IM random fact 2

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  1. Greatest risk factor for Alzheimer'she is age
    Pt with Alzheimer's have cerebral atrophy secondary to neuronal loss and correspondingly enlarged ventricles
  2. Hormone replacement therapy is associated with lower risk of developing Alzhiemer's
    Pt with Alheimer's have decreased acetylcholine synthesis and impaired cortical cholinergic function
  3. Cause of coma:
  4. Criteria to dx brain death: absence of brain and brainstem function (unresponsiveness, apnea despite oxygenation and ventilation, and no brainstem reflexes of pupils, calorics, gag, cornea, doll's eyes)
    Brain death cannot b edx in pt with core body temp <32 (hypothermia)
  5. Infections associated with Guillain-Barre: Campylobacter, CMV< hepatitis, HIV

    Also Hodgkin's, lupus, after surgery, or after HIV seroconversion
    Signs of recovery in 1-3 weeks = good prognosis

    > 6 weeks = chronic relapsing course

    5% di of respiratory failure, PNA, or arrhythmias
  6. Dx made by CSF analysis (elevated protein but normal cell count) and nerve conduction studies
    Never give steroids for tx as are harmful
  7. Respiratory failure can occur within hours in Guillain-Barre syndrome so immediately pt to hospital to monitor
    MG char by skeletal muscular weakness with preservation of sensation and reflexes (may be limited to extraocular muscles in the elderly)
  8. Lambert-Eaton Myasthenic syndrome: autoantibodies directed against presynaptic calcium channels that result in proximal muscle weakness and hyporeflexia
    Associated with small cell lung cancer

    Distinguished from MG because Lambert-Eaton sx improve with repeated muscle stimulation
  9. Meds that worsen MG: antibiotics (aminoglycosides and tetracyclines), beta blockers, and antiarrhythmics (quinidine, procainamide, and lidocaine)
    tx with pyridostigmine

    Possible also thymectomy
  10. Hereditary causes of muscle weakness
    Duchenne's: XLR with no inflammation; serum creatinine phosphokinase elevated

    Beckers: XLR but later onset and less severe

    Mitochondrial d/o: Maternal inheritance and ragged red fibers

    Glycogen storage: McArdles=AR, muscle cramping after exercise due to glycogen phosphorylase deficiency
    Both types neurofibromatosis have seizures, MR/learning disabilities, short height, and macrocephalic
  11. Prognosis in neurofibromatosis depends on type and  number of tumors and location
    Tuberous sclerosis: Ad with cognitive impairment, epilepsy, facial angiofibromas, adenoma sebaceum, retinal hamartomas, renal angiomyolipomas, and rhadomyomas of the heart
  12. Sturge-Weber syndrome: acquired disease with capillar angiomatoses of pia matter, facial vascular nevi (PORT WINE STAIN) epilepsy, and MR
    von Hippel-Lindau: AD with cavernous hemangiomas, renal angiomas, cysts in multiple organs

    associated with RCC and pheochromocytomas
  13. Brown-Sequard syndrome: contralateral loss of pain and temp, ipsilateral hemiparesis, and ipsilateral loss of vibration
    Central vertigo: gradual onset, neurologic findings, CV risk factors, accompanying nystagmus (bidirectional or vertical)
  14. Periheral vertigo: lesions are cochlear or retrocochlear; onset is abrupt with N/V, head position strongly affects sx, brainstem deficits absent (except for tinnitus/hearing loss)
    Use MRI to rule out ischemic event in pt with vertigo
  15. Hearing loss and tinnitus only occur with peripheral vertigo
    Benign positional vertigo is nystagmus without hearing loss of tinnitus
  16. Meclizine is useful for vertigo and as antiemetic; it has anticholinergic and antihistamine effects
    Nystagmus is never peripheral vertigo
  17. Prognosis of syncope is good, unless it is caused by cardiac disease
    • Seizures vs. syncope:
    • Seizures: Duration of unconsciousness longer and bladder control often lost
    • Syncope: Duration of unconsciousness momentary and bladder control often intact
  18. Syncope with exertion = assess for aortic stenosis or hypertrophic cardiomyopathy
    Partial seizure may evolve into generalized seizure (secondary generalization)
  19. Partial seizure means consciousness remains intact
    Generalized means loss of consciousness
  20. Tx partial seizures (complex and simple), and tonic-clonic or myoclonic seizures with phenytoin and carbamazepine
    Tx absence seizures with ethosuximide and valproic acid
  21. Status epilepticus is prolonged, sustained unconsciousness with persistent convulsive activity in seizing pt
    Management of status epilepticus: establish airway, give IV diazepam, IV phenytoin, and 50 mg dextrose

    Tx resistant cases with IV phenobarbital
  22. In early phase of AKI, hyperkalemic cardiac arrest and pulmonary edema are most common mortal complications
    Azotemia = elevatred BUN
  23. Uremia = signs and sx associated with accumulated nitrogenous wastes due to impaired renal function
    ERSD is loss of kidney function leading to lab and clinical findings of uremia (NOT defined by BUN or Cr levels)
  24. Chronic renal insufficiency = renal function is irreversibly compromised but not failed
    Absolute indications for dialysis: Acidosis, electrolytes (K), intoxications (methanol, ethylene glycol, lithium, aspirin), overload not manageable by other means, and uremia (i.e. uremic pericarditis)
  25. Dialyzable substances: salicylic acid, lithium, ethylene glycol, Mg-containing laxatives
    Microscopic hematuria = glomerular disease
  26. Gross hematuria = postrenal causes (trauma, stones, malignancy)
    Gross painless hematuria is sign of bladder or kidney cancer until proven otherwise
  27. Nephrotic syndrome: proteinuria, edema, hypoalbuminemia, hyperlipidemia
    Nephritic: hematuria, HTN, azotemia
  28. Acute AIN causes rapid deterioration in renal function and is associated with eosinophils or lymphocytes
    Chronic AIN has indolent course and is associated with tubulointerstitial fibrosis and atrophy
  29. Renal tubular acidosis = d/o renal tubules that leads to non-angion gap hyperchloremic metabolic acidosis with normal glomerular function
    Type 1 = renal stones and nephrocalcinosis

    Type 2 = increased excretion of bicarb in urine

    Type 4 = hyperkalemia
  30. ADPKD presents with pain, hematuria, infection, HTN, and kidney stones
    Use ACE inhibitors carefully in pt with renovascular HTN
  31. Dx renovascular HTN with renal arteriogram (DO NOT USE CONTRAST DYE IF PT HAS RENAL FAILURE)
    Nephrosclerosis due to HTN is second most common cause of ESRD after diabetes
  32. Calcium stones = radiodense
    Uric acid stones are radiolucent (CANNOT BE SEEN)
  33. Cystine stones = hexagon-shaped cyrstals due to cystinuria (AR disease)
    Hematuria plus pyuria = stone with concomitant infection
  34. It pt has acute obstruction and UTI intervene immediately with renal US or excretory urogram and relieve obstruction
    PSA > 10 = TRUS with bx
  35. Abnormal digital rectal exam (DRE) = TRUS with bx
    PSA < 4 and negative DRE = annual f/u
  36. PSA 4.1-10 and DRE is negative, bx recommended
    Classic triad of RCC: Hematuria, flank pain, and abdominal pain (happens in <10% of pt)
  37. Epididymitis can be differentiated from testiular torsion in that torsion has more acute onset and epididymitis is associated with fever
    Do not combine bolus fluids with dextrose (leads to hyperglycemia) or potassium (leads to hyperkalemia)
  38. Calculation of maintenance fluids:
    100/50/20 rule: 100 mL/kg for first 10 kg, 50 for second 10 kg, and 20 mL for every kg past that then divide by 24

    4/2/1 rule: 4 mL/kg for first 10 kg, 2 mL for next 10, and 1 for ever kg over that

    both give you mL/hr
    Aldosterone increases sodium resorption
  39. ADH increases water resorption
    Hyponatremia and hypernatremia are caused by too much or too little water
  40. Hypervolemia and hypervolemia are caused by too little or too much sodium
    Calculating free water deficit: TBW (1 - actual sodium divided by desired sodium)

    TBW * (1-Na[actual] / Na[desired])
  41. Hypercalcemia = shortening of QT interval
    Hypocalcemia = prolongation of QT interval
  42. Alkalosis can lead to hypokalemia
    Acidosis can lead to hyperkalemia
  43. Hypokalemia: Urine potassium is low with GI losses (<20)
    Hypokalemia: urine potassium is high with renal losses (>20)
  44. If pt is hypertensive and hypokalemic, excessive aldosterone activity is likely
    If pt is normotensive and hypokalemic, GI or renal loss if more likely
  45. EKG changes in hypokalemia:
    T wave flattens out (inverts in severe cases)
    U wave appears
    Hypokalemia predisposes to digoxin toxicity
  46. Hyperkalemia inhibits renal ammonia synthesis and reabsorption -> impaired acid excretion 0> metabolic acidosis -> worsening of hyperkalemia as K shifts out of cells
    EtOH abuse and DKA are most common causes of severe hypophosphatemia
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IM random fact 2
random facts for internal medicine
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