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Advanced Pathophysiology > Cellular and Molecular Biology and Genetics > Flashcards

Cellular and Molecular Biology and Genetics Flashcards

1
Q

Ribosomes are:

A

The sites for cellular protein sythesis in either rough ER or cytoplasm

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2
Q

Activities occurring in cytosol include:

A

Ribosomal protein synthesis
Intermediary metabolism
Glycogen storage

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3
Q

Why do O2 and CO2 diffuse easily through the cell membrane?

A

They’re small size allows them to move through cell membrane

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4
Q

Why are glucose and H+ unable to diffuse through the cell membrane passively?

A

Glucose molecules are too large to diffuse through the membrane. H+ cannot moving against an opposing charge. Both need a transporter across the cell membrane.

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5
Q

The plasma membrane is composed primarily of:

A

Amphipathic molecules hydrophobic (inner, tails) and hydrophillic (outer, heads)

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6
Q

Define passive transport

A

Movement with a gradient; from high concentration to low concentration. Examples: Diffusion, Filtration, and Osmosis

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7
Q

Define active transport

A

Transport requiring and energy source, often ATP. Examples: Na-K pump and Ca channel pump

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8
Q

Which mode of cellular transport can move substances against the concentration gradient?

A

Active transport

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9
Q

Describe facilitated diffusion

A

Diffusion that requires carrier proteins which provide a tunnel for hydrophillic molecules to move through. No energy is requires for this mode of transport.

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10
Q

Hypertonic solutions affect the cell how?

A

Hypertonic describes a situation where there is a high concentration of solute outside of the cell which causes water to move out the cell.

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11
Q

Hypotonic solutions affect the cell how?

A

Hypotonic describes a situation where this is a low concentration of solute outside of the cell so the water moves into the cell.

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12
Q

For a cell to engage in active transport processes it requires:

A

An expenditure of energy
Appropriate fuel
ATP

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13
Q

Give an example of bulk transport:

A

Endocytosis and exocytosis

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14
Q

Give three examples of active transport:

A

Bulk transport
Na-K pump
Ca pump

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15
Q

Hypercholesterolemia occurs due to defects in which type of cellular transport?

A

Bulk transport. Problem with endocytosis; the cell is unable to take in the cholesterol from the blood causing high levels of cholesterol in the circulating blood volume.

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16
Q

What does the Nernst Equation calculate?

A

It quantifies the membrane potential by calculating the equilibrium potential for an ion based on the charge of the ion and its concentration gradient across the membrane.

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17
Q

What happens when a cell reaches it’s membrane potential?

A

Voltage gated channels open and the Na+ ions move into the cell, making it more positive (depolarization)

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18
Q

What happens during repolarization of a cell?

A

Na+ gates close and K+ voltage gates open causing K+ to move out of the cell making it more negative

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19
Q

What happens during hyperpolarization of a cell?

A

The cell becomes too negative because the K+ channels releasing positive ions into the extracellular fluid are slow to close. Once K+ channels close the cell settles at its resting membrane potential.

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20
Q

Name the three types of cellular communication.

A
  1. Gap Junction (protein channels)
  2. Direct Contact (plasma mem bound molecules)
  3. Signaling by secreted molecules (over longer distances)
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21
Q

Give some examples of ligands that bind with membrane receptors:

A 
Hormones
Neurotransmitters
Infectious bacteria
Infectious virus
Antigens
Drugs
Metabolites
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22
Q

Name the three major types of cell surface receptor proteins.

A
  1. Ion channel linked receptors (ligand-gated channels.
  2. Enzyme linked receptors
  3. G-protein linked receptors
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23
Q

What are the 2 major second messenger pathways activated following the binding of a G-protein?

A

cAMP and Ca

24
Q

What is normal fluid homeostasis?

A

Equilibrium between hydrostatic and osmotic pressure (Starling forces)

25
Q

Name the three main etiologies of edema.

A
  1. Decreased capillary oncotic pressure (caused by decreased production of plasma protiens ie-malnutrition or cirrhosis)
  2. Increased tissue oncotic pressure (leading to decreased transport of capillary filter protein causing lymph obstruction and decreased absorption of interstitial fluid)
  3. Increased capillary hydrostatic pressure (seen in venous obstruction, Na+ retention, and heart failure)
26
Q

Define hydrostatic pressure.

A

Mechanical force of water pushing against the cellular membrane. (**outward push)

27
Q

Define oncotic pressure.

A

A form of osmotic pressure exerted by proteins in the blood that pulls water into the circulatory system (**inward pull)

28
Q

Describe hyponatremia, its etiology, and clinical manifestation.

A

Too little Na+ in the circulating blood (too much water/dilute). Examples of are SIADH; too much ADH causes the secretion of Na+ and the retention of water. s/s: CNS dysfunction

29
Q

Describe hypernatremia, its etiology, and clinical manifestations.

A

Too much Na+ in the blood volume (too little water/concentrated). Occurs with a gain of more salt than water or loss of more water than salt (severe dehydration). s/s: CNS dysfunction.

30
Q

Describe hypokalemia, its etiology, and clinical manifestations.

A

Low levels of K+ in the plasma. Caused by decreased K intake, shift of K+ from ECF into the cells, increased K+ (diarrhea or diuretics), increased aldosterone. Causes hyperpolarization=less excitable.. s/s: muscle weakness.

31
Q

Describe hypekalemia, its etiology, and clinical manifestations.

A

High levels of K+ in the plasma. From increased K+ intake, K+ shift from cell to ECF, decreased K excretion. Causes hypopolarization=more excitable. s/s: muscle dysfunction

32
Q

Describe hypocalcemia, its etiology, and clinical manifestations.

A

Decreased bound Ca+ in the blood d/t binding to other plasma proteins or organic ions such as citrate (anticoagulant found in blood products). s/s: muscle excitability d/t decreased threshold potential. Trousseau (BP cuff causing spasm)and Chvostek signs (facial twitch

33
Q

Describe hypercalcemia, its etiology, and clinical manifestations.

A

Increased bound Ca+ in the blood. Causes an increased in threshold potential of the cells. s/s: muscle weakness, lethargy.

34
Q

Describe hypomagnesia, its etiology, and clinical manifestations.

A

Decreased bound Mag in blood. Causes by chronic alcoholism. Often cause hypokalemia, must correct K+levels to correct Mag levels. s/s: because Mag depresses the release of acetylcholine a decrease in it will cause increased neuromuscular excitability- Trousseau and Chvostek signs.

35
Q

Describe hypermagnesia, its etiology, and clinical manifestations.

A

Increased Mag in the blood. s/s: Acetylcholine is more depressed causing depressed neuromuscular function. Lethargy

36
Q

Describe hypophosphatemia, its etiology, and clinical manifestations.

A

Decreased phosphate in the plasma. s/s: decreased body functions d/t phosphate being a major component of ATP

37
Q

Describe hyperphosphatemia, its etiology, and clinical manifestations.

A

Increased levels of phosphate in the plasma. Seen in chronic kidney disease which impedes the excretion of phophate and creates calcium phosphate salts s/s: calcium phosphate salts cause aching joints and hypocalcemia=muscle excitability.

38
Q

What are four themes of cell injury?

A
  1. ATP depletion (cells swell d/t increased NaCl)
  2. Free radicals and ROS
  3. Increased intracellular Ca
  4. Defect in the plasma membrane
39
Q

What is the difference between apoptosis and necrosis?

A

Apoptosis is organized cell death and necrosis is disorganized, unplanned cell death resulting in the release of toxins and triggers an inflammatory response.

40
Q

What is dysplasia?

A

Abnormal cells that are not pre-cancerous.

41
Q

What is metaplasia?

A

Change of cell from one type to another, normal or abnormal.

42
Q

How does DNA result in a protein?

A

DNA creates RNA via transcription and then through translation RNA creates a protein.

43
Q

Define a gene.

A

The functional and physical unit of heredity passed from part to offspring. Genes are pieces of DNA and most genes contain the info for making a specific protein.

44
Q

What is deletion?

A

Loss of a piece of DNA from a chromosome.

45
Q

What is duplication?

A

Production of one or more copies of any piece of DNA, including a gene or even an entire chromosome.

46
Q

What is insertion?

A

When a DNA sequence is inserted into a gene disrupting normal structure and function of that gene.

47
Q

What is translocation?

A

Breakage and removal of a large segment of DNA from one chromosome, followed by the segment’s attachment to a different chromosome.

48
Q

What are the four types of necrosis?

A
  1. Coagulative (most common- ischemic cellular injury leading to loss of pl. mem.’s ability to maintain gradient=influx of Ca ions and mitochondrial dysfunction resulting in pl. mem degradation)
  2. Liquefactive (dissolution of dead cells occurs quickly and an area of lysosomal enzymes and dissolved tissues for an abscess or cyst- may be seen in the brain d/t bacterial infection)
  3. Fat (death of adipose tissues usu. d/t pancreatitis or trauma
  4. Caseous (damaged lung tissue d/t tuberculosis)
49
Q

What happens in autosomal recessive inheritance?

A

Two copies of a disease allele are required for an individual to be susceptible to expressing the phenotype. Ex- Cystic fibrosis, albinism, phenylketonuria

50
Q

What is autosomal dominant inheritance?

A

Only one copy of a disease allele is necessary for an individual to be susceptible to expressing the phenotype. Ex-Marfans and Huntingtons

51
Q

What is the difference between homozygous and heterozygous chromosomes?

A

Homozygous chromosomes have two dominant or two recessive alleles. Heterozygous chromosomes have one dominant and one recessive allele (Ex- an autosomal dominant trait is expressed the same if it is homozygous or heterozygous)

52
Q

X-linked recessive inheritance:

A

Both males and females can be affected although males are typically more affected because they only carry one copy of genes found on the X chromosome. Ex-hemophilia

53
Q

Sex linked chromosome disorders include:

A 
Klinefelter (extra X chromosome=more feminine males)
Turner syndrome (monosomy X=only one X chromosome resulting in a female phenotype. Webbed neck, short stature, wide chest, heart defects, lymphedema at birth, failure to dev. sec. sexual characteristics)
Multiple X Femalesand Double Y Males (extra copies of chromosomes. Females may have abnormal menstruation and males may be taller)
54
Q

Non-disjunction syndromes:

A

Occur when homologous chromosomes fail to seperate during meiosis or mitosis.
Ex- Trisomy 21, Trisomy 18(Edward syn), Trisomy 13 (Patau)

55
Q

Deletion disorders include:

A

Cri du Chat which is a deletion of part of chromosome 5 (characterized by laryngeal abnormalities=cat crying as infants)

Advanced Pathophysiology (12 decks)

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