Surgery Rotation 1 Flashcards
What is the problem and presentation of polycythemia vera
Mainly proliferation of RBCs
Presentation:
♣ Increased blood viscosity
• Plethora (flushed face)
• Transient blurred vision
• Headache
• Erythromelalgia (severe, burning pain and red-blue coloration in the extremities due to episodic blood clots in vessels of extremities)
♣ Thrombosis (e.g Budd Chiari)
♣ Bleeding
♣ Itching after bathing (aquagenic pruritis)
♣ Gouty arthritis due to increased RBC turnover
♣ Splenomegaly
Treatment of polycythemia vera
♣ Phlebotomy
♣ Hydroxyurea (if increased risk of thrombus)
What is essential thrombocythemia + presentation
o Mainly a proliferation of platelets o JAK2 kinase mutation o Presentation: ♣ Increased bleeding – dysfunctional platelets ♣ Thrombosis – too many platelets
What is myelofibrosis and findings
o Obliteration of bone marrow with fibrosis due to increased fibroblast activity
o JAK2 kinase mutation
o Findings:
♣ “Teardrop” RBCs – due to marrow fibrosis
♣ Splenomegaly – extra-medullary hematopoiesis
Is EPO high or low in polycythemia vera
o Increased red cell mass, without elevated EPO (unlike other causes of erythrocytsosis)
Cause and presentation of thrombotic thrombocytopenic purpura (TTP)
o Platelets used up in pathologic formation of microthrombi in small vessels
o Due to decreased ADAMTS13, enzyme that normally cleaves vWF for degradation
♣ No vWF degradation = abnormal platelet adhesion = microthrombi
o Findings (Pentad):
♣ Thrombocytopenia = platelets being used up
♣ Microangiopathic hemolytic anemia = RBCs sheared by microthrombi
♣ Renal insufficiency (thrombi involve vessels of the kidney)
♣ Neurological symptoms (confusion, HA, seizures, coma) – thrombi involve vessels of CNS
♣ Fever
Cause and presentation of hemolytic uremic syndrome
o Platelets used up in pathologic formation of microthrombi in small vessels
o Commonly caused by Shiga toxin-producing E. Coli O157:H7 (STEC)
♣ Accompanied with diarrhea
o Findings (triad):
♣ Microangiopathic hemolytic anemia
♣ Renal insufficiency (thrombi involve vessels of the kidney)
♣ Thrombocytopenia
What causes metabolic acidosis
• Anion gap Adding acid to the blood o MUDPILES: ♣ M – Methanol ♣ U – Uremia (renal failure) ♣ D – Diabetic ketoacidosis ♣ P – Propylene glycol/Paraldehyde ♣ I – Isoniazid/Iron ♣ L – Lactic acidosis ♣ E – Ethylene glycol (antifreeze) ♣ S – Salicylates (aspirin) • Non-anion gap Losing excessive HCO3- o Diarrhea, Renal tubular acidosis, Spironolactone, Acetazolamide
What causes metabolic alkalosis
♣ Causes: • Losing H+ excessive vomiting, diuretics, hyperaldosteronism ♣ Differential of metabolic alkalofis (pH > 7.45; HCO3- > 24) • Low urine chloride ♣ Will respond to saline o Vomiting/nasogastric aspiration o Prior diuretic use • High urine chloride o Hypovolemia/euvolemia ♣ Current diuretic use • Will responds to saline ♣ Bartter & Gitelman syndrome • Saline unresponsive o Hypervolemia ♣ Excessive mineralocorticoid activity o Saline unresponsive • Primary hyperaldosteronism • Cushing disease • Ectopic ACTH production
Fluid given for euvolemic hypernatremia
• Free water supplementation
Fluid given for hypovolemic hypernatrermia (both symptomatic and asymptomatic)
• Non-symptomatic
o 5% dextrose
• Symptomatic
o 0.9% saline (isotonic solution) until Euvolemic, then 5% dextrose (hypotonic solution)
Pathogenesis of DKA
♣ Lack of insulin means glucose cannot get into the cell for glycolysis to make ATP cell instead uses fatty acid beta oxidation which breaks down into ketone bodies
♣ Sodium levels will be low
• Hyponatremia due to sodium loss via diuresis
Will Na+ and K+ be high or low in DKA?
♣ Sodium levels will be low
• Hyponatremia due to sodium loss via diuresis (osmotic diuresis due to increased glucose)
♣ High serum potassium but low total body potassium
• Cells will exchange H+ for K+ causing high potassium
• Potassium in the blood will be excreted cause low total body potassium
IV fluids given to treat DKA
♣ 0.9% normal saline initially
♣ Add dextrose 5% when serum glucose <200 mg/dL
Replacement of one cell type by another
Metaplasia
Abnormal cells, lacking differentiation
Dysplasia
What is atelectasis
Collapse of lung
Ptosis, diplopia, weakness
Myasthenia gravis
Clinical presentation of Lambert-Eaton
- Proximal muscle weakness that improves with use
- Autonomic symptoms (dry mouth, impotence)
- Eyes usually spared
Tumor associated with Lambert eaton
Small cell carcinoma of lung
Clinical presentation of Parkinsons
TRAPS + mask-like facies T - Tremor (resting) R - Rigidity (cogwheel) A - Akinesia P - Postural instability S - staggering gait
What is akinesia
Impairment of voluntary movement
Compare histology of Alzheimers, Frontotemporal dementia, Parkinsons dementia, Lewy Body dementia
Alzheimers - Extracellular beta-amyloid plaques; intracellular neurofibrillary tangles made of tau protein
Frontotemporal dementia - Pick bodies (round aggregates of tau protein)
Parkinsons - Lewy bodies (eosinophilic inclusions of alpha-synuclein) within neurons
Lewy Body dementia - Lewy bodies within the cortex (aggregates of a-synuclein)
What is the striatum and where is it located
Striatum = caudate + putamen
Caudate located lateral to ventricles
Putamen located lateral to globus pallidus
(look up image)
