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MS3 > Internal Med 4 > Flashcards

Internal Med 4 Flashcards

1
Q

Outpatient treatment of CAP

A
  • In healthy = Macrolide or Doxycycline

- Comorbidities = Fluoroquinolones or beta-lactam + macrolide
beta-lactams don’t work against atypicals

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2
Q

Inpatient treatment of CAP in non-ICU patients

A
  • Fluoroquinolone (Levo = lung)

- Beta-lactam + Macrolide

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3
Q

Inpatient tx of CAP in ICU patient

A
  • Beta-lactam + macrolide

- Beta-lactam + fluoroquinolone

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4
Q

What will you see on histology of UC vs. Crohns

A

UC = Crypt abscess with neutrophils

Crohns = noncaseating granulomas

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5
Q

What will you see on gross imaging of UC vs. Crohns

A

UC = loss of haustra “lead pipe”

Crohns = Strictures, “string sign”

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6
Q

Which is associated with increased risk of colorectal cancer, UC or Crohns

A

UC

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7
Q

Where would you expect pain and which one has blood diarrhea, UC or Crohn’s

A

UC = LLQ pain (colorectal), bloody

Crohns = RLQ pain (ileum), non-bloody

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8
Q

When and with what, should you treat an HIV+ patient with TB skin test

A
  • 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)
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9
Q

Tx of toxic megacolon

A

IVF, broad-spectrum abx, bowel rest

IV corticosteroids used in IBD-induced toxic megacolon

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10
Q

What is tumor lysis syndrome

A

♣ 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

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11
Q

Describe electrolyte abnormalities in tumor lysis syndrome (K, Na, Phos, Uric acid)

A
  • Hyperkalemia and Hyperphosphatemia (intracellular ions are liberated)
  • Hypocalcemia (phosphate binds and precipitates calcium)
  • Hyperuricemia (nucleic acids are released and metabolized into uric acid)
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12
Q

What are the two main organs that need to be monitored in tumor lysis syndrome

A

♣ Kidney - Acute kidney injury (due to uric acod/calcium phosphorus)
♣ Heart - Cardiac arrhythmias (due to hyperkalemia)

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13
Q

Treatment of tumor lysis syndrome

A

♣ Continious telemetry

♣ Aggressive electrolyte monitoring/treatment

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14
Q

Prophylaxis of tumor lysis syndrome

A

♣ IV fluids (to flush kidneys)

♣ Allopurinol (to metabolize uric acid)

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15
Q

Describe steps of immediate treatment of pt with an acute STEMI

A

♣ 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

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16
Q

What will be done in-hospital in a patient who just had an acute STEMI, in order to improve long-term prognosis

A

♣ 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

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17
Q

What are the 4 classes of drugs recommended as initial treatment for HTN

A
  • Thiazide diuretics
  • ACEi
  • ARBs
  • CCBs
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18
Q

Describe characteristics of small cell carcinoma of lung + tx

A

♣ “S” = smokers, central, secreting

Tx = radiation

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19
Q

What might small cell cancer of the lung produce

A
  • ADH = SIADH
  • ACTH = Cushing’s
  • Antibodies against pre-synaptic Ca2+ channels = Lambert-Eaton
20
Q

Describe characteristics of squamous cell carcinoma of lung + tx

A
  • “S” = smokers, central, secreting
  • Often presents as a hilar mass

Tx = surgery

21
Q

What might squamous cell carcinoma of the lung produe?

A

• May produced PTH = hypercalcemia

22
Q

Describe characteristics of adenocarcinoma of lung + tx

A
  • Non-smokers and female smokers
  • Located in lung periphery may present with pain because it affects the pleura

Tx = surgery

23
Q

Where does carcinoid tumor occur

A

♣ 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

24
Q

Complication of carcinoid tumor

A 
♣	Rarely causes carcinoid syndrome (BFDR)
•	Bronchospasm and wheezing
•	Flushing
•	Diarrhea 
•	R-sided heart lesions
25
Q

Describe transudative pleural effusion + causes

A

• 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)

26
Q

Describe exudative pleural effusion + causes

A

• 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

27
Q

What is Light’s criteria

A

♣ 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

28
Q

When should you NOT tap a pleural effusion

A
  • 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

29
Q

Describe EKG findings of PE

A

• S1Q3T3
o Large S waves in lead I
o Q waves in lead III
o Inverted T waves in lead III

30
Q

What will you see in PE for:

  • pH
  • pCO2
  • pO2
A 
pH = high
pCO2 = low
pO2 = low

Hypoxia will cause hyperventilation, blowing of CO2 = hypoxemic, hypocarbic respiratory alkalosis

31
Q

Describe transporters located in thick ascending limp of loop of Henle

A

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

32
Q

Describe MOA and effects of Furosemide

A

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

33
Q

What are the effects of loop diuretics on Ca2+ and Mg2+

A

♣ 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

34
Q

What are the effects of Loop diuretics on Potassium

A 
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
35
Q

Describe the transporters that Thiazide diuretics work on in the distal convoluted tubule

A

• Inhibits NaCl cotransporter in apical membrane of distal tubule (so NaCl stays in lumen instead of being reabsorbed into cell)

36
Q

Describe effects of Thiazides on calcium

A

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+)

37
Q

Why do Thiazide diuretics work to treat Nephrogenic Diabetes insipidus

A
  • 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
38
Q

What are the effects of thiazide on:

  • Glucose
  • Lipids
  • Uric acid
  • Potassium
A
  • Hyperglycemia
  • Hyperlipidemia
  • Hyperuricemia
  • Hypokalemia
39
Q

Describe the transporters that potassium-sparing diuretics work on in the collecting duct

A

♣ 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

40
Q

What are names of potassium-sparing diuretics

A

Amiloride, Triamterene, Eplerenone, Spironolactone

41
Q

What is the role of Aldosterone in collecting duct

A

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+

42
Q

How does Amiloride and Triamterene work?

A

• Blocks the Na+ ENaC channels on the apical membrane so that sodium cannot be reabsorbed

43
Q

How does Eplerenone work?

A

• Directly antagonizes the mineralocorticoid receptor (so it can no longer increase the activity of ENaC, K+ channels, and Na+/K+ ATPase)

44
Q

How does Spironolactone work?

A

• Directly antagonized the mineralocorticoid receptor

45
Q

Describe stepwise treatment of COPD

A
  • Short acting beta agonist (SABA)
  • Long acting muscarinic antagonist (Tiotropium)
  • Long acting beta agonist (LABA)
  • Inhaled corticosteroids
  • Phosphodiesterase 4 inhibitors
  • Oral steroids
46
Q

How do you treat acute COPD exacerbation

A
  • 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

MS3 (88 decks)

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