Internal Med 4 Flashcards
Outpatient treatment of CAP
- In healthy = Macrolide or Doxycycline
- Comorbidities = Fluoroquinolones or beta-lactam + macrolide
beta-lactams don’t work against atypicals
Inpatient treatment of CAP in non-ICU patients
- Fluoroquinolone (Levo = lung)
- Beta-lactam + Macrolide
Inpatient tx of CAP in ICU patient
- Beta-lactam + macrolide
- Beta-lactam + fluoroquinolone
What will you see on histology of UC vs. Crohns
UC = Crypt abscess with neutrophils
Crohns = noncaseating granulomas
What will you see on gross imaging of UC vs. Crohns
UC = loss of haustra “lead pipe”
Crohns = Strictures, “string sign”
Which is associated with increased risk of colorectal cancer, UC or Crohns
UC
Where would you expect pain and which one has blood diarrhea, UC or Crohn’s
UC = LLQ pain (colorectal), bloody
Crohns = RLQ pain (ileum), non-bloody
When and with what, should you treat an HIV+ patient with TB skin test
- If area of induration >5 mm at 48-72 hours you need to rule out active TB via CXR and sx review
- If no manifestation of active TB, treat for latent TB with 9 months of Isoniazid (+Pyridoxine to prevent peripheral neuropathy)
Tx of toxic megacolon
IVF, broad-spectrum abx, bowel rest
IV corticosteroids used in IBD-induced toxic megacolon
What is tumor lysis syndrome
♣ Patients with aggressive hematologic malignancies who begin cytotoxic chemotherapy
♣ Large-scale cell death increases vascular concentrations of intracellular products, resulting in potentially life-threatening electrolyte and metabolic abnormalities
Describe electrolyte abnormalities in tumor lysis syndrome (K, Na, Phos, Uric acid)
- Hyperkalemia and Hyperphosphatemia (intracellular ions are liberated)
- Hypocalcemia (phosphate binds and precipitates calcium)
- Hyperuricemia (nucleic acids are released and metabolized into uric acid)
What are the two main organs that need to be monitored in tumor lysis syndrome
♣ Kidney - Acute kidney injury (due to uric acod/calcium phosphorus)
♣ Heart - Cardiac arrhythmias (due to hyperkalemia)
Treatment of tumor lysis syndrome
♣ Continious telemetry
♣ Aggressive electrolyte monitoring/treatment
Prophylaxis of tumor lysis syndrome
♣ IV fluids (to flush kidneys)
♣ Allopurinol (to metabolize uric acid)
Describe steps of immediate treatment of pt with an acute STEMI
♣ Oxygen in patients with saturation <90% or other features of hypoxia
♣ Relief of ischemic pain (Nitroglycerine)
♣ Assesssment of hemodynamic state and correction of abnormalities
♣ Initiaion of reperfusion therapy with primary percutaneous coronary intervention (PCI aka stent placement) or fibrinolysis
♣ Antithrombotic therapy to prevent rethrombosis or acute stent thrombosis
♣ Beta blocker therapy to prevent reccurent ischemia and life-threatening ventricular arrhythrmias
What will be done in-hospital in a patient who just had an acute STEMI, in order to improve long-term prognosis
♣ Antiplatelet therapy to reduce risk of recurrent coronary artery thrombosis or, with PCI, coronary artery stent thrombosis
♣ ACEi therapy to prevent remodeling of the left ventricle
♣ Statin therapy
♣ Anticoagulation in the presence of left ventricular thrombus or chronic atrial fibrillation to prevent embolization
What are the 4 classes of drugs recommended as initial treatment for HTN
- Thiazide diuretics
- ACEi
- ARBs
- CCBs
Describe characteristics of small cell carcinoma of lung + tx
♣ “S” = smokers, central, secreting
Tx = radiation
What might small cell cancer of the lung produce
- ADH = SIADH
- ACTH = Cushing’s
- Antibodies against pre-synaptic Ca2+ channels = Lambert-Eaton
Describe characteristics of squamous cell carcinoma of lung + tx
- “S” = smokers, central, secreting
- Often presents as a hilar mass
Tx = surgery
What might squamous cell carcinoma of the lung produe?
• May produced PTH = hypercalcemia
Describe characteristics of adenocarcinoma of lung + tx
- Non-smokers and female smokers
- Located in lung periphery may present with pain because it affects the pleura
Tx = surgery
Where does carcinoid tumor occur
♣ Well-differentiated neuroendocrine cells
• Chromogranin A positive
♣ Location:
• Lung = Classically presents as a polyp-like mass in the bronchus
• GI tract = only causes carcinoid syndrome if metastasis to liver
Complication of carcinoid tumor
♣ Rarely causes carcinoid syndrome (BFDR) • Bronchospasm and wheezing • Flushing • Diarrhea • R-sided heart lesions
Describe transudative pleural effusion + causes
• Low protein content
o THINK: Transudate is more transparent
• Due to increased hydrostatic pressure (e.g. CHF or fluid overload) or decreased oncotic pressure (e.g. cirrhosis, nephrotic syndrome)
Describe exudative pleural effusion + causes
• High protein content, cloudy
o Pleural fluid will have High LDH and low glucose (due to high metabolic activity of leukocytes and bacteria within the fluid)
• Due to pleural and lung inflammation resulting in increased capillary and pleural membrane permeability (e.g. malignancy, pneumonia, TB, trauma, connective tissue disease)
• Must be drained due to risk of infection
What is Light’s criteria
♣ If at least one of the following 3 criteria is true, the fluid is an exudate
• Pleural fluid protein/serum protein ratio > 0.5
• Pleural fluid LDH/serum LDH ratio > 0.6
• Pleural fluid LDH > 2/3 the upper limit of laboratory’s normal serum LDH
When should you NOT tap a pleural effusion
- CHF = You can do just observation instead if the patient has CHF because the likelihood it is transudative from CHF is so high
- If pleural effusino <1 cm you can watch and wait
- If loculated, you need to do a thoracostomy (chest tube) or thoracotomy (surgery)
Other than these exceptions, you should tap any new pleural effusion
Describe EKG findings of PE
• S1Q3T3
o Large S waves in lead I
o Q waves in lead III
o Inverted T waves in lead III
What will you see in PE for:
- pH
- pCO2
- pO2
pH = high pCO2 = low pO2 = low
Hypoxia will cause hyperventilation, blowing of CO2 = hypoxemic, hypocarbic respiratory alkalosis
Describe transporters located in thick ascending limp of loop of Henle
Impermeable to water - this is the diluting segment that only re-absorbs ions but no water
Contains Na+/K+/2Cl- cotransporter (NKCC) - all 3 are reabsorbed. Makes interstitium of kidney salty
Describe MOA and effects of Furosemide
o blocks NKCC on apical membrane of thick ascending limb
♣ Will reduce reabsorption of NaCl, and water will follow – diuresis
♣ Without electrolyte reabsorption in the ascending limb, the interstitium will not be hypertonic and there will be less reabsorption of H2O in the descending limb – diuresis
What are the effects of loop diuretics on Ca2+ and Mg2+
♣ Normally, K+ will come into the cell via NKCC, but then will diffuse back into the lumen, giving the lumen a slightly positive charge, causing other cations such as Magnesium and Calcium to leave the tubule and enter the interstitium down their electric gradient
• Blocking of NKCC will decrease electric gradient, therefore decreasing the reabsorption of Ca2+ and Mg2+
- AKA adverse effect = hypocalcemia and hypomagnesemia
What are the effects of Loop diuretics on Potassium
o Hypokalemia (potassium wasting) ♣ Sodium that is inhibited from being reabsorbed will be taken to the collecting duct where it is reabsorbed by Na+/K+ ATPase, causing increased potassium excretion
Describe the transporters that Thiazide diuretics work on in the distal convoluted tubule
• Inhibits NaCl cotransporter in apical membrane of distal tubule (so NaCl stays in lumen instead of being reabsorbed into cell)
Describe effects of Thiazides on calcium
Hypercalcemia -
Thiazides block NaCl cotransporters = decreased intracellular Na+ will stimulate the Na+/Ca2+ exchanger at basolateral membrane (between cell and interstitium), causing sodium to be brought into the cell and calcium to be pushed out into the interstitial space (increased reabsorption of Ca2+)
Why do Thiazide diuretics work to treat Nephrogenic Diabetes insipidus
- Hypovolemia-induced increase in sodium and water reabsorption in more proximal segments of the nephron
- Now you don’t have to rely on terminal ducts for reabsorption – this is where ADH works
What are the effects of thiazide on:
- Glucose
- Lipids
- Uric acid
- Potassium
- Hyperglycemia
- Hyperlipidemia
- Hyperuricemia
- Hypokalemia
Describe the transporters that potassium-sparing diuretics work on in the collecting duct
♣ Na+ (ENaC) channels – reabsorbs Na+ across the luminal membrane
• Na+ reabsorption creates a negative luminal potential that facilitates K+ excretion via K+ channel
Diuretics block the Na+ ENaC channel so that sodium cannot be reabsorbed. Positive luminal potential of Na+ prevents K+ from being secreted
What are names of potassium-sparing diuretics
Amiloride, Triamterene, Eplerenone, Spironolactone
What is the role of Aldosterone in collecting duct
Aldosterone is produced by adrenal cortex in response to RAAS, and increases activity of ENaC and K+ channels - increases reabsorption of Na+ and excretion of K+
How does Amiloride and Triamterene work?
• Blocks the Na+ ENaC channels on the apical membrane so that sodium cannot be reabsorbed
How does Eplerenone work?
• Directly antagonizes the mineralocorticoid receptor (so it can no longer increase the activity of ENaC, K+ channels, and Na+/K+ ATPase)
How does Spironolactone work?
• Directly antagonized the mineralocorticoid receptor
Describe stepwise treatment of COPD
- Short acting beta agonist (SABA)
- Long acting muscarinic antagonist (Tiotropium)
- Long acting beta agonist (LABA)
- Inhaled corticosteroids
- Phosphodiesterase 4 inhibitors
- Oral steroids
How do you treat acute COPD exacerbation
- Oxygen
- Inhaled bronchodilators (Albuterol, Ipratropium)
- Systemic glucocorticoids (PO Prednisone or IV Methylprednisolone)
- Antibiotics if > 2 cardinal symptoms (increased dyspnea, cough, or sputum production)
- Oseltamivir if evidence of influenza
- NPPV if ventilator failure
- Tracheal intubation if NPPV failed or contraindicated
