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Clinical Med I > Clin Med Final > Flashcards

Clin Med Final Flashcards

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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
A deletion of 4 of the 4 alpha globin chains results in what?
Hydrops fetalis
26
A deletion/absence of 1 of the 2 beta globin chains results in what?
Thalassemia minor | Mild microcytic anemia
27
A deletion/absence of 2 of the 2 beta globin chains results in what?
Thalassemia Major | Severe hemolytic anemia
28
What is the treatment for Thalassemia?
Folic acid supplementation AVOID iron supplementation Regular transfusions (severe) Hematopoietic cell transplant (severe b-Thalassemia)
29
What causes sideroblastic anemia?
``` Acquired -Often a variant of MDS -Chronic alcoholism -Copper deficiency Inherited ```
30
What will a bone marrow aspirate of a person with sideroblastic anemia show?
Ring sideroblasts
31
What will a blood smear of a person with sideroblastic anemia show?
Siderocytes with Pappenheimer bodies
32
Labs show ↑ RDW ↑ Ferritin ↑ Serum Iron Smear shows Microcytic, hypochromic RBCs Pappenheimer bodies What do you suspect?
Sideroblastic anemia
33
Systemic iron overload may be indistinguishable from what?
Hereditary hemochromatosis
34
What is the treatment of sideroblastic anemia?
``` Patient education- refer to hematology Treat underlying cause Discontinue offending drug Pyridoxine (vit B6) Transfusion ```
35
What is the second most common cause of anemia and is due to a reduction of RBC production?
Anemia of chronic disease
36
What is a contributing factor to anemia of chronic disease?
Hepcidin-induced alteration in iron metabolism
37
``` 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?
Anemia of chronic disease
38
What is the treatment for anemia of chronic disease?
Treat underlying disease | Erythropoietin
39
How long does it take folate deficiency to develop into anemia?
Folate total body stores are small, and have a short half-life so, 4-5 months deprivation can result in anemia
40
What are some dietary sources of folate?
Fresh leafy vegetables Citrus fruits Meat Fortified cereals, rice
41
Where is folate absorbed?
Jejunum
42
What are the clinical presentations of folate deficiency anemia?
Glossitis Vague GI symptoms NO neurologic abnormalitie
43
What can folate deficiency in pregnancy cause?
Neural tube defects
44
Labs show ↓ Serum folate ↑ Homocysteine Serum methylmalonic acid is normal Smear shows Macro-ovalocytes, hypersegmented neutrophils What do you suspect?
Folate deficiency anemia
45
What is the treatment for folate deficiency?
Treat underlying cause Replacement therapy -1mg PO daily
46
What must you always rule out when diagnosis folate deficiency anemia?
Coexisting B12 deficiency
47
Why must you always rule out a coexisting B12 deficiency when diagnosis folate deficiency anemia?
If b12 is not also replaced, pt may develop irreversible neurological damage called subacute combined degeneration of the spinal cord
48
What are sources of vitamin B12?
Only available from diet | Animal sources
49
What is the most common cause of a vitamin B12 deficiency?
Malabsoption
50
How long does it take a vitamin B12 deficiency to develop into anemia?
Body has large stores for B12 so anemia typically takes years to develop
51
Where is vitamin B12 absorbed? Where is it stored?
Absorbed in the ileum | Stored in the liver
52
What are common causes of vitamin B12 deficiency anemia?
Pernicious anemia Decreased intake (vegan diet) Medications
53
What is pernicious anemia?
Autoimmune disorder that causes impaired IF secretion
54
What are the clinical presentations of vitamin B12 deficiency anemia?
Glossitis GI symptoms Neurologic symptoms -defective myelin synthesis in CNS
55
Labs show ↓ Serum vitamin B12 ↑ Homocysteine ↑ Serum methylmalonic acid Smear shows Macro-ovalocytes, hypersegmented neutrophils Ansiocytosis Poikilocytosis What do you suspect?
Vitamin B12 deficiency anemia
56
Labs show antibodies to IF, parietal cells, and ↑ gastrin. What do you suspect?
Pernicious anemia
57
What is the treatment for vitamin B12 deficiency anemia?
Parenteral Vitamin B12 Treat reversible causes PO repletion for mild disease Monitor potassium levels
58
What is the normal survival time for RBCs? What survival . time can the marrow not compensate for?
Normal= 120 days | Cannot compensate for survival less than 20 days
59
What are clinical presentations of hemolytic anemia?
Jaundice Gallstones Dark urine
60
``` 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?
Hemolytic anemia
61
In addition to labs and blood smear, what test can be done to help distinguish between hemolytic anemias?
Direct antiglobin (Coombs) test
62
What are the four types of extravascular hemolytic anemias?
G6PD deficiency Hereditary spherocytosis Sickle cell Autoimmune
63
What are the two types of intravascular hemolytic anemias?
Hemolytic transfusion reaction | Paroxysmal nocturnal hemoglobinuria
64
What type of hemolysis causes destruction of RBCs in the reticuloendothelial system (spleen)
Extravascular hemolysis
65
What type of hemolysis causes destruction of RBCs within the blood stream?
Intravascular hemolysis
66
What do G6PD enzymes protect RBCs from?
Oxidative stress
67
What type of genetic inheritance does G6PD deficiency anemia follow?
X-linked recessive disorder | Female carries rarely affected
68
What are symptoms of G6PD deficiency anemia during a hemolytic episode?
Back or abdominal pain Splenomegaly Jaundice
69
Labs show ↑ Reticulocytes ↑ Indirect bilirubin ↓ G6PD Smear shows Bite cells Heinz bodies What do you suspect?
G6PD deficiency anemia
70
What is the treatment of G6PD deficiency anemia?
Hemolytic episodes usually self limited | Avoid oxidative drugs
71
What type of genetic inheritance does hereditary spherocytosis anemia follow?
Autosomal dominant disorder with mild hemolytic anemia
72
In hereditary spherocytosis anemia, why is the RBC life-span reduced in patients with a spleen?
RBCs are poorly deformable Get trapped in the splenic sinusoids Phagocytized by splenic macrophages
73
What are the clinical presentations of hereditary spherocytosis anemia?
Often asymptomatic Mild jaundice, scleral icterus Pigmented black gallstones Splenomegaly
74
What diagnostic tests can be used for hereditary spherocytosis anemia? What do they show?
Osmotic Fragility Test | Coombs (negative)
75
What is the treatment for hereditary spherocytosis anemia?
Folate supplement | Splenectomy tx of choice for chronic disease
76
What type of genetic inheritance does sickle cell anemia follow?
``` Autosomal recessive Homozygous form -Sickle cell disease: Symptoms Heterozygous from -Sickle cell trait: Carriers ```
77
What are the clinical presentations of sickle cell anemia?
Vaso-occlusive ischemic tissue injury Pain crisis Acute chest syndrome
78
What is the diagnostic test of choice for sickle cell anemia? What does it show?
Hgb electrophoresis reveals Hb S
79
Blood smear shows Normocytic, normochromic anemia Howell- Jolly bodies What do yo suspect?
Sickle cell anemia
80
What is the treatment for sickle cell anemia?
Avoid precipitating factors (hypoxia) Analgesics, fluid, and oxygen during pain crisis Hydroxyurea to decrease painful crises Bone marrow transplant
81
What type of antibodies would produce "cold" autoimmune hemolytic anemia symptoms?
IgM
82
What type of antibodies would produce "warm" autoimmune hemolytic anemia symptoms?
IgG
83
Smear shows Polychromasia Spherocytosis Positive Coombs What do you suspect?
Autoimmune hemolytic anemia
84
What are the treatments for warm and cold autoimmune hemolytic anemia?
Cold- avoid cold | Warm- corticosteroids
85
Which anemia is caused by antibodies to RBCs being directed against ABO/Rh blood group antigens?
Hemolytic Transfusion Reaction
86
What are some symptoms of hemolytic transfusion reaction anemia?
``` Fever Severe hypotension Severe flank pain Pain at infusion site Chest tightness N/V/D ```
87
What type of anemia is a rare acquired stem cell mutation that may progress to myelodysplastic syndrome or acute myeloid leukemia?
Paroxysmal Nocturnal Hemoglobinuria
88
What tests can be used to diagnose paroxysmal nocturnal hemoglobinuria?
Flow cytometry Osmotic fragility test Coombs (negative)
89
What is the treatment of paroxysmal nocturnal hemoglobinuria?
Monoclonal antibody against complement C5 Steroids Stem cell transplant Folic acid supplementation
90
What type of anemia is an acquired abnormality of hematopoietic stem cells?
Aplastic anemia
91
What is treatment for aplastic anemia?
Bone marrow transplant (preferred treatment) Treat underlying cause Hematology referral Transfusions Immunosuppressants if no bone marrow transplant
92
What is considered a major risk factor for recurrent VTE?
Previous thrombotic event
93
What is Virchow's triad?
Stasis Vessel wall injury Hypercoagulability
94
What are classic symptoms of a DVT?
``` Larger calf diameter Swelling Pain Warmth Erythema Palpable cord ```
95
What can be used to calculate a patients probability of a DVT before any diagnostic tests?
Wells Criteria
96
What are some of the Wells criteria?
``` Bedridden Surgery Swelling Pitting edema Cancer Alternative diagnosis more likely (-2 points) ```
97
If pt has a low or moderate probability for DVT according to Wells score, what should you do next?
D-dimer should be obtained
98
When is a D-dimer useful?
Sensitive, but not specific | Only useful when negative and low clinical suspicion
99
If pt has a low or moderate Wells score and negative D-dimer, what should you do next?
No further workup
100
If pt has a high probability for DVT according to Wells score, what should you do next?
Skip D-dimer | Further workup indicated (compression ultrasound)
101
What is the treatment for a DVT?
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
What is the most common cause of a PE?
DVT
103
What are the four ways in which PEs are classified?
Hemodynamic stability Temporal pattern Anatomic location Presence or absence of symptoms
104
What defines hemodynamic instability (massive PE)?
Systolic BP less than 90mmHg
105
What are signs and symptoms of a PE?
``` Dyspnea Pleuritic pain Symptoms of DVT Cough Tachypnea/Tachycardia ```
106
If you suspect a PE and pt is hemodynamically stable what should you do?
Combine clinical and pretest probability according to Wells criteria, D-dimer, and diagnostic imaging (CTPA)
107
If you suspect a PE and pt is hemodynamically unstable what should you do?
Skip diagnostic imaging (may do bedside echocardiography)
108
If you suspect a PE and pt has low probability (Wells criteria <2), what should you do?
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
If you suspect a PE and pt has intermediate probability (Wells criteria 2-6), what should you do?
D-dimer testing necessary Negative D-dimer = no further workup Positive D-dimer = imaging (CTPA)
110
If you suspect a PE and pt has high probability (Wells criteria >6), what should you do?
Skip D-dimer, go directly to diagnostic imaging (CTPA)
111
What is the definitive diagnostic test of choice for PE?
CT Pulmonary Angiography | CTPA
112
If you suspect a PE and a CTPA cannot be obtained, what can be used instead?
``` Ventilation perfusion (V/Q) Not test of choice because poorly specific and diagnostic dilemma with intermediate probability result ```
113
What is the treatment for PE?
Anticoagulant | Supplemental O2, mechanical ventilation, vasopressors
114
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?
IV Unfractionated heparin
115
What anticoagulant preferred in pregnancy and in pts with active cancer?
Low molecular weight heparin (LMWH)
116
What anticoagulants are used in most patients?
LMWH, Fondaparinux, Rivaroxaban, or Apixaban
117
What can be used to reverse UFH?
Protamine
118
What can be used to reverse LMWH?
Protamine
119
What can be used to reverse warfarin?
Vitamin K and fresh frozen plasma
120
What can be used to reverse factor Xa inhibitors?
Tranexamic acid and maybe andexanet alfa
121
What can be used to reverse direct thrombin inhibitor (Dabigatran)?
Idarucizumab
122
How long should anticoagulants be given for provoked cases?
3 months
123
How long should anticoagulants be given for unprovoked cases?
Consider extending therapy, 6-12 months
124
What can be used as in addition to anticoagulants in tx of DVT and PE?
Thrombolytics “clot buster” -Used for unstable patients with PE IVC Filter Thrombectomy/embolectomy
125
What are the four categories of the innate immune system?
Physical barriers Complement system White blood cells Inflammation
126
``` What type of immune system is: First line of defense Rapid response Non-specific defense No memory defense ```
Innate immune system
127
What are the five cells of the adaptive immune system?
``` Lymphocytes T Cells B Cells Antibodies NK Cells ```
128
``` What type of immune system is: Second line of defense More sophisticated response Long lasting response Highly specific Develops memory with each exposure ```
Acquired immune system
129
What causes activation of the complement system?
Activated when C1 binds to an antigen antibody complex on a bacterial cell
130
Activation of the complement system causes the formation of what enzyme?
C3 convertase
131
In the complement system, C3 convertase converts C3 into C3a and C3b. What does C3b do?
C3b coats the microbe (opsonization) to “tag” it for phagocytosis
132
What causes inflammation in the complement system?
Mast cells and basophils release cytoplasmic granules
133
In the complement system, | what combines on the surface of an antigen, and causes to the cell to disintegrate and the cell to lyse?
Membrane Attack Complex (MAC)
134
In the inflammatory system, tissue damage causes chemical signals to alter what kind of cells?
Endothelial cells
135
In the inflammatory system, what sticks along the capillary walls?
Neutrophils
136
In the inflammatory system, what releases histamine?
Mast cells
137
In the inflammatory system, what causes vasodilation and openings between endothelial cells?
Histamine
138
What is the process of neutrophils squeezing through endothelial openings called?
Extravasation
139
In the inflammatory system, what type of cells are attracted to the damaged site and ingest/destroy bacteria?
Neutrophils
140
What type of cells are first responders and active against bacteria?
Neutrophils
141
What does an increase in band neutrophils indicate?
Bone marrow has been signaled to release WBCs = Leukocytosis with left shift >8% bands signifies a left shift
142
What type of infection does neutrophillia indicate?
Bacterial infection
143
What type of infection does neutropenia indicate?
Viral infection
144
What type of cells target parasite and are numerous in mucous membranes?
Eosinophils
145
What type of cells are active against an allergic response and release histamine and heparin?
Basophils
146
What are the largest type of WBC, often found in the blood and spleen, that migrate to tissues to become macrophages and dendritic cells?
Monocytes
147
What type of cells are active against an anaphylaxis response and release histamine?
Mast cells
148
Where do B-cells and T-cell mature?
B-cells: bone marrow | T-cells: thymus
149
What type of immunity is antibody mediated and has primary defense against extracellular pathogens?
Humoral immunity
150
How are mature naïve B-cells activated?
One step activation | Antigen binds to the mature B-cell
151
What can B-cells differentiate into?
``` Plasma cells (which make antibodies) Memory B-cells ```
152
Which antibody is the first responder, indicates acute or recent infection, and activates the complement system?
IgM
153
Which antibody is the second responder, is good at opsonization, and is the most abundant?
IgG
154
Which antibody eliminates pathogens through mucosa, is a weak opsonizer, and does not activate the complement system?
IgA
155
Which antibody is produced in response to allergens, defends against parasites, and binds to mast cells to release histamine?
IgE
156
What type of antibody activates B-cells?
IgD
157
What type of immunity has direct contact and has primary defense against intracellular pathogens?
Cell-mediated immunity
158
How are T-cells activated?
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
What can T-cells differentiate into? (4)
Helper T cells Cytotoxic T cells Suppressor T cells Memory T cells
160
What type of cell has a CD4 receptor and binds to MCH II?
Helper T cells
161
What type of cell has a CD8 receptor and binds to MCH I?
Cytotoxic T cells
162
What MCH class is on the surface of all nucleated cells?
MCH I
163
What MCH class is only on the surface of B-cells, dendritic cells, and macrophages?
MCH II
164
What is the most common acute leukemia in adults?
Acute Myeloid Leukemia (AML)
165
CBC with dif & Bone marrow aspiration = Myeloid blasts > 20% Peripheral smear = Auer Rods Elevated uric acid and lactate dehydrogenase (LDH) What do you suspect?
Acute Myeloid Leukemia (AML)
166
Myelodysplastic syndrome has a risk for progression to what?
Acute Myeloid Leukemia (AML)
167
What treatment can offer a cure to patients with myelodysplastic syndrome?
Allogenic bone marrow transplant
168
What can cause tumor lysis syndrome?
Initiation of cytotoxic therapy (12-24hr after chemo) | Spontaneous
169
What are the manifestations of tumor lysis syndrome?
Hyperkalemia Hyperphosphatemia Hypocalcemia Hyperuricemia
170
What type of cancer has an accumulation of leukemic blast?
Acute Myeloid Leukemia (AML)
171
What type of cancer has unregulated production and proliferation of granulocytes?
Chronic Myeloid Leukemia (CML)
172
What gene is associated with Chronic Myeloid Leukemia?
BCR-ABL
173
Patient presents with splenomegaly, bleeding, pain over lower sternum, and B Symptoms You identify a Philadelphia chromosome. What do you suspect?
Chronic Myeloid Leukemia (CML)
174
What treatment could offer a cure for Chronic Myeloid Leukemia?
Allogenic stem cell transplant
175
What are possible complications of Chronic Myeloid Leukemia?
Tumor lysis syndrome Hyperleukocytosis (emergency) Hyperviscosity syndrome
176
What is the most common cancer in children and teens with a peak incidence at 2-5 years old?
Acute Lymphoblastic Leukemia (ALL)
177
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?
Acute Lymphoblastic Leukemia (ALL)
178
What is the most common type of Acute Lymphoblastic Leukemia? Favorable or unfavorable prognosis?
Precursor B-cell ALL | Favorable prognosis
179
What type of Acute Lymphoblastic Leukemia has | bulky extramedually disease and CNS symptoms? Favorable or unfavorable prognosis?
Mature B-cell ALL Favorable prognosis **Also called Burkitt cell leukemia/lymphoma
180
What is Mature B-cell ALL also called?
Burkitt cell leukemia/lymphoma
181
What type of Acute Lymphoblastic Leukemia has hyperleukocytosis at dx and is found in older patients? Favorable or unfavorable prognosis?
T-cell ALL | Less favorable prognosis
182
What type of cancer has progressive accumulation of functionally incompetent monoclonal B-cells?
Chronic Lymphocytic Leukemia (CLL)
183
Is Chronic Lymphocytic Leukemia found in children or adults?
Adult leukemia (70 years old)
184
Patient presents wit bone marrow failure, organomegaly, and leukemia cutis. Labs show B Lymphocytes > 30% What do you suspect?
Chronic Lymphocytic Leukemia (CLL)
185
What is the treatment for early stage 1 Chronic Lymphocytic Leukemia?
Observation
186
Which type of lymphoma is less common and most prevent between ages 15 and 34?
Hodgkin Lymphoma (HL)
187
What is a risk factor for Hodgkin Lymphoma?
Epstein-Barr virus
188
Patient presents with painless cervical lymphadenopathy, mediastinal mass, severe pain after alcohol, B Symptoms, and pruritus w/o rash. What do you suspect?
Hodgkin Lymphoma (HL)
189
What blood smear finding is associated with Hodgkin Lymphoma?
Reed-Sternberg cells | Multinucleated B-cells “popcorn cells”
190
What treatment is usually curative for Hodgkin Lymphoma?
Chemotherapy
191
What type of cells are majority of Non-Hodgkin Lymphoma cells derived from?
Can be derived from B or T cells, but 90% are derived from B-cells
192
Patient presents with painless lymphadenopathy, mediastinal mass, extra lymphatic sites, and B symptoms. What do you suspect?
Non-Hodgkin Lymphoma
193
What is used for dx of Non-Hodgkin Lymphoma?
Lymph node biospy
194
What is the treatment of indolent Non-Hodgkin Lymphoma?
Radiation alone
195
What is the treatment of aggressive Non-Hodgkin Lymphoma?
Chemotherapy Immunotherapy Autologous stem cell transplant
196
Which type of cancer is more common in African Americans and is a malignancy of plasma cells?
Multiple myeloma
197
In multiple myeloma, what do plasma cells secrete?
Paraproteins
198
What do paraproteins in the blood lead to?
Hyperviscosity
199
What do paraproteins in the urine lead to?
Renal failure
200
Patient presents with back pain, weakness, paresthesia, bone pain, and weight loss. Protein electrophoresis shows an M spike. What do you suspect?
Multiple myeloma
201
What would you expect an X-ray of a person with Multiple myeloma to show?
Lytic lesions | General osteoporosis
202
What type of cancer is "CRAB" associated with and what does it stand for?
``` Multiple myeloma Calcium Renal insufficiency Anemia Bone lesions ```
203
What is the treatment for Multiple myeloma?
Chemotherapy Vertebroplasty or balloon kyphoplasty IV bisphosphonates Autologous hemopoietic cell transplant
204
What is a powerful, independent predictor of mortality?
Peripheral artery disease (PAD)
205
How does PAD progress?
``` Asymptomatic stenosis (narrowing) Chronic arterial insufficiency Limb-threatening ischemia ```
206
What are risk factors for PAD?
Diabetes, hypertension, dyslipidemia, smoking, age, obesity, family hx
207
What role does diabetes have in association with PAD?
Relationship b/w HgbA1c level and risk of amputation
208
How does atherosclerosis progress?
Development of fatty streaks Fibrous cap, fibrous plaque Atherosclerotic plaque Plaque rupture and thrombose
209
What are contributing factors to atherosclerosis?
Endothelial dysfunction, inflammatory factors, immunologic factors, age
210
What can cause ischemia?
Thrombus or Embolus
211
What is the difference between a thrombus and embolus?
Thrombus- clot formed locally | Embolus- dislodged clot or debris that gets stuck in narrower arteries
212
What classifies an acute limb ischemia?
Sudden decrease in limb perfusion; threat to limb viability
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What classifies a chronic limb ischemia?
Patients who present later than 2 weeks after onset
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What classifies a critical limb ischemia?
Pain in forefoot/toes aggravated by elevation, relieved by dependency Non-healing wounds, ulcers, or gangrene
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What is the clinical presentation of PAD?
``` Claudication- intermittent cramping/aching, induced by exercise and relieved with rest Usually in calf Leriche Syndrome (triad) ```
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What is Leriche Syndrome (triad)?
Claudication Absent/diminished femoral pulses Erectile dysfunction
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What are common physical exam findings with PAD?
Pallor with foot elevation Thin, dry shinning, hairless skin Necrosis/gangrene Ulcers
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What can be used to diagnose PAD?
Ankle Brachial Index -Equal or less than 0.90 Doppler Ultrasound (first) Contrast arteriography (gold standard)
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What is the management of PAD?
Lifestyle modifications Exercise (walking is the most effective tx) Cilostazol (phosphodiesterase inhibitor)
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If critical limb ischemia or disabling symptoms unresponsive to lifestyle modifications, what type of treatment should you consider?
Revascularization
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Where do majority of acute arterial occlusions originate? What causes them?
Majority originate in the heart due to thromboembolism
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What are the 6 Ps of acute arterial occlusion?
``` Paresthesia Pain Pallor Pulselessness Poikilothermia (coolness) Paralysis ```
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What is the management of acute arterial occlusion?
Emergency surgical consultation
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What are risk factors for chronic venous disease?
Age, obesity, smoking, hx of LE trauma, prior venous thrombosis, pregnancy, family hx, standing occupation
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What causes chronic venous disease?
Venous hypertension Dysfunction of valves Obstruction to flow Ineffective “venous pump”
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What are the clinical presentation of chronic venous disease?
``` May be asymptomatic Aching, heaviness, or burning Worse with standing, relived by elevation Swelling Visible varicosities ```
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What causes chronic venous insufficiency?
Due to valvular incompetence or as a result of DVT
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What are more advanced signs of chronic venous insufficiency?
Hemosiderin staining Lipodermatosclerosis Stasis dermatitis
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How is chronic venous insufficiency diagnosed?
``` Doppler ultrasound (first) Venography (gold standard) ```
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What is the management of chronic venous insufficiency?
``` Exercise (walking) Weight loss Elevate legs 30min 3-4x/day Compression therapy Wound care for ulcers Sclerotherapy for small surface veins Vein ligation ```
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What should you do before prescribing compression therapy? Why?
Prior to use, confirm dx | Contraindicated in PAD, cellulitis and acute DVT
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What is an aortic dissection?
Tear in vessel wall creating a false lumen
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What type of aortic dissection involves arch proximal to L. subclavian a. and has a worse prognosis?
Type A
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What type of aortic dissection involves the proximal descending thoracic aorta?
Type B
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What are clinical presentations of an aortic dissection?
Sudden onset of severe, persistent chest pain that radiates to back Hypertensive initially and may become hypotensive (shock) Diminished/unequal pulses
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What can be used to diagnose an aortic dissection?
CT chest and abdomen (widened mediastinum)
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What is the management of an aortic dissection?
Emergency Immediately control BP with beta-blockers Urgent surgical intervention
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What is the cause of most aortic aneurysms? What else can cause them?
Atherosclerosis | Connective tissue disease (Marfan’s, Ehler-Danlos Syndromes)
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What are the clinical presentations of a thoracic aortic aneursym?
``` Usually asymptomatic until rupture Substernal back or neck pain Dyspnea, stridor, cough Edema in neck and arms Distended neck veins Hoarseness ```
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Where is the most common site of an aortic aneurysm?
Abdominal Aortic Aneurysms (AAA)
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What is the clinical presentation of an AAA after rupture?
Excruciating abdominal pain that radiates to the back Pulsatile abdominal mass Tenderness Hypotension
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How is an AAA diagnosed?
Abdominal ultrasound | CT (should be done when near 5.5 cm diameter)
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How is an AAA managed when its less than 4 cm?
Watchful waiting
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How is an AAA managed when its ≥ 4 cm?
Refer to vascular specialist
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How is an AAA managed when its 5.5 cm or has rapid growth?
Repair | Endovascular or surgical
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What are the clinical presentations of a carotid artery stenosis?
``` Transient ischemic attacks Amaurosis fugax Contralateral weakness/numbness of extremity or face Carotid bruit Absent pupillary light response Abnormal funduscopic exam ```
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How is a carotid artery stenosis diagnosed?
``` Carotid duplex ultrasound (first) Cerebral angiography (gold standard) ```

Clinical Med I (24 decks)

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