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definitions > 18B > Flashcards

18B Flashcards

1
Q

dyspepsia

A 
combination of symptoms that indicates an Upper GIT problem
Sx-  Epigastric pain or burning
Early satiation
Post prandial fullness
Belching, bloating, nausea, discomfort
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2
Q

Heartburn

A

a burning sensation in the chest, just behind the sternum or in the epigastrium
The pain often rises in the chest and may radiate to the neck, back, shoulder, throat, or angle of the jaw
~50% of patients with GORD will present with chest pain
It may also be a symptom of ischemic heart disease

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3
Q

Heartburn cont

A

Cardiac and oesophageal causes may share similar symptoms as these two structures have the same nerve supply.
GORD is the most common cause of heartburn
recognized as a symptom of an acute myocardial infarction and angina

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4
Q

chest pain caused by GORD

A

has a distinct ‘burning’ sensation
occurs after eating or at night
worsens when a person lies down or bends over
It also is common in pregnant women
may be triggered by consuming food in large quantities, or specific foods containing certain spices, high fat content, or high acid content.

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5
Q

Heartburn and indigestion – Danger signs

A

Dysphagia
Dyspepsia at any age combined with one or more of the following ‘alarm’ symptoms: Weight loss,Proven anaemia, Vomiting (or haematemesis

Dyspepsia in a patient aged 55 years or more with at least one of the following ‘high-risk’ features: Onset of dyspepsia <1 year previously, Continuous symptoms since onset
Dyspepsia combined with at least one of the following known ‘risk factors’: Family history of upper GI cancer in more than two firstdegree relatives, Pernicious anaemia, Palpable Virchow’s node

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6
Q

Regulation of gastric acid secretion

A

Gastric acid secretion by parietal cells in gastric mucosa stimulated by:
Acetylcholine (induces increase in intracellular calcium)
Histamine (activation of adenylyl cyclase)
Gastrin (induces increase in intracellular calcium)

Gastric acid secretion diminished by
Prostaglandin E2 (inhibits adenylyl cyclase) Somatostatin (inhibits adenylyl cyclase)
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7
Q

factors that can affect gastric acid secretion

A

dicyclomine blocks cholinergic receptor
cimetidine blocks histamine receptor
omeprazole blocks proton pump

misoprostol stimulates prostaglandin receptor

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8
Q

peptic ulcer disease causes

A

NSAIDS (espAspirin)
Infection with Helicobacter pylori- (90% duodenal ulcers)- (70% gastric ulcers)
Increased hydrochloric acid and pepsin secretion
Inadequate mucosal defence against gastric acid

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9
Q

peptic ulcer disease Non-Pharmacological Rx

A

Stop smoking
Avoid ulcerogenic drugs (alcohol, NSAIDS, glucocorticosteroids)
Reduce caffeine intake

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10
Q

peptic ulcer disease Pharmacological Rx

A

Eradicating H.pylori infection- Antimicrobial therapy (amoxicillin, clarithromycin and metronidazole) + PPI (Esomeprazole, Lanzoprazole, Pantoprazole)
Reducing secretion of gastric acid- PPI, H2 receptor antagonists
Providing agents that protect the gastric mucosa from damage- Misoprostol, Sucralfate, alginates, bismuth
Antacids- Aluminum hydroxide, Calcium carbonate, Sodium bicarbonate

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11
Q

Proton Pump Inhibitors facts

A

Inhibit irreversibly H+/K+ – ATPase enzyme (proton pump) thereby suppressing secretion of hydrogen ions into the gastric lumen
Omeprazole inhibits CYP450 : thus inhibits metabolism of warfarin, phenitoin, diazepam, cyclosporine, digoxin

Most potent suppressors of gastric acid secretion
Acid suppression begins on average 1-2 hours after 1st dose
Effect for 2-3 days because of accumulation in gastric canaliculi
Preferred to H2 antagonists

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12
Q

Proton Pump Inhibitors indications

A

short term mx of peptic ulcer disease and GORD
Long term prevention of relapse of GORD
Treatment of Zollinger-Ellison syndrome
Treatment and prevention of NSAID-associated erosions and ulcers
IV PPI useful for high risk bleeding peptic ulcer

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13
Q

Proton Pump Inhibitors adverse effects

A 
Hypomagnesemia (in prolonged use) 
Increased risk of fracture 
Headaches 
Skin rashes 
Diarrhoea
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14
Q

H2-receptor antagonists facts

A

Reduces gastric acid secretion by reversibly blocking the action of histamine at the H2 receptors in the parietal cells of the stomach
Very efficient in nocturnal acid secretion

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15
Q

H2-receptor antagonists indications

A

Peptic ulcers, oesophagitis
Acute stress ulcers
GORD
Hypersecretory states (Zollinger-Ellison syndrome)

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16
Q

H2-receptor antagonists adverse effects

A

Headache, dizziness, diarrhoea, muscular pain
CNS – confusion, hallucinations, slurred speech
Anti-androgenic effect (esp. cimetidine)- Impotence, Gynaecomastia, Galactorrhoea

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17
Q

Cimetidine (H2-receptor antagonists)

A

high potential for drug interactions (inhibits P450)- theophylline, phenytoin, fluorouracil, metformin, diazepam, imipramine (increased effects)
Ketoconazole (increased absorption)

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18
Q

Ranitidine

A

Doesn’t cross BBB as easily, therefore less CNS symptoms
Less potential for drug-drug interactions (no effect on P450)
Little or no anti-androgenic effect compared to cimetidine

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19
Q

Prostaglandins facts

A

inhibits secretion of HCl, stimulates secretion of mucus and bicarbonate and causes vasodilation in the submucosa
Less effective than H2 antagonists or PPI’s
Routine use only in NSAID induced ulcers
Adverse effects-Uterine contractions (Contra indicated with pregnancy), Nausea and diarrhoea

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20
Q

adverse effects of GORD drugs

A

sucralfate- interferes with absorption of Tetracycline & Phenytoin
Bismuth subcitrate- Blackening of the tongue, teeth, stools
Aluminum hydroxide- constipation and faecal impaction
Magnesium (hydroxide and trisilicate)- diarrhoea and N+V
Calcium antacids- Milk-alkali syndrome
Sodium bicarbonate- Liberates CO2, causing belching and flatulence

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21
Q

H.pylori eradication

A

Triple therapy (7-(14) day regimen for eradication therapy)
PPI) PLUS TWO of the following antibiotics
Clarithromycin 500mg bd
Amoxicillin 1g bd
Metronidazole 400mg bd
(Tetracycline)

Quadruple therapy- Ranitidine 300mg dly for 7 days (if PPI contraindicated) PLUS Bismuth subcitrate 120mg 6hrly for 7 days PLUS 2 above antibiotics
PPI may be continued for 1 month or until the ulcer has healed

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22
Q

cause secondary hypertension

A

kidney disease
adrenal disease
thyroid problems
obstructive sleep apnea

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23
Q

Thiazide diuretics

A

inhibit Na+ and Cl- transporter in distal convoluted tubules
increased Na+, Cl- & K+/Mg2+ excretion
decrease Ca2+ excretion
weak inhibitors of carbonic anhydrase, increased HCO3- excretion

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24
Q

side effects Thiazide diuretics

A 
hypokalemia
hypovolemia
hyperuricemia
metabolic ADRs (impaired glucose tolerance and dyslipidemia - mostly after high doses)
erectile dysfunction
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25
Q

Potassium-sparing Diuretics

A

Works in the collecting duct
Binds and blocks aldactone receptors resulting in blocked Na water reabsorption; decreased SVR and BP
Considered a weak diuretic & thus often used in conjunction with more potent K depleting diuretics

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26
Q

side effects Potassium-sparing Diuretics

A 
Monitor K levels closely for hyperkalemia especially with renal impairment, use of potassium supplements, or ACE drugs
gynecomastia
amenorrhea
post-menopausal bleeding
dizziness, cramps, nausea, diarrhea
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27
Q

ACE Inhibitor Side Effects

A 
Cough (15% of patients. Is reversible) 
Taste disturbance (reversible) 
Angiodema 
First-dose hypotension 
Hyperkalaemia (esp. in patients with type II diabetes and renal dysfunction
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28
Q

Angiotensin II receptor blockers

A

Block the binding of Angiotensin II to AT1 receptors on vessels & adrenal gland thereby: -promoting vasodilation / lower aldosterone -decreased SVR and decreased BP

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29
Q

side effects Angiotensin II receptor blockers

A

Minimal side effect profile
Metabolically neutral
No impact on lipids, insulin or K+
Lowers uric acid levels

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30
Q

angiotensin II type 1 receptor effects

A

vessels- vasoconstriction, atherosclerosis, inflammation
heart- hypertrophhy, fibrosis
kidneys- incr aldosterone, salt retention

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31
Q

Calcium Channel Blockers

A

They act by reducing Ca2+ influx through voltage dependant L-type Ca2+ channels – resulting in smooth muscle relaxation and vasodilatation.
Effectively treat systolic hypertension
May be superior to other antihypertensives for stroke prevention
Effective in patients with: Comorbid conditions (Raynauds, migraine)
Particularly effective in- Elderly and African American’s

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32
Q

Calcium Channel Blockers side effects

A

Dihydropyridines- Peripheral edema, reflex tachycardia, flushing/headache, Hypotension
Non dihydropyridines- constipation, conduction abnormalities

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33
Q

Calcium Channel Blockers caategories

A

benzothiazepines, phenylalkylamines & dihydropyridines (1st, 2nd and 3rd gen)

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34
Q

Alpha-Beta Blockers

A

Work by binding to both alpha-1 and beta-1 and/or beta-2

Carvedilol & Labetalol both block: alpha-1 + beta-1+ beta-2

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35
Q

Beta Blockers: CV Pharmacodynamics

A

Reduced: heart rate, force of heart contraction, cardiac output, blood pressure
Decreased renin
Reduction in LVH, arrhythmias

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36
Q

Hypertension in Pregnancy

Pre-existing HPT

A

Drugs with best safety record are: Methyldopa, Nifedipine, Labetalol (also given IV in severe pre-eclampsia)
In the second trimester, although the risk of malformations is lower, diuretics and beta blockers are still contraindicated because they may retard foetal growth and cause electrolyte imbalance in the newborn

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37
Q

Hypertension in Pregnancy

Pre-eclampsia

A

Presents with HPT, oedema, proteinuria or hyperuricaemia in those whose BP had been norma
Complications: convulsions, cerebral haemorrhage, abruptio placentae, pulmonary oedema and renal failure

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38
Q

HT therapy in Special Populations

A

Africans- Responsd best to diuretics & CCB
Angioedema 2 – 4-fold higher
LVH- Aggressive BP control regresses LVH but hydralazine & minoxidil (vasodilators) DO NOT!
Elderly- Thiazide or CCB may be better tolerated
Pregnancy- Avoid ACEI & ARBs
Children/adolescents- Avoid ACEI & ARBs in pregnant or sexually active girls

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39
Q

Alpha Blockers

A

Results in vasodilatation
Fair tolerability; May cause postural effects
Additive agent for older men to decrease BPH symptomatology
Add-on agent only, should never be used as monotherapy due to increased risk of stroke and CHF

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40
Q

Direct Vasodilators

A

Hydralazine – dilates arterioles but not veins
Minoxidil – opens K+ channels in smooth muscles by its active metabolite
Sodium Nitroprusside – powerful vasodilator for treatment of hypertensive emergencies, Works by increasing intracellular GMP and dilates both arteries and veins
Diazoxide – stimulates opening of K+ channels, Can be used for treating hypertensive emergencies

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41
Q

Direct Vasodilators Precautions include

A

tachycardia, significant peripheral oedema and hair growth

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42
Q

centrally acting drugs

A

stimulates central alpha2 receptors which results in: Inhibiting efferent sympathetic activity
Additive agents
Should be used 3rd or 4th line
Caution: sedation, orthostatic hypotension

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43
Q

Clonidine (Centrally Acting drugs)

A

α-2 agonists
Reduces norepinephrine production
Blood vessel dilation results in decreased BP
Adverse effects: Sedation, dry mouth, Na and water retention

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44
Q

α-methyldopa (Centrally Acting drugs)

A

does not alter most of the cardiovascular reflexes
It is a pro-drug that exerts its antihypertensive action via an active metabolite (α-methylnorepinephrine)
Adverse effects- Sedation, lassitude (lack of energy), nightmares and lactation

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45
Q

Pharyngitis Causative organisms

A

Viral- Rhinovirus, corona virus, adenovirus, parainfluenza, influenza, EBV, CMV
Bacterial- Streptococcus pyogenes (GABHS)– 15-30% of cases in children and 5-10% adults, Mycoplasma Pneumoniae

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46
Q

Pharyngitis presentation

A 
Sore throat
Odynophagia
Fever
Anterior Cervical lymphadenopathy
Pharyngotonsillar exudate
Absence of cough
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47
Q

Pharyngitis treatment

A

Penicillin VK orally -10 days
IM penicillin (ie, benzathine penicillin G) for persons who may not be compliant with a 10-day course of oral therapy
Cephalosporins- Only considered first line if patient has a history of recent antibiotic use, recurrent pharyngitis infection or high penicillin failure rate is documented in the community
Macrolides- Only when penicillin or cephalosporins cannot be used

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48
Q

Tonsilitis Causative organisms

A

Viral- EBV, CMV, HSV, adenovirus

Bacterial- Streptococcus pyogenes

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49
Q

Tonsilitis: clinical presentation

A 
Fever
Sore throat
Foul smelling breath
Difficulty swallowing (dysphagia)
Painful swallowing (Odynophagia)
Tender cervical lymph nodes
Tonsillar exudate
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50
Q

Tonsillitis -Complications

A

Peritonsillar abscess (Quinsy)
Peritonsillar cellulitis
Complications due to GABHS: Scarlet fever (bright red tongue,rash), Acute poststreptococcal glomerulonephritis, Rheumatic fever

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51
Q

Tonsilitis- treatment

A

Oral penicillin
Recurrent tonsillitis- Amoxicillin/ clavulanate
Other antibiotics- Cephalosporin, Clindamycin, Macrolides

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52
Q

Bacterial Rhinosinusitis Causative organisms

A 
Strep Pneumonia
Heamophillus Influenzae
Moraxella catarrhalis
Staph aureus
Strep pyogenes
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53
Q

Acute Viral Rhinosinusitis causes

A

Rhinovirus, Influenza virus, Parainfluenza virus

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54
Q

Sinusitis –Clinical presentation

A 
Maxillary sinuses often affected
Pain and pressure over cheek, radiating to frontal region or teeth
Post nasal discharge
Blocked nose (Nasal congestion)
Cough
Discolored nasal discharge
Poor response to decongestants
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55
Q

Sinusitis -complications

A

Orbital cellulitis
Osteomyelitis
Intracranial extension
Carvenous sinus thrombosis - ophthalmoplegia

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56
Q

Sinusitis -Treatment

A

Amoxicillin with or without clavulanate (1st line) or clarithromycin or azithromycin
2nd line – 2nd or 3rd generation cephalosporins, macrolides, fluoroquinolones, clindamycin
Patients with an allergy to penicillin- doxycycline or a respiratory quinolone as first-line therapy

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57
Q

Treatment – Viral Rhinosinusitis

A 
Analgesics and antipyretics (NSAIDS , paracetamol)
Intranasal steroids (relieve facial pain and nasal congestion)
Saline irrigation (thin mucous and improve mucociliary clearance)
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58
Q

Community acquired pneumonia Causative organisms

A

Streptococcus Pneumoniae
Haemophillus Influenzae
Moraxella Catarrhalis

Staph aureus (post-influenza)
Klebsiella Pneumoniae (chronic alcoholism)
Pseudomonas Aeruginosa (bronchiectasis or cystic fibrosis
59
Q

Community acquired pneumonia atypical Causative

A

Chlamydia Pneumoniae
Mycoplasma Pneumoniae
Legionella species

60
Q

Community acquired pneumonia clinical presentation

A

Fever, Productive cough, Pleuritic chest pain (sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling)

61
Q

Community acquired pneumonia home Rx

A

<65 years old, without antibiotic exposure in the past 90 days or comorbidities- oral high dose amoxicillin ≥65 years old, have received antibiotics within the previous 90 days or who have comorbidities- oral amoxicillin-clavulanate or an oral second generation cephalosporin.
In both groups the alternative- oral respiratory fluoroquinolone when there is severe beta-lactam allergy
if beta-lactam allergy is presesnt oral macrolide/azalide

62
Q

Community acquired pneumonia hospital Rx

A

<65 years with no comorbidities- IV ampicillin or penicillin
≥65 years, have recent antibiotic exposure or comorbidities- amoxicillin-clavulanate, cefuroxime or a third generation cephalosporin
An alternative is a respiratory fluoroquinolone which is equally effective given orally or intravenously

63
Q

severe Community acquired pneumonia Rx

A

combo of amoxicillin-clavulanate, cefuroxime or a third generation cephalosporin plus a macrolide/azalide antibiotic
An alternative regimen- respiratory fluoroquinolone, combined with a betalactam
therapy should be initiated within 4–8 hours of hospital arrival

64
Q

acute uncomplicated cystitis cause

A 
Escherichia coli
Klebsiella
Proteus
Enterobacter
Staphylococcus sacrophyticus
Pseudomonas
65
Q

Lower urinary tract symptoms

A

Dysuria, Frequency of micturition, Urinary urgency
Haematuria (sometimes)
Suprapubic dyscomfort (less common

66
Q

acute cystitis Rx

A

First-line- Nitrofurantoin 100mg BD x 5 days
Trimethoprim / sulfamethoxazole 960mg (DS) BD
Fosfomycin Tromeatamol

Second line- Fluoroquinolones
Beta-lactam antibiotics
Cystitis in pregnancy- Penicillins, cephalosporins

67
Q

acute cystitis alternative Rx

A

Augmentin 500 mg/125 mg PO BID for 3-7d OR Augmentin 250 mg/125 mg PO TID for 3-7d

Second & third generation cephalosporins
Cefaclor 500 mg PO TID for 7d or
Cefpodoxime 100 mg PO BID for 7d or
Cefuroxime 250 mg PO BID for 7-10d

68
Q

Pyelonephritis sx and causes

A

sx- fever, flank pain

causes- E coli, Klebsiella, Staph saprophyticus

69
Q

Empiric Outpatient therapy of pyelonephritis

A

If local rates of E. coli fluoroquinolone resistance are low (< 10%):- Ciprofloxacin 500 mg PO twice daily x 7 d
Ciprofloxacin extended release 1000 mg PO x 7 d
Levofloxacin 750 mg orally x 5-7 d

Consider an initial dose of a parenteral agent, particularly if fluoroquinolone resistance is >10%.
Ceftriaxone 1 gm IM or IV x 1
Gentamicin 5 mg/kg IM or IV x 1
Ciprofloxacin 400 mg IV x 1

70
Q

Empiric in-hospital therapy of pyelonephritis

A

If local fluoroquinolone resistance rates < 10% -Ciprofloxacin 400 mg IV q12h OR Levofloxacin 500 mg IV once daily
Ceftriaxone 1 g IV once daily (with or without an aminoglycoside, e.g., gentamicin 5 mg/kg IV daily)
Gentamicin/tobramycin 5 mg/kg IV once daily (with or without ampicillin 2 grams IV q4h)
Piperacillin/tazobactam 3.375 g IV q6h (with or without an aminoglycoside, e.g., gentamicin
Meropenem 2 grams IV q8h
Duration: typically 48h parenteral therapy or until afebrile, then switch to oral therapy based upon susceptibility data to complete 7d (fluoroquinolone) or 14d (TMP-SMX) course

71
Q

Quinolones

A

Inhibits bacterial DNA gyrase
Bioavailability decreased by antacids
Large volume of distribution: including eye, lungs, prostatic fluid, CSF, bone and cartilage
Entero-hepatic cycle: AB in urine 5 days after stopping Rx
t½=4 hours
Less active in acidic urine

72
Q

Quinolones side effects

A 
GIT- nausea, dyspepsia, vomiting
CNS- dizziness, insomnia and headache
Hypersensitivity
QT prolongation/ torsades de pointes
Liver and renal damage
73
Q

Sulfamethoxazole + Trimethoprim

A

Inhibits production of folic acid
Hypersensitivity reaction- Steven Johnson’s Syndrome
Aplastic/ hemolytic anaemia
CI: newborn, porphyria, G6PD deficiency

74
Q

asthma

A

triad of wheeze, cough and breathlessness
symptoms are due to a combination of
constriction of bronchial smooth muscle
oedema of the mucosa lining the small bronchi
plugging of the bronchial lumen with viscous mucus and inflammatory cells

75
Q

Inflammatory mediators implicated in asthma include

A 
Histamine
Several leukotrienes (LTC4/D4 and E4) 5-hydroxytryptamine (serotonin)
Prostaglandin D2
Platelet-activating factor (PAF
Neuropeptides
Tachykinins
76
Q

asthma vs COPD

A

Asthma- Young age onset < 20
Symptoms worse at night, during resp. infections, weather changes, when upset
Marked improvement with beta2 agonist

COPD- Older age onset > 40
Symptoms worsen over long period of time (not rather at night)
Little improvement with beta2 agonist (not fully reversible obstruction)

77
Q

Asthma Classification (4 types)

A

Mild intermittent asthma- Patients have mild symptoms up to two days per week or two nights per month
Mild persistent asthma- Symptoms are still mild but occur more than twice per week
Moderate persistent asthma- Patients have symptoms at least once per day, also at least one night per week
Severe persistent asthma – Patients have symptoms most days and nights & sdesn’t respond well to medications even when taken regularly

78
Q

High probability of asthma

A

1/+ of sx: wheeze, breathlessness, cough, chest tightness – Especially if symptoms are worse at night and early morning
Symptoms in response to exercise, allergen exposure, cold air
Symptoms after taking aspirin or beta-blockers
Low FEV1/PEF
Otherwise unexplained peripheral blood eosinophilia

79
Q

Low probability of asthma

A

Dizziness, light-headed, peripheral tingling
Chronic productive cough, in absence of wheeze or breathlessness
Voice disturbance
Symptoms with cold only
Normal PEF or spirometry when symptomatic

80
Q

Global initiative for Asthma goals (GINA)

A

Achieve and maintain control of symptoms
Maintain normal activity levels, including exercise
Maintain pulmonary function as close to normal as possible
Prevent asthma exacerbations
Avoid adverse effects from asthma medications
Prevent asthma mortality

81
Q

drugs that aggravate asthma

A

beta-blockers (even eyedrops)
aspirin
NSAID”s

82
Q

asthma Treatment classification

A

Preventers- Drugs with anti-inflammatory action to prevent asthma attacks eg Inhaled/ Oral corticosteroids
Controllers-sustained bronchodilator action but weak or unproven anti-inflammatory effect eg Long acting β2 agonists, Methylxanthines, Leukotriene receptor antagonists
Relievers- short acting β2 agonists, Anticholinergic agents, Short acting theophylline

Mast cell stabiliser: Sodium chromoglycate, Ketotifen

83
Q

β2Agonists (Sympathomimetics)

A

used to treat the symptoms of bronchospasm in asthma and COPD
Drugs of choice in the management of acute bronchoconstriction
given via inhalation where possible

84
Q

cAMP phosphorylates a cascade of enzymes which results

A

Relaxation of smooth muscle including bronchial, uterine and vascular
Inhibition of release of inflammatory mediators
Increased mucociliary clearance
Increase in heart rate, force of myocardial contraction
Vasodilatation in muscle

85
Q

Short acting β2 agonists

Salbutamol, Fenoterol, Terbutaline

A 
Work within 15-30 minutes
Peak= 30 -60 minutes
Relief for 4-6 hours
Metered dose inhaler via spacer 
Dry powder/Nebulizer
Symptomatic relief
86
Q

Long acting β2 agonists

Salmeterol, Formoterol

A

Onset of action= 1-2 hours
Duration = 12 hours
Reduces need for additional bronchodilators
Improves lung functions
Reduces exacerbation rate
Combination with long acting anticholinergic agents very effective in COPD as well but very expensive

87
Q

β2 agonists Drug interactions

A

D/I- Corticosteroids (increased risk of hypokalaemia and hyperglycaemia)
Digoxin and diuretics (increased risk of cardiac arrhythmias)

Side effects – Uncommon with inhalation preparations – Fine tremor, nervousness, headache, dizziness, cardiac stimulation (tachycardia and palpitations)

88
Q

Anticholinergic agents

Ipratropium and Tiotropium

A

Are potent inhibitor of vagus-mediated bronchoconstriction and has significant bronchodilator activity
But do not have a significant inhibitory effect on mucociliary clearance
They are not the preferred relievers in asthma
They are more useful in COPD
They may be used in patients (especially the elderly) who cannot tolerate β2 agonist side-effects.

89
Q

Anticholinergic agents

Clinical use and Indications

A

Equal (or better) than β2 agonists in COPD
Relief of bronchospasm in asthma – Less effective than β2 agonists in acute bronchoconstriction – Used as additional bronchodilator in asthmatic patients not controlled on a Long-Acting BetaAgonists (LABA)
Cystic fibrosis

90
Q

Anticholinergic agents

Pharmacokinetics

A

Slow onset of action (>30min) and duration of action 4 hours. (Ipratropium)
Tiotropium – longer acting and only 1x dly inhalation
NOT for use in acute bronchospasm

91
Q

Short acting anticholinergics

Ipratropium

A

Onset of action= 30-60 minutes
Duration= 3-6 hours thus take 3-4 times a day
Longer duration of action than β2 agonists
Metered dose
nebulizer

92
Q

Long acting anticholinergics

Tiotropium

A

Onset of action= 30-60 minutes
Duration= 24-72 hours thus Once daily dosing
Elimination half life=5-6 days

93
Q

anticholinergics side effects

A

Dry mouth and unpleasant bitter taste
Urinary retention in patients with prostate hypertrophy tachycardia
Inhaled ipratropium may precipitate glaucoma in elderly patients
Constipation possible but seldom occurs

94
Q

Phosphodiesterase inhibitors

Methylxanthines: theophylline, aminophylline

A

Second line treatment for acute, severe and chronic persistent asthma
Advantages include: – Oral administration (theophylline), sustained bronchodilator action, mild antiinflammatory actions and a complementary mode of action to other bronchodilators
Once-a-day administration at lower doses
IV administration: aminophylline @ 1ml/min

95
Q

Methylxanthines

A

Inhibit phosphodiesterase and thus ↑cAMP- relaxes smooth muscle and inhibit mediator release from mast cells
Antagonists of Adenosine at A2 receptors
Anti inflammatory activity on T-lymphocytes by ↓ release of PAF

96
Q

Pharmacokinetics of Methylxanthines

A

Variable t½ (3-12hrs)
Good oral absorption
Metabolized by liver (Substrate for CYP1A2 and CYP3A4)
NB – Very narrow therapeutic index (10-20mcg/ml)
The enzyme inducing interaction achieved its maximal effect 6 days after starting

97
Q

Methylxanthines Adverse effects

A

GIT- nausea, vomiting, anorexia
Cardiovascular: – dilatation of vascular smooth muscle – headache, flushing and hypotension; tachycardia and cardiac dysrhythmias (atrial and ventricular)
CNS insomnia, anxiety, agitation, hyperventilation, headache and fits

98
Q

Glucocorticosteroids

A

Used in the treatment of asthma and in severe exacerbations of COPD because of their potent anti-inflammatory effect
Most effective controller therapy available for asthma. Inhaled corticosteroids (ICS) - Beclometasone, Budesonide
Systemic preparations – Prednisone, Betamethasone, Dexamethasone
MOA- Induce the formation of lipocortin-1: inhibits phospholipase A2 – reduce free arachidonic acid and thus leukotriene synthesis

99
Q

Corticosteroids

A

Decrease formation of cytokines (esp Th2), eosinophils, macrophages and T lymphocytes
Reversing mucosal oedema
Inhibit the generation of PGE2 and PGI2 by inhibiting induction of COX2
Decrease permeability of capillaries
Decrease release of leukotrienes and histamine which cause bronchoconstriction
Decrease hyperresponsiveness of airway smooth muscle to sensitive stimuli such as cold, irritants, allergens etc

100
Q

Corticosteroids – Inhaled adverse effects

A

Oral Candidiasis
Irritation and hoarseness of voice
Dryness of mouth
headache, skin reactions skin bruises, psychiatric symptoms
paradoxical bronchoconstriction, hypersensitivity reactions
minimal systemic adverse effects if taken by inhalation, but higher doses can cause adrenal suppression

101
Q

Corticosteroids – Systemic adverse effects

A

Suppression of Hypothalamic-pituitaryadrenal (HPA) axis depends on dose – Oral: prednisone >7.5-10 mg/day, after few months – Inhalational: beclomethasone >2000ug/day after few months

HT
Increased appetite
hirsutism
glaucoms
peptic ulcer
hypookalaemia
102
Q

what mediator antagonists can be used as adjunctive therapy

A

Antihistamines
Anti-leukotrienes
Mast cell stabilizers

103
Q

Histamine acts on 4 types of receptors

A 
H1 = anti-allergic and anti-emetic action
H2 = inhibits acid secretion (GI)
H3 = afferent pain and itch perception
H4 = Inflammatory and immune suppression
104
Q

1st Gen H1 antihistamine (Sedative)

Indications

A 
Allergic conditions
urticaria
angioedema
acute anaphylaxis
motion sickness
common cold and rhinorrhea
105
Q

1st Gen H1 antihistamine (Sedative)

Adverse effect

A

Sedation
hallucinations
precipitation of seizures in epileptics
Anticholinergic effects (sinus tachycardia, dry skin, dry mucous membranes)

106
Q

1st Gen antihistamine (Sedative) facts

A

t½ between 4-8 hours
Crosses BBB, good absorption, metabolized by liver

CNS depressants (effect potentiated)
Anticholinergic agents, antidepressants (anticholinergic effect potentiated)
107
Q

2nd Gen H1 antihistamine (NON sedative) facts

A

t½ 10h (thus daily dosing )
Minimal BBB penetration
Minimal metabolized – excreted by kidney unchanged

Drug interactions- CNS depressants
Drugs with arrhythmogenic potential (ketoconazole, erythromycin, protease inhibitors

108
Q

2nd Gen H1 antihistamine (NON sedative)

Indications

A

Symptomatic treatment for allergic conditions (allergic rhinitis, atopic dermatitis, chronic urticaria)
Not very effective in common colds

109
Q

2nd Gen H1 antihistamine (NON sedative)

Adverse effects

A

Sedation (uncommon
Headache, dizziness, GI disturbances, hypersensitivity reactions
Potential for cardiac arrhythmias (QT prolongation)

110
Q

Leukotrienes facts

A

Leukotrienes are more powerful bronchoconstrictors and longer acting than histamine
Leukotrienes increase bronchial mucus secretion and vascular permeabilit
LTB4, C4 & D4 induce bronchoconstriction and increased bronchial reactivity.

111
Q

Pathophysiology of cysteinyl leukotrienes in asthma

A 
Constriction of bronchiolar smooth muscle
Airway hyperresponsiveness
Plasma exudation
Eosinophilic inflammation
Increased endothelial permeability
Promotion of mucous secretion
112
Q

Anti-Leukotrienes

A

Prophylaxis and prevention of asthma
Inhibits variety of bronchoconstriction causes: allergen induced, Exercise, cold air, aspirin
Reduction in amount of B2 and corticosteroids needed
Improved respiratory function in mild to moderate asthma
Increased compliance in children
No benefit in severe cases of asthma or COPD)

113
Q

Anti-Leukotrienes Pharmacokinetics

A

Good oral absorption
90% plasma protein bound
Undergo biliary excretion
Pharmacological response within 24h

114
Q

Anti-Leukotrienes Adverse effects

A 
Abdominal pain, headache, rash, anaphylaxis
Eosinophilia, vasculitis (Churg Strauss Syndrome)
Liver dysfunction (very rare)
115
Q

anti leukotrienes Drug interactions

A

Zafirlukast extensively metabolized by liver (inhibitor of CYP3A4 and CYP2C9)
Warfarin – anticoagulant effect enhanced
Erythromycin, Theophylline and terfenadine – zafirlukast levels are reduced

116
Q

Mast cell stabilizers Ketotifen

A

MOA- Histamine antagonist, Functional leukotriene antagonist, Phosphodiesterase inhibitor

Indications- Useful adjunct to bronchodilator therapy in highly allergic children <3 years who have atopic eczema or hay-fever in addition to asthma

117
Q

Mast cell stabilizers Adverse reactions

A

somnolence, xerostomia, mild dizziness, and fatigue (reversible with withdrawal)
Weigh gain, increased appetite
Hypersensitivity in immunocompromized patients

118
Q

Mast cell stabilizers Drug interactions

A

oral antidiabetic preparations enhances the risk of reversible thrombocytopenia
potentiates the effect of sedatives, hypnotics, antihistamines and alcohol

119
Q

Mast cell stabilizers: Chromones

A

Drugs – Cromolyn, Nedocromil
cromone molecules used to prevent or control allergic disorder
Have no effect if bronchoconstriction has already occurred
MOA- Block calcium channels essential for mast cell degranulation, stabilizing the cell and thereby preventing the release of histamine and related mediators

120
Q

Mast cell stabilizers

indications, kinetics and adverse effects

A

Indications- Effective prophylactic anti-inflammatory agents (Not for use in acute asthmatic attacks
Useful in allergic rhinitis (nasal sprays)
Allergic conjunctivitis (eye drops)

Kinetics- Efficacy only determined after 4-6 weeks
Short duration of action – TDS, QID dosing

Adverse effects- Minimal adverse effects
mainly transient irritant effects such as pharyngeal irritation, chest tightness, coughing and nasal congestion, mouth dryness

121
Q

Immunomodulatory therapies in asthma

A

Immunosupressive therapy could be considered when ALL other treatments are unsuccessful- Methotrexate, Cyclosporine, IV immunoglobulins
Less effective and more side effects than oral corticosteroids therefor NOT recommended for routine therapy
Anti-IgE receptor therapy (Monoclonal antibodies) – Only omalizumab to be considered
Specific immunotherapy – May have anaphylactic and local reactions

122
Q

Omalizumab

A

Leads to decreased binding of IgE to receptors on mast cells and basophils
Reduces the requirement for oral and inhaled corticosteroids and reduces asthma exacerbations
Not used in acute bronchoconstriction

123
Q

Other Adrenergics acting on the respiratory system

A

Indirect Acting: Causes release of NE from storage vesicles- amphetamine, cocaine
Direct acting agonists on α1 receptors- Pseudoephedrine, Phenylephrine

124
Q

Direct acting agonists

A

Indications- Systemic and topical nasal decongestants
Usually in combination with antihistamines

MOA- Constrict dilated arterioles in nasal mucosa and reduce airway resistance

125
Q

Direct acting agonists C/I and precautions

A

Contraindications- Severe hypertension, Monoamine oxidase inhibitors (MAOI)
Precautions- Cardiovascular disease, hyperthyroidism, diabetes, prostatic hypertrophy, renal and hepatic impairment
Do not use longer than 7 days (rhinitis medicamentosa

126
Q

Direct acting agonists Adverse effects

A

CNS stimulation, anxiety, restlessness, tremors, headache
Reduced appetite, nausea and vomiting
Hypertension, cerebral haemorrhage, pulmonary oedema

127
Q 
Antitussives
Cough suppressants (Opium Alkaloids)
A

MOA- Suppress medullary cough centre in brain by acting on mu opioid receptors in lower doses needed for pain relief

Drug interactions- CNS depressants, Amiodarone, fluoxetine, MAOI (may be fatal)

128
Q 
Antitussives
Cough suppressants (Opium Alkaloids) Side effects
A 
Decreases bronchial secretions (thickens sputum)
Inhibits ciliary activity
Constipation, GI disturbances, dizziness
Respiratory depression
Confusion and sedation
129
Q

Mucolytics

A

Acetylcysteine (ACC), Carbocisteine (Mucospect)
Agents used to reduce disulphide bonds in mucous plugs in order to decrease the viscosity and enhance the mucus expulsion by coughing
Side effects- GIT ulceration

130
Q

Expectorants

A

Guaifenesin (Benylin) • Tinct Ipecacuanha
Agents used to increase the volume of mucus in order to decrease the viscosity and enhance the mucus expulsion by coughing
Enhances the ciliary movements in the respiratory tract
Side effects- Irritation of GI mucous membrane (Can be used as emetic)

131
Q

Inhalants and antiseptics

A

Inhalations: Camphor, menthol, eucalyptus oil, benzoin Antiseptics and anaesthetics in gargles and lozenges and sprays

132
Q

Allergic rhinitis

A

A symptomatic disorder of the nose, induced after allergen exposure, by IgE-mediated inflammation of the nasal mucous membranes
Symptoms – Nasal- sneezing, nasal obstruction/congestion, rhinorrhoea/post nasal drip and pruritis.
– Non-nasal- itchy palate or ears, conjunctivitis

133
Q

Symptoms of Allergic rhinitis are severe when…

A

One or more of the following: abnormal sleep, ↓of daily activities such as sport, leisure problems caused at work or school, symptoms troublesome-patient seeks treatment

134
Q

Allergic rhinitis sx

A

Rhinorrhea
Secretions ↑( mucous glands stimulated)
Vascular permeability increased – plasma exudate
Vasodilatation – congestion and pressure
Sensory nerves stimulated – sneezing and itching
Systemic effects – fatigue, sleepiness, malaise

135
Q

physical s/s of Allergic rhinitis

A

Allergic shiners
allergic salute
Pale boggy blue gray mucosa of nasal turbinates
Dennie Morgan lines, swelling of palpebral conjunctivae
“Cobblestoning”: lymphoid tissue on posterior pharynx

136
Q

Prophylactic treatment of Allergic rhinitis

A

Intranasal corticosteroids –first line treatment
Oral antihistamines (preferably second generation)
Decongestants oral and topical
Ocular antihistamines and cromolyns especially in seasonal allergic rhinitis
Leukotriene receptor antagonists

137
Q

Pharmacological Rx of Allergic rhinitis

A

Intermittent symptoms- Oral antihistamine & Decongestants
Chronic symptoms- Intranasal steroid spray
Other- Ocular / Intranasal antihistamine
Intranasal cromolyn
Short course of oral steroids in severe, acute episode
Leukotriene receptor antagonists if both rhinitis and asthma
dont use 1st generation antihistamines

138
Q

2nd generation antihistamines on Allergic rhinitis

A

Compete with histamine at H1 receptor in blood vessels, GI tract, respiratory tract
Improve rhinorrhea, sneezing, itching
No effect on nasal congestion
Use for seasonal/episodic rhinitis

139
Q

Oral decongestants (pseudoephedrine)

A

α-adrenergic agonists that act by constricting blood vessels in the nasal mucosa
Pseudoephedrine produces weak bronchial relaxation, has no effect on asthma
It can also cause side effects such as tremor, insomnia and nervousness
They should be avoided in males with benign prostatic hyperplasia (BPH) as they can cause urinary retention
Are contraindicated in patients with hypertension and glaucoma

140
Q

Topical decongestants: oxymetazoline and xylometazolin

A

These agents can be used for the symptomatic relief of nasal congestion
Their use should be limited to < 5 days as often secondary vasodilatation follows the initial vasoconstriction giving rise to rebound congestion “rhinitis medicamentosa”
Are long acting α-receptor stimulants which have a vasoconstrictor and decongestive effect on the nasal mucosa
Phenylephrine –has a shorter duration of action, with maximal effects lasting up to 4 hours
Side effects: transient burning or dryness of the mucosa may occur

141
Q

Intranasal corticosteroids e.g. beclomethasone, budesonide, fluticasone, mometasone and triamcinolone

A

They are the most effective maintenance therapy for allergic rhinitis both intermittent and persistent
They are poorly absorbed from the nasal mucosa and have little systemic effect

Side effects: – Transient burning or stinging, headache
Dry nose, sneezing, nasal bleeding, stuffy nose, and Irritation of the throat
Excessive use may lead to adrenal suppression

142
Q

Corticosteroids in allergic rhinitis

A

Relief of all symptoms
More effective than monotherapy with antihistamine/cromolyn
Greater benefit if combined with other agents
Does not Rx eye symptom

143
Q

Intranasal antihistamines eg Azelastine, Levocabastine

A

Intermittent allergic rhinitis
Some effect on nasal congestion
Vasomotor rhinitis
11% of pt- systemic absorption - sedation

144
Q

Immunotherapy allergic rhinitis

A

Success rate 80-90% for certain allergens esp pollen, dust mites, cat
Long term treatment: 3-5 years
Severe systemic allergy can occur

Indications: – Severe disease
– Poor response to treatment
– Presence of co-morbid conditions/Complications

definitions (11 decks)

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