Exam 3 [Diseases Of Blood & Lymph] Flashcards
Clinical Features of Anemias
1) Pallor of Skin & Mucous Membranes
2) Weakness, Fatigue, Lethargy, Dizziness
3) Hyper Dynamic Circulation
4) Anginal Pain or Cardiac Failure
3 Types of Anemias
1) Increased Blood Loss
2) Increased rate of Destruction (Hemolytic)
3) Decreased rate of Production
Acute Anemia Due to Blood loss Features
- Hypovolemia
- Hemodilution
- Reticulocytosis
- Nomocytic
- Normochromic
Chronic Anemia Due to Blood Loss Features
- Iron deficiency
- Hypochromic
- Microcytic
What is Anemia due to Increasd Rate of Destruction (Hemolytic)
- Reduced life span of RBC’s (<120 days)
- Accelerated red cell destruction
Evidence of Hemolysis in Anemia due to Increasd Rate of Destruction (Hemolytic)
1) Increased Unconjugated Bilirubin -> jaundice
2) Damaged Red cells
3) Erythroid Hyperplasia of Bone Marrow
4) Increased Immature red cells in blood
Causes of Anemia due to Increasd Rate of Destruction (Hemolytic)
Intrinsic: red cell deficits
Extrinsic: abnormal hemolytic mechanisms
Hemolytic Anemias due to Intrinsic Causes
1) Sickle cell
2) Thalassemia
3) Hereditary Spherocytosis
4) Glucose 6-Phosphate Dehydrogenase Deficiency
What is Hereditary Spherocytosis
Dominant inheritance of spherical red cells due to alterations in permeability of cell membrane
Childhood Clinical Features of Hereditary Spherocytosis
- Hemolysis
- Decreased red cell life span
Adulthood Clinical Features of Hereditary Spherocytosis
- Hemolysis
- Anemia
- Jaundice & Pigment Gall Stones
- Erythoid Hyerplasia of Bone Marrow
Clinical remission in Hereditary Spherocytosis
Splenectomy produces remission in most cases
What is a “Sickle Cell”
- Contains HbS instead of HbA
- AA substitution causes decreased solubility of hemoglobin
Reduced state HbS =
Long, slender crystalline masses causing distortion of red cell born in Vito and in vitro
Pathogenesis of Sickle Cell Disease
- hemolytic anemia
- capillary obstruction due to thrombosis
Series of events in Sickle Cell Disease
Increased Hypoxia -> Sickling -> RBC Destruction -> Hypoxia -> fatty degeneration of lower kidney & spleen -> enlargement from trapped damaged RBC’s -> forms atrophic fibrous mass (autoplenectomy)
Sickle Cell Disease Findings
1) Normochromic, Normocytic
2) Anisocytosis & Poikilocytosis
3) Increased Reticulocytes & Polymorphs
4) Erythroid Hyperplasia in Marrow
5) + Sickling test
6) Hemoglobin Electrophoretic pattern
Clinical Features of Sickle Cell Disease
- Onset in 2nd year of life
- Susceptible to Pneumococcal Pnuemonia, Salmonella, Osteomyelitis, bacterial meningitis
- Erythroid Hyperplasia
Symptoms of Sickle Cell Disease
- Fever
- Bone, Joint & Abdominal Symptoms
Homozygous vs. Heterozygous Sickle Cell Disease
Homo: 80-100% of Hb is HbS, decreased PO2 Sickling in vivo
Hetero: 10% of black Americans carry HbS gene
.2% have Sickle Cell
Sickle Cell Trait
Heterozygous Hgb
- Increased resistance to malaria parasite
- asymptomatic until exposed to low PO2
- HbS = 25-40% of hemoglobin
What is Thalassemias
- Mediterranean = Sea of Blood
- alpha or beta chain issue
Cells of alpha Thalassemias
- Alpha chain deficiency
- beta & gamma form polymers
- inclusion bodies
- red cells = thinner w/ short life span
Pathogenesis of Beta Thalassemia
- Excessive Hemolysis
- Homozygous: (Cooley’s Anemia)
Clinical Features of Beta Thalassemia
1) Splenomegaly
2) Mild jaundice
3) Erythroid Hyperplasia
4) Pigment Gallstones
5) progressive Anemia
4 Clinical Gene Syndromes of Alpha-Thalassemia
1) -A/AA = asymptomatic carrier
2) -A/A- = thalassemia minor
3) - -/-A = thalassemia major (Hgb H disease)
4) - -/- - = fatal in-utero (hydros fetalis)
G-6-PD Deficiency combined with drugs causing Hemolytic Anemia
Antimalarials: quinine
Antimicrobials: nitrofurantoin & sulfonamides
Analgesics: aspirin & phenacetin
G-6-PD Deficiency Affects:
- 10% American blacks
- “Favinism” in Middle East (eating the bean Vinca Fava)
- Heinz Bodies
Extrinsic Hemolytic Anemias
1) Infections - Malaria
2) Toxins - heavy metals, drugs, exotoxins
3) Autoimmune Hemolytic Disease
4) Blood group incompatibilities
5) Hypersplenism
2 processes that cause Anemia in Malaria
1) parasite grows inside RBC during RBC lysis
2) Increased macrophages -> increased phagocytosis of nonparisited cell -> increased anemia
Mycoplasma Pneumoniae is…
Self-limiting
2 Classifications of Immunohemolytic Anemias
1) Warm antibodies: hemolysis @ body temperature
2) Cold antibodies: Raynaud’s & hemolysis only in the cold
Blood Group Incompatibilities
- Due to Rh incompatibility
- Normal 1st pregnancy
- more pregnancies = greater effect on fetus (erythroblastosis fetalis)
Anemias due to decreased RBC production
1) iron Deficiency
2) Anemia of Chronic Disease
3) Megoblastic
4) Aplastic
5) Marrow Replacement
6) Anemia of Chronic Renal Failure
Iron Deficiency Etiology
- Diet Deficiency
- Increase demand for iron
- malnutrition
- chronic blood loss
Iron deficiency pathology
- Anemia
- hypochromic, microcytic
- atrophy of epithelial surfaces
- Koilonychia
Anemias of Chronic disease
1) Chronic Infections
2) Autoimmune Diseases
3) Malignant Neoplasms
Megaloblastic Anemias Etiology
Vitamin B12 & Folic Acid deficiency
Megaloblastic Anemia Pathology
- Megaloblasts
- Intramedullary hemolysis OR ineffective erythropoiesis
- Macrocytosis with HOWELL-JOYYL BODIES, DNA fragments
- Hypersegmented neutrophils
Aplastic anemias Etiology
Reactions to drugs & chemicals
Aplastic anemias Pathology/Clinical features
- Anemia (normocytic & normochromic)
- Granulocytopenia -> infectious/oral ulceration
- Thrombocytopenia -> bleeding tendency
Polycythemia (Rubra) Vera Etiology
Idiopathic (> 50, M > F)
- All blood elements are increased
- uncontrolled production of marrow elements
Pathology of Polycythemia (Rubra) Vera
Increase blood volume -> organ congestion
Increased blood viscosity -> vascular thrombosis, kidney, spleen, heart infarcts
Polycythemia (Rubra) Vera: Bleeding Tendency
Defective platelet function
Increased platelets, but dont work properly
Polycythemia (Rubra) Vera: Increased acid in Blood due to…
Turnover of Nucleic acids from normoblasts & megakaryocytes
(Gout in minority of patients)
Polycythemia (Rubra) Vera: Clinical Features
-Dark, Dusty red color on face
- prominent temporal artery
- big eye vessels on retina
- Cyanosis
Etiology of Infectious Mononucleosus
Epstein-Barr Virus
Clinical Presentation of Infectious Mononucleosus
- Swollen Lymph
- Fever
- sore throat
- extreme fatigue
Pathology of Infectious Mononucleosus
-EBV infects B lymphocytes
- Abnormal lymphocytes develop from CD8+ T cells
Acute Lymphoblastic Leukemia: Age Group & Cell Type
- Young children (3-4 years old)
- Lymphoblasts
Acute Myeloblastic Leukemia: Age Group & Cell Type
- Young Adults (15-20 years old)
- Myeloblasts: Auer’s Rods
**May not have lymph node involvement
Chronic Lymphocytic Leukemia: Age Group & Cell Type
> 60 years
Small mature lymphocytes (usually B-cell)
Organ Enlargement
**Most Benign of 4 major leukemias
Chronic Myelocytic Leukemia: Age Group & Cell Type
- (40-50 years old)
- Mature neutrophils
** Massive Splenomegaly
Karyotype of Chronic Myelocytic Leukemia
Philidelphia Chromosome
- part of Chromosome 22 translocated to chromosome 9
Chronic Phase of Chronic Myelocytic Leukemia
- (3-10 years)
- 60-80% go into blasting crisis
Hodkin’s Disease: Cell Type & Etiology
Reed-Sternberg cell
- large bi-nucleated cell w/ prominent nucleate
Viral including EBV
Staging of Hodkin’s Disease
Stage 1: single node region
Stage 2: 2 node regions on same side of diaphragm
Stage 3: Both sides of diaphragm
Stage 4: extra lymphoid organs
Systemic symptoms of Hodgkin’s Disease
- Fever
- Night sweats
- Weight loss
Non-Hodgkin’s Lymphomas: What is it & Etiology
Neoplasticism proliferation of Lymphoid tissue w/o Reed-Sternberg Cells
Etiology: viruses (Burkitt’s, Epstein Barr, Herpes Type 4, autoimmune & immunodeficiencies)
Plasma Cell Dyscrasia
- Growth of a clone of plasma cells
- Middle aged-elderly
Multiple Myeloma: Cell Type
IgG (MC) & IgA
(Immunoglobins accumulate)
Multiple Myeloma: Urine
- Can have Bence-Jones proteins
- Calcium
- Polyuria
Multiple Myeloma: Symtoms
- Anemia
- Bone Pain
- Path fractures
- weakness, Lethargy
- Renal stones & insufficiency
Multiple Myeloma: Pathology
Medullary Cavity Erosion -> Ca2+ in blood -> hypercalcemia
- Increased susceptibility to infection
Histiocytosis X facts
(A.k.a. Langerhans cells histiocytosis)
HX Body: Birbeck’s granules on EM
Histiocytosis X Diseases
1) Eosinophilic Granuloma
2) Hand-Schuller-Christian Disease
3) Letterer-Siwe Disease
Eosinophilic Granuloma
- Unifocal or Singular
- Bone Marrow
- Males: Skull or Ribs
Hand-Schuller-Christian Disease
- Multifocal proptosis
- Bone lesions in Skull
- Diabetes Insipidus
- ADH
Lettered-Siwe Disease
- Acute Disseminated form of Histiocytosis X
- Lesions of Bone + Lymphoid Tissue
- Children
- Fever, skin rashes, splenomegaly, lymphadenopathy
Diseases of Hemostasis
1) Senile Purpura
2) Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome)
3) Symptomatic purpura
4) Hypersensitivity Angiitis (anaphylactoid purpura)
Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome): Presentation
- Disease of venules & capillaries
- around mouth & in oral cavity/sinuses
- recurrent hemorrhages getting worse with age
- Initially: Epistaxis
- Later: G.I. Hemorrhage
Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome): Genetics
Autosomal Dominant
Hypersensitivity Angiitis (anaphylactoid purpura): How it Shows up & Population
- allergic damage to vessel wall
- follows streptococcal infections
- adults with exposure to drugs
Senile Purpura: What is it? & Population
- Lack of Collagen supporting the blood vessel
- Elderly
Symptomatic PurPura is seen with
Other Diseases like Septicemias
Etiology of Disseminated Intravascular Coagulation
Caused by inflammation from an infection, injury or illness
- (MC: sepsis)
- Surgery/trauma
- cancer
- blood infections
- pancreatitis
Pathology of Disseminated Intravascular Coagulation
- massive systemic intravascular activation of coagulation
- widespread deposition of “fibrin” in circulation compromising blood supply to various organs
Disseminated Intravascular Coagulation leads to…
Consumptive Coagulopathy
What is Thrombocytopenia?
Decreased platelets below 150,000/ml
(Below 50,000 produces hemorrhage)
Cause of Thrombocytopenia
1) Decreased Production
2) Increase Destruction
3) Splenic Sequestration
Thrombocytopenia caused by Decreased Production
Aplastic Anemia
leukemias
Radiation/Chemicals
Thrombocytopenia caused by Increased Destruction
2 forms of Idiopathic Thrombocytopenia Purpura
2 forms of Idiopathic Thrombocytopenia Purpura
1) Acute ITP in Childhood
2) Chronic ITP in Adulthood
Acute ITP in Childhood
- Follows viral illness
- Platelet count = < 20,000/ml
- Sudden onset of Petechial & Purpura
- Major Risk: Intracranial Hemorrhage
Chronic ITP in Adults
- Associated w/ Collagen Disease
- Platelet count = < 100,000/ml
- Bleeding episodes (not life-threatening)
- Improved w/ Glucocorticoids
Drug Induced Increased Destruction Seen in Idiopathic Thrombocytopenia Purpura
[Quinidine, Sulfonamides, Cimetidine]
- Idiosyncratic Response
- Appears weeks or months after agent
Thrombocytopenia is severe & symptomatic with count of…
20,000/ml
Hemophilia A: Genetics & Factors Involved
- X linked recessive
- Gene for the VIII OR IX protein (produces too little)
[LACK OR TOTAL ABSENCE OF COAGULATION VIII]
Hemophilia B: Genetics & Factors Involved
- X linked recessive
- Gene for the VIII OR IX protein (produces too little)
[SHORTAGE OF COAGULATION FACTOR IX]
Von Willebrand: Genetics & Source
-On Autosomal Chromosome 12
- Mutation of the VWF gene
Von Willebrand: Features of Deficiency
- VWF gene makes blood clotting protein called Von Willebrand Factor
- Slows the blood clotting process
- Prolonged bleeding after an injury
Von Willebrand: Function
Formation of blood clots to prevent further blood loss
Function of Thromboxane A
- Amplifies platelet aggregation to the site of injury
- Blood Clot Formation (Thrombosis)
Thromboxane A’s Relationship w/ Aspirin
Low-dose long-term aspirin use irreversibly blocks formation of Thromboxane A2 in platelets
(Producing inhibitory effect on platelet aggregation)
Congenital Diseases of Blood Vessels
1) Developmental Aneurysms
2) A-V Fistulas
3) Hemangiomas
4) Coarctation of the Aorta
5) Marfan’s
6) Developmental Aneurysms
Berry Aneurysms
- Circle of Willis
- Vessel stretches from increased BP
- hemorrhage inside the Skull
A-V Fistulas or Malformations
- Arterial vessels connect directly to venous vessels
- Veins have increased pressure -> may rupture
- Rupture likely w/ hypertension
A-V Fistulas or Malformations: MC Location
Branches of Middle Cerebral
Hemangiomas: 2 Types
Capillary & Cavernous
Hemangiomas associated with what Syndrome?
Sturgeon-Weber
Infantile (pre-ductal) Coarctation of the Aorta
- Narrowing of Aorta proximal to Ductus
- Lower 1/2 of body is supplied by Pulmonary Artery through Ductus Arteriosus
- Cyanotic
Adult (post-ductal) Coarctation of the Aorta: More Common in patients…
1) w/ Turner’s Syndrome
2) that are Male
Adult (post-ductal) Coarctation of the Aorta: Pathological features
- Coarctation after Ductus Arteriosus
- Lower body gets blood from narrowed Aorta & collateral circulations
- Asymptomatic until Adult
Adult (post-ductal) Coarctation of the Aorta: Clinical Signs/Symptoms
- Delayed & Low Pressure Femoral Pulse
- Intermittent Claudication w/ exercise
- Hypertension from Renin production
- Notching of the Ribs (on X-Ray)
Adult (post-ductal) Coarctation of the Aorta: Associations
1) Bicuspid Aortic Valve
2) Berry Aneurysms
Marfan’s Syndrome: What is it?
- CT Disease w/ production issue of Fibrillin
Marfan’s Syndrome: Areas MCly Affected
- Aorta
- Cardiac Valves
- Eyes
- Skeletal System
Marfan’s a Syndrome: Tests
Steinberg: thumb extends beyond flexed fingers
Walker-Murdough: thumb & 5th finger overlap around wrist
Marfan’s Syndrome: Eye Pathology
Dislocation of the Lens from the Suspensory Ligament
Marfan’s Syndrome: Cardio pathology
Myxomatosis change in Tunica Media of Aorta: aneurysm of aortic root, aortic valve incompetence, dissecting aneurysm of aorta
Myxomatosis change in tunica Media of Mitral valve: mitral valve incompetence
Ehlers-Danilo’s Syndrome: Pathological Effects
- Affect collagen formation
- hyperexstensible skin & joints
Ehler’s-Danlos Syndrome: Clinical Signs
- Bleeding, poor healing, retinal detachment, dislocated lens, mitral valve prolapse, aneurysms, blue sclera
- Large scars over knees/elbows
Hurler’s Syndrome: AKA’s & Genetics
- AKA gargoylism & Mucopolysaccharidosis I
- Autosomal Recessive
What is Hurler’s Syndrome?
Enzyme deficiency leading to excessive GAG’s in bone, brain & liver
Hurler’s Syndrome: Clinical Features
- Facial Chgs
- organomegally
- corneal opacity
- severe MR
Hurler’s syndrome: Life expectancy
10 years (Death 2nd to cardio respiratory disease)
Hurler’s syndrome: Medications
Chondroitin, Dermatan & Heparan Sulfate
Arteriosclerosis: 3 diseases
1) Medial Calcification Sclerosis (Mockenberg’s)
2) Arteriosclerosis
3) Atherosclerosis
(2 & 3 are interchangeable)
Monckeberg’s Medial Calcification Sclerosis: Affects what and who?
- Tunica Media of muscular arteries (does not obstruct)
- People over 50
Monckeberg’s Medial Calcification Sclerosis: Pathological Findings
- Calcium presence can be seen on X-Ray
- Doesn’t produce clinical problems
- Artery may have atherosclerosis
Hyaline Arteriolosclerosis
- Accumulation of abnormal material in the Intima of ARTERIOLES (narrows the Lumen)
- Associated w/ DM & Hypertension
Hyperplastic Arteriosclerosis
- Thickening of MEDIA, Narrows LUMEN, stiffens WALL
- Associated w/ rapid increasing hypertension (malignant hypertension: Diastolic >120)
Gruel “Hardening”: MC What?
Most important form of arteriosclerosis as cause of mortality (in the west: 50% of deaths, 5x higher than Japan)
“Disease of Affluence”
Gruel “Hardening”: Incidence
Incidence of Atherosclerosis is tracked using the incidence of IHD
- Peak death of IHD was in 1968
Gruel “Hardening”: Pathogenesis (Historical Theories)
1) Insudation Hypothesis (Source of LDL’s)
2) Reaction to Chronic Endothelial Injury (PDGF)
3) Monoclonal Hypothesis (source of smooth m. Cells)
4) Encrustation Hypothesis (thrombus > atherosclerosis)
5) Hemodynamic Hypothesis (atherosclerosis accelerated w/ HTN)
Atherosclerosis: Pathology
- Fatty streak
- Simple fibrous atheromatous plaque
Atherosclerosis: Complicated Plaque Complications
1) Plaque Rupture
2) Plaque Ulceration
3) Thrombus Formation
4) Hemorrhage into Plaque
5) Calcification
6) Aneurysm Formation
Atherosclerosis: General Complications
- chronic endothelial injury
- monocytes & smooth muscle cells in the Intima
- Insudation of fats
- Macrophages produce cytokines
What do Myointimal cells do in the unifying hypothesis of Atherosclerosis?
- engulf lipid -> fatty streak
- form cap over lesion -> lipid accumulates producing atheromatous plaque
Atherosclerosis: Risk factors
- Old age
- Male > Female
- Heredity
- Hyperlipidemia
- DM, HTN & Obesity
- Smoking
Levels of HTN, Smoking, Cholesterol, triglycerides, LDL, HDL & LDL/HDL ratio as Risk Factors for Atherosclerosis (increased IHD risk)
HTN: increases 60%
Smoking: 1 pack/day increases 200%
Cholesterol: > 240mg/dl
Triglycerides: > 250mg/dl
LDL: > 160 mg/dl
HDL: < 35mg/dl
LDL/HDL ratio: < 3.7
Atherosclerosis: Protective factors
1) Exercise
2) Estrogens
3) Low Alcohol consumption
Atherosclerosis: Locations in the Body
(1) Abdominal Aorta
(2) Coronary Arteries
(3) Popliteal Arteries
(4) Internal Carotid Arteries
(5) Circle of Willis
Atherosclerosis: Clinical Features
1) Sudden Narrowing
2) Chronic Occlusion
3) Embolism
4) Aneurysm
Systemic Hypertension: Definition
Diastolic: > 90mm/Hg
Systolic: > 140mm/Hg
Systemic Hypertension: Epidemiology
- 25% of population
- Older people
- females > males
- blacks > caucasians
Primary Hypertension (“essential”)
- Multifactorial in Origin (genetics & environment)
- 95% of all systemic hypertension
- Different factors in different patients
Secondary Hypertension: Origin, % of cases
- Renal Origiin
- 5% of all systemic hypertension’s
Secondary Hypertension: Other Causes & Treatment
- Endocrine, Vascular & Neurogenic causes
- BCP & allergy meds
Benign Hypertension: % of cases, Complications
- 90% of all patients
- compatible w/ life
- Cardiac, CVA & renal complications
- accelerates Atherosclerosis
Malignant Hypertension: % of cases, What is it & what it produces
- 5% of cases
- rapid rising BP (diastolic > 120mm/Hg)
- Produces Renal Failure & Retinal changes
- Risk for cerebral hemorrhage
Regulation of Normal BP Equations
BP = CO * PR
BP = (HR * SV) * PR
& Renin-Angiotensin System
Benign vs Malignant Arteriosclerosis
Benign: Hyaline
Malignant: Hyperplastic
Arteriosclerosis: Clinical Features
- Asymptomatic
- HTN Heart Disease
- Hypertensive Retinopathy (Cotton wool spots)
- ATHEROSCLEROTIC THROMBOSIS/INFARCTION
- CEREBRAL HEMORRHAGE (strokes)
- L. VENTRICULAR FAILURE
- MALIGNANT NEPHROSCLEROSIS (renal failure)
Examples of Saccular Aneurysms
Mytotic & Congenital
Examples of Fusiform Aneurysms
Atherosclerosis & Syphilitic Aortits
Example of Dissecting Aneurysms
Cystic Medial Necrosis
Aneurysms: Clinical Consequences
1) Rupture/Hemorrhage
2) Thrombosis/Embolism
3) Compression of Surrounding Structures
4) Circle of Willis-compress cranial nn.
5) Abdominal Aneurysm-bone erosion
6) Syphilitic aneurysm-erode sternum
7) trachea-dyspnea
8) esophagus-dysphagia
Vasculitides: 2 MC Pathogenic Mechanisms
1) immune mediated inflammation
2) direct vascular invasion by pathogens
Vasculitides: Refers to & type of condition
- Arteries, Veins & Venule WALLS
- Immune complex type of condition
Vasculitides: Immune Complex Mechanism Details
- found in biopsies lesion along w/ complement & virus antigens
- Hep B surface antigen (some patients)
- HCV/RNA & Cryoprecipitates (some patients)
Major Vasculitis Syndromes
1) Polyarteritis nodosa
2) Wegener’s granulomatosis
3) Hypersensitivity angiitis
4) Temporal arteritis
5) Kawasaki’s arteritis
6) Thromboangiitis obliterans
7) Takayasu’s disease
8) Syphilitic aortitis
Raynaud Disease
- primary condition
- young females initially
- no underlying condition
- vessels over-react to the cold & SPASM (do not vasoconstrict)
Raynaud Phenomenon
- secondary condition
- any age in either male or female
- Seen w/ Bronchogenic Carcinoma
- Seen w/ Collagen diseases (SLE, RA)
- Cryoglobulins present
Varicose Veins: Etiology
- Myxomatous degeneration of the valve
- Increased abdominal pressure
Varicose Veins: Effects
- Varicose or Stasis Dermatitis
- Varicose Ulcers
- Thrombophlebitis
What are Hemorrhoids?
Abnormal downward displacement of anal cushions causing venous dilation
What are Esophageal varices?
- Develop when normal blood flow to liver is blocked by clot or scar
- Increased Portal pressure (can rupture)
What is Varicocele?
- MC cause of primary & secondary infertility in men
- Vascular abnormality of testicular venous drainage
- mass in veins of pampiniform & cremasteric venous plexus
Phlebothrombosis: What is it?
Thrombosis without inflammation
- usually in deep veins of legs produced by immobilization (especially in hypercoagulability)
Phlebothrombosis: Associated with…
1) Cardiac failure
2) Pregnancy
3) Oral COntraceptives
4) Post Surgery
5) Trauma
Thrombophlebitis: Occurs…
- thrombosis produced secondary to vein inflammation
- in varicose veins of legs
- in association with vasculitis
Migratory Thrombophlebitis Occurs in association with:
Neoplasms such as Carcinoma of the Pancreas
What is a Capillary Hemangioma?
- Benign vascular lesion
- Hamartomatous proliferation of vascular endothelial cells
What is a Cavernous Hemangioma?
- Solitary usually
- composed of: multivascular channels lined by single layer of flat epithelium
- supported by: fibrous septa
Examples of Capillary Hemangiomas
- Juvenile hemangioma
- Pyogenic Granuloma
Examples of Cavernous Hemangiomas
- Retina
- Brain
- Spinal
What is a Glomus Tumor?
Tumor of neuromyoarterial temperature receptor often found under nails & is extremely painful
Angiosarcoma: Etiology
- Endothelial cells that line sinusoids
- Result of a chemical exposure
- Often occur in the Liver
Angiosarcoma: Chemical involvement
Chemical exposure to: Thorotrast & PVC
Arsenics may involve the skin
Kaposi Sarcomas: Associated with
AIDS due to HIV Infection
4 major types of Kaposi Sarcomas
1) Classic European KS
2) African KS
3) Transplant KS
4) AIDS associated KS
Elephantiasis: Etiology
Caused by infection of parasite Nematodes (roundworms) that is transmitted through mosquito bites
Elephantiasis: Clinical Features
- Gross enlargement/Swelling of area of the body due to accumulation of fluid
- Arms & Legs MC
- Skin can be: dry, thick, ulcerated, dark & pitted
Kaposi Sarcoma: Clinical Features
- Painess purplish spots on the legs, feet or face
- can lead to painful swelling of legs & feet
