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Greatest risk factor for Alzheimer'she is age
Pt with Alzheimer's have cerebral atrophy secondary to neuronal loss and correspondingly enlarged ventricles
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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
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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)
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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
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Dx made by CSF analysis (elevated protein but normal cell count) and nerve conduction studies
Never give steroids for tx as are harmful
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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)
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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
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Meds that worsen MG: antibiotics (aminoglycosides and tetracyclines), beta blockers, and antiarrhythmics (quinidine, procainamide, and lidocaine)
tx with pyridostigmine
Possible also thymectomy
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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
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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
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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
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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)
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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
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Hearing loss and tinnitus only occur with peripheral vertigo
Benign positional vertigo is nystagmus without hearing loss of tinnitus
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Meclizine is useful for vertigo and as antiemetic; it has anticholinergic and antihistamine effects
Nystagmus is never peripheral vertigo
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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
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Syncope with exertion = assess for aortic stenosis or hypertrophic cardiomyopathy
Partial seizure may evolve into generalized seizure (secondary generalization)
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Partial seizure means consciousness remains intact
Generalized means loss of consciousness
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Tx partial seizures (complex and simple), and tonic-clonic or myoclonic seizures with phenytoin and carbamazepine
Tx absence seizures with ethosuximide and valproic acid
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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
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In early phase of AKI, hyperkalemic cardiac arrest and pulmonary edema are most common mortal complications
Azotemia = elevatred BUN
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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)
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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)
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Dialyzable substances: salicylic acid, lithium, ethylene glycol, Mg-containing laxatives
Microscopic hematuria = glomerular disease
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Gross hematuria = postrenal causes (trauma, stones, malignancy)
Gross painless hematuria is sign of bladder or kidney cancer until proven otherwise
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Nephrotic syndrome: proteinuria, edema, hypoalbuminemia, hyperlipidemia
Nephritic: hematuria, HTN, azotemia
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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
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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
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ADPKD presents with pain, hematuria, infection, HTN, and kidney stones
Use ACE inhibitors carefully in pt with renovascular HTN
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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
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Calcium stones = radiodense
Uric acid stones are radiolucent (CANNOT BE SEEN)
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Cystine stones = hexagon-shaped cyrstals due to cystinuria (AR disease)
Hematuria plus pyuria = stone with concomitant infection
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It pt has acute obstruction and UTI intervene immediately with renal US or excretory urogram and relieve obstruction
PSA > 10 = TRUS with bx
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Abnormal digital rectal exam (DRE) = TRUS with bx
PSA < 4 and negative DRE = annual f/u
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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)
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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)
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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
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ADH increases water resorption
Hyponatremia and hypernatremia are caused by too much or too little water
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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])
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Hypercalcemia = shortening of QT interval
Hypocalcemia = prolongation of QT interval
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Alkalosis can lead to hypokalemia
Acidosis can lead to hyperkalemia
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Hypokalemia: Urine potassium is low with GI losses (<20)
Hypokalemia: urine potassium is high with renal losses (>20)
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If pt is hypertensive and hypokalemic, excessive aldosterone activity is likely
If pt is normotensive and hypokalemic, GI or renal loss if more likely
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EKG changes in hypokalemia:
T wave flattens out (inverts in severe cases)
U wave appears
Hypokalemia predisposes to digoxin toxicity
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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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