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med school pre Rough Review > Exam 1 Summary > Flashcards

Exam 1 Summary Flashcards

1
Q

Describe the function of Golgi apparatus

A

Especially well developed in secretory cells

  • plasma cells-antibodies
  • pancreatic acinar cells- digestive enzymes

Transport between rER and Golgi

  • Coatamer-coated vesicles
  • COP-II: Anterograde
  • COP-I: Retrograde

Vesicular trafficking

  1. Constitutive
  2. Regulated
  3. Lysosomal
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2
Q

Summarize exocytosis

A
  1. Regulated
    - secretory
    - stimulus-induced
    - Ca2+ influx
    - fusion of secretory vesicles
  2. Constitutive
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3
Q

Summarize peroxisomes

A
  • degrade ROS (hepatocytes)
  • Converts water to oxygen and water
  • fat metabolism
  • peroxisomes proteins synthesized by free ribosome
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4
Q

What is Zellwegger syndrome?

A

Pathology: mutation in gene for peroxisome function or protein import

Affects: peroxisomes

Impact: dysfunctional peroxisome activity/ detoxification

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5
Q

Describe the lysosome

A

Targeting proteins for lysosomes
A) hydrolase precursors covalently modified by addition of mannose 6-phosphate (M6P)

B) Binding to M6P receptor 

C) Precursors transported to lysosome 

D) M6P receptor recycled  -Protons pump help reduce pH
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6
Q

What is Tay-Sachs?

A

Pathology: mutation in HEXA gene for lysosome enzymes

Affects: lysosomes

Impact: death of neurons in brain and spinal cord

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7
Q

What is autophagy ?

A
  • Double membrane vacuole

- essential role in starvation, cell differentiation, cell death and ageing

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8
Q

What are proteasomes?

A
  • destroy proteins without involving lysosomes

- tagged with ubiquitin

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9
Q

Summarize lipids in the plasma membrane

A

-Amphipathic
-3 classes
A) Phospholipid
-most abundant
I. Phosphatidylcholine
II. Sphingomyelin
III. Phosphotidylserine
IV. Phosphatidylethanolamine
V. Phosphatidylinositol

B) Cholesterol- membranes inside the cell don’t contain cholesterol

C) glycolipids

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10
Q

Describe proteins of the plasma membrane

A 
2 classes
A) integral
     I. Transmembrane 
         a. Pumps/carriers/transporters
         b. Channels 
         c. Receptors
         d. Linkers
         e. Enzymes
         f. Structural proteins
  II. Anchored

B) Peripheral
-Noncovalent association with integral membrane proteins

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11
Q

Summarize membrane biochemistry

A
  • lipoprotein membrane allows transfer of non-polar lipids into blood
  • fluidity is determined by fatty acids found in polar lipids
  • shorter fatty acids and unsaturated fatty acids make membrane more fluid
    - I.e. arachidonic acid and DHA
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12
Q

Describe the glycocalyx

A

Carbohydrate rich zones

A) glycolipids

B) glycoproteins

C) proteoglycans

  • help establish micro environmental cell surface
  • protection
  • cell recognition
  • cell-to-cell interactions(lectins)
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13
Q

What are lipid rafts?

A
  • specialized cholesterol enriched micro domain

- signal transduction, virus infection and endocytosis

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14
Q

Summarize receptor-mediated endocytosis

A
  • clathrin-dependent
  • cargo-specific
-selective uptake 
Clathrin-coated pits
  A) Receptor recycled, ligand degraded
  B) Receptor and ligand recycled
  C) Receptor and ligand degraded
  D) Receptor and ligand trans-cytosis
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15
Q

Summarize vesicle targeting

A

I. Rab-GTPase interact with tethering protein

II. Docking complex

III. Accurate targeting via:

 a. v-SNARE
 b. t-SNARE
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16
Q

What are the functions of an endosome?

A

-Endosomal processing
I. Early endosome
-sorts and r3cycles

II. Late endosome

 - Receives protein for degradation 
 - Receives new lysosomal enzymes
 - Matures to lysosome  - Lysosome digestion
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17
Q

Summarize pinocytosis

A
  • Clathrin-independent
  • Non-specific
  • Constitutive
  • Fusion with lysosomes
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18
Q

Summarize phagocytosis

A
  • Actin-dependent
  • Cargo-specific
  • Performed by macrophage/neutrophils
  • Psuedopodia extension
  • Fuse with lysosome
  • Residual body of indigestible substances
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19
Q

Sumarrize the types of Actin

A

G actin- free actin

F actin- polymerized and ATP dependent

  • polarized structure(+) (fast) and (-) (slow)
  • bundle, network, single,
  • cell function
  • anchorage
  • Core of microvilli and stereocilia
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20
Q

What is the type and function of the drug, phalloidin?

A

Type: Binds F-actin more tightly

Action: promotes excessive polymerization and inhibits de polymerization

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21
Q

What is the type and function of the drug Cytochalasins?

A

Type: blocks polymerization of actin

Action: inhibit cell movement, division, and induce programmed cell death

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22
Q

What is the function of Myosin ?

A

Myosin 2
Motor and skeletal contraction

  • tail to tail interactions result in bipolar thick filaments
  • each head binds

Stage 1: attachment

Stage 2: release
-ATP binding

Stage 3: Bending
-ATP hydrolysis

Stage 4: force generation
-Pi released followed by power stroke

Stage 5: reattachment

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23
Q

Comeback to page 5

A

Not yet

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24
Q

What are the pathology and organelle affect by myoclonic epilepsy ragged red fibers?

A

Pathology: mutation in tRNA

Affected organelle: mitochondria

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25
Q

What is the pathology and organelle affected in Leber hereditary optic neuropathy?

A

Pathology: mutations in mitochondrial gene

Affected organelle: mitochondria

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26
Q

Summarize neutrophil migration

A

Extravasion

  1. Rolling
  2. Activation
  3. Adhesion
  4. Transemdothelial migration via diapedesis
    • pass through basement membrane
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27
Q

What are the 6 classes of intermediate filaments?

A

1 & 2: keratin (epithelial)

3: vimentin & vimentin-like (meso-derived cells, muscle cells, glial & astrocytes)
4: neurofilaments (neurons)
5: lamins(nucleus): lamin A & B
6: beaded filaments: (eye-liens specific)

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28
Q

Describe intermediate filaments

A
  • rope-like filaments
  • non-polar and highly variable subunits
  • functions
  • structural
  • stabilize cell structure
  • maintain the position of nucleus and other organelles
  • essential for integrity of cell-cell & cell-ECM junctions
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29
Q

What is the purpose of chemotaxis?

A
  • seeks out inflammation

- N-formulated peptide attach to matrix

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30
Q

What is the pathology, affected organelle and impact of cystic fibrosis?

A

Pathology: mutation in gene coding for CFTR impairs proper transport of Cl- into and out of epithelial cells

Affected organelle: cystic fibrosis transmembrane conductance regular CFTR

Impact: salty tasting skin, poor growth, and poor weight gain despite normal food intake, accumulation of thick, sticky mucus, frequent chest infections, and coughing or shortness of breath

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31
Q

What is the function of the inner membrane of the mitochondria?

A

3 major functions:

  • oxidative reactions
  • synthesize ATP
  • regulate metabolite transport in and out of the matrix
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32
Q

What is the function of the matrix of the mitochondria?

A
  • Oxidation of pyruvate and fatty acids
  • Citric acid cycle
  • matrix granule storage of Ca2+
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33
Q

What is the function of the outer membrane of the mitochondria?

A

-contains porins, Phospholipase, and Acetyl coenzyme A synthase

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34
Q

What is the function of the inter membrane space of the mitochondria?

A

Enzymes that use ATP

  • creative kinase
  • adenylate kinase
  • cytochrome C
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35
Q

What are the 3 lipid classification?

A
  1. Simple lipids- triacylglycerol
  2. Derived lipids- fatty acids(saturated and unsaturated)
  3. Complex lipids-phospholipids and glycolipids
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36
Q

Describe the structure and function of cholesterol

A

Dietary lipids= troacylglecerol (TAG)
-27C atom

  • amphipathic because of —OH
  • present in membrane with—OH group towards the aqueous side
  • both leaflets
  • precursor to bile acid/bile salt synthesis
  • precursor for Vit. D
37
Q

State the structure, function of saturated fatty acids

A
  • no. Double bond
  • palmitic acid (18C) and stearic acid (18C) (most abundant in humans)
  • saturated fatty acids bad for cardiovascular

Short(below 6 C) = mostly in milk

Medium= 6-10C

Long = 12-20 C (mostly in humans)

38
Q

Give the structure, function of lipids in general

A

Dietary lipids= Triacylglycerol(TAG)

  • 90%-95% of dietary lipids are TAGs
    • provides 20%-30% of calories
  • stored in adipose tissue
  • structural components of: cell membrane, myelin
  • cholesterol precursor to steroids and vit D
  • prostaglandins (Eicosanoids) derived from fatty acids
  • lipoprotein important for transfer of triacylglycerol and cholesterol esters
  • ketone bodies derived from incomplete oxidation of the fatty acids in TAGs
39
Q

Describe the structure of phospholipids

A
  • base component is phosphatidic acid
  • have non-lipid component
  • all amphipathic
  • presence of unsaturated fatty acid makes membrane susceptible to free radicals

Two types:

  • phospholipids
  • glycolipids
40
Q

What are the 7 types of glycerophospholipids?

A
  1. Phosphatidylcholine(lecithin)- present on inner and outer leaflet
  2. Phosphatidylethanolamine
  3. Phosphatidylserine
4. Phosphatidylinositosol
Derivatives include: 
-PIP2: Phosphatidylinositol biphosphate 
-IP3: inositol triphosphate
-DAG: Diacylglycerol
  1. Cardiolipin
    - most abundant in inner mitochondrial membrane
  2. Plasmalogens and platelet activating factor( PAF)
  3. Dipalmitolphosphatidylcholine (dipalmitoyl lecithin) (DPPC)
    - important component of surfactant
    - high risk of RDS in premature neonates
    - Lecithin-sphingomyelin ratio (L/S) measured to determine lung maturity
    • L/S> 2= mature
    • L/S<1.5= immature
      • Maternal steroid injections improve lung maturation
41
Q

What are the types of glycolipids?

A
  1. Cerebroside = ceramide + monosaccharide
  2. Sulfatide= ceramide + monosaccharide+ sulfate
  3. Globoside= ceramide + oligosaccharide
  4. Ganglioside= ceramide+ oligosaccharide containing NANA
42
Q

Summarize glycolipids basics glycosphingolipids

A
  • ceramide+ carbohydrate
  • found mainly on outer leaflet
  • glycolipids + glycoprotein = glycocalyx
43
Q

What are the categories of unsaturated fats?

A

Monounsaturated+ polyunsaturated

44
Q

What are the essential polyunsaturated fats?

A
  1. Alpha linolenic acid (omega-3)

2. Linoleic acid (omega-6)

45
Q

Where are trans fats found?

A
  • margarine
  • baked goods
  • fried goods
46
Q

What are the derivatives of alpha linolenic acid?what are their uses?

A

1st derivative- eicosapentaenoic acid(EPA) uses- anti-inflammatory, cardio protective

2nd derovative- decosahexaenoic acid (DHA)- neural brain development and vision

47
Q

What are the derivatives of linoleic acid?what are their uses?

A

1st derivative- arachadonic acid uses: formation of eicosanojds

48
Q

What are the types of eicosanoids and their uses?

A
  1. Prostaglandins
    - PGE: mediators of inflammation
    - thromboxane: platelet aggregation
  2. Leukotrienes
    - Mediator of allergic response that cause bronchoconstriction and itching
49
Q

After what carbon in unsaturated fatty acids, can humans not add a bond?

A

After C 9

50
Q

What does nutritional deficiency of fatty acids lead to?

A

Nutritional deficiency of essential fatty acids leads to scaly dermatitis, rough and dry skin, loss of hair

51
Q

What are the high affinity Glucose transporters? What are the low affinity glucose transporters?

A

High affinity- glut 1, 3, 4

Low affinity- glut. 2 and 5

52
Q

Where are GLUT 1 located?

A

Brain, RBC, kidneys

53
Q

Where are GLUT 2 located?

A

Intestine, hepatocytes, renal tubules cells, B cell/pancreas,

Transports large amounts of glucose @high glucose concentration

  • Intestines/mucosal cells: release of sugar
  • Hepaatocytes: takes up glucose at high glucose levels
  • Renal tubular cells: reuptake of glucose
  • B-cells: transports large amounts and measures glucose levels
54
Q

Where is GLUT 5 located? It’s function?

A

Intestines luminal side, seminal vesicles

  • transports fructose (and glucose only when very high)
  • release fructose —> glucose—> used for energy by sperm
55
Q

Where are GLUT 3? What is the function?

A

Brain, neuron

-constant rate with normal and lower blood glucose concentrations

56
Q

Where are GLUT 4 located? What is its function?

A

Fat cells, skeletal muscle, heart

  • insulin dependent
  • insulin mobilizes transport of GLUT-4 to membrane via endosome
  • Insulin injection can lead to hypoglycemia due to rapid uptake
57
Q

What are the major differences between GLUT and SGLT transporters?

A

GLUT- Na independent, facilitated diffusion

SGLT- Na-dependent, secondary active transport

58
Q

Where are SGLT 1 used?

A

Intestinal mucosal cells

-symporters Na+ glucose/galactose against gradient

59
Q

Where are SGLT 2. used?

A

Kidney

-symporter Na+ + glucose

60
Q

What causes microencephaly?

A

Pathology: GLUT-1 deficiency

Affected organelle: GLUT-1 transporter

Impact:

  • epilepsy like seizures
  • ataxia
  • delayed psychomotor response
  • movement disorder
  • impaired speech
61
Q

What is the rate of diffusion determined by in carrier mediated diffusion?

A
  1. Saturation
  2. Number of transporters
  3. Conformational change
  4. Gradient
62
Q

What does the flux depend on in simple diffusion?

A
  1. 🔼C
  2. Electrical gradient
  3. Temperature
  4. Surface area of membrane
  5. Molecule mass
  6. Membrane permeability
  7. Can be positive or negative

Net flux=0
Fick’s law= flux

63
Q

How are hydrogen bonds broken in amino acids?

A

Heat, 5-10M urea, salt

64
Q

How are ionic bonds broken in amino acids?

A

Strong acids and bases

65
Q

How are hydrophobic interactions in amino acids?

A

1-2% detergent

66
Q

How are disulfide bonds broken in amino acids ?

A

B-mercaptoethanol

2-mercaptoethanol

67
Q

What are the liver function tests?

A
  • ammonium
  • albumin
  • bilirubin
68
Q

What are the indicators of decreased cellular integrity(for the liver)?

A
  • ALT and AST used by not very specific
  • Even though hepatocyte is damaged it can still function
  • High ALT levels indicate liver damage (AST/ALT<2)
69
Q

What is the cause of bile duct obstruction ?

A

Obstructed by gallstones or tumors

70
Q

What are the indicators of bile duct obstruction?

A
  • ALP-1
  • GGT
  • Conjugated bilirubin
  • Increase in both ALP-1 and GGT can indicate bile duct issue (but not either alone)
71
Q

What are the causes of pancreatitis?

A
  • Acute: heavy alcohol intake , gallstones

- Chronic: CF, hypertriacylglycerolemia, ethanol abuse

72
Q

What are the indicators of pancreatitis?

A
  • Serum amylase (a-amylase)

- Lipase (pancreatic lipase)

73
Q

What are the alcohol abuse and Cirrhosis indicators?

A
  • AST/ALT >2 indicates cirrhosis or alcohol abuse
  • High ALP levels can be due to cirrhosis due to fibrosis of intrahepatic bile ducts
  • Lipase /Amylase >2 indicates damage due to alcohol
74
Q

What is alanine aminotransferase (ALT)?

A

Enzyme needed for gluconeogenesis and urea cycle

-ALT higher concentration in hepatocytes

75
Q

Where is Aspartate aminotransferase found?

A

High concentration in liver, heart

76
Q

What is the Alkaline phosphates (ALP)?

A

Creates alkaline pH of bile

-hepatic bile canaculi cells and biliary duct cells have high concentration ALP

77
Q

What are the two types of ALP?

A
  • ALP 1: Indicator of bile duct obstruction
  • ALP 2: indicator of bone disease (Padgett disease or bone tumor ) or found at high levels in growing children and pregnant women
78
Q

What is y-glutamyl transferase (transpeptidase) (GGT) ? What does it do?

A

-transports AA into cell

  • uses glutathione (GSH)
    - glutathione has peptide bond located at y carbon and not a carbon

-can increase due to enzyme induction by ethanol

79
Q

What is creative kinase and how is it formed?

A
  • catalyzes reversible reaction
  • At high ATP levels, creative phosphate (CrP) is formed
  • At low ATP levels, ATP formed from CrP
80
Q

Where is creative kinase found?

A

CK found in cytosol and mitichondria
-Isozymes of CK

  • CK-BB(CK1) - found mostly in brain and intestines
  • CK-MB(CK2)- found in heart (30%) and skeletal muscle (2%)
  • CK-MM(CK3)- found in heart (70%) and (98%)
    - elevated CK-MM indicative of rhabdomyolysis or muscular dystrophy
81
Q

What is troponin?

A

Not an enzyme

-two types: cTnl and cTnT

82
Q

What are the disease indicators of myocardial infarction?

A
  • CK-MB >3% indicates that MI has occurred
  • CK-MB/total CK indicates severity of MI
  • LDH can be used if CK, CK-MB and cTnl/cTnT not available or many days have passed (half life of 5 days)
  • “flipped” LDH-1/LDH-2 ratio (LDH-1>LDH-2)
83
Q

If cellular injury leads to increased levels of specific enzymes in serum, how much would be mild, moderate, and marked?

A

Mild: 2-3 times

Moderate: 3-20 times

Marked: >20 times

84
Q

What are the cons of stem cell tech?

A
  • ESCs genetically different from patient

- Transplant may induce immune response

85
Q

How is cloning done with stem cell tech?

A

Create cloned embryo with donor nucleus

86
Q

What are the cons of using stem cells for cloning?

A
  • inefficient
  • deleterious effects and die early
  • premature aging
  • abnormal embryonic development
87
Q

How can stem cell cloning be used for therapeutic reasons?

A
  • generate organ

- correct genetic error

88
Q

What are the cons for cloning for therapeutic reasons?

A
  • inefficient
  • large number of eggs needed
  • excessive hormone therapy
  • surgery to retrieve eggs

med school pre Rough Review (7 decks)

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