DOCUMENT CODE: BIOCHEM-2021-01

SUBJECT: Page 1 of 2

WEEK 2 CASE VIGNETTE TRIGGER/GUIDE QUESTIONS LEARNING OUTCOMES REFERENCE

Mr. and Mrs. Gottleib brought 1. What are the major substances I. MEMBRANES: STRUCTURE & FUNCTION Harper’s
their nine-month-old infant, Jeremy, to found in sweat? Where are these A. Basic features and major components Illustrated
the emergency room for episodes of substances located in the body? of membranes. Biochemsitry.
31st Edition
cough and diarrhea for almost a week. 2. The cell and its organelles are B. Role of membrane proteins and
Parents claimed that Jeremy would enclosed in a membrane membrane asymmetry.
Others:
sometimes “wheeze” a lot more than structure, enumerate its C. Fluid mosaic model of membrane 1. Textbook of
they thought was normal for a child composition and their biologic structure and its specialized features. Biochemistry
with “just a cold”. The pediatrician importance. D. Movement, transport of materials with Clinical
noted that patient was small for his 3. Describe the properties and and selectivity across membranes. Correlation. 7th
age, salt crystals were present on the characteristics of a membranes. 1. Passive diffusion 2. Lehninger’s
skin, and chest auscultation revealed 4. In the patient, salt crystals 2. Facilitated diffusion Prinicples of
abnormal breath sounds. Chest Xray appear on the skin. How does 3. Active transport Biochemistry
. 6th Edition.
and sweat test were taken. salt seep through the membrane 4. Endocytosis and Exocytosis
3. Marks’
The primary attending of the skin – by what transport
Basic
physician (AP) had a family conference mechanism does it apply? How is II. THE EXTRACELLULAR MATRIX
Medical
with the Gottleibs. Jeremy’s diagnosis it different from the other A. 3 major classes of biomolecules Biochemistr
was disclosed to the family. The AP transport mechanism in the comprising the extracellular matrix y: A Clinical
explained that, Cystic fibrosis (CF) is an body? One prominent symptoms and function. Approach. 4th
inherited disease of the glands that of CF patients are thick and B. Pathway in the biosynthesis and post- Edition
make mucus and sweat. Sweat test tenacious mucous secretions translational modification of
revealed that chloride levels were produced by the lining collagens-the most abundant protein
higher than normal. Patients with CF epithelium of the respiratory in mammals, and elastin.
get a defective gene from both parents. tracts. C. Major components of the basal
People who have one defective gene 5. Tabulate the major classes and lamina and basement membrane and
from one parent are called carriers. function of the connective tissue its role in maintaining overall
Thus, don't have the disease. found underneath this lining
 CF affects a cell protein called epithelium. structure.
CFTR (cystic fibrosis transmembrane 6. Outline how the most abundant D. Properties and general features of the
regulator). CFTR controls the flow of protein is formed and give synthesis and degradation of
water and certain salts in and out of examples of disorders associated glycosaminoglycans and
the body's cells. As the movement of with mutations in synthesis. proteoglycans.
salt and water in and out of cells is 7. Differentiate the various E. Examples of inborn errors of
changed, the mucus that many cells glycosaminoglycans and its metabolism.
normally make gets thicker. This thicker functions. F. Principal proteins found in bone.
mucus can affect many organs and 8. Identify the glycoprotein found G. Examples of diseases of the bone due
body systems. This explains Jeremy’s in respiratory tracts. Enumerate to metabolic and genetic mutations.
respiratory symptoms were his airways the major classes of
became distended by thick and glycoproteins and its role in III. GLYCOPROTEINS
tenacious mucus secretions which biologic processes and diseases. A. Structure of glycoproteins and the
cannot be normally cleared from the 9. Outline the distinct pathways of principal sugars involved.
airways in patients with CF. the synthesis and degradation of B. Types of glycosidic bonds and its
glycoproteins. physiologic role.
C. Features of glycoprotein biosynthesis
and degradation.
D. Definition and pathologic
consequence of advanced glycation
end products (AGEs).
E. Diseases resulting to abnormalities in
glycoprotein synthesis.