins in the urine lead to?

A

Renal failure

200
Q

Patient presents with back pain, weakness, paresthesia, bone pain, and weight loss.

Protein electrophoresis shows an M spike.

What do you suspect?

A

Multiple myeloma

201
Q

What would you expect an X-ray of a person with Multiple myeloma to show?

A

Lytic lesions

General osteoporosis

202
Q

What type of cancer is “CRAB” associated with and what does it stand for?

A 
Multiple myeloma
Calcium
Renal insufficiency
Anemia
Bone lesions
203
Q

What is the treatment for Multiple myeloma?

A

Chemotherapy
Vertebroplasty or balloon kyphoplasty
IV bisphosphonates
Autologous hemopoietic cell transplant

204
Q

What is a powerful, independent predictor of mortality?

A

Peripheral artery disease (PAD)

205
Q

How does PAD progress?

A 
Asymptomatic stenosis (narrowing)
Chronic arterial insufficiency Limb-threatening ischemia
206
Q

What are risk factors for PAD?

A

Diabetes, hypertension, dyslipidemia, smoking, age, obesity, family hx

207
Q

What role does diabetes have in association with PAD?

A

Relationship b/w HgbA1c level and risk of amputation

208
Q

How does atherosclerosis progress?

A

Development of fatty streaks Fibrous cap, fibrous plaque Atherosclerotic plaque
Plaque rupture and thrombose

209
Q

What are contributing factors to atherosclerosis?

A

Endothelial dysfunction, inflammatory factors, immunologic factors, age

210
Q

What can cause ischemia?

A

Thrombus or Embolus

211
Q

What is the difference between a thrombus and embolus?

A

Thrombus- clot formed locally

Embolus- dislodged clot or debris that gets stuck in narrower arteries

212
Q

What classifies an acute limb ischemia?

A

Sudden decrease in limb perfusion; threat to limb viability

213
Q

What classifies a chronic limb ischemia?

A

Patients who present later than 2 weeks after onset

214
Q

What classifies a critical limb ischemia?

A

Pain in forefoot/toes aggravated by elevation, relieved by dependency
Non-healing wounds, ulcers, or gangrene

215
Q

What is the clinical presentation of PAD?

A 
Claudication- intermittent cramping/aching, induced by exercise and relieved with rest
Usually in calf
Leriche Syndrome (triad)
216
Q

What is Leriche Syndrome (triad)?

A

Claudication
Absent/diminished femoral pulses
Erectile dysfunction

217
Q

What are common physical exam findings with PAD?

A

Pallor with foot elevation
Thin, dry shinning, hairless skin
Necrosis/gangrene
Ulcers

218
Q

What can be used to diagnose PAD?

A

Ankle Brachial Index
-Equal or less than 0.90
Doppler Ultrasound (first)
Contrast arteriography (gold standard)

219
Q

What is the management of PAD?

A

Lifestyle modifications
Exercise (walking is the most effective tx)
Cilostazol (phosphodiesterase inhibitor)

220
Q

If critical limb ischemia or disabling symptoms unresponsive to lifestyle modifications, what type of treatment should you consider?

A

Revascularization

221
Q

Where do majority of acute arterial occlusions originate? What causes them?

A

Majority originate in the heart due to thromboembolism

222
Q

What are the 6 Ps of acute arterial occlusion?

A 
Paresthesia
Pain 
Pallor
Pulselessness
Poikilothermia (coolness)
Paralysis
223
Q

What is the management of acute arterial occlusion?

A

Emergency surgical consultation

224
Q

What are risk factors for chronic venous disease?

A

Age, obesity, smoking, hx of LE trauma, prior venous thrombosis, pregnancy, family hx, standing occupation

225
Q

What causes chronic venous disease?

A

Venous hypertension
Dysfunction of valves
Obstruction to flow
Ineffective “venous pump”

226
Q

What are the clinical presentation of chronic venous disease?

A 
May be asymptomatic
Aching, heaviness, or burning
Worse with standing, relived by elevation
Swelling
Visible varicosities
227
Q

What causes chronic venous insufficiency?

A

Due to valvular incompetence or as a result of DVT

228
Q

What are more advanced signs of chronic venous insufficiency?

A

Hemosiderin staining
Lipodermatosclerosis
Stasis dermatitis

229
Q

How is chronic venous insufficiency diagnosed?

A 
Doppler ultrasound (first)
Venography (gold standard)
230
Q

What is the management of chronic venous insufficiency?

A 
Exercise (walking)
Weight loss
Elevate legs 30min 3-4x/day
Compression therapy
Wound care for ulcers
Sclerotherapy for small surface veins
Vein ligation
231
Q

What should you do before prescribing compression therapy? Why?

A

Prior to use, confirm dx

Contraindicated in PAD, cellulitis and acute DVT

232
Q

What is an aortic dissection?

A

Tear in vessel wall creating a false lumen

233
Q

What type of aortic dissection involves arch proximal to L. subclavian a. and has a worse prognosis?

234
Q

What type of aortic dissection involves the proximal descending thoracic aorta?

235
Q

What are clinical presentations of an aortic dissection?

A

Sudden onset of severe, persistent chest pain that radiates to back
Hypertensive initially and may become hypotensive (shock)
Diminished/unequal pulses

236
Q

What can be used to diagnose an aortic dissection?

A

CT chest and abdomen (widened mediastinum)

237
Q

What is the management of an aortic dissection?

A

Emergency
Immediately control BP with beta-blockers
Urgent surgical intervention

238
Q

What is the cause of most aortic aneurysms? What else can cause them?

A

Atherosclerosis

Connective tissue disease (Marfan’s, Ehler-Danlos Syndromes)

239
Q

What are the clinical presentations of a thoracic aortic aneursym?

A 
Usually asymptomatic until rupture
Substernal back or neck pain
Dyspnea, stridor, cough
Edema in neck and arms
Distended neck veins
Hoarseness
240
Q

Where is the most common site of an aortic aneurysm?

A

Abdominal Aortic Aneurysms (AAA)

241
Q

What is the clinical presentation of an AAA after rupture?

A

Excruciating abdominal pain that radiates to the back
Pulsatile abdominal mass
Tenderness
Hypotension

242
Q

How is an AAA diagnosed?

A

Abdominal ultrasound

CT (should be done when near 5.5 cm diameter)

243
Q

How is an AAA managed when its less than 4 cm?

A

Watchful waiting

244
Q

How is an AAA managed when its ≥ 4 cm?

A

Refer to vascular specialist

245
Q

How is an AAA managed when its 5.5 cm or has rapid growth?

A

Repair

Endovascular or surgical

246
Q

What are the clinical presentations of a carotid artery stenosis?

A 
Transient ischemic attacks
Amaurosis fugax
Contralateral weakness/numbness of extremity or face
Carotid bruit
Absent pupillary light response
Abnormal funduscopic exam
247
Q

How is a carotid artery stenosis diagnosed?

A 
Carotid duplex ultrasound (first)
Cerebral angiography (gold standard)

Clinical Med I (24 decks)

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