Exam 2: L7-8 Hemodynamics Flashcards
1
Q
- Compare/contrast exudates with transudates as to causes and lab findings
A
a. Exudates-high in protein. Fibrin, other large molecules present
i. WBCS, LD increased.
ii. Causes-infection, inflammation, repair:angiogenesis malignancy:angiogenesis
b. Transudates-low protein
i. few cells, LD doesn’t exceed plasma level.
ii. Causes-hydrostatic pressure increased, osmotic pressure decreased, lymphatic obstruction, primary retention of Na and water.
2
Q
- What are some locations and what are the causes of local edema due to increased hydrostatic pressure?
A
a. Impaired venous outflow
b. Localized increased pressure-dependent edema, DVT.
c. Generalized heart failure
3
Q
- Describe the pathogenesis of edema in heart failure. Compare with mechanism of edema in renal disease; liver failure; nutrition (figure 4-2, Robbins)
A
a. Heart failure-decreased CO→decreased effective arterial blood flow→increase renin→aldosterone→increase renal Na+ reabsorption→increase renal retention of Na and H2O→increase plasma volume→increase transudation→EDEMA
b. Renal disease, liver failure, nutrition
i. Decrease plasma albumin→decreased plasma oncotic pressure→EDEMA
4
Q
- List causes of decreased colloid osmotic pressure. What is a frequent initial manifestation of edema related to decreased osmotic pressure?
A
a. Decreased colloid osmotic pressure
i. Increased protein loss-nephrotic syndrome, protein losing enteropathy.
ii. Decreased protein/albumin production-severe liver disease, malnutrition.
b. Frequent initial manifestation-periorbital edema
5
Q
- Define lymphedema. List causes. What is the description given to advanced lymphedema?
A
a. Lymphedema-impaired lymphatic drainage leading to edema.
b. Causes:
i. Primary-inherited or development defect of lymph vessles or nodes. Milroy’s Disease.
ii. Secondary
1. Trauma to lymphatics
2. Radiation injury to lymphatics
3. Cancer metastatic to lymphatics
4. Extrinsic pressure on lymphatics
5. Infections of lymphatics
c. Peau d’orange-thickened skin due to advanced lymphedema of all causes
6
Q
- What are the causes and morphology of pulmonary edema? What would you expect for clinical symptoms?
A
a. Causes:
i. Left ventricular failure-common
ii. Renal failure, ARDS, pulmonary infections
b. Morphology:
i. Lungs 2-3x increase in weight
ii. Frothy blood tinged fluid
iii. Dilated and full of blood
iv. Alveoli-fluid instead of air.
v. Edematous septae.
vi. Chronic-Siderophages in alveoli, red blood cells break down and release iron.
7
Q
- Define hyperemia. What are the causes?
A
a. Hyperemia-erythema-local increased volume of blood.
b. Causes-exercise, inflammation (cytokines).
8
Q
- Define congestion. What are some causes? What is the morphology of chronic pulmonary congestion? What is the morphology of chronic lower extremity edema? What complication may occur?
A
a. Congestion-local increased volume of blood. Passive process-impaired venous outfow
b. Causes: heart failure, local venous obstruction
c. pulmonary congestion-rubbery, brown
d. chronic lower extremity edema - Brown Induration & Ulceration
e. Can have capillary rupture with focal hemorrhages, accumulation of siderophages
9
Q
- What is the cause and morphology of hepatic congestion? What are causes of congestive splenomegaly?
A
a. Cause hepatic congestion
i. Right heart failure
b. Morphology-red-brown depressed areas→cardiac cirrhosis
i. Nutmeg liver-siderophages
c. Congestive splenomegaly
i. Right heart failure, hepatic cirrhosis, portal vein occlusion.
10
Q
a. Hematoma
A
mass of blood confined within an organ, tissue or internal space
11
Q
b. Contusion
A
bruise/ecchymosis-blunt force injury-damages small blood vessels without disruption of continuity of tissue
12
Q
c. Ecchymosis
A
large areas (>1-2 cm). changes from red-blue→blue green (heme→bilirubin)→gold-brown (hemosiderin)
13
Q
d. Petechiae
A
punctate hemorrhages. Causes: thrombocytopenia, dysfunctional platelets
14
Q
e. Purpura
A
confluent petechiae. Similar to causes above plus vascular inflammation, trauma
15
Q
f. Hemarthrosis
A
bleeding into joint
16
Q
h. Laceration
A
tear due to blunt force trauma, bridging strands of fibrous tissue or blood vessels
17
Q
i. Incision
A
sharp cutting object
18
Q
j. Abrasion
A
scrape, superficial dermis torn off
19
Q
k. Epistaxis
A
nosebleed
20
Q
l. Hemoptysis
A
coughing up blood
21
Q
m. Hematemesis
A
vomiting up blood
22
Q
n. Hematochezia
A
bright red blood in stool
23
Q
o. Melena
A
black/digested blood in stool
24
Q
p. Hematuria
A
blood in urine
25
q. Menorrhagia
excessive menstrual bleeding
26
11. What are the components of primary hemostasis?
i. Immediate response to vascular injury
ii. Vascular wall-endothelial cells and underlying CT.
iii. Platelets.
27
11. What are signs and symptoms of defects of primary hemostasis?
i. Epistaxis, bleeding from gums
ii. Bleeding from/into GI tract and skin
1. Petechiae, purpura, ecchymosis
iii. Bleeding from GU tract.
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a. Prothrombotic
i. Platelet adhesion
| ii. Exposure of membrane bound tissue factor→extrinsic coagulation sequence
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b. Antithrombotic
i. Heparin-like molecule
ii. Tissue factor pathway inhibitor
iii. Thrombin binding to thrombin receptor→endothelial effect→fibrinolytic cascade, inhibit platelet aggregation
iv. Thrombin binding to thrombomodulin→Active protein C→active proteolysis of Va and VIIIa
30
13. Describe and know in order, the events involved in primary hemostasis (figure4-5). List factors involved in each step.
a. Vasoconstriction
b. Platelet adhesion
c. Platelet degranulation-ADP and TXA2
d. Recruitment of additional platelets
e. Platelet aggregation and formation of primary hemostatic plug
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a. Vasoconstriction
i. Reflex neural stimulation
| ii. Endothelin release from endothelial cells
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b. Platelet adhesion
i. Platelets (have Gp1b receptor) adhere via vonWillebrand factor and exposure to collagen.
1. vW factor from WP bodies of endothelial cells and alpha-granules of platelets.
ii. Adhesion induces shape change in platelets→degranulation
1. Shape change by binding ADP to its receptor
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c. Platelet degranulation-ADP and TXA2
i. Alpha granules
1. P-selectin
2. Fibrinogen, fibronectin, factors V and VIII
3. Heparin binding factor, PF4
4. Growth factors: PDGF, TGF-B
ii. Dense granules have products for metabolism, recruitment
1. ADP, serotonin, epinephrine, calcium, others.
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e. Platelet aggregation and formation of primary hemostatic plug
1. ADP, TXA2
2. Thrombin (via receptor (PAR) on platelets)
3. Via GPIIb/IIIa-binds fibrinogen
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14. With respect to platelets what are the actions? Be specific regarding mediators and order of actions.
a. Get activated, granule release. Recruit other platelets.
b. ADP, TXA2 released from platelets
i. ADP→exposes GPIIB/IIIa receptor on platelets.
ii. TXA2→promotes platelet aggregation.
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15. What are the hereditary platelet diseases? Be familiar with the clinical features (refer to signs and symptoms of diseases of primary hemostasis).
a. Von Willebrand disease- Platelet unable to adhere
b. Bernard-Soulier syndrome-defect in Gp1b
c. Clinical features-signs and symptoms of diseases in primary hemostasis.
d. Defect in platelet function-Glansmann thombasthenia (defect in GpIIb/IIIa. Platelet aggregation affected.
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16. List and describe as to action, the antiplatelet drugs.
a. Used to prevent recurrent thrombosis
b. ADP receptor PY2 inhibitors-activation of platelets and eventual crosslinking by fibrinogen
c. GpIIbIIIa inhibitors
d. Aspirin, NSAIDS-block cyclooxygenase pathway on AA→prevent TXA2 production.
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17. What are other acquired, nonpharmaceutical defects of platelets?
a. Thrombocytopenia-decreased numbers
i. Decreased platelet production in bone marrow
ii. Increased peripheral destruction
1. Autoimmune-ITP, HIV
b. Dysfunctional platelets
i. Uremia, drugs
c. Prostacyclin-PGI2-from endothelial cell
i. Vasodilation, inhibits platelet aggregation
d. Thromboxane-from platelet
i. Vasoconstriction, stimulates platelet aggregation
e. NO-from endothelium
i. Vasodilation, inhibits platelet aggregation
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18. What labs are used to assess primary hemostasis?
a. CBC for platelet count
b. Platelet function analyzer
i. Measure time to form platelet plug, analogous to bleeding time.
c. Bleeding time (poor reproducibility)
d. Test for vW disease
e. Platelet aggregation studies
40
19. Review coagulation (secondary hemostasis). Know how each factor is activated and where it acts in the “coagulation cascade”. Define tenase complex and prothrombinase complex. Memorize vitamin K dependent factors.
a. Enzymatic reactions terminating in activated thrombin.
i. Thrombin proteolyzes fibrinogen→fibrin
b. Fibrin monomers polymerize into soluble gel that encases platelets to form definitive secondary plug.
c. Factor XIII cross-links and stabilizes fibrin polymers.
d. Fibrinogen (Factor I)
i. Acted upon by 2 enzymes
1. Thrombin-releases fibrin monomers from inactive fibrinogen
2. Plasmin-enzyme that proteolyzes fibrin/fibrinogen into peptides=fibrinolysis
a. Products of fibrinolysis-fibrin degradation products, d-dimer.
ii. Factor XIIIa cross-links fibrin
e. Thrombin (Factor II)
i. Activated from prothombin via prothrombinase
ii. Converts fibrinogen to fibrin-clot.
iii. Amplifies formation of additional thrombin
iv. Activates platelets, factor XIII
v. Inhibits thrombin formation via feedback
vi. Actions on inflammation-
1. Proinflammatory and anti-inflammatory
vii. Affects repair-healing
f. Tissue Factor-Factor III
i. Sources-walls of blood vessels, endothelial cells, cells in CT, circulating monocytes.
ii. Actions
1. Only initiator of coagulation
iii. Blocked by tissue factor pathway inhibitor from endothelial cells.
g. iX, VIII-tenase component.
h. X,V-prothombinase component.
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20. Be able to interpret PT and PTT to screen patients for cause of bleeding diathesis.
a. PT
i. Extrinsic and common pathway
ii. Monitor coumadin therapy.
iii. deficiencies in VII, X, V, II, I
b. PTT
i. Intrinsic and common pathway
ii. Monitor heparin therapy
iii. XII, XI, IX, VIII, X, V, II, I
42
21. List coagulation factor deficiencies. Describe etiology.
a. Factors VIII, IX--X-linked.
b. vonWillebrand disease-Autosomal Dominant
c. remaining-autosomal recessive
d. Vitamin K Deficiency-
i. Procoagulants II, VII, IX, X,
ii. Anticoagulants -proteins C and S
iii. Caused by
1. Malabsorption
2. Antibiotic therapy
3. Dietary deficiency
4. Coumadin therapy
5. Deficient in many neonates; given at birth
e. Coumadin/warfarin-blood thinner
i. Vitamin K antagonist
43
22. Compare/contrast clinical features of bleeding due to defects of primary hemostasis with coagulation factor deficiencies. (see chart)
(see chart)
44
23. List the natural anticoagulants. Describe the anticoagulant pathophysiology of each. What condition is associated with deficiency or defect of a natural anticoagulant?
a. Anticoagulants
i. Antiplatelet activity of endothelium-physically inhibits platelet adhesion.
ii. Mediators→release secondary to thrombin binding, vasodilation
1. PGI2 (prostacyclin), NO, ADPase
iii. Fibrinolytic activity-source of tissue plasminogen activator
1. From endothelial cells→lyses newly formed clot.
2. Activates plasminogen→plasmin→lysis fibrin/fibrinogen
iv. Heparin-like molecule-cofactor for antithrombin
v. Thrombomodulin binding-inhibits thrombin and activates protein C→inactivates Va and VIIIa.
vi. Tissue factor pathway inhibitor-inactivates VIIa
b. Natural anticoagulants-restict coagulation to site of exposed phospholipid.
i. Deficiencies→abnormal tendency to clot.
ii. Antithrombin III
1. Activated by binding to heparin like molecules on endothelial cells or by therapeutic heparin injections
2. ATIII-heparin complex
a. Inhibits thrombin & IXa,Xa,XIa
3. ATIII deficiency very rare
iii. Protein S
1. Vitamin K dependent cofactor of protein C .
a. Source: endothelial cells, liver, others.
iv. Protein C
1. Vitamin K dependednt
a. Source: liver
b. Activated by binding of thrombin to endothelial thrombomodulin.
v. Activated Protein C (+S)
1. Inactivates Va and VIIIa
45
24. Define fibrinolysis as to actions, labs. What are the inhibitors of fibrinolysis?
a. Action-breakdown of fibrin to yield firbin split products, FDPs and d-dimer.
b. Labs- pTor PTT?? D-dimer
c. Inhibitors of fibrinolysis- PAI
46
25. Define thrombosis. What is Virchow’s triad? Refer to examples of each arm. Recognize morphologic examples of thrombi.
a. Thrombosis-pathologic process-formation of a clot within intact vascular system
b. Virchow’s triad-endothelial injury, stasis or turbulence of blood, blood hypercoagulability.
i. Endothelial injury-
1. Cigarette smoke - products toxic to endothelium
2. Sepsis – (systemic response to infection) - activates endothelium
a. Favors Thrombosis (DIC)
3. Malignancy (DIC)
ii. Turbulence of blood-aneurysms, sickle cell anemia
iii. Hypercoagulability
1. Polycythemia
2. Hereditary Thrombophilia (Increases risk of DIC)
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26. List the hereditary thrombophilias. Which are most common? In order:
a. Factor V, Leiden Mutation
b. Prothrombin 20210A mutation
c. Hyperhomocystenemia (quite common)
d. Protein C deficiency
e. Protein S deficiency
f. Anti-thrombin III deficiency
48
27. What are the features of factor V Leiden?
a. 60%-recurrent DVT
b. single AA substitution results in -
i. Factor Va that is resistant to digestion by activated protein C
c. Lab tests-
i. Activated protein C resistance
ii. Genetic testing for mutation
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28. Describe prothrombin 20210A mutation.
a. Mutation results in increased levels of prothrombin
b. Increases prothrombin leads to more fibrinogen→fibrin
c. 3x increased risk of venous thrombosis
50
29. What are the features of hyperhomocysteinemia?
a. Mutation in methyltetrahydrofolate reductase
b. Inhibits ATIII activity and thrombomodulin
c. Contributes to formation of atherosclerosis
d. Acquired form-B12 or folate deficiency
51
30. Learn the list of secondary/acquired hypercoagulable disorders. Which confer the highest risk for thrombosis?
a. Prolonged bed rest, immobilization
b. MI, atrial fib
c. Tissue damage
d. Cancer
e. Prosthetic heart valves
f. Disseminated intravascular coagulation
g. Antiphospholipid antibody syndrome
h. Prior thrombosis
i. Increasing age; >60 years old
j. Hyperestrogenic states: pregnancy, exogenous estrogens and tamoxifen
k. Oral contraceptive use
l. Sickle cell anemia
m. Smoking
n. Obesity
52
31. Describe HIT including pathogenesis and clinical features.
a. Heaprin-induced Thrombocytopenia
i. Antibodies form to unfractionated heparin
ii. Recognize complexes of heparin-platelet factor 4.
iii. Binding activates platelets→formation of platelet rich thrombi.
iv. Thrombocytopenia due to platelet consumption
v. Thrombosis occlude vessels, produce hypoxic tissue injury
53
32. Define antiphospholipid antibody syndrome, listing clinical associations
a. May be primary-solitary autoimmune defect.
i. Or secondary-systemic lupus erythematous (SLE)
b. Recurrent venous or arterial thrombi
i. Arterial thrombosis: stroke, MI
ii. DVT with pulmonary emboli
iii. Renovascular disease; bowel infarct.
c. Repeated spontaneous abortions
i. Antibody mediated inhibition of tPA→no throphoblastic invasion of endometrium
ii. Cardiac valvular vegetations-Libman-Sachs
iii. Thrombocytopenia – Cause keep froming clots
iv. Catastrophic antiphospholipid syndrome
1. Widespread small vessel thrombi
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33. Know the definitions of phlebothrombosis and thrombophlebitis. What are the clinical features of saphenous vein thrombophlebitis? What is the most common source of pulmonary thromboemboli? What are signs of DVT?
a. Phlebothrombosis-clot in vein
b. Thrombophlebitis-clots that incite inflammatoin
c. Clinical features of saphenous vein thrombophlebitis
i. Local congestion, pain, swelling
ii. Varicose ulcers
d. Common source of pulmonary thromboemboli
i. Deep veins of legs (DVT)
e. Signs of DVT
i. Edema, swelling of leg
ii. Homan’s sign-pain in calf on dorsiflexion
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34. Review morphology of thrombi. What are associations?
a. Occur anywhere in cardiovascular system
b. Venous thrombi-extend in direction of blood flow.
c. Arterial thrombi-extend retrograde
i. Lines of Zahn-alternating layers of RBCs and platelets in thrombi-formed in heart and aorta.
d. Associations
i. Atherosclerosis is most common cause
1. Turbulence: occur at bifurcations
2. Endothelial injury: ulcerated plaque
ii. Coronary artery→MI
iii. Cerebral artery thrombosis→stroke
iv. Femoral artery→gangrene of leg
v. Mural thrombus (within chamber of heart)→systemic emboli
vi. Aneurysms predispose to thrombosis
e. Fate
i. Propagation-continue to enlarge
ii. Embolization-travel to distant site
iii. Dissolution-removal by fibrinolysis
iv. Organization and recanalization
1. Organization-thickens wall, narrows lumen
2. Recanalization-small channels in fibrous stroma-reduced blood flow
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35. Define: Embolus. Which is most common? Recognize morphology. Thomboembolism, infarction, cor pulmonale.
a. Embolus-detached solid, liquid, or gaseous mass that is carried by blood to site distant from its point of origin.
b. Thromboembolism-embolus of blood clot (thrombus)
i. Thrombi most common
c. Infarction-ischemic necrosis of tissue
d. Cor pulmonale-hypertrophy of right ventricle due to lung disease; leads to right heart failure.
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36. What are sources and morphology of atheroemboli (Hollenhorst plaques and figure 20-43)
a. Sources
i. Deep veins of the leg above popliteal fossa
b. Outcomes
i. Fatal pulmonary emboli
1. Saddle embolus-occludes bifurcation of the main pulmonary artery.
2. Produces electrical mechanical dissociation
ii. Massive simultaneous emboli involving 60% of pulmonary circulation-obstructive shock
c. Other Outcomes
i. Most clinically silent (small size)
ii. Pulmonary infarction (uncommon-occurs with occlusion of small end-arteriolar branches)
iii. Pulmonary hemorrhages-emboli in medium sized arteries, can produce hemoptysis.
iv. Pulmonary hypertension with cardiorespiratory compromise may occur later.
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38. Define systemic thromboembolism. What are sources? Recognize morphology, figure 4-13 and microscopic description. Review sites and consequences of systemic thromboembolism.
a. Systemic thromboembolism-emboli travelling within arterial circulation
b. Sources
i. Intracardiac mural thrombi
ii. Aortic aneurysm
iii. Thrombi from ulcerated atherosclerosis
iv. Valvular vegetation
v. Paradoxical embolus-right to left shunt in heart→venous thrombus enters arteries.
c. Sites and consequences-
i. Lower extremities, brain, intestines, kidneys, spleen, retina
d. Consequences
i. Gangrene of leg/arm
ii. Cerebral vascular accident
iii. Infarction of intestines, kidney, spleen
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39. What are some causes and clinical presentations, including labs, of acute DIC? What is a common cause and what are the clinical features of chronic DIC?
a. Acute DIC
i. Thrombo-hemorrhagic disorder
1. Occurs in obstetrical accidents, sepsis, others
2. Coagulation pathways activated systemically-thrombi form throughout microcirculation
3. Secondary complication of variety of diseases
ii. Presents with hemorrhages from multiple sites
1. Post recovery sequelae-related to ischemic injury of multiple organs.
b. Chronic DIC
i. Not bleeding-clotting. Hypercoaguable. Get DVT.
ii. Venous thrombi, nonbacterial thrombotic endocarditis.
iii. Trousseau syndrome
1. Migratory thrombophlebitis in a patient with pancreatic cancer.
60
40. What are the origin, morphology and clinical features of traumatic fat embolism?
a. Origin-from bone marrow. Fracture long bones, the fat of the bone marrow elements gets into circulation.
b. Morphology- embolus with clear vacuoles that are fat.
c. Clinical features-shortness of breath, confusion, coma, 1-3 days after fracture.
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41. What are causes and consequences of air embolism?
a. Causes
i. Clinical settings-exogenous air
1. Obstetric procedures-delivery/abortion: contractions for air into uterine veins
2. Treatment of pneumothorax
3. Lung/chest wall injury opens large vein, admitting air during inspiration
ii. Endogenous air
1. Scuba/deep sea divers
2. Underwater caisson workers
3. Unpressurized aircraft in rapid ascent.
iii. Gas emboli occlude arteries→ischemia
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42. Describe clinical features and describe and recognize morphology of amniotic fluid embolism
a. Mechanism-infusion of amniotic fluid into maternal circulation via tear in membranes and uterine wall.
b. Morphology-fetal squames, hair, vernix fat, and meconium in pulmonary vessels.
c. Clinical-shortness of breath, shock, followed by seizures, coma, DIC; neurologic sequelae in 85%
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43. Describe infarction. Classify by color and correlate color with cause and/or location. Recognize morphologies. What type of necrosis is present?
a. Infarction-area of ischemic necrosis caused by occlusion of either the arterial supply or venous drainage of a tissue.
b. Red or hemorrhagic
i. Venous occlusions – Twisted Ovaries, Testes
ii. Arterial occlusions in loos tissues (lungs) - Blood collects in infracted zone
iii. Arterial occlusions in tissue with dual circulation – Lung & Intestines
iv. Occlusion in tissues previously congested
v. Occlusions where blood flow is re-established
c. White infarcts
i. Arterial occlusion in solid organs-heart, spleen, kidney.
ii. Density of tissue limits seepage from adjoining capillaries.
d. Coagulative necrosis
e. Prussian blue-positive
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44. Review and understand factors that influence development of an infarct.
a. Dual blood supply reduces vulnerability of tissues to occlusion
i. Uncommon in lungs, liver, hand-forearm
b. More likely when blood passes through a set of capillaries before tissue perfusion.
c. Rate of development of occlusion: slowly progressing occlusions develop collaterals.
d. Oxygen content of blood
i. Infarction more likely with anemia, cyanosis
ii. Congestive heart failure-impaired circulation and ventilation-more likely to have infarct.
e. Vulnerability to hypoxia
i. Neurons-irreversible injury 3-4 minutes
ii. Cardiac myocytes-begin to die after 20-30 minutes
iii. Fibroblasts and muscle can tolerate hours of ischemia.
a. Dual blood supply reduces vulnerability of tissues to occlusion
i. Uncommon in lungs, liver, hand-forearm
b. More likely when blood passes through a set of capillaries before tissue perfusion.
c. Rate of development of occlusion: slowly progressing occlusions develop collaterals.
d. Oxygen content of blood
i. Infarction more likely with anemia, cyanosis
ii. Congestive heart failure-impaired circulation and ventilation-more likely to have infarct.
e. Vulnerability to hypoxia
i. Neurons-irreversible injury 3-4 minutes
ii. Cardiac myocytes-begin to die after 20-30 minutes
iii. Fibroblasts and muscle can tolerate hours of ischemia.
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45. Review and understand lipid metabolism, especially cholesterol hepatic pathways.
a. Cholesterol suppresses further synthesis of cholesterol by inhibiting HMG-CoA reductase (rate limiting enzyme in cholesterol synthesis).
b. Cholesterol activates ACAT→esterification and storage of cholesterol
c. Cholesterol downregulates synthesis of LDL receptors (protects from further accumulation within the cell)
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46. What is the most common familial hyperlipidemia and what is the cause?
a. Familial Hypercholesterolemia due to defective LDL receptor.
i. LDL receptor-inadequate uptake of LDL, increased serum level.
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47. What are the labs and clinical findings of familial hypercholesterolemia? Know the goals of serum lipid levels.
a. Clinical findings
i. Heterozygotes
1. Plasma cholesterol increased from birth 2-3x
2. Cutaneous xanthomas (maybe)
3. Premature atherosclerosis develops in adults
ii. Homozygotes
1. Plasma cholesterol 5-6 x normal
2. Skin and tendinous xanthomas
3. Coronary, cerebral, and peripheral vascular atherosclerosis in childhood, adolescence.
b. Serum lipid levels
i. Total cholesterol-45
iii. LDL cholesterol-<100
