
Renal pharmacology 2- Diuretics
o Hypokalemia is a commonly seen Side Effect of most Diuretics except Mannitol.
o Sulfonamide have a common Side effect of Skin rashes/ Allergy
o What are the most Common
o Carbonic Anhydrase Inhibitors
 Acetazolamide decreases Bicarbonate and Sodium Reabsorption by Inhibiting
PCT Luminal CA + Na+/H antiporter
 Acetazolamide cannot be used in the setting of Chronic Kidney Disease; Use
Loop Diuretics instead
 What is the drug used to treat mountain sickness and Glaucoma?
Acetazolamide, A carbonic Anhydrase Inhibitor
 Since carbonic Anhydrase inhibitors increase Bicarbonate Excretion in Urine, A
major side effect would be Hyperchloremic Metabolic Acidosis.
 Other Side Effects are Bone Marrow Suppression
 Urine alkalinization can treat weak Acid overdose and prevent Uric or Cysteine
stones. Carbonic Anhydrase inhibitors can be used to induce Urine
Alkalinization
o Osmotic Diuretics
 Mannitol, An osmotic diuretic, increases Na and H20 excretion at PCT to
Descending LOH.
 Mannitol can be used for High ICP/Glaucoma and is safe for Oliguric states
(Shock+ trauma)
 Pulmonary Edema is a key Toxicity for Mannitol
o Loop Diuretics
 Ethacrynic Acid is an ototoxic loop d
 Which loop diuretic do you avoid in Liver Cirrhosis? Furosemide b/c albumin is
needed for it’s absorbption.
 Loop diuretics work by Blocking NKCC2 Channel
 Loop Diuretics cause Ototoxicity and Calcium stones SFx
 Inherited Defect of Thick ascending loop of Henle that mimics Loop Diuretic OD
 Barter Syndrome (Mutation of NKCC2 – “3 Ions for 1 channel Barter”)
o Thiazide Diuretics
 Thiazides block NCC at the DCT
 Inherited Defect of DCT that mimics Thiazide OD
 Gitelman Syndrome ( Gitelman’s THIghs- Sounds like a mythical Strip
club named Gentleman’s Thighs)
o K+ Sparing Diuretics
 Spironolactone is the treatment of choice for Conn Syndrome
(Hyperaldosteronism)
 Spironolactone and Eplerenone antagonizes aldosterone binding at the MR
(Aldosterone receptor) to cause Sodium Excretion and K+ reabsorption.
 Spironolactone or Eplenerone causes Amennorhea in women and
Gynecomastia in Men.

o

Amiloride and Trimaterene loop diuretics work directly on Epithelial Na intake
channels at CCT
 Triad of Hypertension, Hypokalemia, and Metabolic alkalosis caused by
activated ENaC at the Collecting tubules. What Syndrome?
 Liddle Syndrome or Pseudo-hyperaldosteronism (Aldosterone binds MR
causing Na Reabsorption and K wasting
 Liddle Syndrome is Tx’ed with Amiloride or triamterene
 K- Sparing diuretics are given with Loop or Thiazide diuretics to prevent
Hypokalemia
ADH antagonists
 Conivaptan-IV / Tolvaptan are used to treat SIADH.
 Conivaptan/Tolvaptan MOA? Block ADH Receptor V2
 Central Diabetes Insipidus is treated by Aquaporin-2 agonists
(Desmopressin/Vasopressin). Nephrogenic Diabetes Insipidus treated with
Thiazides
Mycobacteria
o Zieh Nielsen Acid fast organisms retain Carbolfuchsin.
 Carbolfuchsin, Alcohol, and then methylene Blue counter stain.
o M. Tuberculosis is Acid Fast Positive, Uniquely forms Cords , and is Pathogenic in
Guinea Pigs.
o What is the Cytokine necessary to coordinate a CMI response for TB latency)? TNF
alpha. Can be blocked by Remicade causing TB reactivation
o Pulmonary TB or ghon complex consists of a Hilar Lymph Node granuloma and Lobar
Granuloma.
o How does TB establish Extrapulmonary foci? Hematogenous Spread in Naïve
Macrophages
o What is the Preferred method for culture samples in pediatric TB? Gastric Aspirates
o PPD and IGRA (Interferon Gamma release Assay) detect a previous CMI response to TB.
o TB therapy requires Directly Observed multidrug Therapy with RIPE (Rifampin, Isoniazid
, pyrazinamide and Ethambutol)
o Isoniazid Blocks Mycolic Acid Synthesis with Side effect of Hepatitis.
o Ethambutol blocks Synthesis of TB cell wall with Side effect of Optic Neuritis.
o Previous BCG vaccination or exposure can cause a false Positive TST.
o A CMI response is required to clear leprosy. What are the specific types of CMI
responses that result in Leprosy?
 Strong TH1 response leads to Tuberculoid.
 Th2 antibody production leads to Lepromatous.
o Lepromatous leprosy will test Lepromatin PPD Negative and Show Anti- Glycoplid1
antibodies. Tuberculoid will test Lepromatin PPD Positive and LMIT positive
(Lymphocyte Migration Inhibition Test) .
o M. Leprae is treated with Dapsone and Rifampin for 2 or more years.
o Erythema Nodosum rxn to M. Leprae treatment can be treated with thaliodimide
o
o
Atypical Mycobacteria are environmental, Not Lethal in Guinea Pigs, and test negative
for TST.
Four groups of Atypical Mycobacteria are : Photochromogens produce pigment in light.
Scotochromogens produce pigment in dark or light. Non-Chromogens produce no
pigment, and Rapidly growing Mycobacteria.

Bacterial Pneumonia 2
o How does legionella Infect and survive Inside Alveolar Macrophages?

Type IV Secretion System(Alters endosome) And Protease to escape
endosome.
o What are the risk factors for Legionnaires disease?
 Older, Immunosuppressed, Smoker/Drinker
o Legionella is Diagnosed with a Urine Antigen Test or Special Culture Media (Buffered
Charcoal Yeast agar)
o Compared to other causes of Atypical Pneumonia, Legionnaire’s pneumonia includes GI
and Renal involvement.
o Legionella Pneumonia and Mycoplasma Pneumonia are treated with Respiratory
fluoroquinolones ( Levofloxacin and Moxifloxacin).
o What is the Typical Presentation of Q Fever/ Coxiella Burnetti zoonosis by
aerosolization?
 presents with Pneumonia and Hepatitis.
o What is the treatment for Coxiella Burnettii Atypical Pneumonia ?
 Doxycyline or Flouroquinolones
o Name the Bacteria that lacks a peptidoglycan cell wall, Has a cholesterol based Plasma
membrane and Causes atypical/ walking Pneumonia?
 Mycoplasma Pneumoniae
o 2 key Virulence factors for Mycoplasma Pneumonia are :
 Adhesin for Binding to Respiratory cells; CARDS Exotoxin that causes Ciliostasis
o A key serological finding of Mycoplasma Walking Pneumonia is High Cold Agglutinin
Titers that causes Anemia
o A wild young seemingly healthy patient presents with a mild pneumonia and alarming
patchy infiltrates on chest X-ray would increase suspicion for Mycoplasma Walking
Pneumonia

CAD Pharmacotherapy
o STEMIs are seen with complete Coronary Artery occlusion causing epicardial and
endocardial ischemia.
o NSTEMIs are seen w/ partial coronary occlusion leading to endocardial ischemia.
o Acute management of STEMIs mainly involves Reperfusion therapy with PCI
angioplasty or Fibrinolytics ( tPA-Alteplase) if unavailable.
o Fibrinolytics are contraindicated with recent surgery or Stroke, Brain Tumor, or Past
history of Intracranial Bleeding
o Heparin is used for Chronic management after Fibrinolytics in STEMI. Used separately in
NSTEMI.
o
o
o
o
o

Heparin dosing is determined by aPTT or Anti-Xa Assay . Unfractionated Heparin is
administered more often than LMWH.
Bleeding and Heparin Induced Thrombocytopenia are key side effects of Heparin Use.
What are other therapeutic approaches for Acute management of STEMI?
 MONA (Morphine, Oxygen, Nitrates, and Aspirin)
Define Chest Jaw or Arm Discomfort that worsens with stress or exertion and Improves
with Nitroglycerin.
 Angina
Adjuvant therapy for ACS ( MI or Unstable Angina) includes :
 beta blockers to reduce Myocardial O2 demand
 ACE Inhibitors or ARB to reduce mortality and Aneurysm formation/ wall
remodeling
 Statins to lower cholesterol Levels
o All of the following are contraindications of Beta Blocker Use in acute MI
 Hypotension, Bradycardia, Asthma, Heart Block, Hypertension
o Unstable Angina and NSTEMI are treated with Heparin ( to prevent clot formation) and
Antiplatelet agents.
o Antiplatelet agents used in NSTEMI are ADP receptor Blockers and Direct GP2/3a
blockers
o Name 2 Irreversible ADP receptor ( P2Y12) blockers that block platelet aggregation
 Clopidrogrel 1st line antiplatelet agent and Prasugrel ( More powerful; Increased
bleeding risk )
o Name the Anitplatelet that is Safe only in patients < 75 YO weighing over 60 Kg without
a history of Stroke or TIA
 Prasugrel
o Ticagrelor is a reversible ADP receptor Blocker that is dosed twice daily
o Abciximab, Eptifibatide and tirofiban are examples of direct Gp IIb/IIIa receptor
blockers ( Prevents Platelet Aggregation)
Syncope Evaluation and Management
o Transient and complete loss of consciousness with loss of postural tone
 Syncope
o Syncope occurs when there is decreased cerebral perfusion
o 3 etiologies of Syncope : Neural/Reflex, Orthostatic Hypotension, and Cardiac.
o A premonition, then drop in blood pressure followed by Bradycardia indicates Neural
Syncope caused by loss of Sympathetic tone
o A Drop in BP followed by Tachycardia indicates Orthostatic Hypotension
 Decreased peripheral Vasoconstriction triggered by DAAD( Drugs, Autonomic
Dysfn, Alcohol and Dehydration)
o Describe the presentation of Cardiac Syncope
 Sudden Drop attack due to Arrhythmia and Structural Heart disease
o Syncope after sudden noise or extreme emotion indicates Cardiac Syncope ( Long QTSyndrome)
o
o
o
 Long QT shows low Magnesium. Treated by Administering IV Magnesium
Tilt table testing is used to confirm Neural/Vasovagal syncope. Cardiac Syncope is
Confirmed with cardiac event monitors
How are neural and orthostatic Hypotension Syncope managed?
 Primarily lifestyle Modifications to avoid triggers and dehydration.
 Stockings for counterpressure
 Alpha agonists (Midodrine)
Bradycardic Cardiac Syncope is treated with Pacemaker implantation while
Tachyarrhythmic cardiac syncope is treated with AICD (Defibrillation)