Exam 4 Review Flashcards
(128 cards)
1
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
Thrombogenesis begins with vascular injury, exposing collagen and von Willebrand factor (vWF) beneath the endothelium. Platelets adhere to these exposed elements via receptors (GP Ia for collagen and GP Ib for vWF). Adhesion activates platelets, causing them to release ADP, thromboxane A₂ (TXA₂), and serotonin (5-HT), which recruit and activate additional platelets. ADP and TXA₂ enhance aggregation, while 5-HT promotes vasoconstriction, helping to reduce blood flow to the area. Platelets link together through fibrinogen binding to GP IIb/IIIa receptors, forming a platelet plug. Thrombin then converts fibrinogen to fibrin, creating a stable clot. Prostacyclin (PGI₂), released from intact endothelial cells, inhibits platelet aggregation in uninjured areas, keeping the clot localized.
2
Q
Intrinsic coag pathway
A
Collagen exposure → Factor XII → XIIa → Factor XI → XIa → Factor IX → IXa (+ Factor VIII and Ca²⁺) → Factor X.
3
Q
Extrinsic coag pathway
A
Tissue damage → TF + Factor VII → VIIa → Factor X.
4
Q
Common coag pathway
A
Factor X → Xa (+ Factor V and Ca²⁺) → Prothrombin (II) → Thrombin (IIa) → Fibrinogen (I) → Fibrin → (+ Factor XIII) Stable Fibrin Clot.
5
Q
Describe the causative factors of DVT and the difference between white and red thrombi/thromboemboli.
A
Causes: Stasis (immobility), hypercoagulability, endothelial inury.
White: formed in high pressure arteries, mainly composed of platelets/fibrin.
Red: Forms in low-pressure veins with trapped red cells around a fibrin-platelet core, with a tail that can detach and cause embolism.
6
Q
List the risk factors for DVT
A
Inherited conditions such as antithrombin III deficiency, protein C/S deficiency, sickle cell anemia, activated protein C resistance.
Acquired risks: bedridden, surgery/trauma, obesity, estrogen use, malignancies, chronic venous insufficiency.
7
Q
DIC, include causes and treatments
A
DIC: disseminated intravascular coagulation, overstimulation of clotting leads to excessive clot formation, depletion of platelets, and bleeding.
Causes: massive tissue injury, malignancy and sepsis.
Tx involves plasma transfusion and addressing underlying cause.
8
Q
HIT, Include causes and treatments
A
Heparin-induced thrombocytopenia
Immune response to heparin resulting in low platelet count and increased bleeding risk. Treatment includes discontinuation of heparin and possibly using alternative coags.
9
Q
TTP, Include causes and treatments
A
Thrombotic thrombocytopenic Purpura
Widespread platelet aggregation and small clots in microcirculation, leading to thrombocytopenia and hemolytic anemia. Tx involves plasma exchange.
10
Q
Draw the pathway for fibrinolysis including the mediators involved
A
t-pa, urokinase, streptokinase binds to plasminogen -> converts it into plasmin -> plasmin breaks down fibrin into fibrin degradation products (FDPs) including D-dimers.
11
Q
List the four classes of coagulation modifier drugs, and examples of each.
A
Anticoagulants: warfarin, heparin
Antiplatelet drugs: aspirin, clopidogrel
Thrombolytics: Streptokinase, urokinase
Hemostatic/antifibrinolytic drugs: Aminocaproic acid, Tranexamic acid
12
Q
Differentiate the indirect and direct thrombin inhibitors and briefly describe how each function to inhibit thrombin.
A
indirect: heparin and LMWH, enhance antithrombin activity, inactivating thrombin and Factor Xa.
Direct: bind directly to thrombins active sites, inhibiting thrombin without needing antithrombin.
13
Q
Explain the difference between HMW, LMW, and Fondaparinux heparins, and the use of each.
A
High molecular weight: broad activity, less specific for factor Xa
LMW: more specific for factor Xa with fewer side effects
Fondaparinux: synthetic, selectively inhibits factor Xa, useful in HIT patients with less bleeding risk
14
Q
List the toxicity and contraindications of HMW heparin and treatment
A
Toxicity: bleeding and thrombocytopenia
Contraindications: active bleeding, hemophilia, severe hypertension, intracranial hemorrhage, TB, hepatic disease
Tx: d/c heparin, use of protamine sulfate for reversal
15
Q
Describe the laboratory testing for coagulation pathways and normal values.
A
prothrombin time: assesses extrinsic and common pathways, normal INR = 0.8 - 1.2
advanced partial thromboplastin time (aPTT): evaluates intrinsic and common pathways, normal = 35-45 seconds
16
Q
List the oral anticoagulants, their MOA, and treatment considerations.
A
warfarin: blocks vitamin k recycling, reducing clotting factor synthesis. Requires close monitoring of INR and dosage adjustments.
17
Q
Discuss treatment considerations and pharmacogenomics of warfarin treatment.
A
Considerations: start low and adjust based on INR, drug interactions, risk of bleeding.
Pharmacogenomics: variability in warfarin metabolism due to genetic differences can influence dosing and response.
18
Q
List non-warfarin anticoagulant drugs and their targets.
A
Factor Xa inhibitors: apixaban, rivaroxaban
Direct thrombin inhibitors: dabigatran
19
Q
List the various fibrinolytic drugs.
A
Streptokinase, urokinase, tPA (alteplase) activate plasminogen to plasmin, leading to fibrin clot breakdown
20
Q
Describe the targets for the antiplatelet aggregation drugs aspiring, Plavix, Ticlid, and
abiciximab.
A
aspirin: inhibits thromboxane A2, reducing platelet aggregation.
Clopidogrel (plavix) and Ticlopidine (Ticlid): inhibit ADP receptors on platelets, preventing aggregation.
Abciximab: monoclonal antibody blocking the llb/llla receptor on platelets
21
Q
Describe how bleeding disorders can be treated with Vit. K, plasma fractions,
desmopressin, aminocaproic acid, and tranexamic acid
A
Vit K: essential for clotting factor production
Plasma fractions: used to treat clotting factor deficiencies
Desmopressin: increases Factor VIII in mild hemophilia and von willebrand disease
Aminocaproic acid and TXA: inhibit plasminogen activation, reducing fibrinolysis in bleeding conditions.
22
Q
Describe the exocrine and endocrine functions of the pancreas.
A
exocrine: pancreas acts as an exocrine gland by producing digestive enzymes, which are released into the duodenum to aid in the breakdown of proteins, fats, and carbs.
Endocrine: Involves the islets of langerhans, which contain different cell types, including beta cells that release insulin and alpha cells that release glucagon. These hormones regulate blood glucose in the body.
23
Q
Contrast the roles of insulin and glucagon on blood glucose levels.
A
Insulin: released from pancreatic beta cells in response to high blood glucose levels, insulin facilitates glucose uptake by cells, thus lowering blood glucose. It also promoted glycogen storage in the liver.
Glucagon: secreted by pancreatic alpha cells when BG levels are low, glucagon increases blood blucose by stimulating glycogen breakdown in the liver (Glycogenolysis) and glucose production.
24
Q
List the four main types of diabetes mellitus.
A
I: insulin dependent, caused by destruction of beta cells, leading to severe insulin deficiency. Auto-immune.
II: Non-insulin-dependent, commonly associated with insulin resistance and often linked to obesity.
III: Secondary to other conditions like pancreatitis, drug therapy.
IV: Gestational diabetes, during pregnancy due to insulin resistance from pregnancy hormones.
25
List the three cardinal symptoms of diabetes.
Polydipsia (Thirst), polyuria (urination), polyphagia (Hunger)
26
Describe the sorbitol pathway, and why it leads to peripheral neuropathy and blindness.
Conversion of excess glucose into sorbitol anf fructose. High BG levels lead to increased sorbitol in cells such as those in the lens, nerves, RBCs, resulting in osmotic stress as water is drawn in. Causes cell damage, contributing to peripheral neuropathy and blindness due to cellular swelling and rupture.
27
Differentiate the two types of diabetes tests.
Fasting BG test: measures BG after overnight fast to assess baseline glucose levels
Glucose tolerance test: after fasting, consumes high glucose drink, and blood samples are taken every hour over several hours to measure glucose tolerance.
28
Describe the structure of insulin, and the role of insulin secretagogues in its release.
Structure: peptide hormone with an alpha and beta chain connected by disulfide bonds. Inactive form (Proinsulin) it includes a C-peptide that is cleaved to activate insulin.
Secretagogues: glucose, certain amino acids, and incretins that stimulate insulin release by depolarizing the beta cell membrane, allowing calcium influx and vesicle fusion to release insulin.
29
8. Delineate the insulin receptor pathway and the various types of glucose transporter
(GLUT).
Pathway: insulin binds to receptor, a tyrosine kinase, initiating phosphorylation that leads to multiple intracellular signaling cascades. This action results in GLUT translocation to the cell membrane, allowing glucose uptake.
GLUT2: found beta cells and liver; low affinity, active at high glucose levels.
GLUT 4: Common in muscle and adipose tissue; moderate affinity, responsive to insulin.
GLUT1/3: high affinity, found in brain and RBCs, enables uptake under low-glucose conditions.
30
List the four types of insulin preparation, and examples of each.
Rapid: lispro, aspart, glulisine
Short: regular insulin (humulin, novolin)
Intermediate: Neutral protamine hagedorn (NPH)
Long: glargine, detemir
31
Describe the types of insulin dosing regimens.
intensive: basal + bolus, using long acting for baseline and rapid acting for meal coverage.
Conventional: premixed insulin (70:30 mix) for less precise but easier dosing.
Insulin pump: provides continous subcutaneous insulin for tight control, adjusting for basal and bolus needs.
32
Calculate the units of insulin required given an example scenario.
If a patient is consuming 60g of carbs, and 1 unit of rapid acting insulin covers 15g of carbs, they need 4 units of insulin.
Correction factor: if glucose is 200mg/dL, and each unit lowers it by 50mg/dL, administer 2 units to reach target of 100mg/dL
33
List problems and treatments for hypoglycemia.
Problems: anxiety, blurred vision, sweating, slurred speech, shakiness, confusion.
Tx: 3-4 glucose tablets, 1/2 can of soda, glucagon injection if severe. (1mg IM, IV, SQ, repeat if needed)
34
List the eight classes of oral antidiabetic medications, their MOA, potential side effects, and examples of each.
Biguanides: Reduces hepatic glucose production. Example: Metformin. Side effects: GI upset.
Insulin Secretagogues: Increase insulin release by blocking potassium channels. Examples: Sulfonylureas, Meglitinides. Side effects: Hypoglycemia, cardiovascular risks.
Thiazolidinediones (TZDs): Enhance insulin sensitivity via PPAR activation. Example: Rosiglitazone. Side effects: Risk of MI.
Alpha-glucosidase Inhibitors: Delay carbohydrate absorption. Example: Acarbose. Side effects: GI issues.
Bile Acid Binding Resins: Reduce glucose reabsorption. Example: Colesevelam. Side effects: GI upset.
Amylin Analog: Suppress glucagon, reduce blood glucose. Example: Pramlintide. Side effects: Nausea.
Incretin-based Therapies: Enhance insulin release and inhibit glucagon. Examples: GLP-1 agonists (e.g., Semaglutide), DPP-4 inhibitors. Side effects: Risk of pancreatic issues.
SGLT2 Inhibitors: Increase glucose excretion in urine. Examples: Dapagliflozin, Canagliflozin. Side effects: Dehydration, weight loss.
35
Describe adjunctive therapies that may be useful in pre-diabetes.
lfiestyle modifications (diet control and exercise)
medications such as metformin
CV protection: blood pressure control with ACE inhibitors or ARBs
Lipid management: statins for LDL control, dietary fiber, and omega-3 fatty acids.
36
Diagram a treatment algorithm for patients with Type II diabetes.
initial step: lifestyle interventions
First line med: metformin
Second-line: sulfonylurea, TZD, or DPP-4 inhibitor
Third line or combo therapy: Add SGLT2 inhibitor, GLP-1 agonist, basal insulin
Regular monitoring of A1C, adjust treatment as necessary based on glucose levels and patient response.
37
Diagram the process of atherogenesis.
Endothelial injury: damage caused by things like high LDL, smoking, hypertension, diabetes
Lipid entry: LDL enters vessel wall and oxidizes
Monocyte activation: monocytes migrate, turn into macrophages, and engulf oxidized LDL to form foam cells
Fatty streak: foam cell accumulation creates early lesions
Smooth muscle migration: smooth muscle cells move to the intimate, proliferate, and form a fibrous cap
Plaque formation: a lipid core and fibrous cap reduce the vessel lumen
Plaque rupture: Cap rupture exposes the core, leading to thrombus formation and potential blockage.
38
Describe the difference between triglycerides and cholesterol.
Triglycerides: energy storage molecule made of glycerol +3 fatty acids, stored in adipose tissue. They are broken down into free fatty acids and glycerol for energy during fasting or in between meals.
Cholesterol: sterol used as precursors for cell membranes, hormones, bile acids, vitamin D. Not used as energy but is vital for structural and metabolic functions.
39
Differentiate free and esterified cholesterol.
Free: active form found in cell membranes and blood plasma. Helps maintain membrane fluidity.
Esterified: Cholesterol combined with fatty acids for storage and transport
40
List the two sources of cholesterol, and key elements of the mevalonate pathway.
Dietary (eggs, meat, dairy) which are absorbed in the intestine and transported via chylomicrons.
Also, liver synthesis (de novo).
Key pathway elements: Acetyl-CoA formation is the starting point -> HMG-CoA synthase converts acetyl-coa into HMG-CoA -> HMG-CoA reductase converts HMG-CoA into mevalonate (reductase is the target for statins)
Lastly, Mevalonate is processed into isoprenoids and squalene. Squalene is cyclized to form lanosterol, which is then converted into cholesterol.
41
Describe the different types of lipoproteins including their structure, how they are formed, and their role in lipid transport.
Chylomicrons: Largest lipoprotein. formed in intestinal cells called enterocytes, transport dietary triglycerides/cholesterol to tissues.
VLDL: formed in liver, transport glycerides to tissues
IDL: derived from VLDL after triglyceride delivery. Intermediate form; precursor to LDL
LDL: formed from IDL, "cholesterol rich" bad cholesterol; delivers cholesterol to tissues
HDL: synthesized in liver/intestines, protein rich, good cholesterol, removes cholesterol to the liver for excretion
42
Calculate coronary artery disease risk using the LDL/HDL ratio.
LDL divided by HDL = CAD risk.
Males:
1.0 = low risk
3.55 = moderate risk (average)
6.25 = high risk (twice the average)
7.99 = Very high risk (3 times average risk)
Females:
1.47 = low risk
3.22 = moderate risk
5.03 = high risk
6.14 = very high risk
43
List target levels of total cholesterol, HDL, LDL, and triglycerides.
Total: <200
LDL: <130
HDL: men >40, women >50
Triglycerides: <120
44
Differentiate between primary hypercholesterolemias and secondary causes.
Primary: Genetic mutations (familial caused by LDL receptor mutations). Key feature is extremely high LDL levels from birth, resulting in early-onset atherosclerosis
Secondary: Result of conditions or lifestyle factors, such as:
-Obesity
-DMII
-Hypothyroidism
-CKD
-Meds such as steroids or beta-blockers
45
Explain why dietary control of lipid intake may not be sufficient to lower cholesterol, and some dietary strategies.
Reason: liver compensates by increasing endogenous cholesterol synthesis when dietary cholesterol is reduced.
Strategies for dietary management:
-increase soluble fiber such as oats and legumes to reduce cholesterol absorption.
-consume omega-3 fatty acids (fish, flaxseed) to lower triglycerides
-Limit saturated fats and trans fats to reduce LDL protection
-Plant sterols and stanols, which will compete with cholesterol for absorption
46
List the six hyperlipidemia drug classes, their MOA, examples, and side effects of each.
Statins: inhibit HMG-CoA reductase to decrease cholesterol synthesis. Ex: atorvastatin, rosuvastatin. SE: muscle pain, liver enzyme elevation.
Niacin (Vit B3): reduces VLDL and LDL synthesis; increases HDL. Ex: Niaspan. SE: flushing, GI upset, liver tox
Fibrates: Activate PPAR-alpha to enhance triglyceride metabolism. Ex: fenofibrate, gemfibrozil. SE: GI upset, gallstones
Bile acid resins: Bind bile acids in intestine, forcing liver to use cholesterol to produce more bile acids. Ex: cholestyramine, colestipol. SE: constipation, bloating
Cholesterol absorption inhibitors: Inhibit NPC1L1 transporter to block dietary cholesterol absorption. Ex: ezetimibe. SE: GI upset, rare liver tox
PCSK9 inhibitors: monoclonal antibodies prevent LDL receptor degradation, increasing LDL clearance. Ex: evolocumab, alirocumab. SE: injection site reactions
47
Explain the novel MOA of PCSK9 inhibitors.
PCSK9 binds to LDL receptors and promotes their degradation. So, the Inhibitors block PCSK9 activity, preserving LDL receptors on the livers surface, enabling more LDL to be removed from the bloodstream. LDL reduction up to 65% when combined with statins
48
List possible risks of hypocholesterolemia
-increased cancer risk due to impaired cell repair
-hemorrhagic stroke
-anxiety and depression (cholesterol needed for brain function)
-preterm birth and low birth weight
-impaired wound healing
49
Define NSAIDs and give examples.
Relieve pain, fever, inflammation by inhibiting cyclooxygenase enzymes. Aspirin, ibuprofen, naproxen, diclofenac, celecoxib
50
Diagram the major cell damage pathways (COX, LOX).
COX pathway: converts arichidonic acid to prostaglandins which mediate pain fever and inflammation.
LOX pathway: converts arachidonic acid to leukotrienes which are involved in bronchoconstriction and vascular permeability
51
Differentiate the two COX isoforms.
COX-1: constitutive, widely distributed, involved in homeostatic functions like gastric protection and platelet aggregation.
COX-2: inducible, expressed during inflammation, promotes inflammatory response.
52
List the pharmacokinetic properties of NSAIDs, and their major side effects.
weak acids, well absorbed, highly protein-bound, metabolized in liver and excreted renally. Causes GI irritation/ulcers, nephrotoxicity, hepatotoxicity, hypersensitivity reactions.
53
Describe the MOA of aspirin irreversible inhibition.
Aspirin acetylates the COX enzyme, irreversibly inhibiting its activity, reducing prostaglandin and thromboxane synthesis for the lifetime of the platelet.
54
Categorize the NSAIDs based on effects on COX-1 and COX-2
Nonselective: ibuprofen and naproxen
Cox-1 preferential: aspirin
Cox-2 selective: celecoxib
55
Describe the effects of NSAIDs on vasoconstriction and peripheral vasodilation to reduce fever.
Reduce fever by inhibiting prostaglandin E2 synthesis, which reverses hypothalamic-mediated vasodilation and heat dissipation
56
Define the MOA for GI upset with all NSAIDs.
inhibit cox-1, reducing protective gastric prostaglandins, leading to mucosal irritation and ulcers.
57
List blackbox warnings associated with NSAIDs.
increased risk of CV events and GI bleeding, ulceration, perforation.
58
Determine toxicity of aspirin from nomogram.
aspirin toxicity is evaluated using serum salicylate levels and time since ingestion. Symptoms include tinnitus, metabolic acidosis, hyperventilation. Treat with emergent dialysis
59
Describe the benefits and drawbacks of COX-2 selective inhibitors.
Benefits: reduced GI toxicity compared to nonselective NSAIDs.
drawbacks: increased CV risk due to reduced prostacyclin without inhibiting thromboxane A2.
60
Define specific applications for diclofenac and indomethacin.
diclofenac: osteoarthritis, rheumatoid arthritis, anykylosing spondylitis.
Indomethacin: gout, patent ductus arteriosus.
61
Explain the selection criteria for NSAIDs.
Based on patient-specific factors such as GI risk (use cox-2-I) renal function, CV risk, cost.
62
Describe why acetaminophen is not an NSAID
Lacks significant anti-inflammatory activity as it weakly inhibits COX in peripheral tissues.
63
Associate acute and chronic effects of glucocorticoids.
Acute: anti-inflammatory, immune suppresion, improved cognitive function.
Chronic: immunosuppresion, diabetes, HTN, osteroporosis, muscle wasting
64
Define the MOA of glucocorticoids.
Glucocorticoids bind to glucocorticoid receptors, modulating transcription of anti-inflammatory genes and suppressing pro-inflammatory mediators like cytokines.
65
List the endogenous opioids and their targets.
opioids: endorphins, enkephalins, dynorphins.
Targets: Mu, delta, kappa receptors.
66
Define DMARDs, and list 3 important DMARDs and their effects
Disease-modifying anti-rheumatic drugs reduce inflammation and slow disease progression. Ex: abatacept (T cell activation), rituximab (depletes B lymphocytes), adalimumab (anti-TNFa)
67
Differentiate the three main fibers for transmission of sensation.
A-beta: large, myelinated; transmit non painful stimuli.
A-delta: small, myelinated; transmit sharp pain
C-fibers: unmyelinated, transmit dull achy pain
68
Describe the three tracts in the CNS, and the importance of the PAG.
Spinothalamic: pain perception
Spinoreticular: emotional response
Spinomesencephalic: PAG pain modulation
PAG releases endogenous opioids to suppress pain signals
69
Describe the components of pain and pain signaling.
pain has sensory (nociceptive) and emotional components, transmitted via nociceptors to CNS, modulated by neurotransmitters like substance P
70
List the pharmacokinetic properties and organ system effects of the opioids.
Well-absorbed, metabolized by liver, excreted in urine. Analgesia, euphoria, resp depression, constipation.
71
Describe specific applications for opioids.
Severe pain, obstetrics, acute coronary syndrome, palliative care, cough suppression.
72
Define opioid toxicity.
resp depression, pinpoint pupils, sedation, nausea. Treated with naloxone.
73
Differentiate tolerance and withdrawal, and list degrees of tolerance to various effects.
Tolerance: reduced response to repeated doses. Fairly rapid.
High: analgesia, euphoria, sedation, resp depression.
Moderate: bradycardia
Minimal: constipation, miosis, convulsions.
Withdrawal: symptoms include anxiety, muscle aches, nausea, diarrhea.
74
List at least two drugs in each of the opioid structure classes, as well as opioid antagonists.
Phenanthrenes: morphine and hydromorphone
Phenylpiperidines: fentanyl, meperidine
Phenylheptylamines: methadone
Antagonists: naloxone, naltrexone
75
Define post-op shivering and treatments.
treated with meperidine or serotonin receptor antagonist like ondansetron
76
Discuss the important differences between Gram (+) and Gram (-) structure.
Gram (+): thick peptidoglycan layer, contains teichoic acid, no outer membrane, stains purple in gram staining
Gram (-): thin peptidoglycan layer, outer membrane with lipopolysaccharides (LPS, contains porins, stains pink in gram staining
77
List the five general properties of antimicrobial agents.
solubility in body fluids, selective toxicity, stable and resistance to degradation, spectrum of activity, limited side effects.
78
List examples of Gram (+), Gram (-), and atypical bacteria, and the diseases they cause.
Gram (+): staphylococcus aureus, streptococcus pyogenes, clostridium difficile. Diseases: skin infections, strep throat, pseudomembranous colitis.
Gram (-): escherichia coli, pseudomonas aeruginosa, neisseria gonorrhoeae. Diseases: UTIs, hospital-acquired infections, gonorrhea.
Atypical: mycoplasma pneumoniae, chlamydia trachomatis, rickettsia spp. Diseases: atypical pneumonia, STIs, rocky mountain spotted fever
79
Differentiate spectrum of activity and selective toxicity.
spectrum: range of pathogens an antibiotic can target (narrow vs broad-spectrum)
Toxicity: ability of a drug to target bacterial processes without harming host cells.
80
Describe the five main targets of antimicrobial agents, and give examples of drugs that
work by that mechanism.
Cell wall synthesis: penicillins, cephalosporins.
Cell membrane: polymyxins
protein synthesis: tetracyclines, macrolides
Nucleic acid synthesis: fluoroquinolones
Folic acid synthesis: sulfonamides, trimethoprim
81
Describe the mechanism of antibacterial action of beta-lactam antibiotics.
Beta-lactams inhibit transpeptidase enzymes, preventing cross-linking of peptidoglycan chains, leading to bacterial cell lysis.
82
Describe mechanisms underlying the resistance of bacteria to beta-lactam antibiotics.
production of beta-lactamases (enzymes that hydrolyze the beta-lactam ring)
Alteration of penicillin-binding proteins (PBPs)
Decreased permeability due to porin mutations in gram-negative bacteria
83
Identify the prototype drugs in each subclass of beta lactams, and describe their antibacterial activity and clinical uses.
Penicillins: penicillin G (narrow spectrum, gram +) Strep, C-diff, meningitis.
Cephalosporins: Cephalexin (1st gen, gram +) skin and soft tissue infections (staph/strep), UTIS.
Carbapenems: imipenem (Broad spectrum) seriosu hosp-acquired infections, sepsis, pneumonia, intra-abdominal infections, polymicrobial infections
Monobactams: aztreonam (gram -) UTIs, lower resp tract, sepsis caused by gram -.
84
List the major adverse effects of the penicillins and the cephalosporins.
penicillins: allergic reaction, GI upset, interstitial nephritis.
Cephalosporins: hypersensitivity, bleeding disorders, superinfections.
85
Identify the important features of imipenem, and meropenem.
imipenem: Broad spectrum, effective against gram +, gram -, and anaerobic bacteria. Requires co-admin with cilastatin to prevent renal degradation.
meropenem is similar, just less nephrotoxic.
86
Discuss the effects of premature termination of antibiotics.
Encourages development of resistance, leads to incomplete eradication of infection causing relapse or persistence.
87
Describe the clinical uses and toxicities of vancomycin.
MRSA, penicillin resistant gram+ infections.
Toxicities: red man syndrome, nephrotoxicity, ototoxicity.
88
Describe the MOA of polymyxins and their bacterial target.
bind to phospholipids in bacterial membranes, disrupting membrane integrity. effective against gram- bacteria.
89
Describe why inhibitors of protein synthesis are broad spectrum, their MOA, and toxicities.
Bacterial ribosomes (70S) differ from human ribosomes (80S), allowing drugs like tetracyclines and macrolides to target a wide range of bacteria. They bind to ribosomal subunits and inhibit them. ototoxicity and nephrotoxicity.
Tetracyclines can cause DEVILS CAP: Dentition, epigastric pain N/V/D (SEVERE), vestibular toxicity, insipidus diabetes, liver damage, (c)kidney damage, superinfection, anti-anabolic effect, phototoxicity
90
List examples of tetracyclines, macrolides, and additional inhibitors of protein synthesis.
tetracyclines: doxycycline, tetracycline.
Macrolides: azithromycin, erythromycin
Others: clindamycin, linezolid
91
Describe how sulfonamides and trimethoprim affect bacterial folic acid synthesis.
sulfonamides inhibit dihydropteroate synthase.
Trimethoprim inhibits dihydrofolate reductase.
Both disrupting bacterial folic acid synthesis.
92
Identify major clinical uses of sulfonamides and trimethoprim.
UTIs, pnuemocystis pneumonia, toxoplasmosis
93
Describe how fluoroquinolones inhibit nucleic acid synthesis.
inhibit bacterial DNA gyrase and topoisomerase IV, preventing DNA replication and transcription.
94
Discuss how disruption of normal microflora may be problematic.
leads to superinfections (c-diff colitis), yeast infections, and reduced competition for pathogens.
95
Identify key questions in deciding which antibiotic to use for which illness.
Clinical diagnosis, causative organism, antimicrobial susceptibility, narrow or broad spectrum required, patient specific factors (allergies, renal function)
96
Recognize components of viruses, and describe their importance.
Capsid: protein shell that protects viral genome and aids in host cell attachment.
Envelope (some viruses): lipid bilayer derived from host cell membrane, with embedded glycoproteins for host cell entry.
Nucleic acids: either DNA or RNA, encodes viral proteins.
Spikes: glycoproteins on the envelope or capsid that mediate host cell attachment and entry.
97
List examples of DNA and RNA viruses, and the diseases they cause.
DNA: HSV, Hep B, varicella zoster. Cause cold sores, chickenpox, hepatitis.
RNA: influenza, hep C, HIV. Flu, hepatitis, aids.
98
Explain the viral replication cycle and why viruses are considered obligate intracellular parasites.
Adsorption: virus attaches to host cell receptors via spikes
Penetration: entry into host cell via endocytosis or fusion
Uncoating: release of viral genome into host cytoplasm
Synthesis: host machinery produces new viral proteins and nucleic acids
Assembly: formation of new virions
Release: virions exit the cell (lysis or budding)
They're intracellular parasites because viruses rely on host cellular machinery for replication as they lack enzymes for nucleic acid synthesis and energy production.
99
Describe the infection cycle of the rotavirus.
Attachment to intestinal epithelial cells -> entry into cells via endocytosis -> uncoating and replication in cytoplasm -> production of double-layered particles -> release into intestinal lumen, causing diarrhea by disrupting epithelial function.
100
Outline the various drugs used for HBV and HIV, including their targets.
HBV: tenofovir, entecavir: inhibit HBV DNA polymerase.
Interferon-alpha: modulates immune response.
HIV: nucleoside reverse transcriptase inhibitors (NRTIs) ex: zidovudine.
Non-nucleoside reverse transcriptase inhibitors (NNRTIs) ex: efavirenz
Protease inhibitors: lopinavir
Fusion inhibitors: enfuvirtide
101
List signs and symptoms associated with the Ebola virus.
Fevere, headache, muscle pain.
NVD.
unexplained bleeding or bruising.
High mortality rate due to multiorgan failure and shock.
102
Explain the MOA of acyclovir in DNA chain termination.
acyclovir is phosphorylated by viral thymidine kinase to acyclovir triphosphate.
Incorporated into viral DNA by DNA polymerase. Lacks a 3'-OH group, causing premature DNA chain termination. Selective for infected cells due to reliance on viral thymidine kinase.
103
List uses for acyclovir and ganciclovir.
Acyclovir: HSV-1 and 2, VZV (chickenpox/shingles), prophylaxis in immunocompromised patients.
Ganciclovir: cytomegalovirus (CMV), particularly in immunocompromised people.
104
List and describe the three types of influenza antivirals.
Neuraminidase inhibitors: tamiflu and relenza, which block viral neuraminidase, preventing release of new virions.
Cap-dependent endonuclease inhibitors: Xofluza, inhibits viral RNA polymerase, blocking replication.
Adamantanes: amantadine, inhibit viral uncoating and only effective against flu A)
105
Contrast the two main types of influenza.
Flu A: humans and animals, associated with pandemics due to antigenic shift, subtypes based on hemagglutinin and neuraminidase.
Flu B: infects humans only, milder illness, no antigenic shift, less variable.
106
List different types of coronaviruses.
SARS-CoV: severe acute respiratory syndrome
MERS-CoV: middle east respiratory syndrome
SARS-CoV-2: Covid 19
ranges from mild colds to severe pneumonia
107
Describe the treatment of COVID-19 and the MOA of remdesivir, including possible side effects.
Vaccination, oxygen therapy, corticosteroids. Antivirals such as remdesivir and paxlovid.
MOA: nucleotide analog that inhibits RNA-dependent RNA polymerase, terminating viral replication. SE include Nausea, liver enzyme elevation, potential renal tox.
108
Define the following terms: Tremor, chorea, ballismus, athetosis, dystonia.
tremor: rhythmic, involuntary, common in parkinsons.
Chorea: irregular, rapid, jerky movements that impair voluntary control, associated with huntingtons disease.
Ballismus: violent, flinging movements of a limb, caused by damage to subthalamic nucleus.
Athetosis: slow, writhing movements, typically of hands and fingers.
Dystonia: sustained, involuntary muscle contractions causing abnormal postures or repetitive movements.
109
Explain the relationship between the basal ganglia, motor cortex, and thalamus; and describe the pathology in movement related disorders.
Basal ganglia: regulates motor activities by inhibiting or facilitating signals.
Motor cortex: execute voluntary movement.
Thalamus: relays sensors and motor signals betwween basal ganglia and motor cortex.
pathology: for parkinsons, dopaminergic neuron degeneration in the substantia nigra, leads to decreased dopamine in basal ganglia. Huntingtons has loss of GABAergic neurons in basal ganglia, resulting in excessive movement.
110
List the most common signs of Parkinson’s disease, and risk factors.
signs: tremors at rest, bradykinesia, rigidity, postural instability.
Risk: age 60+, male, genetic predisposition (SNCA gene mutation), environmental exposure such as pesticides and heavy metals.
111
Describe the function of synuclein and disorders associated with Parkinson’s.
alpha-synuclein is involved in synaptic vesicle regulation and neurotransmitter release.
Parkinsons: misfolded alpha-synuclein forms lewy bodies, leading to neurodegeneration.
112
List non-pharmacologic treatments for Parkinson’s.
exercise: improves motor function and reduces rigidity.
PT: focus on balance and gait training
OT: aids in daily tasks
113
Describe the role of Levodopa and its adjunct carbidopa.
Levodopa: converts to dopamine in brain, restoring dopaminergic activity.
Carbidopa: inhibits peripheral conversion of levodopa, increasing its bioavailability and reducing side effects like nausea.
114
List common side effects of levodopa and treatments for these.
levodopa: N/V, dyskinesia (involuntary movements), hallucinations.
Treatments: antiemetics, adjusting dose for dyskinesia, pimavanserin for hallucinations.
115
Draw the pathway for levodopa metabolism and targets for dopamine receptor agonists, MAO-B antagonists, and COMT inhibitors.
Levodopa -> dopamine via dopa decarboxylase. Targets dopamine receptors to activate receptors directly (pramipexole)
MAO-B inhibitors: reduce dopamine breakdown (selegiline)
COMT inhibitors: prevent peripheral breakdown of levodopa (entacapone)
116
List additional treatments for Parkinson’s and describe “On-Off” periods.
dopamine agonists, MAO-B inhibitors, amantadine for dyskinesia.
On-off: fluctuations between mobility and immobility, managed with dose adjustments or continous infusions.
117
Contrast other movement disorders (essential tremor, benign hereditary chorea, tardive
dyskinesia) in terms of symptoms and treatments.
Essential tremor: symmetrical tremor that is treated with beta-blockers
Benign hereditary chorea: childhood onset, non-progressive. Treated with tetrabenazine.
Tardive dyskinesia: repetitive involuntary movements from antipsychotics; treated with valbenazine
118
Describe the most common causes of cerebral palsy, assessments in infant, and
treatment.
causes: perinatal trauma, anoxia, infection
assessments: abnormal reflexes, delayed milestones, hyper/hypotonia.
tx: botulinum toxin, PT, intrathecal baclofen.
119
Describe the most common type of muscular dystrophy, the gene involved, and treatment. What is “Gower’s sign”?
most common: duchenne MD
Gene: dystrophin gene mutation
Tx: corticosteroids, PT
Gowers sign: use of hands to push on legs to stand up d/t weak proximal muscles.
120
Distinguish additional movement disorders (Huntington’s, ALS, Alzheimer’s) from Parkinson’s including causes and treatment
Huntingtons: GABA neuron loss, tetrabenazine.
ALS: motor neuron degeneration, riluzole.
Alzheimers: amyloid plaques and tau tangles; treated with cholinesterase inhibitors.
121
Describe the roles of the FDA and FTC in regulating OTC and Herbal Supplements.
FDA: approves OTC drugs, ensures safety and efficacy, monitors dietary supps.
FTC: regulates advertising of OTC drugs and supps.
122
Differentiate prescription, OTC, and “behind the counter” drugs.
prescription: provider approval required
OTC: available to public, deemed safe for self-use.
BTC: dispensed by pharmacists without a prescription (pseudoephedrine)
123
List the different phases of clinical testing in drug development and describe the
differences between phases.
P1: safety in healthy volunteers
P2: efficacy in small patient groups
P3: large scale trials for safety/efficacy
P4: post-marketing surveillance
124
Define GRASE.
Generally recognized as safe and effective. Used for OTC drug ingredients.
125
Describe the difficulties in regulating dietary supplement claims.
Lack of requirement for pre-market approval, and burden on FDA to prove harm.
126
List the purported benefits of echinacea, garlic, ginkgo, and St. John’s wort.
echinacea: immune stimulation
Garlic: CV health
Ginkgo: memory improvement
St johns wort: depression treatment
127
List the purported benefits of ginseng, milk thistle, saw palmetto, kombucha, kava kava,
aloe, and black cohosh (potential matching type question).
Ginseng: energy boost
Milk thistle: liver health
Saw palmetto: prostate health
Kombucha: gut health
Kava: anxiety relief
Aloe: wound healing
Black cohosh: menstrual relief
128
Recall the benefits and potential uses of vitamins and minerals.
Vit C: antioxidant, immune health
Vit d: bone health
iron: anemia treatment
Zinc: wound healing, immune function.
