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Pharm (Marcus) > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

List the effects seen in the Triple Response of allergy testing and mediators.

A

a. Response:
i. Microcirculation becomes leaky leading to redness.
ii. Capillaries become leaky leading to swelling.
iii. Sensory nerve endings have a flare response leading irregular welt borders

b. Mediators:
i. Eggs, peanuts

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2
Q

Describe the pharmacology of the 2 groups of H1 antihistamines; list prototypical agents for each group.

A

a. 1st Gen:
i. Most have anticholinergic activity, marked sedation & anti-motion sickness activity
ii. Benadryl, Dramamine, Periactin, Phenergan
b. 2nd Gen:
i. No anticholinergic effects or sedation
ii. Allegra, Clartitin, Zyrtec

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3
Q

Recall the major indications for 1st generation antihistamines, and contrast 1st and 2nd generation antihistamine.

A

a. 1st Gen:
i. Can cross the BBB causing mild sedation, have effects on H1 & H3.
ii. Sleep aids
iii. Anti-nausea/antiemetic
b. 2nd Gen:
i. Same efficacy as Gen 1 without crossing BBB. No sedation

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4
Q

List the uses of the H2 antihistamines, contrast PPIs, and name 2 members of this group.

A

a. H2:
i. Use: Bind to histamine receptors & decreases H+/K+ ATPase pump activity. For mild acid reflux.
ii. Zantac, Pepcid
b. PPI’s:
i. Use: Directly inhibit H+/K+ ATPase pump
ii. Omeprazole (Nexium, Prilosec)

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5
Q

Describe serotonin effects in neural and non-neural tissues.

A

a. Neural:
i. Mood, sleep, temp regulation, blood pressure, vomiting, depression anxiety, migraines
b. Non-neural:
i. GI: Facilitates peristalsis. Overproduction –> diarrhea
ii. Respiratory: Facilitates ACh release –> constriction
iii. CV: Contraction of vascular smooth muscle, except heart & skeletal muscle.

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6
Q

What produces, breaks-down serotonin?

A

a. Serotonin is produces from tryptophan (an amino acid)
b. Serotonin is broken down by MAO into 5-HIAA
i. High amounts of 5-HIAA levels in the blood are indicative of an enterochromaffin tumor

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7
Q

List the source of serotonin in the brain, three main 5-HT agonist targets, two main 5-HT antagonist targets, and drugs in each category.

A

a. Source:
i. Raphe nuclei
b. Agonist targets:
i. 5-HT1A
1. Buspar (partial agonist). Used for anxiety & OCD. Slows down serotonin release.
ii. 5-HT1B
1. Sumatriptan for migraines
iii. 5-HT1D
1. Sumatriptan
c. Antagonsit targets:
i. 5-HT2A:
1. Platelets, smooth muscle: Phenoxybenzamine, Cyproheptadine
ii. 5-HT3 (Ion channel):
1. Area postrema: Zofran will block nausea

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8
Q

Compare and contrast preventatives and treatments for migraine headache.

A

a. Preventatives:
i. Glucocorticoids, Beta-blockers, CCB’s, ACEi, antidepressants, anti-seizure meds, Botox, MAbs (Aimovig, blocks CGRP-r)
b. Treatments:
i. Triptans (#1), anti-nausea, pain relief

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9
Q

Describe the action and indication for the use of sumatriptan.

A

a. Action:
i. Bind to 5-HT1D/1B in cranial blood vessels & prevent dilation & stretching of pain endings.
b. Toxicity:
i. Recurrence of migraines
ii. Coronary vasospasm (rare)
iii. Serotonin syndrome (If taking with SSRI’s, MAOI’s)

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10
Q

List the three categories of hyperthermia disorders, contributing factors, and treatments.

A

a. Serotonin Syndrome:
i. Precipitation: SSRI’s, antidepressants, tramadol, ondansetron, fentanyl, sumatriptan, LSD, ginseng, St John’s Wort
ii. S/S: Hyperthermia within hours, coma or death if not treated.
iii. Tx: Sedation, paralytics, intubation & ventilation
b. Neuroleptic Malignant Syndrome:
i. Precipitation: D2-blocking antipsychotics
ii. S/S: Hyperthermia, HTN onset over 1-3 days
iii. Tx: IV Benadryl, cooling, sedation with benzos
c. Malignant Hyperthermia:
i. Precipitation: Anesthetics
ii. S/S: Hyperthermia, tachycardia, HTN, muscle rigidity within minutes
iii. Tx: Dantrolene, cooling

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11
Q

Differentiate between anxiety and depression, and list major types of each.

A

a. Anxiety:
i. Activity based.
ii. GAD, OCD, PTSD, social phobia
b. Depression:
i. Sadness.
ii. Dysthymia, psychosis, bipolar, seasonal affective disorder, postpartum

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12
Q

List the four categories of antidepressant medications in order of treatment severity.

A

a. SSRI’s
b. SNRI’s
c. TCA’s
d. MAOI’s

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13
Q

Describe the primary MOA and use for the major anti-seizure drugs.

A

a. Ion conductance modification: Na+, K+, Ca++
b. Enhance GABA
c. Inhibit Glutamate

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14
Q

Describe the most common automatisms seen with seizures.

A

Lip smacking, swallowing, fumbling, scratching, walking about

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15
Q

Differentiate tonic and clonic.

A

Tonic: Increased muscle tone/stiffness.

Clonic: Rapid movement/jerking

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16
Q

List the drugs of choice for focal seizures, generalized tonic-clonic seizures, absence and myoclonic seizures, and status epilepticus.

A

a. Focal: Carbamazepine
b. Generalized tonic-clonic: Phenytoin
c. Absence: Ethosuxamide
d. Myoclonic: Valproic Acid (Depakene)
e. Status epilepticus: Lorazepam, Diazepam

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17
Q

Identify the mechanisms of antiseizure drug action at the levels of specific ion channels or neurotransmitter systems.

A

a. Block Na+ channels
b. Enhance GABA
c. Decrease Glutamate
d. K+
e. Ca2+ channel inhibition (Ethosuxamide)

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18
Q

Describe what is meant by competing for binding sites on albumin, and potential problems for free phenytoin levels.

A

a. Phenytoin (Dilantin), carbamazepine, valproic acid, & sulfonamides (Abx) all bind to plasma albumin. If multiple meds compete for same binding sites that will increase free plasma drug levels, which can cross BBB & be harmful.
b. Valproic acid competes & dislodges phenytoin from albumin.

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19
Q

Indicate why benzodiazepines are rarely used in the chronic therapy of seizure states but are valuable in status epilepticus.

A

a. Due to the CNS depressant/drowsy effect.
b. They are available in IV form and very effective quickly.

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20
Q

Identify the main treatment targets in infantile spasms.

A

a. Vigabatrin (GABA analog)
b. Zonisamide (Zonergan)
c. Corticotropins

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21
Q

Describe major considerations in status epilepticus.

A

a. Pt history, EEG, Eyewitness
b. Klonipin for long-term use but only available in PO form.

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22
Q

Perioperative Considerations for patients with seizure disorders.

A

a. Chronic phenytoin use makes patients more resistant to NDM-Blockers
b. If actively taking phenytoin then it will enhance NDMB
c. Avoid Methohexital, sevoflurane, & Demerol as they could stimulate seizure activity

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23
Q

List alternative therapies for seizure management.

A

a. Vagus nerve stimulation (increase PSNS)
b. Ketogenic diet (switch from carbs to more fatty diet)
c. Medical Marijuana (Cannabinoids)
d. Surgery (foci resection)

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24
Q

Describe the main pharmacokinetic features, and list the adverse effects of carbamazepine.

A

i. MOA:
Blocks Na+ channels, enhances GABA, decreases glutamate
ii. Use:
1. Drug of choice for focal seizures*
2. In conjunction with phenytoin.
3. Trigeminal neuralgia
4. Bipolar disorders
iii. Kinetics:
Peak in 6-8hrs. T1/2 is 36hrs but drops to 20hrs with continued use.
iv. Interactions:
Affects all anti-seizure meds

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25
Q

Describe the main pharmacokinetic features, and list the adverse effects of phenytoin,

A

i. MOA:
1. Alters Na+, K+, * Ca2+ conductance. Enhances GABA & decreases Glutamate.
ii. Fosphenytoin:
1. More soluble prodrug & can cross BBB. Can be given IM.
iii. Use:
1. Very effective for tonic-clonic, focal
iv. Toxicity:
1. Nystagmus, diplopia, ataxia, sedation
2. Gingival hyperplasia, Hirsutism, coarsening of facial features.
3. Decrease dose in pregnancy as it can affect fetus.
4. Give folic acid (B-9) supplement to avoid some toxicities.

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26
Q

Describe the main pharmacokinetic features, and list the adverse effects of lacosamide.

A

i. MOA:
1. Blocks Na+ channels
ii. Use:
1. Focal seizures
iii. Toxicity:
1. Dizziness, nausea, HA, diplopia
2. Minimal drug interactions

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27
Q

Describe the main pharmacokinetic features, and list the adverse effects of phenobarbital.

A

i. MOA:
1. Enhances GABA, decreases excitatory transmission. Sedative-hypnotic
ii. Use:
1. Generalized tonic-clonic, focal-declining,
2. Drug of choice for infants*
3. Injection for status epilepticus
iii. Not useful in:
1. Absence seizures, atonic attacks, infantile spasms
iv. Toxicity:
1. Sedation
2. Overdose: unsteady gait, slurred speech, confusion, respiratory depression

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28
Q

Describe the main pharmacokinetic features, and list the adverse effects of ethosuximide.

A

i. MOA:
1. Ca2+ channel inhibition
ii. Use:
1. Drug of choice* for Absence seizures
iii. Toxicity:
1. Minimal pain, gastric distress
2. Lethargy at high doses

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29
Q

Describe the main pharmacokinetic features, and list the adverse effects of valproic acid.

A

i. MOA:
1. Unknown but probably All (increase GABA, decrease glutamate, increase K+ conductance, blocks high frequency firing).
ii. Use:
1. Absence, tonic-clonic, clonic, bipolar, migraine (Broad spectrum)
iii. Toxicity
1. #1 is GI (N/V, pain, heartburn)
2. Competes with phenytoin on albumin binding sites

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30
Q

Differentiate between sedation and hypnosis.

A

a. Sedation:
i. Sedation but not sleep
b. Hypnosis:
i. Inducing sleep (Ambien, Lunesta)

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31
Q

Identify the major subgroups of sedative hypnotics, and major drugs in each sedative-hypnotic subgroup, and their receptor target.

A

a. Benzodiazepines:
i. Diazepam, Midazolam, lorazepam
b. Barbiturates:
i. Phenobarbital, thiopental, methohexital
c. Sleep aids:
i. Zolpidem
d. Anxiolytics:
i. Buspirone
e. Ethanol:

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32
Q

Summarize characteristic pharmacodynamic and pharmacokinetic properties of ethanol.

A

a. Dynamics:
i. Enhances GABA. Inhibits glutamate from opening NMDA channel.
b. Kinetics:
i. Rapid onset & distribution. Metabolized in the liver

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33
Q

List the molecular targets of ethanol.

A

a. Neurotransmitter receptors: Amines, amino acids, opioids, neuropeptides
b. Enzymes: Na+/K+ ATPase, adenylyl cyclase, phospholipase C

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34
Q

Recall the management of acute alcohol intoxication.

A

a. Prevent respiratory depression & aspiration.
b. Correct electrolyte imbalance (Thiamine, magnesium, multivitamin, potassium glucose)

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35
Q

Outline the pharmacotherapy of (1) the alcohol withdrawal syndrome and (2) alcohol-use disorders.

A

a. Mild:
i. Tachycardia, HTN, tremors, anxiety, insomnia (last 1-2 days)
b. Severe:
i. Withdrawal seizures, hallucinations (last 1-5days)
c. Delirium tremens:
i. Delirium, agitation low grade fever, diaphoresis

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36
Q

Diagram the process of thrombogenesis including the platelet phases and the roles of the various mediators (PGI2, collagen vWF, ADP, TXA2, 5-HT).

A

a. Prostacyclin (PGI2): Released from EC lining to prevent clots.
b. Collagen & vWF: Bind to GP Ia & Ib activating the platelets, which release ADP, TXA-2, & 5-HT
c. Phases:
i. Adhesion: Platelets adhere to wounded area
ii. Aggregation: Upregulate surface proteins to bind together.
iii. Secretion: Pro-coagulation proteins to stabilize the clot.
iv. Cross-linking of adjacent platelets

37
Q

Draw the coagulation cascade including the intrinsic pathway.

A

Damaged surface activates Factor XII to XIIa. Factor XIIa activates Factor XI to Xia. Factor Xia activates Factor IX to IXa. Factor IXa activates Factor X to Xa.

38
Q

Draw the coagulation cascade including the extrinsic pathway.

A

Tissue factor activates Factor VII into VIIa. Factor VIIa activates Factor X into Xa. Factor Xa converts Prothrombin to thrombin. Thrombin converts fibrinogen to fibrin. Fibrin with help of Factor XIIIa develops Cross-linked fibrin clot.

39
Q

What are the functions of Factor VIII, TFPI, antithrombin, & active protein C in the coagulation pathway?

A

d. Factor VIII:
i. Activated by thrombin to Factor VIIIa, which then activates Factor X to Xa.
e. TFPI:
i. Inhibits conversion of Factor VII to VIIa
f. Antithrombin:
i. Inhibits conversion of Factor VIIa to Factor X & inhibits thrombin.
g. Active Protein C:
i. Inhibits conversions of Factor VIII to VIIIa & Factor V to Va.

40
Q

List the inherited & acquired risk factors for DVT.

A

a. Inherited:
i. Antithrombin III deficiency, Protein C & Protein S deficiencies, Sickle cell anemia, Activated Protein C resistance.
b. Acquired:
i. Bedridden, obesity, surgery, trauma, estrogen use, malignancies

41
Q

Define the following conditions: DIC. Include causes and treatments.

A

i. Causes:
1. Massive tissue injury, malignancy, bacterial sepsis, abruptio placentae
2. Overstimulation & consumption of clotting factors & platelets.
ii. Treatment:
1. Plasma transfusions & Factor replacement
2. Treat underlying cause.

42
Q

Define the following conditions: HIT. Include causes and treatments.

A

i. Cause:
1. The body makes antibodies to HMW heparin in the system, which bind to heparin & platelets  low platelet count.
ii. Treatment:
1. Fondaparinux

43
Q

Draw the pathway for fibrinolysis including the mediators involved.

A

a. T-pa or urokinase convert Plasminogen into Plasmin. Plasmin breaks down fibrinogen into degradation products & breaks down Fibrin into fibrin split products.
b. Streptokinase can be given in case of DVT or PE. It activates plasminogen.
c. Aminocaproic acid blocks plasminogen to stabilize clot.

44
Q

List the four classes of coagulation modifier drugs, and examples of each.

A

a. Anticoagulants:
i. Heparin & Warfarin
b. Antiplatelet:
i. Aspirin, Plavix, Abciximab
c. Thrombolytic (Fibrinolytic):
i. Streptokinase (break down thrombi), t-pA
d. Hemostatic or Antifibrinolytic:
i. Vitamin K, Plasma, Aminocaproic acid

45
Q

Differentiate the indirect and direct thrombin inhibitors and briefly describe how each functions to inhibit thrombin.

A

a. Indirect:
i. They enhance antithrombin activity, which inhibits thrombin & conversion of Factor VIIa to Factor X.
b. Direct:
i. Angiomax & Hirudin: Bind to both active & substrate recognition sites of thrombin.
ii. Argatroban: Bind only to thrombin active sites

46
Q

Explain Fondaparinux heparin and the use.

A

Targets & binds to antithrombin directly, which binds with factor Xa blocking factor II.

47
Q

Explain LMW and the use.

A

i. Only contain active components but are less effective.
ii. More specific to factor Xa.

48
Q

List the toxicity and contraindications of HMW heparin and treatment.

A

a. Toxicity:
i. Bleeding
b. Contraindications:
i. Hemophilia, severe HTN, hemorrhage, infective endocarditis, active TB, GI ulcers, advanced hepatic disease
ii. Elderly & renal failure patients are more prone to hemorrhage
c. Treatment:
i. Protamine sulfate binds to & inactivates heparin

49
Q

Describe the laboratory testing for coagulation pathways and normal values.

A

a. Tests:
i. PT assess the function of extrinsic system & common pathway of coagulation cascade.
ii. aPTT assess intrinsic & common pathway of coagulation cascade.
b. Values:
i. INR normal is 0.8 – 1.2
ii. aPTT normal is 35 – 45sec

50
Q

What are the MOA treatment considerations, & reversal for Warfarin?

A

i. MOA:
1. Blocks carboxylation of factors. Reduce prothrombin activity to 25% of normal.
2. 8-12hr delay in onset of action.
ii. Consideration:
1. 99% protein binding= may dislodge antiseizure meds
2. Birth defects, hemorrhagic disorder in the fetus, cutaneous necrosis.
3. Reduce dose or D/C if prothrombin activity is < 20% of normal.
iii. Reversal:
1. Stop drug. Large dose Vit-K. FFP, Factor IX concentrates

51
Q

List non-warfarin anticoagulant drugs and their targets.

A

a. Xarelto, Eliquis, Bevyxxad:
i. Target Factor Xa
b. Pradaxa:
i. Targets thrombin

52
Q

List the various fibrinolytic drugs.

A

a. Streptokinase
b. Urokinase:
i. synthesized by the kidney
ii. Lyses thrombi from within
c. Tissue plasminogen activators (t-PA):
i. Activates plasminogen that is bound to fibrin

53
Q

Describe the targets for the antiplatelet aggregation drugs Aspirin, Plavix, Ticlid, and abiciximab.

A

a. ASA: Platelet prostaglandin
b. Plavix & Ticlid: InhibitADP receptor
c. Abciximab: Factor IIb/IIIa

54
Q

Describe how bleeding disorders can be treated with Vit. K, plasma fractions, desmopressin, aminocaproic acid, and tranexamic acid.

A

a. Vit-K:
i. Activity to produce factors VII, IX, & X  normal factor production
b. Plasma fractions:
i. Replenishes factors  normal clotting cascade
c. Desmopressin:
i. Increases factor VIII activity
d. Aminocaproic acid:
i. Completely inhibits plasminogen activity  clot stabilization
e. Tranexamic acid:
i. Inhibits plasminogen to plasmin conversion  clot stabilization

55
Q

Describe the exocrine and endocrine functions of the pancreas.

A

a. Exocrine:
i. Produces digestive enzymes, which empty into the duodenum.
b. Endocrine:
i. Islet cell release insulin & glucagon into bloodstream.

56
Q

Contrast the roles of insulin and glucagon on blood glucose levels.

A

a. Insulin:
i. Pre to Pro-Insulin, C-peptide gets cleaved making insulin.
ii. Beta cells release insulin
b. Glucagon:
i. Alpha cell produce glucagon when low BG.

57
Q

List the four main types of diabetes mellitus.

A

a. Type I= Insulin dependent
b. Type II= Non-insulin dependent
c. Type III= temporary due to other causes like pancreatitis, drug therapy, anti-cancer drugs, etc.
d. Type IV= Gestational (hormone fluctuating)

58
Q

List the three cardinal symptoms of diabetes.

A

a. Polyphagia, polyuria, polydipsia

59
Q

Describe the sorbitol pathway, and why it leads to peripheral neuropathy and blindness.

A

Glucose enters cells & some is converted into Sorbitol & fructose. Those two cannot leave the cell, which leads to a change in osmolality. H2O diffuses into the cell and eventually the cell bursts.

60
Q

Differentiate the two types of diabetes tests.

A

a. Fasting BG:
i. 8hrs no food and test should be <100mg/dL
b. Glucose tolerance test:
i. Take blood & urine then drink very sugar heavy drink then check BG level at 30mins, 1, 2, & 3 hrs.
ii. If BG >126mg/dL after 1 -2hrs then definitive for diabetes

61
Q

Describe the structure of insulin.

A

Alpha-chain, Beta-chain are connect at cystines. Also C-Peptide chain present, which can be cleaved.

62
Q

Delineate the insulin receptor pathway.

A

Insulin binds to tyrosine kinase receptor  phosphorylates activities downstream incl. IRS  increased protein production, which are responsible for membrane translocation of GLUT transporters.

63
Q

List problems and treatments for hypoglycemia.

A

a. Problems:
i. Anxiety, blurred vision, palpitations, shakiness, sweating, slurred speech
b. Treatment:
i. Glucose, soda, glucagon injection

64
Q

What are the MOA, potential side effects, and examples of Biguanides?

A

i. MOA: Decrease hepatic glucose production
ii. Side effects: GI
iii. Example: metformin (Glucophage)

65
Q

What are the MOA, potential side effects, and examples of Insulin secretagogues?

A

i. MOA: Bind to & close K+r channels  more insulin release
ii. Side effects: Cardiac with Tolbutamide
iii. Example: Sulfonylureas, Meglitinide, Phenylalanine

66
Q

What are the MOA, potential side effects, and examples of c. Thiazolidinediones (TZDs)

A

i. MOA: Increases production of gene products associated with insulin receptor. Increase GLUT-4 without insulin binding.
ii. Side effects: Risk of MI, especially with insulin & nitrates
iii. Example: Avandia

67
Q

What are the MOA, potential side effects, and examples of Alpha-glucosidase Inhibitors:

A

i. MOA: Prevents glucose uptake in the intestine (beneficial in Pre-diabetics)
ii. Side effects: Flatulence, diarrhea, abdominal pain (Less in countries eating low sugar)
iii. Example: Acarbose

68
Q

What are the MOA, potential side effects of Bile Acid Sequestrant

A

i. MOA: Surround food & prevents glucose & cholesterol uptake into body
ii. Side effects: GI related

69
Q

What are the MOA, potential side effects, and examples of Amylin Analogs

A

i. MOA: Suppresses glucagon & insulin release  decreased circulating glucose.
ii. Side effects: Parenteral only
iii. Example: Symlin

70
Q

What are the MOA, potential side effects, and examples of Incretin-based Therapies?

A

i. MOA:
1. GLP-1 agonists  stimulates insulin release & decrease glucagon release.
2. DPP-4 Antagonist  inhibit enzyme that breaks down GLP & Incretins
ii. Side effects: Pancreatic cancer
iii. Example: Trulicity (GLDP-1 agonist), Januvia (DDP-4 antagonist / from lizard saliva)

71
Q

What are the MOA, potential side effects, and examples of SGLT2 Inhibitors?

A

i. MOA:
1. Prevent glucose reabsorption in PCT
2. Blocks SGLT-2 receptor in the S-1 segment of the PCT.
ii. Side effects: dehydration, weight loss, perineum necrosis in bedridden patients.
iii. Example: -liflozin medications

72
Q

Describe adjunctive therapies that may be useful in pre-diabetes.

A

a. Exercise & diet. ACEi & SBP <130 for patients with CV disease
b. LDL <100mg/dL, antiplatelet agents

73
Q

Diagram a treatment algorithm for patients with Type II diabetes.

A

a. First line:
i. Exercise & lifestyle. Fasting BG >126  metformin.
b. Second line:
i. Sulfonylurea, metformin or others
c. Third line:
i. Basal insulin or pre-mixed. Or GLP-1 agonist
d. Fourth line:
i. Same as Type 1 DM

74
Q

Diagram the process of atherogenesis.

A

Excess cholesterol & triglycerides are deposited between smooth muscle & endothelial cells then become oxidized & are more pro-inflammatory. WBC’s migrate to area & absorb cholesterol, which gets stuck inside WBC’s. That increases inflammation. Over time cholesterol becomes crystallizes & foam cell bursts releasing cytokines. The process starts over. Over time a necrotic core forms pushing from inside making artery smaller.

75
Q

Describe the difference between triglycerides and cholesterol.

A

a. Triglycerides:
i. Main type of fat. Can be used for energy. Fat build up.
b. Cholesterol:
i. Plaque formation. Important precursor.

76
Q

Differentiate free and esterified cholesterol.

A

a. Free cholesterol:
i. Is biological active and has cytotoxic effect.
b. Esterified cholesterol:
i. Is the protective form for storage in the cell & transport in plasma

77
Q

List the two sources of cholesterol, and key elements of the mevalonate pathway.

A

a. Produced in liver (De novo synthesis)
b. Dietary intake (animal products)
c. Statins block mevalonate.

78
Q

Describe the different types of lipoproteins including their structure, how they are formed, and their role in lipid transport.

A

a. Apolipoproteins are on the surface & fat is carried on the inside.
b. Chylomicron is only made from diet in the intestine, becomes smaller as it moves thru the body.
c. VLDL made in the liver then converted to LDL thru endogenous pathway

79
Q

List target levels of total cholesterol, HDL, LDL, and triglycerides.

A

a. Total: <200
b. HDL: Men >40 & Women >50
c. LDL: <130
d. Triglycerides: <120

80
Q

Differentiate between primary hypercholesterolemias and secondary causes.

A

a. Primary:
i. Genetic disorders
b. Secondary:
i. DM, EtOH, hypothyroidism, obesity.

81
Q

Explain why dietary control of lipid intake may not be sufficient to lower cholesterol, and some dietary strategies.

A

a. Avoid animal products, alcohol, excess calories, sucrose, fructose.
b. We produce cholesterol on our own in the liver.

82
Q

List the MOA, side effects & examples for statins.

A

i. MOA: Decrease cellular cholesterol synthesis & increase LDL receptors.
ii. Side effects: Avoid in pregnancy, lactating & children. Elevated liver enzymes. They also increase PCSK9, which leads to less LDL-receptor recycling.
iii. Example: simvastatin

83
Q

List the MOA, side effects & examples for Niacin.

A

i. MOA: Reduce VLDL secretion from liver
ii. Side effects: Flushing, rash, dry skin, nausea, abdominal discomfort
iii. Examples: Niaspan

84
Q

List the MOA, side effects & examples for Fibrates

A

i. MOA: Decrease VLDL & LDL
ii. Side effects: Upset GI
iii. Examples: Lopid

85
Q

List the MOA, side effects & examples for Bile acid binding resins

A

i. MOA: Bind bile acids
ii. Side effects: Constipation, bloating, steatorrhea.
iii. Examples: Welchol

86
Q

List the MOA, side effects & examples for absorption inhibitors

A

i. MOA: Target & block NPC1L1. Cholesterol cannot enter & gets excreted.
ii. Side effects: Hepatic?
iii. Examples: Zetia

87
Q

List the MOA, side effects & examples for monoclonal antibodies

A

i. MOA:
1. LDL binds to receptor and gets internalized. Once inside contents are released and receptor is recycled to surface. The injected antibodies bind to PCSK9 and inhibit them from binding to the LDL receptors, so they do not get digested by lysosomes in the cell.
ii. Side effects: Mild nasopharyngitis, rhinitis
iii. Examples: Repatha

88
Q

List possible risks of hypocholesterolemia.

A

Cancer, hemorrhagic stroke, depression, anxiety, preterm birth and low birth weight.

89
Q

Explain the novel MOA of PCSK9 inhibitors.

A

The antibodies bind to PCSK9 and prevent them from binding to LDL receptors, allowing receptor recycling

Pharm (Marcus) (8 decks)

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