test 8 Flashcards
1
Q
increased hydrostatic pressure can be caused by
A
CHF, portal HTN, renal retention of salt and water, venous thrombosis
2
Q
hypoalbuminemia and decreased colloid osmotic pressure are caused by
A
liver disease, nephrotic syndrome, kwashiorkor
3
Q
lymphatic obstruction (lymphedema) caused by
A
tumor, surgical removal of lymph nodes, parasitic infestation (filariasis-> elephantiasis)
4
Q
increased endothelial permeability caused by
A
inflammation/histamine, type I hypersensitivity runs, drugs
5
Q
increased interstitial sodium caused by
A
increase Na+ intake, renal failure, primary hyperaldosteronism
6
Q
myxedema
A
specialized form of tissue swelling due to increased extracellular glycosaminoglycans
(from thyroid disease)
7
Q
anasarca
A
severe generalized edema
8
Q
effusion
A
fluid w/in body cavities (tends to collect into potential spaces; i.e. pleural space)
9
Q
types of edema fluid
A
transudate; exudate
10
Q
transudate
A
edema w/ low protein content
clear/pale no tissue fragments; thin alkaline low cell count low enzyme count no bacteria
11
Q
exudate
A
edema fluid w/ high protein content & cells
cloudy, white, yellow, or red thick; tissue fragments acidic many WBCs and RBCs may have bacteria
12
Q
types of exudates (4)
A
purulent (pus)
fibrinous
serous
hemorrhagic (sanguineous)
13
Q
fibrinous exudate
A
collagen exudates in body cavities
14
Q
sanguineous exudate
A
blood in exudate
15
Q
purulent (suppurative) exudate
A
increased art of pus and/or neutrophils; necrotic cells and edematous fluid; i.e. meningitis, cephalitis
16
Q
serous exudate
A
thin fluid derived from either serum or secretions of mesothelial cells (effusion)
often combines w/ sanguineous
17
Q
ascites
A
gastroenterological term for an accumulation of fluid in the peritoneal cavity
18
Q
condition that leads to ascites
A
cirrhosis
19
Q
exudates… pitting or not
A
no pitting
20
Q
hyperemia
A
active increase in the volume of blood in tissues
21
Q
causes of hyperemia
A
arteriolar dilation
22
Q
congestion
A
passive increase in the volume of blood in tissues; us. accompanied by edema
23
Q
causes of congestion
A
impaired venous flow from tissues eg cardiac failure, venous obstruction
24
Q
complications of congestion
A
cyanosis/hypoxia
25
hemostasis
sequence of events leading to the cessation of bleeding by the formation of a stable fibrin-platelet hemostatic plug
involves interactions b/w the vascular wall, platelets, and coagulation system
26
clotting is a balance b/w which 2 opposing forces
1. formation of a stable thrombus; 2. factors causing fibrinolysis of the clot
27
transient vasoconstriction is mediated by
endothelin-1
28
5 thrombogenic factors
changes in BF cause turbulence and stasis, which favors clot formation
release of tissue factor from injured cell activates factor VII (extrinsic pathway) from damaged cells
exposure of thrombogenic sub endothelial collagen activates factor XII (intrinsic pathway) always in blood
release of vWF which binds to exposed collagen and facilitates platelet adhesion
decreased endothelial synthesis of antithrombogenic substances (prostacyclin, NO2, TPA, and thrombomodulin)-->allows for clots
29
endothelin does what 5 things
proliferation
fibrosis
vasoconstriction
hypertrophic
inflammation
30
3 steps of platelets
platelet adhesion
platelet activation
platelet aggregation
31
platelet adhesion
vWF adheres to sub endothelial collagen
platelets then adhere to vWF by **glycoprotein Ib**
32
platelet activation
platelet undergo a shape change and degranulation occurs
platelet synthesis of **thromboxane A2***
membrane expression of phospholipid complex which is an important substrate for coagulation cascade
33
platelet aggregation
additional platelets are recruited from bloodstream
ADP and thromboxane A2 are potent mediators of aggregation
platelets bind to each other by binding to fibrinogen using **Gp IIb-IIIa***
34
bernard-soulier syndrome
autosomal recessive
deficiency of platelet **Gp Ib**
**defective platelet adhesion**
35
glanzmann thrombasthenia
AR
deficiency of **Gp IIb-IIIa**
**defective platelet aggregation**
36
asprin
irreversibly acetylates cyclooxybenase
**prevents platelet production of thromboxane A2**
37
Immune Thrombocytopenia Purpura
Autoimmune mediated attack (typically IgG antiplatelet antibodies) against platelets leading to decreased platelets (thrombocytopenia)
• Results in petechiae, purpura (bruises), and a bleeding diathesis (e.g. hematomas)
38
etiology of Immune Thrombocytopenia Purpura
* Antiplatelet antibodies against platelet antigens such as Gp IIb-IIIa and Gp Ib-IX (type II hypersensitivity reaction)
* Antibodies are made in the spleen
* Platelets are destroyed peripherally in the spleen by macrophages which have Fc receptors that bind IgG-coated platelets
39
acute ITP
Seen in children following a viral
infection
• Self-limited disorder
40
chronic ITP
Usually seen in women in their
childbearing years
• May be the first manifestation of SLE
• Petechiae, ecchymoses, menorrhagia, and nosebleeds
41
lab diagnostics of ITP
Decreased platelet count and prolonged bleeding time
• Normal prothrombin time (PT) and partial thromboplastin time (PTT)
• Peripheral blood smear shows thrombocytopenia with enlarged immature platelets (megathrombocytes)
• Bone marrow biopsy shows increased numbers of megakaryocytes with immature forms
42
treatments of ITP
Corticosteroids, which decrease antibody production
• Immunoglobulin therapy, which floods Fc receptors on splenic macrophages
• Splenectomy, which removes the site of platelet destruction and antibody production
43
thrombotic Thrombocytopenic Purpura (TTP)
Rare disorder of hemostasis where there is widespread intravascular formation of fibrin- platelet thrombi due to a deficiency/inhibition of the enzyme ADAMTS13, which is responsible for cleaving large multimers of von Willebrand factor
44
thrombotic Thrombocytopenic Purpura (TTP) clinical findings
```
Most often affects adult women
• Pentad of characteristic signs
• Fever
• Thrombocytopenia
• Microangiopathic hemolytic
anemia (intravascular hemolysis)
• Neurologic symptoms
• Renal failure
```
45
lab diagnosis of thrombotic Thrombocytopenic Purpura (TTP)
* Decreased platelet count and prolonged bleeding time
* Normal PT and PTT
* Peripheral blood smear shows thrombocytopenia and schistocytes, and reticulocytosis
46
pathology of thrombotic Thrombocytopenic Purpura (TTP)
Widespread formation of platelet thrombi with fibrin (hyaline thrombi) leading to intravascular hemolysis (thrombotic microangiopathy)
47
Hemolytic Uremic Syndrome (HUS)
* A form of thrombotic microangiopathy due to endothelial cell damage
* Occurs most commonly in children
* Follows a gastroenteritis with bloody diarrhea
* Organism: verotoxin- producing E. coli 0157:H7
```
Pentad of characteristic signs
• Fever
• Thrombocytopenia
• Microangiopathic hemolytic
anemia (intravascular hemolysis)
• Neurologic symptoms
• Renal failure
```
48
vitamin k required for these clotting factors
clotting factors 2, 7, 9, 10
49
The majority of the clotting factors are produced by...
the liver
50
The factors are ... that must be converted to the active form, some on... and require...
proenzymes
on a phospholipid surface
Ca++
51
The extrinsic coagulation pathway is activated by the release of
tissue factor
52
The intrinsic coagulation pathway is activated by
contact factors:
• Contact with subendothelial collagen
• High molecular weight kininogen (HMWK)
53
prothrombin time (PT) tests
* Tests the extrinsic and common coagulation pathways
* Tests factors VII, X, V, prothrombin, fibrinogen
* International normalized ratio (INR) standardizes the PT test so that results throughout the world can be compared
54
Partial thromboplastin time (PTT) tests
Tests the intrinsic and common coagulation pathways
| • Tests factors XII, XI, IX, VIII, X, V, prothrombin, fibrinogen
55
Fibrin degradation products (FDP) tests
fibrinolytic system (increased with DIC)
56
Thrombin time (TT) tests
adequate fibrinogen levels
57
Disseminated
Intravascular
Coagulation (DIC) causes
* Obstetric complications (placental tissue factor activates clotting)
* Gram-negative sepsis (TNF) activates clotting
* Microorganisms (especially meningococcus and rickettsiae)
* AML M3 (cytoplasmic granules in neoplastic promyelocytes activate clotting)
* Adenocarcinomas (mucin activates clotting)
58
Disseminated
Intravascular
Coagulation (DIC) pathology
* Results in widespread microthrombi
| * Consumption of platelets and clotting factors causes hemorrhages
59
Disseminated
Intravascular
Coagulation (DIC) lab
* Platelet count is decreased
* Prolonged PT/PTT
* Decreased fibrinogen
* Elevated fibrin split products (D-dimers)
* Treatment: treat the underlying disorder
60
Hemophilia A
Deficiency of factor VIII
| X-linked recessive
61
Hemophilia A features
• Predominately affects males
• Symptoms are variable dependent on
the degree of deficiency
• Newborns may develop bleeding at the time of circumcision
• Spontaneous hemorrhages into joints (hemarthrosis)
• Easy bruising and hematoma formation after minor trauma
• Severe prolonged bleeding after surgery or lacerations
• *****No petechiae or ecchymoses***
62
Hemophilia A tests
* Normal platelet count and bleeding time
| * Normal PT and prolonged PTT
63
Hemophilia A features
• Factor VIII concentrate
64
Hemophilia B
* Deficiency of factor IX
* X-linked recessive
* Clinically identical to hemophilia A
65
Vitamin K deficiency leading to and caused by
* Decreased synthesis of factors II, VII, IX, X, and protein C & S
* Caused by liver disease and the resulting decreased synthesis of virtually all clotting factors
66
Von Willebrand Disease
Inherited bleeding disorder characterized by either a deficiency or a qualitative defect in von Willebrand factor
• vWF is normally produced by endothelial cells and megakaryocytes
67
Von Willebrand Disease genetics
Types I-III genetic
Type I AD 75% (most mild)
II AR – intermediate severity 4 subtypes III AR – rare and severe
“Type 4” acquired
68
Von Willebrand Disease labs
* Normal platelet count and a prolonged bleeding time
* Normal PT with often a prolonged PTT
* Abnormal platelet response to ristocetin (adhesion defect) is an important diagnostic test
69
Von Willebrand Disease features
* Spontaneous bleeding from mucous membranes
* Prolonged bleeding from wounds
* Menorrhagiainyoungfemales
* Hemarthrosis is uncommon
70
Von Willebrand Disease treatment
* Treat mid cases (type I) with desmopressin (an antidiuretic hormone {ADH} analog)
* It releases vWF from Weibel-Palade bodies of endothelial cells
71
Thrombosis
pathologic formation of an intravascular fibrin-platelet thrombus during life
72
Thrombosis outcomes
* Vascular occlusion and infarction • Embolism
* Thrombolysis
* Organizationandrecanalization
73
Thrombosis locations
• Coronaryandcerebralarteries
• Heart chambers atrial fibrillation or post-MI
(mural thrombus)
• Aortic aneurysms
• Heart valves (vegetations) • Deep leg veins (DVTs)
74
Factors involved in thrombus formation (Virchow’s Triad
stasis, vascular injury, hyper coagulability
* Endothelial injury
* Atherosclerosis
* Vasculitis
* Many others
75
Hypercoagulabilityofblood caused by
• Clotting disorders (factor V Leiden, deficiency of
antithrombin III, protein C, or protein S)
• Tissue injury (postoperative and trauma)
• Neoplasia
• Nephrotic syndrome
• Advanced age
• Pregnancy
• Oral contraceptives (estrogen increases synthetic activity of the liver, including clotting factors
76
Embolism
Is any intravascular mass that has been carried down the bloodstream from its site of origin resulting in the occlusion of a vessel
77
Embolism composition
* Thromboemboli - most common (98%) type of emboli
* Atheromatous emboli – severe atherosclerosis
* Fat emboli – bone fractures
* Bone marrow emboli – bone fractures and CPR
78
gas emboli
• Decompression sickness “the bends”
• Rapid ascent results in nitrogen gas
bubbles in the blood vessels
79
Amniotic fluid emboli
• Complication of labor
• Fetal squamous cells are seen in the
maternal pulmonary vessels
• May result in DIC
80
Pulmonary Emboli (PE) pathology
* 95% of PEs arise from DVTs
* Pelvic venous plexuses of the prostate and uterus
* Right side of the heart
81
Pulmonary Emboli (PE) diagnosis
* Doppler ultrasound of the leg veins to detect DVT (do first)
* V/Q scan shows mismatch
* Spiral CT
* Plasma D-dimer ELISA test is elevated ($1000 and cannot be used after surgery)
* Pulmonary angiogram GS
82
PE outcomes
No sequelae (75%)
• Asymptomatic or transient dyspnea/tachypnea
• No infarction (dual blood supply)
• Complete resolution
Infarctions (15%)
• More common in patients with cardiopulmonary compromise
• SOB, hemoptysis, pleuritic chest pain, pleural effusion
• Hemorrhagic wedge-shaped infarct (x-ray Hamptons
hump)
```
Sudden death (5%)
• Large emboli may lodge in the bifurcation (saddle embolus) or large pulmonary artery branches and cause sudden death
• Obstruction of >50% of the pulmonary circulation
```
Chronic secondary pulmonary HTN (3%)
• Caused by recurrent PEs
• Increased pulmonary resistance
• Lead to secondary pulmonary HTN
83
Systemic Arterial Emboli
• Most arise in the heart
• Most arterial emboli cause
infarction
• Common sites of infarction include the LE, brain, intestine, kidney, and spleen
84
paradoxical emboli
Any venous embolus that gains access to the systemic circulation by crossing over from the right to the left side of the heart through a septal defect
85
Infarction
Localized area of necrosis secondary to ischemia
86
Factors predicting development of infarct:
* Vulnerability of the tissue to hypoxia
* Degree of occlusion
* Rate of occlusion
* Presence of dual blood supply
* Decreased oxygen carrying capacity (anemia, CO, etc.)
87
General sequence of tissue changes after infarction:
Ischemia-Coagulative necrosis- inflammation- granulation tissue -fibrous scar
88
Shock
* Vascular collapse and widespread hypoperfusion of cells and tissue due to reduced blood volume, cardiac output (CO) or vascular tone
* Cellular injury is initially reversible
* If the hypoxia persists, the cellular injury becomes irreversible, leading to the death of cells and the patient
89
Cardiogenic shock
```
(pump failure)
• MI
• Arrhythmias
• PE
• Cardiac tamponade
```
90
Hypovolemic shock
(reduced blood
volume)
• Hemorrhage
• Fluid loss due to burns • Severe dehydration
91
septic shock
(bacterial infection)
• Gram-negative septicemia
• Release of endotoxins (bacterial wall LPS
‘lipopolysaccharides’ )
```
High levels of endotoxin results in
• Production of cytokines TNF, IL-1, IL-6, and IL-8
• Vasodilationandhypotension
• Acuterespiratorydistresssyndrome(ARDS)
• DIC
• Multiple organ dysfunction syndrome
• Mortality rate: 50%
```
92
Anaphylactic shock
(generalized vasodilation – type I hypersensitivity reaction)
93
Neurogenic shock
(generalized vasodilation) • Anesthesia
| • Brain or spinal cord injury
94
stage 1 of shock
Compensation, in which perfusion to vital organs is maintained by reflex mechanisms
• Increased sympathetic tone
• Releaseofcatecholamines
• Activationoftherenin-angiotensinsystem
95
stage 2 of shock
Decompensation
• Progressivedecreaseintissueperfusion
• Potentiallyreversibletissueinjuryoccurs
• Developmentofametabolic(lactic) acidosis, electrolyte imbalances, and renal insufficiency
96
stage 3 of shock
Irreversible
• Irreversibletissueinjuryandorganfailure
• Ultimately resulting in death
97
kidney shock pahtology
* Acute tubular necrosis (acute renal failure)
| * Oliguria and electrolyte imbalances occur
98
lung shock pathology
Undergo diffuse alveolar damage (“shock lung”)
99
intestines shock pathology
* Superficial mucosal ischemic necrosis and hemorrhages
| * Prolonged injury may lead to sepsis with bowel flora
100
liver shock pathology
Undergoes centrilobular necrosis (“shock liver ”)
101
adrenal shock
* Undergo the Waterhouse-Friderichsen syndrome
* Commonly associated with meningococcal septic shock
* Bilateral hemorrhagic infarction
* Acute adrenal insufficiency
102
NON-Specific Vascular Wall
| Response to Injury
* Endothelial “activation”
* Smooth Muscle cell roles
Development, growth, Remodeling
• Intimal “thickening”
103
arteriosclerosis
thickening and loss of elasticity in arterial walls (general)
104
monckeberg medial calcific sclerosis
calcific deposits in muscular arteries in persons over 50
105
function of endothelial cells (9)
Maintenance of Permeability Barrier
• ElaborationofAnticoagulant,Antithrombotic, Fibrinolytic Regulators: Prostacyclin, Thrombomodulin, Heparin, Plasminogen •ElaborationofProthromboticMolecules: vWF, TF, Plasminogen activator inhibitor
• Extracellular Matrix Production (collagen,
proteoglycans)
• Modulation of Blood Flow and Vascular Reactivity
• Vasoconstrictors: endothelin, ACE
• Vasodilators: NO, Prostacyclin
• Regulation of Inflammation and Immunity
• Regulation of Cell Growth
• OxidationofLDL
106
Prostacyclin ... platelet activation
INHIBITS
107
Thrombomodulin ... thrombin
inhibits
108
body’s main anticoagulant
heparin
109
plasminogen is a precursor of what and what is its function?
precursor of plasmin dissolves fibrin!
110
vessel growth and remodeling (5 aspects)
The sum total of all the factors and processes involved in tissue injury and the body’s ability to grow vessels, develop new pathways, and re- perfuse areas in response to tissue and/or blood vessel injury.
111
intimal thickening
Intimal thickening is a NON-specific response to vascular (chiefly arterial) injury, and is they KEY feature in atherosclerosis as well.
112
ArterioVenous Malformation (AVM)
= Arteriovenous fistulas (can be surgically produced for dialysis)
• Also called ArterioVenous Malformation (AVM)
• Common factor is abnormal communication between high pressure arteries and low pressure veins
• Usually congenital (malformation), but can be acquired by trauma or inflammation
• Most often described in the brain as an AVM
• Often asymptomatic or with hemorrhage or pressure effects
113
Arteriolosclerosis
involving small arteries and arterioles, generally regarded as NOT strictly being part of atherosclerosis, but more related to hypertension and/or diabetes
114
3 stages of Atherosclerosis
1) FATTY STREAK non-palpable, but a visible YELLOW streak)
2) ATHEROMA (plaque) (palpable)
3) THROMBUS (non-functional, symptomatic)
115
morphologic progression of artheriosclerosis
• Macrophages (really monocytes) infiltrate
• Intimal “Thickening”
• Lipid Accumulation
• Streak
• Atheroma
• Smooth Muscle Hyperplasia and
Migration
• Fibrosis
• Calcification
• Aneurysm*
• Thrombosis
116
Cholesterol (really cholesterol esters) makes macrophages
“foamy” and cause “clefts” extracellularly.
117
pathogenesis of arterioschlerosis
Chronic endothelial injury
• LDL, Cholesterol in arterial WALL
• OXIDATION of lipoproteins
• Monocytes migrateendothelium*
• Platelet adhesion and activation
• Migration of SMOOTH MUSCLE from media to intima to activate macrophages (foam cells)
• Proliferation of SMOOTH MUSCLE and ECM
• Accumulation of lipids in cells and ECM
118
major risk factors for arterioschlerosis
NON-modifiable
Increasing age
Male gender
Family history Genetic abnormalities
Modifiable
Hyperlipidemia Hypertension Cigarette smoking Diabetes
119
minor factors for artheriosclerosis
Modifiable
Obesity
Physical inactivity
Stress ("type A" personality)
Postmenopausal estrogen deficiency
High carbohydrate intake
Alcohol
Lipoprotein Lp(a)
Hardened (trans)unsaturated fat intake Chlamydia pneumoniae
120
Hyperlipidemia – Foamy Macrophage
Chiefly CHOLESTEROL, LDL>>>>HDL
• HDL mobilizes cholesterol FROM atheromas to liver
• Low Cholesterol Diet Is Good
• Unsaturated Fatty Acids Good
• Omega-3 Fatty Acids Good
• Exercise Good
121
cholesterol clefts/esters
• Needle shaped washed out spaces in arteries, are cholesterol clefts, and can be nothing else, and like all other fat, yellow grossly, white microscopically.
122
NON ATHEROSCLEROSIS VASCULAR DISEASES (5)
•HYPERTENSION •ANEURYSMS
•VASCULITIDES • VEIN DISORDERS
• NEOPLASMS
123
Causes of renal hypertension (7)
Renal
• Acute glomerulonephritis
• Chronic renal disease
• Polycystic disease
• Renal artery stenosis
• Renal artery fibromuscular dysplasia
• Renal vasculitis
• Renin-producing tumors
124
causes of endocrine hypertension
Endocrine
• •
•
•
•
Adrenocortical hyperfunction
(Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, licorice ingestion)
Exogenous hormones (glucocorticoids, estrogen [including pregnancy- induced and oral contraceptives], sympathomimetics and tyramine- containing foods, monoamine oxidase inhibitors)
Pheochromocytoma, acromegaly, HYPO-thyroidism (myxedema), HYPER-thyroidism
pregnancy-induced
125
causes of cardiovascular hypertension
• Coarctation of aorta, polyarteritis nodosa (or other vasculitis)
• Increased intravascular volume
126
CO is influenced by (4)
BLOOD VOLUME
atriopeptin
Na
mineralocorticoids
CARDIAC FACTORS
127
what constricts? (5)
```
angiotensin II
catecholamines
thromboxane
endothelin
leukotrines
```
128
dilators (3)
NO
kinins
prostoglandins
129
local factors that affect peripheral resistance
pH, hypoxia
| autoregulation
130
local factors that affect peripheral resistance
pH, hypoxia
| autoregulation
131
neural factors that affect peripheral resistance
dilators-alpha adrenergic
constrictors-beta adrenergic
132
the juxtaglomerular cells release the enzyme renin....
If the perfusion of the juxtaglomerular apparatus in the kidneys decreases
133
renin cleaves
• Renin cleaves an inactive peptide called
angiotensinogen, converting it into angiotensin I.
134
Angiotensin I is then converted to angiotensin II by
angiotensin-converting enzyme (ACE), which is found mainly in lung capillaries.
135
Angiotensin II is the major bioactive product of the renin-angiotensin system. Angiotensin II acts as
an endocrine, autocrine/ paracrine, and intracrine hormone.
136
Often, benign or “malignant” hypertension is described as two different types of changes in arterioles, usually renal. These are described as...
1)Benign: Hyalization of arteriole wall
2)Malignant: Fibrinoid necrosis and “onion skinning” of arteriole wal
137
true v false aneurysm
difference between a TRUE (endothelial expansion) and FALSE (NO endothelial expansion) aneurysm
138
Non-atherosclerotic causes of aneurysms (5)
Congenital
• Luetic(Syphilitic)
• Traumatic
• “Mycotic”(Mis-leadingTerm) • 2° To Vasculitis
139
Non-atherosclerotic causes of aneurysms
Congenital
• Luetic(Syphilitic)
• Traumatic
• “Mycotic”(Mis-leadingTerm) • 2° To Vasculitis
140
2 main causes of aneurysms
1) atherosclerosis
2) cystic medial degeneration (necrosis), can be familial
141
Most abdominal aortic aneurysms (AAA) occur
between the renal arteries and the bifurcation of the aorta
142
Dissection
i.e., blood or hemorrhage disrupting the wall of a large artery) can be both a cause or an effect of an aneurysm.
143
Vasculitides
inflammation of the blood vessels that causes changes in the blood vessel walls.
144
Why are arteritides highly linked to autoimmune diseases
Because there are rarely any known causative external (i.e., infectious) pathogens, and many are associated with known auto- antibodies.
145
“Temporal” Arteritis aka, Giant Cell Arteritis, GCA
• Mainly Arteries Of The Head And Temporal Arteries Are The Most Visibly, Palpably, And Surgically Accessible
• Blindness Most Feared Sequelae
• Granulomatous Wall Inflammation Diagnostic
• Often Associated With Marked ESR Elevation To Be Then Known As Polymyalgia Rheumatica
• Anti-neutrophil Ab’s Often Positive
146
Takayasu Arteritis
• Involves aortic arch and other heavily elastic arteries, i.e., chief thoracic aorta branches, most commonly young Asian women
• FEMALES
