Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Systems Pathology > Exam 3 [Diseases Of Blood & Lymph] > Flashcards

Exam 3 [Diseases Of Blood & Lymph] Flashcards

1
Q

Clinical Features of Anemias

A

1) Pallor of Skin & Mucous Membranes
2) Weakness, Fatigue, Lethargy, Dizziness
3) Hyper Dynamic Circulation
4) Anginal Pain or Cardiac Failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

3 Types of Anemias

A

1) Increased Blood Loss
2) Increased rate of Destruction (Hemolytic)
3) Decreased rate of Production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acute Anemia Due to Blood loss Features

A
  • Hypovolemia
  • Hemodilution
  • Reticulocytosis
  • Nomocytic
  • Normochromic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Chronic Anemia Due to Blood Loss Features

A
  • Iron deficiency
  • Hypochromic
  • Microcytic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Anemia due to Increasd Rate of Destruction (Hemolytic)

A
  • Reduced life span of RBC’s (<120 days)
  • Accelerated red cell destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Evidence of Hemolysis in Anemia due to Increasd Rate of Destruction (Hemolytic)

A

1) Increased Unconjugated Bilirubin -> jaundice
2) Damaged Red cells
3) Erythroid Hyperplasia of Bone Marrow
4) Increased Immature red cells in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of Anemia due to Increasd Rate of Destruction (Hemolytic)

A

Intrinsic: red cell deficits
Extrinsic: abnormal hemolytic mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hemolytic Anemias due to Intrinsic Causes

A

1) Sickle cell
2) Thalassemia
3) Hereditary Spherocytosis
4) Glucose 6-Phosphate Dehydrogenase Deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is Hereditary Spherocytosis

A

Dominant inheritance of spherical red cells due to alterations in permeability of cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Childhood Clinical Features of Hereditary Spherocytosis

A
  • Hemolysis
  • Decreased red cell life span
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Adulthood Clinical Features of Hereditary Spherocytosis

A
  • Hemolysis
  • Anemia
  • Jaundice & Pigment Gall Stones
  • Erythoid Hyerplasia of Bone Marrow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Clinical remission in Hereditary Spherocytosis

A

Splenectomy produces remission in most cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a “Sickle Cell”

A
  • Contains HbS instead of HbA
  • AA substitution causes decreased solubility of hemoglobin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Reduced state HbS =

A

Long, slender crystalline masses causing distortion of red cell born in Vito and in vitro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pathogenesis of Sickle Cell Disease

A
  • hemolytic anemia
  • capillary obstruction due to thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Series of events in Sickle Cell Disease

A

Increased Hypoxia -> Sickling -> RBC Destruction -> Hypoxia -> fatty degeneration of lower kidney & spleen -> enlargement from trapped damaged RBC’s -> forms atrophic fibrous mass (autoplenectomy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Sickle Cell Disease Findings

A

1) Normochromic, Normocytic
2) Anisocytosis & Poikilocytosis
3) Increased Reticulocytes & Polymorphs
4) Erythroid Hyperplasia in Marrow
5) + Sickling test
6) Hemoglobin Electrophoretic pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Clinical Features of Sickle Cell Disease

A
  • Onset in 2nd year of life
  • Susceptible to Pneumococcal Pnuemonia, Salmonella, Osteomyelitis, bacterial meningitis
  • Erythroid Hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Symptoms of Sickle Cell Disease

A
  • Fever
  • Bone, Joint & Abdominal Symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Homozygous vs. Heterozygous Sickle Cell Disease

A

Homo: 80-100% of Hb is HbS, decreased PO2 Sickling in vivo
Hetero: 10% of black Americans carry HbS gene
.2% have Sickle Cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Sickle Cell Trait

A

Heterozygous Hgb
- Increased resistance to malaria parasite
- asymptomatic until exposed to low PO2
- HbS = 25-40% of hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Thalassemias

A
  • Mediterranean = Sea of Blood
  • alpha or beta chain issue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cells of alpha Thalassemias

A
  • Alpha chain deficiency
  • beta & gamma form polymers
  • inclusion bodies
  • red cells = thinner w/ short life span
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pathogenesis of Beta Thalassemia

A
  • Excessive Hemolysis
  • Homozygous: (Cooley’s Anemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Clinical Features of Beta Thalassemia

A

1) Splenomegaly
2) Mild jaundice
3) Erythroid Hyperplasia
4) Pigment Gallstones
5) progressive Anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

4 Clinical Gene Syndromes of Alpha-Thalassemia

A

1) -A/AA = asymptomatic carrier
2) -A/A- = thalassemia minor
3) - -/-A = thalassemia major (Hgb H disease)
4) - -/- - = fatal in-utero (hydros fetalis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

G-6-PD Deficiency combined with drugs causing Hemolytic Anemia

A

Antimalarials: quinine
Antimicrobials: nitrofurantoin & sulfonamides
Analgesics: aspirin & phenacetin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

G-6-PD Deficiency Affects:

A
  • 10% American blacks
  • “Favinism” in Middle East (eating the bean Vinca Fava)
  • Heinz Bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Extrinsic Hemolytic Anemias

A

1) Infections - Malaria
2) Toxins - heavy metals, drugs, exotoxins
3) Autoimmune Hemolytic Disease
4) Blood group incompatibilities
5) Hypersplenism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

2 processes that cause Anemia in Malaria

A

1) parasite grows inside RBC during RBC lysis
2) Increased macrophages -> increased phagocytosis of nonparisited cell -> increased anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Mycoplasma Pneumoniae is…

A

Self-limiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

2 Classifications of Immunohemolytic Anemias

A

1) Warm antibodies: hemolysis @ body temperature
2) Cold antibodies: Raynaud’s & hemolysis only in the cold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Blood Group Incompatibilities

A
  • Due to Rh incompatibility
  • Normal 1st pregnancy
  • more pregnancies = greater effect on fetus (erythroblastosis fetalis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Anemias due to decreased RBC production

A

1) iron Deficiency
2) Anemia of Chronic Disease
3) Megoblastic
4) Aplastic
5) Marrow Replacement
6) Anemia of Chronic Renal Failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Iron Deficiency Etiology

A
  • Diet Deficiency
  • Increase demand for iron
  • malnutrition
  • chronic blood loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Iron deficiency pathology

A
  • Anemia
  • hypochromic, microcytic
  • atrophy of epithelial surfaces
  • Koilonychia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Anemias of Chronic disease

A

1) Chronic Infections
2) Autoimmune Diseases
3) Malignant Neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Megaloblastic Anemias Etiology

A

Vitamin B12 & Folic Acid deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Megaloblastic Anemia Pathology

A
  • Megaloblasts
  • Intramedullary hemolysis OR ineffective erythropoiesis
  • Macrocytosis with HOWELL-JOYYL BODIES, DNA fragments
  • Hypersegmented neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Aplastic anemias Etiology

A

Reactions to drugs & chemicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Aplastic anemias Pathology/Clinical features

A
  • Anemia (normocytic & normochromic)
  • Granulocytopenia -> infectious/oral ulceration
  • Thrombocytopenia -> bleeding tendency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Polycythemia (Rubra) Vera Etiology

A

Idiopathic (> 50, M > F)
- All blood elements are increased
- uncontrolled production of marrow elements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Pathology of Polycythemia (Rubra) Vera

A

Increase blood volume -> organ congestion
Increased blood viscosity -> vascular thrombosis, kidney, spleen, heart infarcts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Polycythemia (Rubra) Vera: Bleeding Tendency

A

Defective platelet function
Increased platelets, but dont work properly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Polycythemia (Rubra) Vera: Increased acid in Blood due to…

A

Turnover of Nucleic acids from normoblasts & megakaryocytes
(Gout in minority of patients)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Polycythemia (Rubra) Vera: Clinical Features

A

-Dark, Dusty red color on face
- prominent temporal artery
- big eye vessels on retina
- Cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Etiology of Infectious Mononucleosus

A

Epstein-Barr Virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Clinical Presentation of Infectious Mononucleosus

A
  • Swollen Lymph
  • Fever
  • sore throat
  • extreme fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Pathology of Infectious Mononucleosus

A

-EBV infects B lymphocytes
- Abnormal lymphocytes develop from CD8+ T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Acute Lymphoblastic Leukemia: Age Group & Cell Type

A
  • Young children (3-4 years old)
  • Lymphoblasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Acute Myeloblastic Leukemia: Age Group & Cell Type

A
  • Young Adults (15-20 years old)
  • Myeloblasts: Auer’s Rods
    **May not have lymph node involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Chronic Lymphocytic Leukemia: Age Group & Cell Type

A

> 60 years
Small mature lymphocytes (usually B-cell)
Organ Enlargement
**Most Benign of 4 major leukemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Chronic Myelocytic Leukemia: Age Group & Cell Type

A
  • (40-50 years old)
  • Mature neutrophils
    ** Massive Splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Karyotype of Chronic Myelocytic Leukemia

A

Philidelphia Chromosome
- part of Chromosome 22 translocated to chromosome 9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Chronic Phase of Chronic Myelocytic Leukemia

A
  • (3-10 years)
  • 60-80% go into blasting crisis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Hodkin’s Disease: Cell Type & Etiology

A

Reed-Sternberg cell
- large bi-nucleated cell w/ prominent nucleate

Viral including EBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Staging of Hodkin’s Disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Systemic symptoms of Hodgkin’s Disease

A
  • Fever
  • Night sweats
  • Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Non-Hodgkin’s Lymphomas: What is it & Etiology

A

Neoplasticism proliferation of Lymphoid tissue w/o Reed-Sternberg Cells

Etiology: viruses (Burkitt’s, Epstein Barr, Herpes Type 4, autoimmune & immunodeficiencies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Plasma Cell Dyscrasia

A
  • Growth of a clone of plasma cells
  • Middle aged-elderly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Multiple Myeloma: Cell Type

A

IgG (MC) & IgA
(Immunoglobins accumulate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Multiple Myeloma: Urine

A
  • Can have Bence-Jones proteins
  • Calcium
  • Polyuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Multiple Myeloma: Symtoms

A
  • Anemia
  • Bone Pain
  • Path fractures
  • weakness, Lethargy
  • Renal stones & insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Multiple Myeloma: Pathology

A

Medullary Cavity Erosion -> Ca2+ in blood -> hypercalcemia

  • Increased susceptibility to infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Histiocytosis X facts

A

(A.k.a. Langerhans cells histiocytosis)
HX Body: Birbeck’s granules on EM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Histiocytosis X Diseases

A

1) Eosinophilic Granuloma
2) Hand-Schuller-Christian Disease
3) Letterer-Siwe Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Eosinophilic Granuloma

A
  • Unifocal or Singular
  • Bone Marrow
  • Males: Skull or Ribs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Hand-Schuller-Christian Disease

A
  • Multifocal proptosis
  • Bone lesions in Skull
  • Diabetes Insipidus
  • ADH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Lettered-Siwe Disease

A
  • Acute Disseminated form of Histiocytosis X
  • Lesions of Bone + Lymphoid Tissue
  • Children
  • Fever, skin rashes, splenomegaly, lymphadenopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Diseases of Hemostasis

A

1) Senile Purpura
2) Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome)
3) Symptomatic purpura
4) Hypersensitivity Angiitis (anaphylactoid purpura)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome): Presentation

A
  • Disease of venules & capillaries
  • around mouth & in oral cavity/sinuses
  • recurrent hemorrhages getting worse with age
  • Initially: Epistaxis
  • Later: G.I. Hemorrhage
72
Q

Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome): Genetics

A

Autosomal Dominant

73
Q

Hypersensitivity Angiitis (anaphylactoid purpura): How it Shows up & Population

A
  • allergic damage to vessel wall
  • follows streptococcal infections
  • adults with exposure to drugs
74
Q

Senile Purpura: What is it? & Population

A
  • Lack of Collagen supporting the blood vessel
  • Elderly
75
Q

Symptomatic PurPura is seen with

A

Other Diseases like Septicemias

76
Q

Etiology of Disseminated Intravascular Coagulation

A

Caused by inflammation from an infection, injury or illness
- (MC: sepsis)
- Surgery/trauma
- cancer
- blood infections
- pancreatitis

77
Q

Pathology of Disseminated Intravascular Coagulation

A
  • massive systemic intravascular activation of coagulation
  • widespread deposition of “fibrin” in circulation compromising blood supply to various organs
78
Q

Disseminated Intravascular Coagulation leads to…

A

Consumptive Coagulopathy

79
Q

What is Thrombocytopenia?

A

Decreased platelets below 150,000/ml
(Below 50,000 produces hemorrhage)

80
Q

Cause of Thrombocytopenia

A

1) Decreased Production
2) Increase Destruction
3) Splenic Sequestration

81
Q

Thrombocytopenia caused by Decreased Production

A

Aplastic Anemia
leukemias
Radiation/Chemicals

82
Q

Thrombocytopenia caused by Increased Destruction

A

2 forms of Idiopathic Thrombocytopenia Purpura

83
Q

2 forms of Idiopathic Thrombocytopenia Purpura

A

1) Acute ITP in Childhood
2) Chronic ITP in Adulthood

84
Q

Acute ITP in Childhood

A
  • Follows viral illness
  • Platelet count = < 20,000/ml
  • Sudden onset of Petechial & Purpura
  • Major Risk: Intracranial Hemorrhage
85
Q

Chronic ITP in Adults

A
  • Associated w/ Collagen Disease
  • Platelet count = < 100,000/ml
  • Bleeding episodes (not life-threatening)
  • Improved w/ Glucocorticoids
86
Q

Drug Induced Increased Destruction Seen in Idiopathic Thrombocytopenia Purpura

A

[Quinidine, Sulfonamides, Cimetidine]
- Idiosyncratic Response
- Appears weeks or months after agent

87
Q

Thrombocytopenia is severe & symptomatic with count of…

A

20,000/ml

88
Q

Hemophilia A: Genetics & Factors Involved

A
  • X linked recessive
  • Gene for the VIII OR IX protein (produces too little)
    [LACK OR TOTAL ABSENCE OF COAGULATION VIII]
89
Q

Hemophilia B: Genetics & Factors Involved

A
  • X linked recessive
  • Gene for the VIII OR IX protein (produces too little)
    [SHORTAGE OF COAGULATION FACTOR IX]
90
Q

Von Willebrand: Genetics & Source

A

-On Autosomal Chromosome 12
- Mutation of the VWF gene

91
Q

Von Willebrand: Features of Deficiency

A
  • VWF gene makes blood clotting protein called Von Willebrand Factor
  • Slows the blood clotting process
  • Prolonged bleeding after an injury
92
Q

Von Willebrand: Function

A

Formation of blood clots to prevent further blood loss

93
Q

Function of Thromboxane A

A
  • Amplifies platelet aggregation to the site of injury
  • Blood Clot Formation (Thrombosis)
94
Q

Thromboxane A’s Relationship w/ Aspirin

A

Low-dose long-term aspirin use irreversibly blocks formation of Thromboxane A2 in platelets
(Producing inhibitory effect on platelet aggregation)

95
Q

Congenital Diseases of Blood Vessels

A

1) Developmental Aneurysms
2) A-V Fistulas
3) Hemangiomas
4) Coarctation of the Aorta
5) Marfan’s
6) Developmental Aneurysms

96
Q

Berry Aneurysms

A
  • Circle of Willis
  • Vessel stretches from increased BP
  • hemorrhage inside the Skull
97
Q

A-V Fistulas or Malformations

A
  • Arterial vessels connect directly to venous vessels
  • Veins have increased pressure -> may rupture
  • Rupture likely w/ hypertension
98
Q

A-V Fistulas or Malformations: MC Location

A

Branches of Middle Cerebral

99
Q

Hemangiomas: 2 Types

A

Capillary & Cavernous

100
Q

Hemangiomas associated with what Syndrome?

A

Sturgeon-Weber

101
Q

Infantile (pre-ductal) Coarctation of the Aorta

A
  • Narrowing of Aorta proximal to Ductus
  • Lower 1/2 of body is supplied by Pulmonary Artery through Ductus Arteriosus
  • Cyanotic
102
Q

Adult (post-ductal) Coarctation of the Aorta: More Common in patients…

A

1) w/ Turner’s Syndrome
2) that are Male

103
Q

Adult (post-ductal) Coarctation of the Aorta: Pathological features

A
  • Coarctation after Ductus Arteriosus
  • Lower body gets blood from narrowed Aorta & collateral circulations
  • Asymptomatic until Adult
104
Q

Adult (post-ductal) Coarctation of the Aorta: Clinical Signs/Symptoms

A
  • Delayed & Low Pressure Femoral Pulse
  • Intermittent Claudication w/ exercise
  • Hypertension from Renin production
  • Notching of the Ribs (on X-Ray)
105
Q

Adult (post-ductal) Coarctation of the Aorta: Associations

A

1) Bicuspid Aortic Valve
2) Berry Aneurysms

106
Q

Marfan’s Syndrome: What is it?

A
  • CT Disease w/ production issue of Fibrillin
107
Q

Marfan’s Syndrome: Areas MCly Affected

A
  • Aorta
  • Cardiac Valves
  • Eyes
  • Skeletal System
108
Q

Marfan’s a Syndrome: Tests

A

Steinberg: thumb extends beyond flexed fingers
Walker-Murdough: thumb & 5th finger overlap around wrist

109
Q

Marfan’s Syndrome: Eye Pathology

A

Dislocation of the Lens from the Suspensory Ligament

110
Q

Marfan’s Syndrome: Cardio pathology

A

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

111
Q

Ehlers-Danilo’s Syndrome: Pathological Effects

A
  • Affect collagen formation
  • hyperexstensible skin & joints
112
Q

Ehler’s-Danlos Syndrome: Clinical Signs

A
  • Bleeding, poor healing, retinal detachment, dislocated lens, mitral valve prolapse, aneurysms, blue sclera
  • Large scars over knees/elbows
113
Q

Hurler’s Syndrome: AKA’s & Genetics

A
  • AKA gargoylism & Mucopolysaccharidosis I
  • Autosomal Recessive
114
Q

What is Hurler’s Syndrome?

A

Enzyme deficiency leading to excessive GAG’s in bone, brain & liver

115
Q

Hurler’s Syndrome: Clinical Features

A
  • Facial Chgs
  • organomegally
  • corneal opacity
  • severe MR
116
Q

Hurler’s syndrome: Life expectancy

A

10 years (Death 2nd to cardio respiratory disease)

117
Q

Hurler’s syndrome: Medications

A

Chondroitin, Dermatan & Heparan Sulfate

118
Q

Arteriosclerosis: 3 diseases

A

1) Medial Calcification Sclerosis (Mockenberg’s)
2) Arteriosclerosis
3) Atherosclerosis
(2 & 3 are interchangeable)

119
Q

Monckeberg’s Medial Calcification Sclerosis: Affects what and who?

A
  • Tunica Media of muscular arteries (does not obstruct)
  • People over 50
120
Q

Monckeberg’s Medial Calcification Sclerosis: Pathological Findings

A
  • Calcium presence can be seen on X-Ray
  • Doesn’t produce clinical problems
  • Artery may have atherosclerosis
121
Q

Hyaline Arteriolosclerosis

A
  • Accumulation of abnormal material in the Intima of ARTERIOLES (narrows the Lumen)
  • Associated w/ DM & Hypertension
122
Q

Hyperplastic Arteriosclerosis

A
  • Thickening of MEDIA, Narrows LUMEN, stiffens WALL
  • Associated w/ rapid increasing hypertension (malignant hypertension: Diastolic >120)
123
Q

Gruel “Hardening”: MC What?

A

Most important form of arteriosclerosis as cause of mortality (in the west: 50% of deaths, 5x higher than Japan)
“Disease of Affluence”

124
Q

Gruel “Hardening”: Incidence

A

Incidence of Atherosclerosis is tracked using the incidence of IHD
- Peak death of IHD was in 1968

125
Q

Gruel “Hardening”: Pathogenesis (Historical Theories)

A

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)

126
Q

Atherosclerosis: Pathology

A
  • Fatty streak
  • Simple fibrous atheromatous plaque
127
Q

Atherosclerosis: Complicated Plaque Complications

A

1) Plaque Rupture
2) Plaque Ulceration
3) Thrombus Formation
4) Hemorrhage into Plaque
5) Calcification
6) Aneurysm Formation

128
Q

Atherosclerosis: General Complications

A
  • chronic endothelial injury
  • monocytes & smooth muscle cells in the Intima
  • Insudation of fats
  • Macrophages produce cytokines
129
Q

What do Myointimal cells do in the unifying hypothesis of Atherosclerosis?

A
  • engulf lipid -> fatty streak
  • form cap over lesion -> lipid accumulates producing atheromatous plaque
130
Q

Atherosclerosis: Risk factors

A
  • Old age
  • Male > Female
  • Heredity
  • Hyperlipidemia
  • DM, HTN & Obesity
  • Smoking
131
Q

Levels of HTN, Smoking, Cholesterol, triglycerides, LDL, HDL & LDL/HDL ratio as Risk Factors for Atherosclerosis (increased IHD risk)

A

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

132
Q

Atherosclerosis: Protective factors

A

1) Exercise
2) Estrogens
3) Low Alcohol consumption

133
Q

Atherosclerosis: Locations in the Body

A

(1) Abdominal Aorta
(2) Coronary Arteries
(3) Popliteal Arteries
(4) Internal Carotid Arteries
(5) Circle of Willis

134
Q

Atherosclerosis: Clinical Features

A

1) Sudden Narrowing
2) Chronic Occlusion
3) Embolism
4) Aneurysm

135
Q

Systemic Hypertension: Definition

A

Diastolic: > 90mm/Hg
Systolic: > 140mm/Hg

136
Q

Systemic Hypertension: Epidemiology

A
  • 25% of population
  • Older people
  • females > males
  • blacks > caucasians
137
Q

Primary Hypertension (“essential”)

A
  • Multifactorial in Origin (genetics & environment)
  • 95% of all systemic hypertension
  • Different factors in different patients
138
Q

Secondary Hypertension: Origin, % of cases

A
  • Renal Origiin
  • 5% of all systemic hypertension’s
139
Q

Secondary Hypertension: Other Causes & Treatment

A
  • Endocrine, Vascular & Neurogenic causes
  • BCP & allergy meds
140
Q

Benign Hypertension: % of cases, Complications

A
  • 90% of all patients
  • compatible w/ life
  • Cardiac, CVA & renal complications
  • accelerates Atherosclerosis
141
Q

Malignant Hypertension: % of cases, What is it & what it produces

A
  • 5% of cases
  • rapid rising BP (diastolic > 120mm/Hg)
  • Produces Renal Failure & Retinal changes
  • Risk for cerebral hemorrhage
142
Q

Regulation of Normal BP Equations

A

BP = CO * PR
BP = (HR * SV) * PR
& Renin-Angiotensin System

143
Q

Benign vs Malignant Arteriosclerosis

A

Benign: Hyaline
Malignant: Hyperplastic

144
Q

Arteriosclerosis: Clinical Features

A
  • Asymptomatic
  • HTN Heart Disease
  • Hypertensive Retinopathy (Cotton wool spots)
  • ATHEROSCLEROTIC THROMBOSIS/INFARCTION
  • CEREBRAL HEMORRHAGE (strokes)
  • L. VENTRICULAR FAILURE
  • MALIGNANT NEPHROSCLEROSIS (renal failure)
145
Q

Examples of Saccular Aneurysms

A

Mytotic & Congenital

146
Q

Examples of Fusiform Aneurysms

A

Atherosclerosis & Syphilitic Aortits

147
Q

Example of Dissecting Aneurysms

A

Cystic Medial Necrosis

148
Q

Aneurysms: Clinical Consequences

A

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

149
Q

Vasculitides: 2 MC Pathogenic Mechanisms

A

1) immune mediated inflammation
2) direct vascular invasion by pathogens

150
Q

Vasculitides: Refers to & type of condition

A
  • Arteries, Veins & Venule WALLS
  • Immune complex type of condition
151
Q

Vasculitides: Immune Complex Mechanism Details

A
  • found in biopsies lesion along w/ complement & virus antigens
  • Hep B surface antigen (some patients)
  • HCV/RNA & Cryoprecipitates (some patients)
152
Q

Major Vasculitis Syndromes

A

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

153
Q

Raynaud Disease

A
  • primary condition
  • young females initially
  • no underlying condition
  • vessels over-react to the cold & SPASM (do not vasoconstrict)
154
Q

Raynaud Phenomenon

A
  • secondary condition
  • any age in either male or female
  • Seen w/ Bronchogenic Carcinoma
  • Seen w/ Collagen diseases (SLE, RA)
  • Cryoglobulins present
155
Q

Varicose Veins: Etiology

A
  • Myxomatous degeneration of the valve
  • Increased abdominal pressure
156
Q

Varicose Veins: Effects

A
  • Varicose or Stasis Dermatitis
  • Varicose Ulcers
  • Thrombophlebitis
157
Q

What are Hemorrhoids?

A

Abnormal downward displacement of anal cushions causing venous dilation

158
Q

What are Esophageal varices?

A
  • Develop when normal blood flow to liver is blocked by clot or scar
  • Increased Portal pressure (can rupture)
159
Q

What is Varicocele?

A
  • MC cause of primary & secondary infertility in men
  • Vascular abnormality of testicular venous drainage
  • mass in veins of pampiniform & cremasteric venous plexus
160
Q

Phlebothrombosis: What is it?

A

Thrombosis without inflammation
- usually in deep veins of legs produced by immobilization (especially in hypercoagulability)

161
Q

Phlebothrombosis: Associated with…

A

1) Cardiac failure
2) Pregnancy
3) Oral COntraceptives
4) Post Surgery
5) Trauma

162
Q

Thrombophlebitis: Occurs…

A
  • thrombosis produced secondary to vein inflammation
  • in varicose veins of legs
  • in association with vasculitis
163
Q

Migratory Thrombophlebitis Occurs in association with:

A

Neoplasms such as Carcinoma of the Pancreas

164
Q

What is a Capillary Hemangioma?

A
  • Benign vascular lesion
  • Hamartomatous proliferation of vascular endothelial cells
165
Q

What is a Cavernous Hemangioma?

A
  • Solitary usually
  • composed of: multivascular channels lined by single layer of flat epithelium
  • supported by: fibrous septa
166
Q

Examples of Capillary Hemangiomas

A
  • Juvenile hemangioma
  • Pyogenic Granuloma
167
Q

Examples of Cavernous Hemangiomas

A
  • Retina
  • Brain
  • Spinal
168
Q

What is a Glomus Tumor?

A

Tumor of neuromyoarterial temperature receptor often found under nails & is extremely painful

169
Q

Angiosarcoma: Etiology

A
  • Endothelial cells that line sinusoids
  • Result of a chemical exposure
  • Often occur in the Liver
170
Q

Angiosarcoma: Chemical involvement

A

Chemical exposure to: Thorotrast & PVC
Arsenics may involve the skin

171
Q

Kaposi Sarcomas: Associated with

A

AIDS due to HIV Infection

172
Q

4 major types of Kaposi Sarcomas

A

1) Classic European KS
2) African KS
3) Transplant KS
4) AIDS associated KS

173
Q

Elephantiasis: Etiology

A

Caused by infection of parasite Nematodes (roundworms) that is transmitted through mosquito bites

174
Q

Elephantiasis: Clinical Features

A
  • Gross enlargement/Swelling of area of the body due to accumulation of fluid
  • Arms & Legs MC
  • Skin can be: dry, thick, ulcerated, dark & pitted
175
Q

Kaposi Sarcoma: Clinical Features

A
  • Painess purplish spots on the legs, feet or face
  • can lead to painful swelling of legs & feet

Systems Pathology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions