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Exam 3 Material Flashcards

1
Q

Symptoms & Factors Involved Airway Obstruction: Asthma

A

-Airway walls are inflamed
-During an asthma attack, mucosal walls are thickened, air is trapped in alveoli, and smooth muscles are constricted.

-Wheezing, breathlessness, chest tighness, coughing. Increased at night and early AM

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2
Q

Symptoms & Factors Involved Airway Obstruction: Croup

A

-Acute laryngotracheobronchitis
-Usually viral
-Common in youth 6mos-5yrs
-Seal-like barking cough

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3
Q

Symptoms & Factors Involved Airway Obstruction: COPD

A

-Hypersecretion of mucus and chronic productive cough
-Inspired irritants increase mucus production along with the size and number of mucus glands

-Wheezing, chronic cough, breathlessness

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4
Q

Symptoms & Factors Involved Airway Obstruction: Emphysema & Bronchitis

A

-Abnormal, permanent enlargement of the gas exchange in airways accompanied by destruction/rupture of alveoli. Loss of elastic recoil in the lungs
-Cough, difficulty breathing, wheezing

-Bronchitis: Inflammation of bronchi. Can be acute or chronic

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5
Q

Airway Function Tests: FEV1

A

-Bronchial hyperreactivity testing.
-The fall in forced expiratory volume, in one second, provoked by inhaling increased concentrations of histamine or methacholine

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6
Q

Airway Function Tests: PEF

A

-Peak Expiratory Flow
-Measures maximum flow of forced expiration.
-This increases as we age

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7
Q

Immune response to allergens: Dendritic cells, T-cells, B-cells, Plasma Cells, Mast Cells, Neutrophils, Eosinophils

A

-Dendritic cells are located in the lining of the respiratory tract; first exposure to allergen. Antigen-presenting cell
-T-cells are activated, release IL-4 –> B-cells are then released by IL-4
-B-cells turn into plasma cells and produce IgE antibodies against the allergen
-IgE binds to the surface of mast cells and is irreversibly bound. On 2nd exposure to allergen, antibodies bind to IgE on mast cells, mast cells degranulate and release histamine, prostaglandins, leukotrienes
-Neutrophils & Eosinophils rush to the area due to a foreign substance being present, further exacerbating inflammation

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8
Q

Mediators released in early & late stages of asthma and their effects

A

Early stages: Histamine & Prostaglandins. Cause immediate bronchoconstriction from muscular contraction and vascular leakage

Later Stages: Leukotrienes. Liberated from the lungs during inflammation. Cause bronchospasm, mucus secretion, microvascular permeability, and airway edema

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9
Q

ANS & it’s effects on airway diameter

What role do the SNS and PNS play?

A

-Airway is innervated by nerves in the PNS, SNS, as well as NANC

-Normal resting tone of the airway smooth muscle is maintained by vagal stimulation

-SNS: Bronchiolar smooth muscle is relaxed when B2 cells are stimulated; however, the PNS system will fire in response causing constriction of the airway

-We see more of a response from circulating catecholamines than from direct innervation of the vagus nerve

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10
Q

MOA, SABA & LABA, Toxicity

Beta 2 Agonists

Short Term Relievers- Asthma & COPD

A

-Bronchodilators

-Nebulized Epi & Isoproterenol: Non-specific for beta cells. Can cause tachycardia and arryhthmias

-Albuterol (SABA): B2 selective. Aerosol. Takes effect in 30 mins, lasts 3-4 hours

-Salmeterol/Formotorol (LABA): B2 Selective. Aerosol. Lipid soluble, lasts 12 hours. Only 10-20% delivered due to droplet size

Toxicity: Skeletal muscle tremors

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11
Q

MOA? Toxicity?

Methylxanthines

Short term relievers- Asthma & COPD

A

-Inhibits PDE & adenosine receptors resulting in mild bronchodilation
-Theophylline: Most effective methylxanthine, found in natural tea.
-Toxicity: CNS stimulation, (+) chronotropy and ionotropy in heart, tremors

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12
Q

Muscarinic (M3) Antagonists

Short Term Relievers- COPD

A

-Bronchodilators
-Atropine: Given IV
-Ipratropium Bromide: Inhaled, can combine with B2 agonists
-Titroprium: Inhaled, long acting
-No CNS effects

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13
Q

Corticosteroids & Glucocorticoids

Long Term Controllers- Asthma

A

-Glucocoritcoids: Inhibit immune response by blocking DNA transcription/translation
-Cortico: Reduce bronchial activity, increase airway caliber, reduce frequency of exacerbations

-S/E: Increased risk of osteoporosis, slow growth rate in children, oropharyngeal candida & other opportunistic infections

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14
Q

Leukotriene Pathway Inhibitors

Long Term Controllers- Asthma

A

-Inhibit 5-Lipoxygenase: Zileuton
-Inhibit synthesis of leukotriene: -ukast
-Both improve aspirin induced asthma

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15
Q

Renal Corpuscle

Parts of the Nephron

A

-Glomerulus & Glomerular Capsule; In the medulla
-Filtration

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16
Q

Transporters in this area?

Proximal Convoluted Tubule

Parts of the Nephron

A

Reabsorption of 65% of Na+, K+, Ca++, Mg++
85% of NaHCO3-
Nearly all glucose and amino acids
Primary Xporters: NHE3, carbonic anhydrase, SGLT2

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17
Q

Proximule Tubule, Straigh Segments

Parts of the nephron

A

Secretion and reabsorption of organic acids and bases, including uric acid and diuretics

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18
Q

Thin Descending Loop & Thick Ascending Loop

Parts of the nephron

A

Descending loop: Passive reabsorption of water

Ascending loop: Active reabsorption of 15-25% of filtered Na+, K+, and Cl-. Secondary reabsorption of Ca++ and Mg ++

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19
Q

Distal Convoluted Tubule

Parts of the nephron

A

Active reabsorption of 4-8% of filtered Na+, Cl-, and Ca++ reabsorption under PTH control

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20
Q

What is secreted here?

Cortical Collecting Tubule

Parts of the Nephron

A

2-5% Na+ reabsorption coupled with K+ and H+ secretion

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21
Q

Medullary Collecting Duct (End of Nephron)

Parts of the nephron

A

Water reabsorption under vasopressin control

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22
Q

Macula Densa Cells

A

Monitors the osmolality and volume of the fluid in the distal tubule.
Transmits that information to the JG cells.
Located in vascular pole of the renal corpuscle

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23
Q

Juxtaglomerular Apparatus & GFR Regulation

A

-GFR regulation is done through adjusting BP:
-Altering capillary surface rea
-Controling arteriole diameter
-Autoregulation & Hormonal Regulation: RAAS
-Neuronal Regulation: NE and Epi release

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24
Q

Function of NHE3 & Carbonic Anhydrase in Na and HCO3- reabsorption

A

-NaHCO3 reabsorption is initiated by the action of the Na+/H+ Exchanger (NHE3)
-This system allows Na+ to enter the cell from the tubular lumen in exchange for an H+ from inside the cell (Na+ moves in, H+ moves out)
-Na+/K+/ATPase pump pumps reabsorbed Na+ back into the interstituem in order to main a low intracelluar Na+ concentration
-Secreted H+ & HCO3- combine to form carbonic acid –> broken down into CO2 & H2O by carbonic anhydrase

HCO3- reabsorption is dependent upon the activity of carbonic anhydrase

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25
Q

Inhibition of what at the loop?

Loop Diuretics

A

-Inhibition of the Na+/K+/Cl- (NKCC2) transporter in the ascending Loop of Henle. Na+ is pushed down and absorbed into the collecting duct, causing excess potassium to be secreted
-Hypokalemic metabolic alkalosis
-Sulfa drugs. Caution with sulfa allergies

-Lasix, Bumex, Ethacrynic Acid

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26
Q

Carbonic Anhydrase Inhibitors

A

-Inhibition of carbonic anhydrase in the PCT, meaning carbonic acid is not broken down into HCO3- & CO2
-Currently used for glaucoma, mountain sickness, edema w/ alkalosis
-Toxicity: Metabolic acidosis, renal stones

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27
Q

Potassium Sparing Diuretics

A

-Aldosterone Receptor Antagonists
-Spironolactone: Blocks aldosterone receptors
-Amiloride: Inhibits Na+ flux through ion channels in luminal membrane

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28
Q

Potassium Wasting w/ Diuretics

A

Potassium wasting occurs because of an increase in Na+ (w/ HCO3-) being driven to the collecting duct. This creates a lumen-negative electrical potential, causing an increase in K+ secretion

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29
Q

Thiazides

A

-Inhibits NaCl transport via the NCC transporter in the DCT
-Sulfa drug

30
Q

Agents that alter water excretion

A

-Mannitol: Used mainly to reduce ICP. Works mainly in the PCT
Urine output increases, reduced ICP, decreased IOP, hyponatremia and then hypernatremia
Toxicity: N/V, HA

-Conivaptin: ADH Antagonist. Reduces water reabsoprtion, increases plasma Na+ concentration

31
Q

Thiazide Diuretics & DI

A

Thiazide diuretics work by decreasing plasma volume and decreasing GFR. Macula densa cells sense this loss of volume and increase Na+ and H2O reabsorption at the PCT leading to decreased UOP

32
Q

How many types of histamine receptors?

Organ System Effects of Histamine

CNS, CV, GI/stomach, Lungs

A

CNS: Stimulates pain & itching
CV: Vasodilation (H1), increased HR
GI/Stomach: Release of HCl, contraction
Lungs: Bronchoconstriction (H1)

4 types- GPCR

33
Q

Organ Effects of Serotonin

CV, Respiratory, GI, Brain

A

CV: Vasocontriction, platelet aggregation

Respiratory: ACh release –> bronchoconstriction, hyperventilation

GI: Overproduction causes diarrhea

Brain: Melatonin precursor. Mood, appetite, temperature regulation, pain perception, migraines, vomitting reflex, BP

34
Q

Triple Response of Histamine Reaction

A

-Used for allergy testing
-Increased blood flow to capillary endothelium (redness)
-Flare: Widespread dilation of surrounding arterioles
-Wheal: Local swelling due to increased permeability in the walls of surrounding vessels

35
Q

1st & 2nd Generation Histamines

Drugs, Uses, Toxicity

A

1st: Benadryl, Phenergan, Dramamine
-Used for motion sickness, nausea, anesthesia
-Cause sedation

2nd: Zyrtec, Claritin, Allegra
-Used for allergic response, seasonal allergies, urticaria
-No CNS effects. Near equal efficacy to first gen

Toxicity: Sedation, urinary retention, blurred vision, convulsions, postural hypotension

36
Q

H2 Antagonists

Use, drug names

A

-Reduce the amount of HCl produced in the stomach
-Not as effective as PPI
-Zantac, Pepcid

37
Q

Serotonin is made where?

How many 5-HT families?

A

90% of body’s serotonin is created in the enterochromaffin cells. 10% from the Raphne Nuclei in the pons

-Seven Families of 5-HT. 6 are GPCR, 5-HT3 is an ion channel

38
Q

5-HT Agonists

Buspar, Triptans

A

-Buspirone; 5-HT1a. Non-benzo anxiolytic, GAD, OCD

-Sumatriptan; 5-HT1D/1B agonist. Tx for migraines. Non-prophylactic. Bind 5-HT in cranial blood vessels, preventing dilation and stretching of pain nerve endings.

-Toxicity: Recurrence of migraine, coronary vasospasm (rare), serotonin syndrome if taking triptans + SSRI, MAOI

39
Q

5-HT Antagonists

Cyproheptadine, Phenoxybenzamine, Zofran

A

-Cyproheptadine & Phenoxybenzamine: 5-HT2.
Carcinoid tumors and cold induced urticaria

-Zofran: 5-HT3
N/V

40
Q

Migraine Prevention

A
  • Beta-Blockers, CCBs, ACE-I
  • Antidepressants- SSRI, TCAs
  • AED- Valproate & Topiramate
  • Botox
  • Mab- Aimovig
41
Q

Migraine Treatment

A
  • Pain Relief: ASA, Nsaids, ASA + Caffeine, Opiods
  • Triptans (not preventative)
  • Ergotramine- not as effective as triptans
  • Anti-nausea meds: Chlorpromazine, ondansetron
  • Glucocorticoids- prednisone
42
Q

Hyperthermia Disorders

Serotonin, Neuroleptic, Malignant. S/S, causes, Tx

A
  • Serotonin Syndrome: HTN, hyperreflexia, clonus
    -Contributing Factors: SSRIs, MAOIs, Triptans, MDMA, St. John’s Wort
    -Tx: Sedation with benzos, 5-HT block with cyproheptadine or chlorpromazine
  • Neuroleptic Malignant Syndrome: HT, Hyperthermia, acute, sever parkinsonism
    -D2 blocking antipsychotics
    -Tx: IV diphenhydramine, cooling, sedation w/ benzos
  • Malignant Hyperthermia: HTN, hyperthermia, muscle rigidity
    -Volatile anesthetics & succinylcholine
    -Dantrolene, cooling
43
Q

Tryptophan Pathway

A

-Tryptophan hydroxylase converts tryptophan into 5-hydroxytryptophan
-5-HT is converted by decarboxylase into serotonin

-Tryptophan is essential in the production of melatonin

44
Q

Dopamine Mesolimbic Reinforcement

A

This system originates in the ventral tegmental area of the brain that projects to the limbic system. The VTA releases large quantities of dopamine when stimulated (and pretty much all addictive drugs activate the VTA) creating a strong reinforcement for this behavior

45
Q

Depression Disorders vs Anxiety

A
  • Depression:
    -Dysthmia
    -Psychosis
    -Postpartum
    -Seasonal Affective Disorder
    -Bipolar
  • Anxiety:
    -Generalized Anxiety Disorder
    -OCD
    -PTSD
    -Social
46
Q

Four Categories of anti-depressants, drugs in them, and side effects

A
  • SSRIs- Most common, first line
    -Inhibition of SERT
    -Fluoxetine, Citalopram, Paroxetine, Sertraline, Escitalopram
  • SNRIs- Used for major depression & pain disorders
    -Inhibition of SERT and NET
    -Desvenlafaxine, Duloxetine
  • TCAs- Supplanted by SSRIs
    -Amitrypyline
  • MAOIs- Rarely used, lethal drug interactions. For refractory depression
    -Irreversible: Phenelzine
    -Selegiline
  • All work by increasing monoamine neurotransmitter levels within the synapse
  • Adverse effects: Suicidal ideation, drug interactions, N/V/D, sexual dysfunction
47
Q

Alternative Therapies for Depression

A
  • Buproprion, Solriamfetol
  • Benzos
  • Antipsychotics
  • Pyscotherapy
  • ECT
  • St John’s Wort
48
Q

Partial/Focal Seizures

3 types

A

-Start in small area of the brain
1. Simple: Not aware of occurence
2. Complex: LOC, automatisms
3. Secondarily generalzed: Just like general

49
Q

General Seizures

5 subtypes

A
  • Start all over the brain
    1. Tonic Clonic: Grand Mal
    i. Aura- Seizure- Post-ictal
    ii. Tonic - clonic (usually <5 mins)
    2. Absence: Petite mal
    3. Drop Attacks: Tonic, Atonic
    4. Clonic: Jerking & myoclonus (twitching)
    5. Infatile spasms: Indicative of underlying pathology
50
Q

Principle MOA of AEDS

A

Principle MOA involves modification of Na+, K+, Ca++ voltage-operated ion channels
-enhancing inhibition through GABA
-inhibiting excitatory function (glutamate)

51
Q

Tonic vs. Clonic

A

-Tonic: Increased tone, stiffening of muscles

-Clonic: Muscle jerking, twitching

52
Q

MOA? Toxicity?

Phenytoin

Focal & Tonic Clonic

A

-Oldest non-sedative AED
-Alters Na+, K+, and Ca++ conductance
-Enhances gaba, inhibits glutamate

-Highly protein bound: competes with carbamazepine, valproic acid, sulfonamides

-Fosphenytoin- More soluble prodrug of phenytoin; can be given IV

-Accumulates in brain, liver, muscle, and fat
-Approaches zero order kinetics
-Highly Toxic; dose related- nystagmus, loss of extraocular movement, diplopia, ataxia, sedation, gingival hyperplasia, hirsuitism

53
Q

MOA? Toxicity?

Carbamazepine

What does it do specifially to metabolism?

A

MOA is similar to Phenytoin, but blocks Na+ channels at therapeutic levels

-TCA

-DOC for focal seizures, can also be used in bipolar disorder, effective in trigeminal neuralgia

-Can be used with Phenytoin

-Induces CYP450, increasing it’s own metabolic rate with prolonged use
-Enhances metabolic rate of other AEDS

A/E: Diplopia, ataxia

54
Q

Phenobarbital

A

-MOA Unknown. We think enhancing GABA
-Sedative
-Can worsen absence, drop, or infantile seizures
-DOC in infants

-Toxicity: Sedation, increase in hepatic enzymes

55
Q

Lacosamine, Lamotrigine, Vigabatrin

A

Lacosamide: Focal Seizures
Lamotrigine: Partial & Absence Seizures.
-MOA; Ion channel
Vigabatrin: GABA analog

56
Q

Ethosuximide

MOA?

A

-DOC for absence seizures
-Syrup
-Ca++ channel inhibition
-A/E: GI upset, sedation, tremor, hepatotoxicity

57
Q

Works for two types of seizures and what othr 2 conditions?

Valproic Acid

A

-MOA: Blocks sustained high frequency firing. Effects Na+ channels, increases GABA, increases K+ conductance
-Absence seizures
-Generalized tonic-clonic
-Bipolar
-Migraine
Displaces phenytoin from proteins

-Inhibits metabolism of phenobarb, phenytoin, carbamazepine
-Toxicity: GI upset, n/v, abdominal pain, heartburn.

58
Q

Major Considerations for Status Epilepticus

How do we treat?

A
  • Most common form in generalized tonic-clonic
  • Requires immediate management
  • always requires IV anti-seizure meds
    -IV Benzodiazepines
    -IV Fosphenytoin or Valproic Acid or Keppra
    -Large dose phenobarb if unresponsive to above
    -Burst suppression
59
Q

Tx of Infantile Spasms

A

Determine underlying pathology

*Palliative care
* IM prednisone
* Vigabatrin- GABA analog

60
Q

Alternative Therapies for Seizures

A
  • Resection of epileptic foci
  • Vagus nerve stimulator
  • Ketogenic Diet (children)
  • Medical THC
61
Q

Anesthesia & AEDS

What three drugs should be avoided?

A
  1. Need adequate AED management during surgery
  2. Phenytoin blocks NMB at lower doses, but can enhance NMB at higher/chronic doses
  3. Avoid methohexital, sevo, demerol
62
Q

Sedatives vs Hypnotics

A
  • Sedative: Decreases activity, reduce anxiety, help with muscle relaxation
  • Hypnotic: Specifically aimed at inducing a sleep state
63
Q

Major Subgroups of Sedative-Hypnotics

Which receptor do they work on? Classes and drug names

A
  • Benzodiazepines
    -Diazepam, midazolam
  • Barbituates
    -Phenobarbitol, Thiopental (replaced by propofol), methohexital
  • Sleep Aids
    -Zolpidem
  • Anxiolytics
    -Buspar
  • Ethanol

These are all GABAa Receptor agonists. Potentiate inhibition at all levels of the CNS
-Increase flow through GABA receptor
-Increase channel opening time

64
Q

Management of Acute ETOH Intoxication

A
  • Goal is to prevent respiratory depression and aspiration of vomit
  • Correct electrolyte imbalances and hypoglycemia
  • Avg blood alcohol in fatal cases >0.4%
65
Q

Toxic Effects of ETOH

A

-Liver & GI Tract damage
-Alcoholic fatty liver –> alcoholic hepatitis –> cirrhosis –> liver failure

-Generalized symmetic peripheral nerve injury
-Parasthesias of hand and feet
-Gait disturbances, ataxia, dementia
-Wernicke-Korsakoff Syndrome (Thiamine defiency)
-Paralysis of external eye muscles, ataxia, confusion, psychosis, coma, death

66
Q

Tolerance, Dependence, Addiction

A

-Tolerance: More of the drug is needed to get the same initial effect

-Dependence: Body is now reliant on drug

-Addiction: Behavior; will seek out drug regardless of negative consequences

67
Q

Management of ETOH W/d- Symptoms

A

-Mild Symptoms (6-8hrs after consumption): Tachycardia, HTN, tremor, anxiety, diaphoresis

-Severe: Seizures (most common cause of seizures in adults), low grade fever, auditory/visual hallucinations

-Delirium Tremens: ANS instability, extreme agitation

68
Q

Tx of ETOH W/d

A

-Prevent seizures, delirium, arrhythmias
-Replace electrolyes & thiamine
-Give benzos, taper off benzos
-Takes months for nervous system function to return to normal, especially sleep

69
Q

Treatment of Alcoholism

A

-Rehab
-Naltrexone; Approved by FDA to tx ETOH dependance. Opioid- antagonists
-Can cause acute opioid w/d in a patient physically dependent on opioids
-Acamprosate: Reduces urge to drink. Adjunct therapy, used in Europe
-Disulfiram

70
Q

ETOH Pathway & where Disulfiram acts

A
  1. Ethanol goes through a redox reaction where alcohol dehydrogenase converts ethanol into acetaldehyde
    -This pathway creates calories from ETOH, causing weight gain
  2. With chronic ETOH use, overtime the body begins to metabolize ETOH via the microsomal ethanol-oxidizing system. This system does not produce calories, chronic alcoholics will be thinner

-Acetaldehyde is converted into acetate via aldehyde dehydrogenase

-Disulfiram inhibits aldehyde dehydrogenase, causing acetaldehyde accumulation (hang over symptoms)

71
Q

ETOH & Sleep

A

-Induces sleepiness via GabaA
-Suppresses REM in early sleeping causing a deep sleep, difficult to wake up
-Increased wakefulness later in sleep
-Prolonged REM in second half of sleep, bizarre & intense dreams

72
Q

Biochemical Pathways For ETOH

A

Advanced Pharm (7 decks)

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