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Pharm Formulas > Regulatory Enzymes You gotta know > Flashcards

Regulatory Enzymes You gotta know Flashcards

1
Q

What activates pyruvate carboxylase?

A

Requires biotin and ATP Activated by acetyl CoA

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2
Q

What does pyruvate carboxylase do?

A

Pyruvate to oxaloacetate

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3
Q

What does PEP carboxykinase do?

A

Oxaloacetate to PEP requiring GTP

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4
Q

What does Fructose 1,6 bisphosphatase do?

A

Fructose 1,6 bisphosphate to fructose 6 phosphate

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5
Q

What activates fructose 1,6 bisphosphate?

A

Citrate

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6
Q

What deactivates fructose 1,6 bisphosphatase

A

AMP F2,6Bisphosphate

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7
Q

What is the action of glucose 6 phosphate

A

Glucose 6 phosphate to glucose

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8
Q

What is the finding of pyruvate dehydrogenase deficiency?

A

Neurologic defects Lactic acidosis Increased serum alanine

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9
Q

What is the treatment for pyruvate dehydrogenase deficiency?

A

Increased intake of ketogenic nutrients (high fat content or increased ketogenic amino acids lysine and leucine)

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10
Q

What activates pyruvate dehydrogenase complex?

A

NAD+ ADP Ca2+

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11
Q

What is the difference between hexokinase and glucokinase?

A

Hexokinase is found in most tissues except liver and pancreatic beta cells with a lower affinity and lower capacity Hexokinase is unaffected by insulin It is inhibited by glucose 6 phosphate

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12
Q

What is the activator of glycolysis?

A

AMP, F26BP

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13
Q

What is the inhibitor of glycolysis?

A

ATP, citrate

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14
Q

What is the activator of gluconeognesis?

A

Citrate

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15
Q

What is the inhibitor of gluconeogenesis?

A

AMP, fructose 2,6 bisphosphate

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16
Q

What is the activator of the TCA cycle?

A

ADP

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17
Q

What is the inhibitor of the TCA cycle?

A

ATP, NADH

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18
Q

What are the inhibitors of glycogenesis?

A

GLucose 6 phosphate, insulin, cortisol

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19
Q

What is the inhibitor of glycogenesis?

A

Epinephrine, glucagon

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20
Q

What is the activator of glycogenolysis?

A

Epinephrine, glucagon, AMP

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21
Q

What is the inhibitor of glycogenolysis?

A

Glucose6 phosphate, insulin, ATP

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22
Q

What are the activators and inhibtors of the HMP shunt?

A

Glucose 6 phosphate dehydrogenase NADP+ activates NADPH inhibits

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23
Q

What are the inhibitors of de novo purine synthesis?

A

AMP, IMP, GMP

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24
Q

What is the activator of the urea cycle?

A

N-acetylglutamate

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25
Q

What is the activators of fatty acid synthesis?

A

Insulin, citrate activate

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26
Q

What is the inhibitors of fatty acid synthesis?

A

Glucagon and palmitoyl-CoA

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27
Q

What is the inhibitor of fatty acid oxidation

A

Malonyl-CoA

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28
Q

What is the activator of cholesterol synthesis?

A

Insulin, thyroxine

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29
Q

What are the inhibitors of cholesterol synthesis?

A

Glucagon, cholesterol

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30
Q

What are the activators of de novo pyrimidine synthesis?

A

ATP, PRPP

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31
Q

What are the inhibitors of de novo pyrimidine synthesis?

A

UTP

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32
Q

What process is affected by a lack of vitamin C?

A
  1. Antioxidation 2. Decreased iron absorption 3. Hydroxylation of proline and lysine in collagen synthesis 4. Decreased dopamine beta hyroxylase activity
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33
Q

What diseases are inherited by trinucleotide repeat expansion?

A

Huntington (CAG) Myotonic dystrophy (CTG) Fragile X syndrome (CGG) Fredreich ataxia (GAA)

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34
Q

What are the X recessive disorders?

A

Oblivious Females Will Often Give Her Boys Her x-Linked Disorders Ornitine transcarbamylase deficiency Fabry disease Wiskott-Aldrich syndrome Ocular albinism G6PD deficiency Hunter syndrome Bruton agammaglobulinemia Hemophilia (A and B) Lesch-BNyhan syndrome Duchenne muscular dystrophy

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35
Q

What are the areas where type 1 collagen may be found?

A

Bone, skin, tendon dentin, fascia, cornea, late wound repair White stuff

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36
Q

What are the areas where type 2 ollagen may be found?

A

Cartilage, vitreous body, nucleus pulposus CarTWOlage

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37
Q

What area where type 3 collagen are found?

A

Reticulin - skin, blood vessels, uterus, fetal tissue, granulaiton tissue Defective in Ehlers, Danlos syndrome

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38
Q

What area is type 4 collagen found?

A

Basement membranes, basal lamina, lens

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39
Q

What is the defect if I cell disease?

A

defect in N-acetylglucosaminyl-1-phosphotransferase leading to a failure of the Golgi to phosphorylate mannose residues leading to proteins being secreted extracellualrly rather than being delivered to lysosomes

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40
Q

What is the manifestation of I cell disease?

A

Coarse facial features, clouded corneas, crestricted joint movement, and high plasma levels of lysosomal enzymes

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41
Q

alpha amantin does what?

A

inhibits RNA polymerase 2 which makes mRNA

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42
Q

What are the sizes of RNAs relative to each other?

A

rRNA is the most numerous mRNA is the most massive tRNA is the tiniest

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43
Q

What enzymes carry out base excision repair?

A

GEL PLease 1. Glycosylase removes altered bases and creats an AP site 2. One or more nucleotides are removed by AP-Endonuclease, which cleaves the 5’ end 3. Lyase cleaves the 3’ end 4. DNA Polymerase-beta fills the gap 5. Lyase seals it

44
Q

What is the defect that occurs in adenosine deaminase deficiency?

A

ADA is required for degradation of adenosine and deoxyadenosine If this enzyme is deficient lymphocytes die from increased dATP

45
Q

What are the symptoms of HGPRT deficiency (Lesch-Nyhan

A

Hyperuricemia Gout Pissed off Retardation dysTonia

46
Q

What is the built up substance in lesch-Nyhan?

A

Decreased purine salvage leading to increased conversion of xanthine to uric acid, which causes hyperuricemia and subsequent issues

47
Q

What is the structure of cilia?

A

9 doublet + 2 singlet arrangement of microtubules connected to a basal body consisting of 9 triplets

48
Q

What is Menkes disease?

A

X-recessive connective tissue diesease caused by impaired copper absorption and transport due to Menkes protein defect. Leads to decreased activity of lysyl oxidase and brittle kinky hair, growth retardation and hypotonia

49
Q

What is the order of intermediates in the porphyrin pathway?

A

Ala Placed in Urine Cup Produces Heme Aminolevulinic Acid Porphobilinogen Uroporphyrinogen Coproporphyrinogen Protoporphyrin Heme

50
Q

What are the order of enzymes in the porphyrin pathway?

A

Some Doctors Prescribe Unlimited F(ph)enobarbitol S = Ala synthase D = Ala Dehydratase P = Porphobilinogen deaminase U = Uroporphyrinogen decarboxylase F = ferrocheletase

51
Q

What is the order of porphyrin diseases?

A

SLAP Sideroblastic anemia Lead Poisoning Acute intermittent Porphyria Porphyria cutanea tarda

52
Q

What occurs in antiphospholipid syndrome?

A

Anticardiolipin antibodies cause false positive RPR and lupus anticoagulant Can also cause prolonged PTT which is not corrected by the addition of normal platelet-free plasma

53
Q

What are the symptoms of antiphospholipid syndrome?

A

Diagnose based on history of thrombosis, or spontaneous abortion Lupus anticoagulant, anticardiolipin, anti-b2 glycoprotein antibodies

54
Q

What is the difference between boerhaave and mallory weiss?

A

Boerhaave syndrome - transmural distal esophageal rupture with pneumomediastinum due to violent retching

Mallory Weiss - Partial thickness mucosal lacerations at gastroesophageal junction due to severe vomiting. Presents with hematemesis and may be misdiagnosed as ruptured esophageal varices

55
Q

What is trousseau syndrome?

A

Redness and tendernes on palpation of extremities

56
Q

What is the mechanism of metoclopramide?

A

D2 receptor antagonist leading to increased resting tone, contractility, LES tone, motility

This promotes gastric emptying, but does not influence colon transport time

Used for diabetic and postsurgery gastroparesis, antiemetic, persistent GERD

57
Q

What is the mechanism and use of aprepitant?

A

Mech: Substance P antagonist. Blocks NK1 receptors in the brain

Use: antiemetic for chemotherapy induced nausea and vomiting

58
Q

What is power?

A

1-beta

beta = type II error

59
Q

What is the function of the glossopharyngeal nerve?

A
  • Taste and sensation from posterior 1/3 of tongue
  • Salivation from parotid
  • Carotid body and sinus monitoring
  • Elevation of the pharynx and larynx via stylopharyngeus
60
Q

What is the function of the facial nerve?

A
  • Facial movement
  • Taste in anterior 2/3 tongue
  • Lacrimaiton and salivation (submandibular and sublingual glands)
  • Eyelid closing (orbicularis oculi)
  • Auditory volume modulation (stapedius)
61
Q

What are the functions of the vagus nerve?

A
  • Taste from supraglottic region
  • Swallowing
  • Soft palate elevation
  • Midline uvula
  • Talking
  • Cough reflex
  • Parasympathetic to thoracoabdominal viscera
  • Monitoring of aortic arch chemo and baroreceptors
62
Q

What are the functions of the trigeminal nerve?

A
  • Mastication
  • Facial sensation (opthalmic, maxillary, mandibular divisions)
  • Somatosensation from anterior 2/3 of tongue
63
Q

Monckeberg sclerosis

A

Medium sized artery calcification of internal elastic lamina and media of arteries leading to stiffening without obstruction

Pipestem appearance on x-ray and does not obstruct blood flow

Intima not involved

64
Q

Brugada syndrome

A

Autosomal dominant disorder most common in asian males where an ECG pattern of pseudo=right bundle branch block and ST elevation in V1-V3

Increased risk of ventricular tachyarrhythmias and SCD

65
Q

What are the results of a C3 deficiency?

A

Increases risk of severe pyogenic sinus and respiratory tract infections

Increased susceptibility to type III hypersensitivity reactions

66
Q

What are the results of C5-C9 deficiencies?

A

Terminal complement deficiency increases susceptibility to recurrent Neisseria bacteremia

67
Q

What is the consequence of C1 esterase inhibitor deficiency?

A

Causes hereditary angioedema due to unregulaed activation of Kallikrein leading to increases bradykinin

Decreased C4 levels

DONT USE ACE INHIBITORS

68
Q

What are the consequences of CD55 deficiency?

A

DAF deficiency leading to complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria

69
Q

What are the activators of each version of the complement pathway?

A
  • Alternative - spontaneous and microbial surfaces
  • Lectin - microbial surfaces
  • Classic - antigen antibody complexes
70
Q

What are the results of beta and glucagon receptor activation?

A
  1. cAMP formation
  2. PKA activation
  3. Glycogen phosphotrylase kinase activation
  4. Phosphorylation and activation of glycogen phosphorylase
71
Q

What are the results of insulin receptor activation?

A
  1. Tyrosine kinase dimer receptor activation
  2. Glycogen synthase activation
  3. Glycogen formation
72
Q

What are the main characteristics of kartagener syndrome?

A

Primary: Dynein arm defect leading to immotile cilia.

Resultant:

  • Decreased male and female fertility tue to immotile sperm and decreased cilia action in the fallopian tube.
  • Because of this decreased motility, ectopic pregnancy is frequent in females
  • Mucociliary escalator affected leading to bronchiectasis and recurrent sinusitis
  • Dextrocardia (reversal of internal organs)
73
Q

What two elements are required to sinthesize niacin?

A

Typtophan

B2 and B6

74
Q

What are the resultant features of hyperacute graft rejection?

A

Widespread thrombosis of graft vessels leading to ischemia and necrosis from pre existing antibodies to donor antigen

REQUIRES IMMEDIATE REMOVAL

75
Q

What are the features of acute rejection?

A

CD8 mediated activity against donor MHCs

Vasculitis of graft vessels with interstitial lymphocytic infiltrate

76
Q

What are the features of chronic rejection?

A

CD4+ cells respond to recipient APCs presenting donor peptides

Recipient T cells secrete cytokines leading to proliferation of vascular smooth muscle, parenchymal atrophy, interstitial fibrosis and arteriosclerosis

77
Q

What are the features of chronic rejection in

Lungs

Heart

Kidney

Liver

A

Lung: Bronchiolitis

Heart: Accelerated atherosclerosis

Kidney: Chronic graft nephropathy

Liver: Vanishing bile duct syndrome

78
Q

What are the features of graft versus host disease?

A

Maculopapular rash, jaundice, diarrhea, hepatosplenomegaly

Usually occurs in bonemarrow and liver transplants

Beneficial in bone marrow transplant for leukemia

79
Q

What drugs elicit a sulfa drug reaction?

A

Scary Sulfa Pharm FACTS

Sulfonamide antiiotics

Sulfasalazine

Probenicid

Furosemide

Acetazolamide

Celecoxib

Thiazides

sulfonylureas

80
Q

Where does the PDA arise? What does it supply?

A

Right coronary artery

Supplies: AV node, posterior 1/3 of interventricular septum, posterior 2/3 of walls of ventricles, posteromedial papillary muscle

81
Q

What is supplied by the left anterior descending artery?

A

Anterior 2/3 of interventricular septum, anterolateral pappilary muscle, and anterior surface of left ventricle

82
Q

Salivary gland tumors can effect what nerve?

A

Facial nerve

83
Q

What inhibits the rate limiting step of ALA synthase?

A

Glucose, heme

84
Q

What are some of the resultant effects of osteopetrosis?

A

Bone fractures

Thrombocytopenia, anemia, leukopenia with extramedullary hematopoiesis due to bony replacement of the marrow

Vision impairment from impingement of cranial nerves

Hydrocephalus from narrowing of foramen magnum

RTA from lack of carbonic anhydrase leading to decreased reabsorption of HCO3- leading to metabolic acidosis

85
Q

What is the major difference with how Lambert Eaton and Myasthenia gravis appears?

A

Muscle weakness worsens with use in myasathenia gravis as opposed to Lambert eaton which gets better with use. Lambert eaton doesnt affect the face either

86
Q

What are the main effects of cortisol?

A

A BIG FIB

  • Appetitie
  • Blood pressure increase (alpha1 arteriole upregulation)
  • Insulin resistance
  • Gluconeogenesis, lipolysis, and proteolysis
  • Fibroblast activity decreased
  • Inflammatory and immune response decrease
  • Bone formation decrease
87
Q

What are the reasons for parathyroid disease for decreased Calcium despite increased PTH

A

vitamin D deficiency

Decreased calcium intake

Chronic renal failure

88
Q

What are the reasons for decreased PTH and calcium

A

Surgical resection of parathyroid

Autoimmune destruction of parathyroid

89
Q

What is the reason for increased PTH and Ca2+?

A

hyperplasia of parathyroid

Adenoma of parathyroid

Carcinoma

90
Q

What is the reason for decreased PTH but high levels of calcium?

A

Excess Ca2+ intake

Cancer

Increased vitamin D

91
Q

Whta are the three destinies for CO2 as it enters the plasma?

A
  1. Combines with CO2 to create H+ and HCO3- which diffuses out of the cell in exchange for Cl-
  2. Addition to Hb to form HbCO2
  3. Stays dissolved in the serum
92
Q

What are the characteristics of strep bovis?

A

Gram + cocci, colonizes the gut

Can cause bacteremia and subacute endocarditis and is associated with colon cancer

(Bovis in the blood gives you Cancer in the Colon)

93
Q

What is scabies?

A

Sarcoptes scabei infection of the skin leading to pruritus and serpinginous burrows (lines) in the webspace of the hands and feet. Common in children and crowded populations

94
Q

Common causes of osteomyelitis in patients who are sexualy active

A

Neisseria gonorrhoeae (rare)

Septic arthritis more common

95
Q

Common causes of osteomyelitis in patients who have sickle cell disease

A

Salmonella and Staph Aureus

96
Q

Common causes of osteomyelitis in patients who have had joint replacement

A

S aureus and staph epidermidis

97
Q

Common causes of osteomyelitis in patients who have vertebral involvement

A

S aureus and mycobacterium tuberculosis (Pott)

98
Q

Common causes of osteomyelitis in patients who have had a cat bite

A

Pasteurella mutocida

99
Q

Common causes of osteomyelitis in patients who have been abusing IV drugs

A

Pseudomonas, candida, S aureus

100
Q

Microscopic appearance of acute inflammation

A
  • Neutrophil, eosinophil, antibody, mast cell, basophil mediated
  • Rapid onset and short duration
  • Can completely risolve, form abscess, or progress to chronic inflammation
101
Q

Microscopic appearance of chronic inflammation

A

Mononuclear cells and fibroblases

Persistent destruction and repair. Associated with blood vessel proliferation, fibrosis. Granuloma: Nodular collections of epithelioid macrophages and giant cells. Outcomes include scarring, amyloidosis, and neoplastic transformation

102
Q

Difference between primary and secondary amyloidosis?

A

AL: deposition of proteins from Ig Light chains. Can occur as a plasma cell disorder or associated with myeloma. Often affects multiple organ systems including renal, cardiac, hematologic, GI, and neurologic

AA: chronic inflammatory conditions such as rheumatoid arthritis, IBD, spondyloarthropathy, familial Mediterranean fever, protracted infection. Fibrils composed of serum Amyloid A. OFten multisystem

103
Q

What is P-glycoprotien?

A

Also known as multidrug resistance protein 1 (MDR1)

Classically seen in adrenocortical carcinoma but also expressed by other cancer cells

Function: Pump out toxins, including chemotherapeutic agents

104
Q

Z values for 95 and 99 percent confidence interval

A

95 = 1.96

99 = 2.58

105
Q
A

Pharm Formulas (10 decks)

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