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FOM Final Review > Week 3 > Flashcards

Week 3 Flashcards

0
Q

When glycogen is being made. . .

A

Insulin is high. Insulin activates protein phosphatase1 which dephosphorylates glycogen synthase and activates it. Then glycogen synthase adds UDP-glucse onto the non-reducing end of glycogen chain with n residues.

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1
Q

Before Glucose is added to the Glycogen chain. . .

A

Hexokinase makes glucose into glucose 6-phosphate. Then phosphoglucomutase makes glucose 6-phosphate into glucose 1-phosphate. Last, UDP glucose phosphorylase makes glucose 1-phosphate into UDP-glucose.

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2
Q

After 11 units of UDP-glucose have been added to glycogen. . .

A

branching enzyme will break a 1:4 bond about 7 glucoses in and make a 1:6 bond several units down. Both chains extend with 1:4 bonds until they are 11 units long and the process restarts.

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3
Q

Advantages to glycogen branching:

A
  1. increased solubility

2. more active ends (so glycogenolysis and glycogenesis can happen rapidly)

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4
Q

Glycogen’s function in the liver:

A

Serves as a glucose buffer for blood and all peripheral tissues

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5
Q

Glycogen’s function in the heart & skeletal muscle:

A

Glucose serves as a buffer for glucose 6-phosphate- glucose that can only be used within the cell

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6
Q

Defects in glycogen metabolism present as:

A

Fasting hypoglycemia (low glucose) & muscle pain during exercise

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7
Q

GSD 0: Causes and symptoms:

A

Cause: Glycogen synthase deficiency
Symptoms: Exercise intolerance, cardiac & muscle hypertrophy (increase size in cells) - failure to make glycogen at all

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8
Q

GSD I, Von Gierke’s disease - Causes, Treatment & Symptoms

A

Cause: Glucose 6-Phosphate deficiency - not a problem in glycogen synthesis or breakdown
Treatment: Avoid fasting, have frequent meals that take a long time to digest (injections of uncooked cornstarch)
Symptoms: Fasting hypoglycemia, lactic acidosis, hepatomegaly (due to glycogen accumulation in the liver - can’t export glucose from liver), hyperuricemia & hyperlipidemia (liver fails so you can’t package fat anymore)

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9
Q

GSD IIIa, Coris Disease - Cause, Treatment, Symptoms:

A

Cause: Deficiency of 1,6 glucosidase activity of debranching enzyeme
Treatment: Freq, high carb meals, avoid fasting, can’t consume many excess calorie
Symptoms: Affects liver & muscle, fasting hypoglycemia & ketoacidosis, hyperlipidemia, hepatomegaly, with elevated AST/ALT, patient will get liver, cardiac problems & muscle pain during exercise

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10
Q

GDS IIIb, Coris Disease: Cause, Treatment, Symptoms

A

Cause: deficiency of 1,6-glucosidase activity of debranching enzyme
Treatment: Freq. high carb meals, avoid fasted state, can’t consume excess calories
Symptoms: Affects only liver, fasting hypoglycemia & ketoacidosis, hyperlipidemia, hepatomegaly with elevated AST/ALT [accumulation of glycogen bc you can only break it down to the ‘stump’], can grow out of this form - distended stomach

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11
Q

GSD IV - Causes and Symptoms:

A

Cause: Deficiency in branching enzyme 4,6 transferase
Symptoms: Failure to thrive, hepatomegaly, liver failure, fatal

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12
Q

GSD V, McArdle’s disease - Causes, Treatment, Symptoms

A

Causes: Muscle glycogen phosphorylase deficiency
Treatment: Avoid exercise and try to build up tolerance
Symptoms: Late childhood onset exercise intolerance, myoglobinuria (myoglobin in urine) after exercise, fasting hypoglycemia, causes tissue damage - because the cell loses structure and shape
–Increases creatine kinase, exaggerated increase of creatine kinase and ammonia after exercise [Can’t use sugar so you degrade a.a. to meet energy needs]

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13
Q

Describe Glycogen synthesis (glyconeogenesis):

A
  1. Glycogen synthase (GSD 0) adds UDP glucose molecules until 11 units long
  2. Then 4:6 transferase (GSD IV) branches the glycogen core (adds a unit branch that glycogen synthase can then add 11 units onto)
  3. Glycogen synthase continues with glycogen synthesis
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14
Q

Describe Glycogen degradation (glycogenolysis):

A
  1. Glycogen phosphorylase (GSD 5) removes glucose units
  2. Then when 4 units away from branch, 4:4 transferase (debranching enzyme) removes 3 units
  3. Then alpha-1,6-glucosidase (GSD III) removes a branch point glucose from the chain.
  4. Then glycogen phosphrylase (GSD 5) continues to remove UDP glucose units/degrades glycogen
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15
Q

What two molecules regulate glycogen metabolism in the fasted state?

A

Epinephrine & glucagon

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16
Q

What molecule regulates glycogen metabolism in the fed state?

A

Insulin

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17
Q

What are the effects of glucagon in a liver cell while fasting?

A
  1. Glucagon causes cAMP to activate PKA
  2. PKA phosphorylates glycogen synthase (halts gluconeogenesis)
  3. PKA phosphorylates (activates) glycogen phosphorylase kinase which phosphorylates (activates) glycogen phosphorylase
  4. This causes glycogenolysis and glucose production.
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18
Q

What are the effects of epinephrine on the liver cell in the fasted state?

A
  1. Epinephrine activates PLC
  2. PLC activates DAG and IP3
  3. Then DAG activates PKC and IP3 activates Ca++ and calmodulin dependent kinase.
  4. PKC and Ca++/kinase phosphorylate glycogen synthase (inhibits glycogenogenesis) and activates glycogen phosphorylase kinase (active) which phosphorylates glycogen phosphorylase which causes glycogenolysis to occur (production of glucose)
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19
Q

How does insulin affect the liver cell in the fed state?

A
  1. Insulin activates IRS-1 which activates PI3K which activates PDK which activates PKB (Akt)
  2. PKB (Akt) phosphorylates protein phosphatase-1 (active) and glycogen synthase kinase-3 (inactive)
  3. This means that glycogen synthase is active and promoting glycogenogenesis (making glycogen)
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20
Q

What is the difference in metabolism between liver and sketal muscle?

A
  • Skeletal has no glucagon receptor
  • Skeletal has nerve impulse effects (Ca++ release)
  • Work done in skeletal muscle –> releases AMP –> AMP-K –> glucose release
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21
Q

Virion

A

an extracellular virus waiting to encounter the next host cell

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22
Q

Some viruses can be segmented, meaning that they. . .

A

can re-assort when they are repackaged. This means that a virus can have different strains and that a particular animal can be infected with different types of flu at the same time.

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23
Q

Top strand of DNA=

Bottom strand of DNA=

A 
Coding/sense strand (+)
Template strand (-)
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24
Q

Top strand of RNA=

Bottom strand of RNA=

A

(+) [translatable RNA]

-

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25
Q

Categories of Virus Classes using Pneumonic:

A

Hungry (Herpesvirus), Potbellied (Parvovirus), Red (Reovirus), Person (Picornavirus-Flu), Outside (Orthomyxovirus), Religious (Retrovirus), House (Hepadnovirus)

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26
Q

Class I & VII

A

dsDNA (+/-) virus

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27
Q

Class II Virus

A

(+) ssDNA

28
Q

Class III Viruses

A

dsRNA (+/-)

29
Q

Class IV Viruses

A

(+) ssRNA

30
Q

Class V

A

(-) ssRNA

31
Q

Class V Viruse

A

(+) ssRNA

32
Q

What is reverse transcriptase?

A

RNA dependent DNA polymerase - makes copies of DNA from RNA

33
Q

What is a plaque in the plaque assay?

A

1 plaque = 1 virus particle

-A plaque is a hole in bacterial cell growth that is caused by the virus - if no virus, the plate is covered in bacteria

34
Q

Transformation (Bacteria)

A

-The induction of inheritable changes in a cell causing changes in the growth phenotype and immortalisation

35
Q

Persistance

A

the inability of the host to completely rid itself of the virus (ex:HIV)

36
Q

Cell Fusion

A
  • important cellular process in which several uninuclear cells combine to form a multinuclear cell - cell fusion is a necessary event in cell maturation so they maintain their specific functions
  • Some viruses have the ability to make the cells fuse together - causes giant dinucleated cells in infections
37
Q

Virulent - virus trait

A

-Virus can only go down the lytic pathway

38
Q

Temperate -viral trait

A

-Virus that can utilize both lytic and lysogenic pathways

39
Q

Prophage

A

Bacterial genome - latent form of the phage
-Upon host cell damage, prophage is excised from the host cell genome (through prophage induction) and the lytic cycle begins

40
Q

Intrinsic Resistance

A

An absence of inaccessibility of the target for the drug action. For example, mycoplasma lack cell walls so they are intrinsically resistant to cell wall inhibitors - no change in bacterial genetics

41
Q

Acquired Resistance

A

Genetic variability exists in the population and resistant forms are able to preferential grow in the presence of the antibiotic [drug itself does not cause the resistance - selecting for bacteria that survive in the presence of the drug]

42
Q

Transposition

A
  • Can cause movement of genetic material (transposable element) within the host genome
  • Transposition could confer resistance to Vancomycin (drug used to treat MRSA)
43
Q

Three ways to transfer DNA in bacteria:

A
  1. Transformation- taking up DNA from outside environment
  2. Transduction- virus injects DNA in new bacterial cells
  3. Conjugation- transfer of R plasmid (can have virulence factors) containing several resistance determinant genes
44
Q

What is superinfection?

A

It is a consequence of overly broad antibiotic treatment.
The broader spectrum of activity and the longer time period of antibiotic treatment - more likely that treatment with antibiotic will cause superinfection.
-Symptoms: range from mild diarrhea to acute enteritis

45
Q 
Prophylaxis-
Pre-emptive-
Empiric Therapy-
Definitive Therapy-
Suppressive Therapy-
A
  • Treating individuals at a high risk of developing an infection to prevent infection (ex: before surgery)
  • Lab test indicates an organism is present but the patient is not symptomatic
  • Empiric therapy - patient is symptomatic but the organisms has not been identified
  • Definitive - pathogen identified (monotherapy, narrow spectrum)
  • Suppressive Therapy - after initial disease is controlled, therapy is continued to prevent recurrance (ex: person with HIV that has a fungal infection- doesn’t have competent immune system)
46
Q

Combined Immunodeficiency (CID)

A

Cause: Purine nucleoside phosphorylase (PNP) deficiency
Symptoms: Low T cells, Normal B cells, chronic infections, FTT, neurological symptoms
Treatment: Bone marrow transplant/hematopoetic stem cell transplant (+/-) chemotherapy
“Ice T got low”

47
Q

Severe Combined Immunodeficiency (SCID)

A

Cause: Deficiency in Adenosine Deaminase (ADA)
Symptoms: Leads to accumulation of 2-deoxyadenosine in the blood which is toxic to lymphocytes, Costrochondral junction dysplasia - skeletal abnormalities, Low T cells & Low B cells
Treatment: Bone marrow transplant/hematopoetic stem cell transplant (+/-) chemotherapy

48
Q

Lesch-Nyhan Diseases (LND)

A

Cause: Inherited deficiency in hypoxanthine-guanine phosphoribosyltransferase (HGPRT) - rare, X-linked syndrome - males only
Symptoms: Self-injury, mental retardation, dystonia (spastic movements), vomiting [often die in 30s due to renal failure - elevated uric acid in urine]
Treatment: Renal failure can be prevented with allopurinol (reduces uric acid) but this doesn’t affect neurological or self-mutilation behaviors

49
Q

Gout

A

Cause: Accumulation of uric acid due to over activity of purin degradation (downstream of salvage pathway) caused by a diet high in organ meats
Symptoms: Uric acid build up as crystals in extremities where temps are lower - extreme, sudden pain, fever
Treatment: Allopurinol (inhibits Xanthine oxidase, reducing uric acid build up)

50
Q

Hereditary Orotic Aciduria

A

Cause: folate deficiency like symptoms caused by deficiency in UMPS enzyme
Symptoms: Excessive urotic acid in urine, megaloblastic anemia, FTT, mental & physical retardation, excessive urotic acid that leads to inhibition of RNA and DNA synthesis,anemia and hyper ammonia
Treatment: Cytidine monophosphate, uradine monophosphate, uradine

51
Q

How is PRPP synthesized?

A

Glucose -> Glucose 6 phosphate - (pentose phosphate pathway) -> ribose 5-phosphate - (PRPP synthetase) -> 5-phosphoribosyl 1-pyrophosphate (PRPP)

52
Q

How are purines degraded?

A

GMP->guanosine->guanine->xanthine->(xanthine oxidase)->uric acid -> urine

AMP->IMP->Inosine->Hypoxanthine->(xanthine oxidase)xanthine->uric acid

Allopurinol blocks the function of xanthine oxidase

53
Q

What happens in Pyrimidine synthesis?

A

CPS II produces carbamoyl phosphate from Glutamine, CO2 and 2ATP. Then Aspartate and carbamoyl phosphate form carbamoyl aspartate which then makes orotic acid which then makes OMP -> UMP -> transformed to make U or C or T for RNA and DNA synthesis.

54
Q

Beta-Lactams

A

Penicillin, Cephalosporin, Carbapenems

  • Bactericidal
  • Target Gram (+) bacteria
  • Bind to penicillin binding proteins which are transpeptidases that catalyze terminal reactions in bact. wall synthesis - this inhibits cross-linking of peptidoglycan - they occupy the D-alanyl-D-alanine substate site of transpeptidase
55
Q

Penicillin Details

A

Side effects: seizure, nausea, diarrhea, hypersensitivity reaction - mild rash due to anaphylaxis, cross-allergenic
Given in forms: Penicillin V (oral) Penicillin G (IV form)
Resistance: Staphylococcal strains & Neisseria gonorrhea produce penicillinases
Notes: Simultaneously administering with probenecid can reduce renal secretion/raise blood levels of drug

Benzathene (what I got!) - longer acting form of penicillin for muscle injection that’s slowly absorbed and associated with irritation and pain

56
Q

Cephalosporin Details

A

Beta Lactam
Side effects: same hypersensitivity as penicillin, seizures, cross-allergenic
-Has 5 different generations that all start with “ceph”
-Dosage must be altered for renal insufficiency since it’s primarily secreted by kidneys

57
Q

Carbapenems Details [imipenem/cilastatin/meropenem]

A

-Broad gram (+) spectrum but MRSA is resistant
Side Effects: seizures, cross allergenic
-Less susceptible to Beta lactamases
-Klebsiella made a carbapenemase

58
Q

Cilastatin

A
  • Decreases cleavage of beta lactam ring and prevents formation of potentially toxic nephrotic metabolite
  • Given with imipenem [which is a carbapenem]
59
Q

Monocyclic Beta-lactam – doesn’t have second ring like other beta-lactams

A

Aztreonam, bactericidal
Targets: gram (-) rods, klebsiella, pseudomonas, serratia
-Works the same as penicillin
Side effects: GI distress, cross allergic, seizures if dose is too high and patient has renal dysfunction

60
Q

What are the three penicillinase-resistant penicillins/beta-lactamases?

A

Nafcillin, Dicloxacillin, Methicillin [not used anymore]

  • Target MSSA- methicillin sensitive staph aureus
  • Mech: similar to penicillins but they have a larger R group so they’re resistant to penicillinases
  • Side effects: Hypersensitivity reactions
  • Anti-staphylococcal penicillins
61
Q

What are the three beta-lactamase inhibitors?

A

Clavulanate (penicillinase), Sulbactam, Tazobactam [bactams]
-Binds irreversibly to penicillinase, allowing penicillins to be effective, must be used with penicillin or penicillin like drug

62
Q

What are the two aminopenicillins?

A

Ampicillin & Amoxicillin
Target: Broad spectrum - gram + and -
Mech: Same as penicillin & inactivated by beta-lactamases
Side effects: Hypersensitivity reactions
Other: water soluble, can pass through porin channels but penicillinase susceptible
Ampicillin -combined with Sulbactam
Amoxicillin - combined with Clavulanate

63
Q

What are the two antipseudomonals?

A

Ticarcillin (combined with clavulanate) & Piperacillin (combined with tazobactam)
Spectrum: Gram (-) bacilli, pseudomonas, broad
Mech: Same as penicillin & inactivated by penicillinases

64
Q

What is Vancomycin?

A

Glycopeptide antibiotic, bactericidal
Tagets: Gram (+), MRSA, C. difficle
Mech: Binds to D-alanyl-D-alanine terminus of cell wall precursor unit, inhibiting the release of the bactoprenol carrier, preventing peptidoglycan synthesis - inhibits transglycosylase reaction
Side effects: Red man syndrome, hypersensitivity, nephrotoxicity-excreted in the kidney
Administered: Oral Vanco is poorly absorbed so its usually given in IV form
Resistance: Enterococci replace the D-alanyl-D-alanine with a D-alanyl-D-lactate/serine to prevent Vanco binding

65
Q

What is Bacitracin? - Like a battery!

A

It prevents dephosphorylation or “recharging” of the bactoprenol carrier that is needed for elongation of peptidoglycan cell wall
SE: Nephrotoxic when given Intramuscularly
Admin: It has poor bioavailability, topical ophthalmic and dermatologic preparations
Resistance is rare and Bacitracin is found in neosporin.

66
Q

What is Polymyxin B?

A

Bactericidal
Spectrum: Multidrug resistant gram (-) bacilli (psedomonas aeruginose & klebsiella pneumoniae)
Mech: Binds to LPS in cell membrane/wall, creating holes leading to the release of cellular contents
Side effects: Nephrotoxicity
“Polymyxin B binds to the LP. . .S”

67
Q

What is Daptomycin?

A

Bafctericidal
-Last resort drug for Gram (+) organisms - VRSA and MRSA
Mech: Binds to the cell membrane and aggregates, creating channels, allowing K+ ions to flow out, depolarizing the membrane and causing cell death

FOM Final Review (4 decks)

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