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Advanced Pharm Fall 24' > Pharm Exam 4 Study Guide > Flashcards

Pharm Exam 4 Study Guide Flashcards

1
Q

What are the key steps in thrombogenesis?

A

Thrombogenesis involves platelet adhesion, activation, and aggregation.

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2
Q

What mediators are involved in platelet activation?

A

ADP, thromboxane A2 (TXA2), and serotonin (5-HT) are released by activated platelets.

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3
Q

What inhibits platelet aggregation?

A

Prostacyclin (PGI2) inhibits platelet aggregation to prevent excessive clotting.

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4
Q

What are the pathways in the coagulation cascade?

A

The intrinsic pathway, extrinsic pathway, and common pathway.

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5
Q

What triggers the intrinsic pathway?

A

The intrinsic pathway is activated by damage inside the vascular system.

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6
Q

What triggers the extrinsic pathway?

A

The extrinsic pathway is triggered by external trauma.

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7
Q

What is Virchow’s triad?

A

Stasis, hypercoagulability, and endothelial injury are the causative factors of DVT.

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8
Q

What is the difference between white and red thrombi?

A

White thrombi are found in high-pressure arteries and are mainly composed of platelets, while red thrombi are found in low-pressure veins and are mainly composed of red blood cells.

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9
Q

What are the risk factors for DVT?

A

Virchow’s triad, Disseminated Intravascular Coagulation (DIC), and imbalances in the fibrinolytic system and antithrombin.

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10
Q

What is Disseminated Intravascular Coagulation (DIC)?

A

DIC is a serious condition characterized by widespread clotting and bleeding, often caused by bacterial sepsis, placental abruption, cancer, or massive tissue injury.

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11
Q

What is Heparin-Induced Thrombocytopenia (HIT)?

A

HIT is a reaction to heparin treatment causing low platelet counts and increased risk of thrombosis.

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12
Q

What is Thrombotic Thrombocytopenic Purpura (TTP)?

A

TTP is a rare blood disorder causing blood clots in small vessels, often due to genetic mutations or autoimmune reactions.

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13
Q

What is the role of tissue plasminogen activator (TPA) in fibrinolysis?

A

TPA activates plasminogen to plasmin, which breaks down fibrin and fibrinogen.

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14
Q

What are the four classes of coagulation modifier drugs?

A

Anticoagulants, anti-platelet drugs, thrombolytics, and hemostatic drugs.

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15
Q

What are indirect thrombin inhibitors?

A

Indirect thrombin inhibitors include heparin and low molecular weight heparin; they enhance the activity of antithrombin.

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16
Q

What are direct thrombin inhibitors?

A

Direct thrombin inhibitors like hirudin and dabigatran directly target and inhibit thrombin.

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17
Q

What is the difference between HMW, LMW, and Fondaparinux heparins?

A

HMW heparin inhibits thrombin and factor Xa, LMW heparin is more specific for factor Xa, and Fondaparinux selectively inhibits factor Xa.

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18
Q

What are the toxicity and contraindications of HMW heparin?

A

Toxicity includes bleeding and thrombocytopenia; contraindications include active bleeding and severe hypertension.

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19
Q

What are the oral anticoagulants and their mechanisms of action?

A

Warfarin blocks vitamin K epoxide reductase; factor Xa inhibitors like apixaban and rivaroxaban are more specific.

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20
Q

What are the cardinal symptoms of diabetes?

A

Polyuria, polydipsia, and polyphagia.

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21
Q

What is the sorbitol pathway?

A

The sorbitol pathway converts glucose to sorbitol via aldose reductase, leading to peripheral neuropathy and blindness.

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22
Q

What are the types of diabetes tests?

A

Fasting Plasma Glucose (FPG) Test and Oral Glucose Tolerance Test (OGTT).

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23
Q

What is the structure of insulin?

A

Insulin is a peptide hormone composed of two chains, A and B, linked by disulfide bonds.

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24
Q

What are insulin secretagogues?

A

Insulin secretagogues are drugs that stimulate the pancreas to secrete more insulin.

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25
Q

What are the types of insulin preparations?

A

Rapid-acting, short-acting, intermediate-acting, and long-acting insulins.

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26
Q

What is the basal-bolus insulin regimen?

A

The basal-bolus regimen involves administering a long-acting insulin for baseline control and rapid-acting insulin for meal coverage.

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27
Q

What are the four types of insulin preparations?

A
  1. Rapid-acting insulin: Examples include insulin lispro, insulin aspart, and insulin glulisine.
  2. Short-acting insulin: Examples include regular insulin (Humulin R, Novolin R).
  3. Intermediate-acting insulin: Examples include NPH insulin (Humulin N, Novolin N).
  4. Long-acting insulin: Examples include insulin glargine, insulin detemir, and insulin degludec.
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28
Q

What is a basal-bolus insulin regimen?

A

It involves a combination of long-acting insulin to provide a constant basal level and rapid-acting insulin taken at mealtimes.

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29
Q

What is a split-mixed insulin regimen?

A

It involves taking a mixture of intermediate-acting and short-acting insulin twice a day.

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30
Q

What is continuous subcutaneous insulin infusion (CSII)?

A

It involves using an insulin pump to deliver a continuous basal dose of insulin with bolus doses at mealtimes.

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31
Q

How do you calculate the units of insulin required?

A

Consider factors such as the patient’s weight, insulin sensitivity, and carbohydrate intake.

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32
Q

What is the correction dose for rapid-acting insulin?

A

1 unit of rapid-acting insulin is needed to drop blood glucose by 50 mg/dL.

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33
Q

What are common causes of hypoglycemia?

A

Hypoglycemia can occur due to excessive insulin administration, missed meals, or increased physical activity.

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34
Q

What are the symptoms of hypoglycemia?

A

Symptoms include shakiness, sweating, confusion, and in severe cases, loss of consciousness.

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35
Q

What is the treatment for hypoglycemia?

A

Treatment involves consuming fast-acting carbohydrates such as glucose tablets, fruit juice, or candy.

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36
Q

What are the eight classes of oral antidiabetic medications?

A
  1. Biguanides (e.g., Metformin)
  2. Thiazolidinediones (e.g., Pioglitazone)
  3. DPP-4 inhibitors (e.g., Sitagliptin)
  4. SGLT2 inhibitors (e.g., Canagliflozin)
  5. Alpha-glucosidase inhibitors (e.g., Acarbose)
  6. Incretin-based therapies (e.g., Semaglutide)
  7. Insulin secretagogues (e.g., Glipizide)
  8. Amylin analogs.
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37
Q

What is the mechanism of action (MOA) of Biguanides?

A

They decrease hepatic glucose production.

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38
Q

What are the side effects of Biguanides?

A

Gastrointestinal upset, lactic acidosis.

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39
Q

What is the MOA of Thiazolidinediones?

A

They increase insulin sensitivity.

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40
Q

What are the side effects of Thiazolidinediones?

A

Weight gain, edema, heart failure.

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41
Q

What is the MOA of DPP-4 inhibitors?

A

They increase incretin levels.

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42
Q

What are the side effects of DPP-4 inhibitors?

A

Nasopharyngitis, pancreatitis.

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43
Q

What is the MOA of SGLT2 inhibitors?

A

They increase urinary glucose excretion.

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44
Q

What are the side effects of SGLT2 inhibitors?

A

Genital infections, dehydration.

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45
Q

What is the MOA of Alpha-glucosidase inhibitors?

A

They delay carbohydrate absorption.

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46
Q

What are the side effects of Alpha-glucosidase inhibitors?

A

Gastrointestinal upset.

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47
Q

What is the MOA of Incretin-based therapies?

A

They increase insulin secretion and decrease glucagon secretion.

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48
Q

What are the side effects of Incretin-based therapies?

A

Nausea, pancreatitis.

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49
Q

What is the MOA of Insulin Secretagogues?

A

They bind to K+ channels, causing depolarization.

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50
Q

What are the side effects of Insulin Secretagogues?

A

Hypoglycemia, weight gain.

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51
Q

What are adjunctive therapies for pre-diabetes?

A

Lifestyle modifications such as diet and exercise, weight loss, and medications like metformin to improve insulin sensitivity.

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52
Q

What is the treatment algorithm for Type II diabetes?

A

It typically starts with lifestyle modifications and metformin. If glycemic control is not achieved, additional medications may be added.

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53
Q

What is atherogenesis?

A

The process of plaque formation in arteries due to endothelial injury, lipid accumulation, inflammation, foam cell formation, and plaque rupture.

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54
Q

What are triglycerides?

A

They are a type of fat found in blood, constituting the majority of neutral fats.

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55
Q

What is cholesterol?

A

A waxy, fat-like substance found in all cells, important for steroid hormones, cell membranes, vitamin D, and bile salts.

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56
Q

What is the difference between free and esterified cholesterol?

A

Free cholesterol is not attached to any fatty acid, while esterified cholesterol is attached to a fatty acid.

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57
Q

What are the two sources of cholesterol?

A
  1. Dietary cholesterol (20% from animal-based foods)
  2. Endogenous cholesterol (80% synthesized by the liver).
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58
Q

What is the mevalonate pathway?

A

A crucial metabolic pathway that produces cholesterol and other isoprenoids, involving Acetyl-CoA and HMG-CoA reductase.

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59
Q

What are chylomicrons?

A

The largest lipoproteins formed in the intestines to transport dietary triglycerides and cholesterol to tissues.

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60
Q

What are Very Low-Density Lipoproteins (VLDL)?

A

Lipoproteins formed in the liver to transport endogenous triglycerides to tissues.

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61
Q

What is Low-Density Lipoprotein (LDL)?

A

Often referred to as ‘bad’ cholesterol, it transports cholesterol to tissues and excess is deposited in arteries.

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62
Q

What is High-Density Lipoprotein (HDL)?

A

Known as ‘good’ cholesterol, it transports cholesterol from tissues back to the liver for excretion.

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63
Q

How is coronary artery disease risk calculated?

A

Using the LDL/HDL ratio; a higher ratio indicates a higher risk of CAD.

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64
Q

What are the target levels for total cholesterol, HDL, LDL, and triglycerides?

A

Total cholesterol: <200 mg/dL, HDL: ≥40 mg/dL (men), ≥50 mg/dL (women), LDL: <100 mg/dL, Triglycerides: <150 mg/dL.

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65
Q

What are primary hypercholesterolemias?

A

Genetic disorders that result in high cholesterol levels, such as familial hypercholesterolemia.

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66
Q

What are secondary causes of hypercholesterolemia?

A

Conditions or lifestyle factors such as hypothyroidism, diabetes, obesity, and certain medications.

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67
Q

Why may dietary control of lipid intake not be sufficient to lower cholesterol?

A

The body also produces cholesterol endogenously, influenced by genetics, age, and overall health.

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68
Q

What are some dietary strategies to help lower cholesterol?

A
  1. Limit calories from fat to 20% of total calories
  2. Use complex carbs and fiber
  3. Weight reduction
  4. Omega-3 fatty acids.
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69
Q

What are the six hyperlipidemia drug classes?

A
  1. Statins
  2. Niacin
  3. Fibrates
  4. Binding Resins
  5. Cholesterol absorption inhibitors
  6. PCSK9 inhibitors.
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70
Q

What is the MOA of Statins?

A

They inhibit HMG-CoA reductase, reducing cholesterol synthesis.

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71
Q

What are the side effects of Statins?

A

Muscle pain, liver damage.

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72
Q

What is the MOA of Niacin?

A

It inhibits the synthesis of VLDL and LDL.

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73
Q

What are the side effects of Niacin?

A

Flushing, liver damage.

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74
Q

What is the MOA of Fibrates?

A

They activate PPAR-alpha, increasing the oxidation of fatty acids.

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75
Q

What are the side effects of Fibrates?

A

Gallstones, muscle pain.

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76
Q

What is the MOA of Binding Resins?

A

They bind bile acids in the intestine, preventing their reabsorption.

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77
Q

What are the side effects of Binding Resins?

A

Gastrointestinal issues.

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78
Q

What is the MOA of cholesterol absorption inhibitors?

A

They inhibit the absorption of cholesterol from the intestine.

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79
Q

What are the side effects of cholesterol absorption inhibitors?

A

Diarrhea, muscle pain.

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80
Q

What is the MOA of PCSK9 inhibitors?

A

They increase the number of LDL receptors on hepatocytes.

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81
Q

What are the side effects of PCSK9 inhibitors?

A

Injection site reactions, flu-like symptoms.

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82
Q

What are the risks of hypocholesterolemia?

A

Increased risk of hemorrhagic stroke, hormonal imbalances, potential links to depression and anxiety, nutrient absorption issues.

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83
Q

What are NSAIDs?

A

Nonsteroidal Anti-Inflammatory Drugs that provide analgesic, antipyretic, and anti-inflammatory effects.

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84
Q

What are examples of NSAIDs?

A

Aspirin, ibuprofen, and naproxen.

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85
Q

What are the major cell damage pathways?

A

The Cyclooxygenase (COX) and Lipoxygenase (LOX) pathways.

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86
Q

What is the role of COX enzymes?

A

They convert arachidonic acid to prostaglandins involved in inflammation and pain.

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87
Q

What is the difference between COX-1 and COX-2?

A

COX-1 is involved in normal cellular processes, while COX-2 is primarily involved in the inflammatory response.

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88
Q

What are the pharmacokinetic properties of NSAIDs?

A

Well-absorbed, widely distributed, metabolized in the liver, and excreted by the kidneys.

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89
Q

What are the major side effects of NSAIDs?

A

Gastrointestinal issues, renal impairment, and increased risk of cardiovascular events.

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90
Q

How does aspirin irreversibly inhibit COX enzymes?

A

By acetylating a serine residue in the active site, blocking the conversion of arachidonic acid.

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91
Q

What are non-selective NSAIDs?

A

They inhibit both COX-1 and COX-2, examples include aspirin, ibuprofen, and naproxen.

92
Q

What are COX-2 selective inhibitors?

A

They primarily inhibit COX-2 with less effect on COX-1, such as celecoxib.

93
Q

How do NSAIDs reduce fever?

A

By inhibiting the production of prostaglandins in the hypothalamus.

94
Q

What are COX-2 selective inhibitors?

A

COX-2 selective inhibitors primarily inhibit COX-2 and have less effect on COX-1.

Examples include celecoxib (only prescribed one currently after Vioxx fiasco). Must consider cardiac risks.

95
Q

How do NSAIDs reduce fever?

A

NSAIDs reduce fever by inhibiting the production of prostaglandins in the hypothalamus, promoting peripheral vasodilation and helping dissipate heat.

96
Q

What is the mechanism of action for GI upset with NSAIDs?

A

The mechanism involves the inhibition of cyclooxygenase (COX) enzymes, leading to a decrease in protective prostaglandins in the stomach lining, making it more susceptible to irritation and ulceration.

97
Q

What are the blackbox warnings associated with NSAIDs?

A

Blackbox warnings include an increased risk of serious cardiovascular thrombotic events, myocardial infarction, stroke, and serious gastrointestinal adverse events like bleeding and ulceration.

98
Q

What are the benefits and drawbacks of COX-2 selective inhibitors?

A

COX-2 selective inhibitors, like celecoxib, reduce gastrointestinal side effects compared to non-selective NSAIDs but still carry a risk of cardiovascular events.

99
Q

What are specific applications for diclofenac?

A

Diclofenac is used for pain and inflammation in conditions like osteoarthritis and rheumatoid arthritis. 20% of patients have adverse GI effects, which can be decreased with Misoprostol (Cytotec).

100
Q

What are specific applications for indomethacin?

A

Indomethacin is used for acute gouty arthritis, rheumatism, and patent ductus arteriosus in neonates. It is a potent COX inhibitor and can reduce PMN migration and T&B cell proliferation.

101
Q

What are the selection criteria for NSAIDs?

A

Selection criteria include the patient’s medical history, specific condition, risk of side effects, and response to previous NSAID therapy. Toxicity Index: Most toxic - Indomethacin, tolmetin; Least toxic - Aspirin and Ibuprofen.

102
Q

Why is acetaminophen not classified as an NSAID?

A

Acetaminophen lacks significant anti-inflammatory properties and does not inhibit COX enzymes in peripheral tissues to the same extent as NSAIDs.

103
Q

What are the acute and chronic effects of glucocorticoids?

A

Acute effects include increased blood glucose levels and fluid retention. Chronic use can lead to osteoporosis, adrenal suppression, increased infection risk, and Cushing’s syndrome.

104
Q

What is the mechanism of action of glucocorticoids?

A

Glucocorticoids bind to receptors in the cytoplasm, translocate to the nucleus, and modulate gene expression, resulting in anti-inflammatory and immunosuppressive effects.

105
Q

What are DMARDs?

A

Disease-modifying antirheumatic drugs (DMARDs) are used to treat inflammatory arthritis by slowing or halting disease progression.

106
Q

What are six important DMARDs?

A
  1. Methotrexate: Adenosine production. 2. Cyclophosphamide: B&T cell suppression. 3. Cyclosporine: Inhibition of interleukins. 4. Abatacept: Blocks T-cell activation. 5. Rituximab: Depletes B-lymphocytes. 6. Adalimumab: anti-TNF.
107
Q

What are endogenous opioids?

A

Endogenous opioids include endorphins, enkephalins, and dynorphins, which bind to opioid receptors in the brain and spinal cord.

108
Q

What are the three main types of opioid receptors?

A
  1. Mu receptors: Responsible for analgesic effects. 2. Delta receptors: Involved in mood regulation. 3. Kappa receptors: Involved in pain relief but can produce dysphoria.
109
Q

What are the components of pain signaling?

A

Pain signaling involves the spinothalamic tract, spinoreticular tract, and spinomesencephalic tract, transmitting pain signals to different brain areas.

110
Q

What are the three main fibers for transmission of sensation?

A

A-delta fibers transmit sharp pain quickly, C fibers transmit dull pain slowly, and A-beta fibers transmit non-painful sensations.

111
Q

What is the importance of the periaqueductal gray (PAG)?

A

The PAG is crucial for pain modulation, containing enkephalin-producing cells that suppress pain and regulate autonomic functions.

112
Q

What are the pharmacokinetic properties of opioids?

A

Opioids are well-absorbed and distributed, metabolized primarily in the liver, and excreted through the kidneys.

113
Q

What are specific applications for opioids?

A

Opioids are used for managing acute and chronic pain, anesthesia, cough suppression, and palliative care.

114
Q

What is opioid toxicity?

A

Opioid toxicity occurs from excessive opioid intake, leading to severe respiratory depression and potentially fatal overdose.

115
Q

What is the difference between tolerance and withdrawal?

A

Tolerance occurs when the body becomes less responsive to opioids, requiring higher doses, while withdrawal occurs with abrupt discontinuation, causing symptoms like anxiety and muscle aches.

116
Q

What are the opioid structure classes?

A
  1. Phenanthrenes: Morphine, codeine. 2. Phenylpiperidines: Fentanyl, meperidine. 3. Diphenylheptanes: Methadone, propoxyphene. Opioid antagonists include naloxone and naltrexone.
117
Q

What is post-operative shivering?

A

Post-operative shivering is involuntary shaking after surgery, often due to anesthesia. Treatments include warming blankets and medications like meperidine, clonidine, and dexmedetomidine.

118
Q

What are the important differences between Gram (+) and Gram (-) bacteria?

A

Gram-positive bacteria have a thick peptidoglycan layer, appearing purple, while Gram-negative bacteria have a thinner layer and an outer membrane, appearing pink.

119
Q

What is the difference between Gram-positive and Gram-negative bacteria?

A

Gram-positive bacteria have a thick idoglycan layer in their cell wall, which retains the crystal violet stain, making them appear purple under a microscope.

Gram-negative bacteria have a thinner peptidoglycan layer and an outer membrane containing lipopolysaccharides, which does not retain the crystal violet stain but takes up the counterstain (safranin), making them appear pink.

120
Q

List examples of Gram-positive bacteria and the diseases they cause.

A

Examples include Staphylococcus aureus (causes skin infections, pneumonia) and Streptococcus pneumoniae (causes pneumonia, meningitis).

121
Q

List examples of Gram-negative bacteria and the diseases they cause.

A

Examples include Escherichia coli (causes urinary tract infections) and Pseudomonas aeruginosa (causes respiratory infections).

122
Q

List examples of atypical bacteria and the diseases they cause.

A

Examples include Mycoplasma pneumoniae (causes atypical pneumonia) and Chlamydia trachomatis (causes chlamydia).

123
Q

What are the five general properties of antimicrobial agents?

A
  1. Selective toxicity: Targets microorganisms without harming the host. 2. Spectrum of activity: Range of microorganisms affected. 3. Bactericidal or bacteriostatic: Kills bacteria or inhibits growth. 4. Mechanism of action: How the agent affects microorganisms. 5. Resistance: Ability of microorganisms to withstand the effects.
124
Q

Differentiate between spectrum of activity and selective toxicity.

A

Spectrum of activity refers to the range of microorganisms an antimicrobial agent can affect, which can be broad-spectrum or narrow-spectrum. Selective toxicity is the ability to target microorganisms without harming the host by exploiting differences between microbial and host cells.

125
Q

What are the five main targets of antimicrobial agents?

A
  1. Cell wall synthesis: Beta-lactam antibiotics (e.g., penicillin). 2. Protein synthesis: Aminoglycosides (e.g., gentamicin). 3. Nucleic acid synthesis: Fluoroquinolones (e.g., ciprofloxacin). 4. Metabolic pathways: Sulfonamides (e.g., sulfamethoxazole). 5. Cell membrane integrity: Polymyxins (e.g., polymyxin B).
126
Q

Describe the mechanism of antibacterial action of beta-lactam antibiotics.

A

Beta-lactam antibiotics inhibit the synthesis of the bacterial cell wall by binding to and inactivating penicillin-binding proteins (PBPs), preventing the cross-linking of peptidoglycan chains, leading to cell lysis and death.

127
Q

What mechanisms underlie the resistance of bacteria to beta-lactam antibiotics?

A
  1. Production of beta-lactamase enzymes that hydrolyze the beta-lactam ring. 2. Alterations in PBPs reduce binding affinity. 3. Changes in permeability of the bacterial cell membrane prevent the antibiotic from reaching its target.
128
Q

Identify the prototype drugs in each subclass of beta-lactams.

A
  1. Penicillins: Penicillin G, effective against gram-positive bacteria and some gram-negative cocci, used for infections like strep throat, syphilis, and meningitis. 2. Cephalosporins: Cephalexin, used for respiratory tract infections, skin infections, and urinary tract infections. 3. Carbapenems: Imipenem, effective against a wide range of bacteria, used for severe infections. 4. Monobactams: Aztreonam, effective against gram-negative bacteria, used for urinary tract infections and respiratory infections.
129
Q

What are the major adverse effects of penicillins?

A

Common adverse effects include allergic reactions (ranging from rash to anaphylaxis), gastrointestinal upset, and, rarely, neurotoxicity.

130
Q

What are the major adverse effects of cephalosporins?

A

Adverse effects include allergic reactions (cross-reactivity with penicillins), gastrointestinal upset, and potential nephrotoxicity.

131
Q

What are important features of imipenem and meropenem?

A

Imipenem is a broad-spectrum beta-lactam antibiotic resistant to most beta-lactamases, often combined with cilastatin to prevent renal degradation. Meropenem is similar but does not require cilastatin and has a slightly broader spectrum.

132
Q

Describe the clinical uses and toxicities of vancomycin.

A

Vancomycin is primarily used to treat serious gram-positive infections, including MRSA and C. difficile-associated diarrhea. Toxicities include nephrotoxicity, ototoxicity, and ‘red man syndrome’ (a histamine release reaction).

133
Q

What are the effects of premature termination of antibiotics?

A

Premature termination can lead to incomplete eradication of bacteria, resulting in relapse of infection and contributes to the development of antibiotic-resistant bacteria.

134
Q

Describe the MOA of polymyxins.

A

Polymyxins disrupt the bacterial cell membrane by interacting with its phospholipids, leading to cell death, primarily effective against gram-negative bacteria.

135
Q

Why are inhibitors of protein synthesis considered broad spectrum?

A

They target the bacterial ribosome, essential for protein production in all bacteria, inhibiting protein synthesis. Toxicities can include gastrointestinal upset, hepatotoxicity, and, in some cases, ototoxicity and nephrotoxicity.

136
Q

List examples of tetracyclines and macrolides.

A

Tetracyclines: Doxycycline, Minocycline. Macrolides: Erythromycin, Azithromycin.

137
Q

How do sulfonamides and trimethoprim affect bacterial folic acid synthesis?

A

Sulfonamides inhibit dihydropteroate synthase, while trimethoprim inhibits dihydrofolate reductase, blocking bacterial growth by inhibiting tetrahydrofolic acid synthesis.

138
Q

What are the major clinical uses of sulfonamides and trimethoprim?

A

They are primarily used to treat bacterial infections, often combined to enhance effectiveness, particularly useful for urinary tract infections, respiratory infections, and certain gastrointestinal infections.

139
Q

How do fluoroquinolones inhibit nucleic acid synthesis?

A

Fluoroquinolones target bacterial DNA gyrase and topoisomerase IV, crucial for DNA replication and transcription, preventing bacteria from replicating and transcribing their DNA.

140
Q

What are the problems associated with disruption of normal microflora?

A

Disruption can lead to overgrowth of pathogenic organisms, resulting in infections such as C. difficile-associated diarrhea, and can weaken the immune response, increasing susceptibility to infections.

141
Q

What key questions should be considered when deciding which antibiotic to use?

A
  1. What is the likely causative organism? 2. What is the susceptibility pattern? 3. What is the site of infection? 4. What are the patient’s allergies and previous antibiotic use? 5. What are the potential side effects and interactions? 6. What is the appropriate dosage and duration?
142
Q

What are the components of viruses?

A
  1. Genetic Material: DNA or RNA containing instructions for new virus particles. 2. Capsid: Protein shell protecting genetic material. 3. Envelope: Lipid membrane helping evade the immune system. 4. Surface Proteins: Crucial for attaching to and entering host cells.
143
Q

List examples of DNA and RNA viruses.

A

DNA Viruses: Herpes Simplex Virus (causes cold sores, genital herpes), Human Papillomavirus (causes warts, cervical cancer). RNA Viruses: Influenza Virus (causes the flu), Human Immunodeficiency Virus (causes AIDS).

144
Q

What is the viral replication cycle?

A
  1. Attachment: Virus binds to host cell receptors. 2. Penetration: Virus enters the host cell. 3. Uncoating: Capsid is removed, releasing genetic material. 4. Replication: Host cell machinery replicates viral genome. 5. Assembly: New viral particles are assembled. 6. Release: New viruses are released, often killing the host cell.
145
Q

Describe the infection cycle of rotavirus.

A

Rotavirus enters through ingestion, replicates in the small intestine lining cells, causing damage and death, and releases new viral particles into the intestinal lumen, leading to diarrhea and dehydration.

146
Q

List drugs used for HBV and their targets.

A

HBV: Entecavir (inhibits HBV DNA polymerase), Tenofovir (inhibits HBV reverse transcriptase).

147
Q

List drugs used for HIV and their targets.

A

HIV: Zidovudine (AZT, inhibits reverse transcriptase), Ritonavir (inhibits protease), Maraviroc (blocks CCR5 receptor, preventing entry).

148
Q

List signs and symptoms associated with the Ebola virus.

A

Fever, severe headache, muscle pain, weakness, fatigue, diarrhea, vomiting, abdominal pain, unexplained hemorrhaging.

149
Q

Explain the MOA of acyclovir in DNA chain termination.

A

Acyclovir inhibits viral DNA synthesis by competing with deoxyguanosine triphosphate for incorporation into viral DNA, acting as a chain terminator due to lacking a 3’-OH group.

150
Q

List uses for acyclovir and ganciclovir.

A

Acyclovir is used for HSV infections, including genital herpes and shingles. Ganciclovir is used for cytomegalovirus infections, particularly in immunocompromised patients.

151
Q

List and describe the three types of influenza antivirals.

A
  1. Neuraminidase inhibitors (e.g., oseltamivir): Block viral neuraminidase, preventing release of new particles. 2. M2 ion channel inhibitors (e.g., amantadine): Inhibit M2 protein involved in uncoating. 3. Polymerase inhibitors (e.g., baloxavir marboxil): Inhibit viral polymerase essential for RNA replication.
152
Q

Contrast the two main types of influenza.

A

Influenza A causes pandemics, divided into subtypes (e.g., H1N1), infects humans and animals. Influenza B primarily infects humans, causes seasonal epidemics, and is less severe.

153
Q

List different types of coronaviruses.

A

SARS-CoV (causes SARS), MERS-CoV (causes MERS), SARS-CoV-2 (causes COVID-19), and other human coronaviruses (HCoV-229E, HCoV-NL63, HCoV-OC43, HCoV-HKU11).

154
Q

Describe the treatment of COVID-19 and the MOA of remdesivir.

A

Treatment includes supportive care and antiviral medications. Remdesivir inhibits viral RNA-dependent RNA polymerase, essential for replication, and may cause nausea, elevated liver enzymes, and allergic reactions.

155
Q

Define tremor.

A

A rhythmic, involuntary oscillatory movement of a body part.

156
Q

Define chorea.

A

Involuntary, irregular, purposeless, non-rhythmic, abrupt, rapid movements that flow from one body part to another.

157
Q

Define ballismus.

A

A severe form of chorea, characterized by violent, flinging movements.

158
Q

Define athetosis.

A

Involuntary, slow, writhing movements, often affecting the hands and feet.

159
Q

Define dystonia.

A

Sustained muscle contractions, abnormal postures, or twisting movements.

160
Q

What are possible side effects of remdesivir?

A

Possible side effects of remdesivir include nausea, elevated liver enzymes, and allergic reactions.

161
Q

Define tremor.

A

Tremor: A rhythmic, involuntary oscillatory movement of a body part.

162
Q

Define chorea.

A

Chorea: Involuntary, irregular, purposeless, non-rhythmic, abrupt, rapid movements that flow from one body part to another.

163
Q

Define ballismus.

A

Ballismus: A severe form of chorea, characterized by violent, flinging movements of the limbs.

164
Q

Define athetosis.

A

Athetosis: Slow, writhing, continuous, and involuntary movements, often seen in the hands and feet.

165
Q

Define dystonia.

A

Dystonia: Sustained or repetitive muscle contractions resulting in twisting and repetitive movements or abnormal fixed postures.

166
Q

What is the relationship between the basal ganglia, motor cortex, and thalamus?

A

The basal ganglia, motor cortex, and thalamus form a complex network that regulates movement.

167
Q

How does the basal ganglia process motor information?

A

The basal ganglia process motor information and send output to the motor cortex via the thalamus.

168
Q

What characterizes Parkinson’s Disease?

A

Parkinson’s Disease is a progressive neurodegenerative disorder characterized by the loss of dopamine-producing neurons in the basal ganglia.

169
Q

What are common symptoms of Parkinson’s Disease?

A

Symptoms include tremors, rigidity, bradykinesia (slowness of movement), and postural instability.

170
Q

What characterizes Huntington’s Disease?

A

Huntington’s Disease is a genetic disorder that causes the progressive breakdown of nerve cells in the brain, particularly affecting the basal ganglia.

171
Q

What are common symptoms of Huntington’s Disease?

A

Symptoms include involuntary jerking or writhing movements (chorea), muscle problems, and cognitive decline.

172
Q

What is dystonia?

A

Dystonia is a movement disorder in which sustained or repetitive muscle contractions result in twisting and repetitive movements or abnormal fixed postures.

173
Q

What is Tourette Syndrome?

A

Tourette Syndrome is a neurological disorder characterized by repetitive, stereotyped, involuntary movements and vocalizations called tics.

174
Q

What are common signs of Parkinson’s disease?

A

Common signs include tremor at rest, bradykinesia (slowness of movement), rigidity, and postural instability.

175
Q

What are risk factors for Parkinson’s disease?

A

Risk factors include age, family history, male gender, exposure to pesticides, and head injuries.

176
Q

What is the function of synuclein in Parkinson’s disease?

A

Synuclein is a protein involved in synaptic function and neurotransmitter release. In Parkinson’s disease, abnormal accumulation of alpha-synuclein forms Lewy bodies, which are associated with neuronal death and the progression of the disease.

177
Q

What are non-pharmacologic treatments for Parkinson’s?

A

Non-pharmacologic treatments include physical therapy, occupational therapy, speech therapy, and exercise programs.

178
Q

What is the role of Levodopa in Parkinson’s treatment?

A

Levodopa is a precursor to dopamine that can cross the blood-brain barrier and is converted to dopamine in the brain, helping to alleviate Parkinson’s symptoms.

179
Q

What is the role of Carbidopa in conjunction with Levodopa?

A

Carbidopa inhibits the peripheral breakdown of levodopa, allowing more of it to reach the brain and reducing side effects like nausea.

180
Q

What are common side effects of levodopa?

A

Common side effects include nausea, vomiting, orthostatic hypotension, dyskinesias (involuntary movements), and hallucinations.

181
Q

What are treatments for levodopa side effects?

A

Treatments include adjusting the dosage, using additional medications to manage side effects, and implementing dietary changes to improve tolerance.

182
Q

What is the pathway for levodopa metabolism?

A

Levodopa is converted to dopamine in the brain by the enzyme aromatic L-amino acid decarboxylase (AADC).

183
Q

What do dopamine receptor agonists do?

A

Dopamine receptor agonists directly stimulate dopamine receptors, mimicking the effects of dopamine.

184
Q

What do MAO-B antagonists do?

A

MAO-B antagonists inhibit monoamine oxidase B, increasing dopamine availability.

185
Q

What do COMT inhibitors do?

A

COMT inhibitors block catechol-O-methyltransferase, prolonging the effect of levodopa.

186
Q

What are additional treatments for Parkinson’s disease?

A

Additional treatments include dopamine agonists, MAO-B inhibitors, COMT inhibitors, anticholinergics, and amantadine.

187
Q

What are ‘On-Off’ periods in Parkinson’s treatment?

A

‘On-off’ periods refer to fluctuations in the effectiveness of Parkinson’s medications, with ‘on’ periods indicating symptom control and ‘off’ periods indicating symptom return.

188
Q

What characterizes essential tremor?

A

Essential tremor is characterized by rhythmic shaking, usually in the hands.

189
Q

What are treatments for essential tremor?

A

Treatments include beta-blockers, anticonvulsants, and sometimes surgery.

190
Q

What is benign hereditary chorea?

A

Benign hereditary chorea is a genetic disorder causing involuntary movements.

191
Q

What is the treatment for benign hereditary chorea?

A

Treatment is symptomatic, often using medications like tetrabenazine.

192
Q

What is tardive dyskinesia?

A

Tardive dyskinesia involves involuntary, repetitive movements, often caused by long-term use of antipsychotic drugs.

193
Q

What are treatments for tardive dyskinesia?

A

Treatments include discontinuing the causative drug and using medications like valbenazine.

194
Q

What is Duchenne Muscular Dystrophy (DMD)?

A

Duchenne Muscular Dystrophy is the most common type of muscular dystrophy, caused by mutations in the dystrophin gene.

195
Q

What are treatments for Duchenne Muscular Dystrophy?

A

Treatments include corticosteroids, physical therapy, and newer gene therapies.

196
Q

What is Gower’s sign?

A

Gower’s sign is a clinical indicator where a child uses their hands to ‘walk’ up their own body from a squatting position due to weakness in the proximal muscles.

197
Q

What are common causes of cerebral palsy?

A

Cerebral palsy is often caused by brain injury or malformation during development.

198
Q

What assessments are done in infants for cerebral palsy?

A

Assessments include monitoring motor skills, muscle tone, and reflexes.

199
Q

What are treatments for cerebral palsy?

A

Treatments focus on improving quality of life and may include physical therapy, occupational therapy, medications, and sometimes surgery.

200
Q

What characterizes Huntington’s Disease?

A

Huntington’s Disease is a genetic disorder causing progressive breakdown of nerve cells in the brain.

201
Q

What are symptoms of ALS?

A

Symptoms of ALS include muscle weakness and atrophy.

202
Q

What is the treatment focus for ALS?

A

Treatments focus on slowing disease progression and managing symptoms.

203
Q

What is Riluzole used for?

A

Riluzole can slow the progression of ALS and prolong survival.

204
Q

What is Edaravone used for?

A

Edaravone helps reduce the decline in daily functioning in people with ALS.

205
Q

What characterizes Alzheimer’s Disease?

A

Alzheimer’s Disease is a neurodegenerative disorder characterized by cognitive decline and memory loss.

206
Q

What are treatments for Alzheimer’s Disease?

A

Treatments include medications to manage symptoms and slow progression.

207
Q

What are cholinesterase inhibitors?

A

Cholinesterase inhibitors, such as donepezil and rivastigmine, increase levels of a chemical messenger involved in memory and judgment.

208
Q

What does Memantine do?

A

Memantine helps regulate the activity of glutamate, a chemical messenger involved in learning and memory.

209
Q

What are anti-amyloid therapies?

A

Anti-amyloid therapies target amyloid plaques in the brain, characteristic of Alzheimer’s.

210
Q

What are the roles of the FDA and FTC in regulating OTC and Herbal Supplements?

A

The FDA regulates the safety and labeling of dietary supplements, while the FTC regulates advertising claims.

211
Q

Differentiate prescription, OTC, and ‘behind the counter’ drugs.

A

Prescription drugs require a doctor’s authorization, OTC drugs can be purchased without a prescription, and ‘behind the counter’ drugs require a pharmacist’s intervention.

212
Q

What are the phases of clinical testing in drug development?

A

Clinical testing phases include Phase 1 (safety), Phase 2 (efficacy), and Phase 3 (confirmation of effectiveness).

213
Q

Define GRASE.

A

GRASE stands for Generally Recognized As Safe and Effective.

214
Q

What are difficulties in regulating dietary supplement claims?

A

Difficulties include lack of pre-market approval and variability in product quality.

215
Q

What are the purported benefits of echinacea?

A

Echinacea is purported to boost the immune system and reduce cold symptoms.

216
Q

What are the purported benefits of garlic?

A

Garlic is believed to have cardiovascular benefits and antimicrobial properties.

217
Q

What are the purported benefits of ginkgo?

A

Ginkgo is often claimed to improve memory and cognitive function.

218
Q

What are the purported benefits of St. John’s wort?

A

St. John’s wort is commonly used for its antidepressant effects.

219
Q

What are the purported benefits of ginseng?

A

Ginseng is believed to enhance energy and reduce stress.

220
Q

What are the purported benefits of milk thistle?

A

Milk thistle is thought to support liver health.

221
Q

What are the purported benefits of saw palmetto?

A

Saw palmetto is often used for prostate health.

222
Q

What are the purported benefits of kombucha?

A

Kombucha is claimed to have probiotic benefits and improve digestion.

223
Q

What are the purported benefits of kava kava?

A

Kava kava is used for its calming effects and anxiety relief.

224
Q

What are the purported benefits of aloe?

A

Aloe is often used for its skin healing properties.

225
Q

What are the purported benefits of black cohosh?

A

Black cohosh is commonly used for menopausal symptoms.

226
Q

What are the benefits of vitamins and minerals?

A

Vitamins and minerals are essential for various bodily functions, including immune support, energy production, and bone health.

Advanced Pharm Fall 24' (16 decks)

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