Normal Circulation and Fluid Balance

Lecture 1: Normal Circulation and Fluid Balance

• Hemostasis involves major components, each with specific functions.
• Petechiae, purpura, and ecchymoses need to be defined.
• Intrinsic and extrinsic pathways each have agents that can initiate clot formation, these must be identified
• Hemostasis occurs in five steps.
• Endothelium has both anticoagulant and procoagulant functions.
• Primary hemostasis differs from secondary hemostasis.
• Platelets contribute to hemostasis through adhesion, release, aggregation, and interaction with the clotting system and knowing the effect of missing processes/components is important.
• Platelet alpha granules and dense bodies have specific contents.
• Thrombin has three functions.
• Three types of naturally occurring anticoagulants exist
• Thrombi can be lysed.

Lecture 2: Fluid Balance

• What causes fluid to exit the vasculature.
• The factors that keep fluid within the vasculature should be known.
• Active hyperemia should be distinguished from congestion (passive hyperemia).
• Hyperemia should be distinguished from hemorrhage.
• Edema and ascites need to be defined.
• The primary causes of edema should be known.
• Transudates and exudates should be compared and contrasted, including contents and causes.
• Cardiac, septic, and hypovolemic shock, their causes, principles, and outcomes, need to be understood.
• There exist three types of fluid distribution disturbances seen in local edema.

Lecture 3: Thrombosis and Embolism

• Clots should be compared to thrombi.
• Localized clot formation should be differentiated from disseminated intravascular coagulation (DIC).
• Virchow's triad consists of three states.
• Injury, trauma, inflammation, and altered blood flow promote thrombosis.
• "Hypercoagulable" means.
• Age, obesity, oral contraceptives, cigarette smoking, and malignancy influence thrombus generation.
• Thrombi relate to emboli and occlusion of blood vessels.
• "Embolism" means.
• Emboli can consist of at least 8 kinds of materials.
• Contributing factors lead to the development of pulmonary emboli.
• Pulmonary emboli are categorized into three groups based on size/clinical impact.
• Systemic and pulmonary emboli can be compared in terms of origin and placement.
• Clinically significant emboli from gasses can form in certain ways, and knowing their composition and size is important.
• Fat can become an embolus via mechanical/biochemical theories.
• Amniotic embolism has a specific clinical picture and specific way of occuring.
• Atherosclerosis can be linked to emboli formation.

Lecture 4: Ischemia and Infarct

• Infarct, ischemia, and hypoxia all need defining.
• Local ischemia has causes.
• The impacts of venous occlusion and arterial obstruction on ischemia need describing.
• Functional and structural evidence indicates ischemia.
• The variables determining the degree of ischemia and their interactions should be known.
• Ischemia relates to infarct.
• Necrosis given at specific anatomical sites of infarct is expected.

Lecture 5: Atherosclerosis

• Arteriosclerosis differs from atherosclerosis.
• Risk factors significantly contribute to atherosclerosis development.
• Atheromatous plaques develop according to the response-to-injury hypothesis.
• Atheroma development leads to clinical manifestations.

Lecture 6: Human Genetics Introduction

• Definitions for:
  • Congenital vs. Hereditary disease
  • Autosomal Dominant
  • Genotype
  • Autosomal Recessive
  • Phenotype
  • Sex-linked Recessive
  • Karyotyping
  • Aneuploidy
  • Mutation
  • Nondisjunction
  • Deletion
  • Cytogenetic
  • Inversion
  • Translocation
• Four main types of genetic abnormalities exist.
• Autosomal and sex-linked disorders differ by chromosomes involved.
• Mutations can give rise to single-gene defects.

Lecture 7: Single Gene Disorders

• Penetrance, incomplete penetrance, and expressivity need defining.
• Ehlers' Danlos Syndrome: mode of inheritance, metabolic alteration, clinical impact.
• Phenylketonuria: inheritance, metabolic pathway, enzyme defect, clinical signs, treatment.
• Hemophilia A: genetic basis, missing clotting factor, consequences, treatment.
• Cystic fibrosis: genetic basis.
• For these genetic diseases, describe inheritance, metabolic pathways, affected enzyme, clinical features, and treatment:
  • Familial Hypercholesterolemia
  • Tay-sachs Disease

Lecture 9: Complex and Chromosomal Disorders

• Down’s Syndrome, Turner Syndrome, and Klinefelter’s Syndrome: define given:
  • Cytogenetic alteration on karyotyping
  • Proposed causative mechanism
  • Main clinical features of each
  • Incidence and relationship with age
  • Life expectancy
  • Prenatal screens
• Alpha-1 antitrypsin deficiency: genetic basis, illness severity prediction, genetic differences, pathogenesis, inheritance.
• Fragile X syndrome: genetic differences, pathogenesis, inheritance.
• Prader-Willi and Angelman syndromes: differences in genomic imprinting.
• Uniparental disomy: define, how does it occur.
• Mitochondrial disorders: mode of inheritance.