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127 Cards in this Set
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SMA-6
a. What, abbreviation for b. Contain |
a. Battery\panel of routine blood test, Sequential multiple analysis
b. 1. Blood urea nitrogen (BUN) 2. Carbon dioxide 3. Chloride 4. Glucose 5. Potassium 6. Sodium (Damjanov) |
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SMA-12
a. What, Abbreviation for b. Components |
a. Battery\panel of routine blood test, Sequential multiple analysis
b. 1. Albumin 2. Alkaline phosphatase 3. Aspartate aminotransferase 4. Bilirubin 5. Calcium 6. Cholesterol 7. Creatinine 8. Glucose 9. Lactate dehydrogenase 10. Phosphorus 11. Protein (total) 12. Uric acid (Damjanov) 1. Albumin |
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Accuracy of a test
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Statistical term reflecting the capacity of the test to measure the true value of an analyte
(Damjanov) |
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Acute-phase proteins
a. Positive acute-phase proteins - what, which (5) b. Negative acute-phase proteins - what, which (1) |
a. Proteins that appear in increased concentration in blood in response to inflammation
1. C-reactive protein 2. Ceruloplasmin 3. Transferrin 4. Fibrinogen 5. Alpha1-antitrypsin b. Proteins that decrease in plasma concentration in response to inflammation - albumin (Damjanov) |
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Alkaline phosphatase
a. What b. Elevated when? (5) |
a. Enzyme that hydrolyze orthophosphoric (ortho-: the most hydrated of an oxoacid: H3PO4) esters
b. 1. Biliary obstruction 2. Growing bones 3. Bone undergoing remodeling - Paget's disease 4. Osteoblastic metastases 5. Bone-forming tumors (Damjanov) |
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Azotemia
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Abnormal increase of urea and other nitrogenous substances in the blood plasma
(Stedman) |
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Lactate dehydrogenase - when is it elevated in blood?
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Its elevated in conditions marked by widespread cell destruction, ie hemolysis
(Damjanov) |
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Precision\reliability of a test
a. What b. precision vs standard deviation c. In most instances the reference range is determined by adding how many SD to the mean? This means that how many % of the results fall in that range? |
a. Statistical term for the consistency with which the same result can be obtained when applying the same test repeatedly to the same sample
b. A high precise test has a low SD (meaning that the results occur within a narrow range) c. 2 SD to the mean. 95% fall in that range and 5%\ 1\20 fall outside it. (Damjanov) |
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Predictive value of a test
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Statistical term estimating the probability that a positive test result will identify a person with a disease (True positives and false positives")
(Damjanov) |
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1. What? used for (1)?
2. What? used for (4)? 3. what? used for (1)? 4. What? used for (2)? why? |
EDTA = ethylenediaminetetraaacetic acid. Also used for folic acid tests
Fluoride oxalate is an inhibitor of glycolysis and is used to measure glucose & lactate because it does not interfere with the measurement of these analytes. |
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How is the sweat test for cystic fibrosis performed?
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Done by stimulating sweating by using pilocarpine.
(Damjanov) |
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What is special about testing for enzyme deficiencies (ie inborn errors of metabolism)?
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They require tissue samples containing cells.
(Damjanov) |
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Statistical requirements of good laboratory tests (4)
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They must be
1. Precise\reliable 2. Accurate 3. High sensitivity 4. High specificity (Damjanov) |
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Specificity of a test
a. What b. Formula c. Mnemonic d. When should tests of high specificity be used |
a. Measure the incidence of true negative results (That means that normal values occur in all tested persons who do not have the disease)
b. Specificity = TN\TN+FP c. SPIN: Specificity = rule in (100% specificity -> 0% false positive. Thus all with positive has the disesae) (a test with high specificity will be always negative in health (100% TN), that is, it will be negative for both FP and TN) d. For final diagnosis (especially if the treatment is risky or could have adverse consequences) (Damjanov) |
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Sensitivity of a test
a. What b. Equation c. Commonly used as d. Mnemonic |
a. Measures the incidence of true positive results among all persons who have the disease, irrespective of whether they tested positively or negatiively, thus representing a sum of TP+FN
b. Sensitivity = TP\(TP+FN) c. Screening test d. SNOUT: Sensitivity = rule out (rule out the healthy, because a test with 100% sensitivity have no FN. Thus negative results always means TN) (Positivity in disease. Tests with a 100% sensitivity will be positive for all those who have a disease and will include all TP and FN) (Damjanov) |
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Predictive value of a test
a. Predictive value of a positive test b. Predictive value of a negative test c. The predictive value of a test depend on? |
a. Predictive value for a positive test = TP\(TP+FP)
b. Predictive value for a negative test = TN\(TN+FN) c. Prevalence. The predictive value decrease as prevalence decrease. (Damjanov) |
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Efficiency of a test
a. What b. Equation |
a. Relates to the number of all correct results
b. Efficiency = (TP + TN)\(TP + TN + FP + FN) |
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Sodium
a. Proportion in different places b. Exchangeable sodium |
a. 50% in ECF, 10% in ICF and 40% in bone
b. All the sodium in the ICF, ECF and 50% of that stored in bone (4.2 mol in a 70 kg man) (Damjanov) |
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What 5 things are in higher concentration in the IC compartment compared to the EC compartment?
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1. K+
2. Mg 3. Proteins 4. PO4 5. SO4 (Damjanov) |
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What 4 physiologic mechanisms regulate the sodium balance
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1. Thirst (↑osmolality in osmoreceptors in the hypothalamus -> thirst, or by ↓intravascular volume)
2. ADH\Arginine vasopressin (↑osmolality in hypothalamus -> ADH, or by↓intravascular volume) 3. Aldosterone 4. Atrial natriuretic peptide (ANP) (Damjanov) |
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Serum osmolality equation
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Serum osmolality = 2 x Na+ (mM) + Glucose (mM) + BUN (mM)
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Causes of altered serum osmolality
a. Increased (3) b. Decreased (1) |
a. Increased serum osmolality
1. Increased content of normal components (Na+, Glu, BUN) 2. Toxic substances 2a. Alchols (ethanol, methanol) 2b. Ethylene glycol\Antifreeze 2c. Acetone 3. Loss of water in excess to sodium (dehydration, diabetes insipidus) b. Decreased serum osmolality -> overhydration <- 1. Loss of sodium in excess to water 2. SIADH (Damjanov) |
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Hyponatremia
a. Definition b. Dilutional causes (6) c. Depletional causes (3) |
a. < 136 mM
b. Dilutional - due to water excess 1. ↑Water intake (neurotic polydipsia, some lung cancer patients who have the paraneoplastic SIADH secretion) 2. Infusion of water 3. Decreased excretion of water (heart failure, renal failure) 4. Hypoproteinemia (cirrhosis\nephrotic syndrome\chronic protein-losing gastroenteropathy -> loss of protein -> loss of oncotic pressure -> shift of water to ISF -> RAS & ADH -> dilutional hyponatremia) 5. Shift of water from cells into the ECV (hyperglycemia, paraproteinemia of multiple myeloma, hyperlipidemia. Due to ↑osmotic substances) 6. SIADH c. Depletional hyponatremia - due to a net loss of sodium 1. Dermal loss in burns 2. GI loss (vomiting, diarrhea, ileus (paralytic), gastrointestinal fistulas) 3. Renal loss (glycosuria of DM, hypercalciuria, salt-wasting kidney diseases (all chronic renal disease with loss of nephron function. The remaining nephrons become overloaded with urea -> osmotic diuresis), diuretics (esp. osmotics), Addison's) (Damjanov) |
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Hyponatremia
a. Sick cell syndrome b. Most common cause b. Most common cause of severe hyponatremia |
a. Mild hyponatremia as a sign of illness, reflecting the inability of cells to maintain the normal gradient and flux of electroclytes across the cell membranes (2-3% of all hospitalized patients)
b. Combined loss of Na+ and water, in which the lost Na+ is not adequately replaced c. Usually a consequence of water intoxication (Damjanov) |
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Hyponatremia
a. Symptoms? b. When do they appear? |
a. Mostly related to depressed transmission of neural or neuromuscular signals: muscle weakness, somnolence, coma. Severe hyponatremia can cause brain injury
b. Rapidly developing hyponatremia of 120-125 mM (Slowly developing dilutional can be as low as 100 mM and cause few if any symptoms) (Damjanov) |
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What is the name of the condition that can develop if hyponatremia is corrected with infusion of salts to rapidly?
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Central pontine myelinolysis (also related to alcoholism)
(Damjanov) |
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Hypernatremia
a. Definition b. Clinically significant hypernatremia develops only in...? c. Most common cause, can be suspected with the additional lab finding |
a. > 150 mM
b. People who have no access to water or are unconscious and cannot drink: comatose, persons in deep anesthesia, very old immobile patients, infants) c. Dehydration, high hematocrit (Damjanov) |
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Causes of hypernatremia
a. Renal loss of water (4) b. Gastrointestinal loss of water (3) c. Dermal loss of water (2) d. Excessive sodium intake or retention (4) |
a. Renal loss of water
1. Central diabetes insipidus (primary: hypothalamic\posterior pituitary injury, secondary to drug treatment like lithium) 2. Nephrogenic diabetes insipidus (consequence of end-stage renal disease) 3. Renal tubular necrosis 4. Diruetics (loop, osmotic) b. GI loss of water 1. Diarrhea 2. Prolonged vomiting 3. Osmotic cathartic agents (agents for emptying bowel\constipation: ie lactulose) c. Dermal loss of water 1. Profuse sweating 2. Extensive burns d. Excessive sodium intake or retention 1. Cushing's syndrome 2. Conn syndrome\primary aldosteronism 3. corticosteroid treatment 4. Infusion (Damjanov) |
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Hypernatremia - symptoms caused by this itself and not hypo-\hypervolemia
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Neurologic symptoms: restlessness, irritability, confusion, agitation
(Damjanov) |
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What is the two metabolic acid-base disorders related to hypochloremia and hyperchloremia
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1. Hyperchloremic metabolic acidosis (depletion of bicarbonate -> Cl- fill anion gap)
2. Hypochloremic metabolic alkalosis (caused by loss of Cl- in the GI tract -> anion gap is filled by bicarbonate) (Otherwise Cl- follows Na+ metabolism) (Damjanov) |
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Potassium
a. How many percent is intracellular and how many is extracellular? |
a. 98% IC, 2& EC
(90% of the IC is in the exchangeable intracellular pool, the rest is structurally bound to bone, neurons, rbcs) (Damjanov) |
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Why is potassium slightly higher in serum than in plasma?
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Because some K+ is released from platelets during coagulation of blood
(Damjanov) |
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Sodium
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(Damjanov)
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Potassium
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(Damjanov)
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How does potassium reenter from the interstitial fluid into the cells of the distal tubules and collecting ducts?
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A small part of it is actively secreted, but mostly K+ enters passively through diffusion (This diffusion occurs in response to the active reabsorption of Na+, this generate an electric membrane gradient, and K+ and H+ cross the membrane to neutralize these electric charges)
(Thus, more Na+ reabsorbed -> more K+ and H+ excreted (K+ and H+ are in balance. In acidosis a higher proportion of H+ are excreted and this is associated with hyperkalemia. The reverse happens in alkalosis. Hypokalemia is typical for renal alkalosis. The opposite is also true: ie hypokalemia can produce alkalosis) (Damjanov) |
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Potassium concentrations during different conditions
a. Damaged cell (ie ischemia) b. Acidosis c. Alkalosis d. Insulin - ↑↓ |
a. Hyperkalemia (inadequate energy of Na-K-ATPase)
b. Hyperkalemia (H+ in, K+ out in an attempt to buffer) c. Hypokalemia (H+ out, K+ in, in an attempt to buffer) d. ↑ -> hypokalemia (influx of K+), ↓-> hyperkalemia (ie DM) (Damjanov) |
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Causes of hypokalemia
a. GI loss (4) b. Renal loss (5) c. Redistribution (3) |
a. All Gi secretions contain K+
1. Vomiting 2. Diarrhea 3. Laxatives 4. Inflamed mucosa (secrete K+) b. Renal loss 1. Osmotic polyuria <- DM 2. Diuretics 3. Cushing's syndrome 4. Conn's syndrome\primary hyperaldosteronism 5.Secondary hyperaldosteronism (<- cirrhosis, heart failure, end-stage kidney disease) c. Redistribution 1. Alkalosis 2. Insulin administration 3. Familial periodic muscle paralysis (due to entry of K+ into muscle cells) (Damjanov) |
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Hypokalemia - symptoms
a. Cardiac (3) b. Neuromuscular (3) c. GI d. Metabolic\renal (2) |
a.
1. Flattening\inversion of T waves 2. ST segment depression 3. U waves (Increased digitalis toxicity) b. Neuromuscular 1. Hypotonia, muscle weakness 2. Lethargy 3. Depression 4. Confusion c. GI: slow peristalsis -> ileus d. Metabolic\renal 1. Alkalosis 2. Polyuria <- decreased concentrating capacity (Damjanov) |
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Hyperkalemia - causes
a. Reduced excretion (4) b. Massive tissue injury or cell lysis (4) c. Other (2) |
a. Reduced excretion
1. End-stage renal failure (>80% of nephrons damaged) 2. Acidosis (ketoacidosis most common) 3. Addison's disease 4. Some antihypertensives (ACE-I, aldosterone antagonist, ATII antagonist) b. Massive tissue injury or cell lysis 1. Burns 2. Crush injuries 3. Rhabdomyolysis 4. Tumor lysis syndrome (post-chemotherapy, esp. for lymphomas) c. Others 1. Infusion\oral 2. Redistribution ICV->ECV (lack of insulin, ketoacidosis, hyperglycemia) |
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Spurious (false) hyperkalemia can result from?
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Release of K+ from hemolyzed red blood in the test tube
(Damjanov) |
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Hyperkalemia - symptoms (3)
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Accelerates the transmission of electric currents. Can be lethal in the heart. Progression:
1. Initially peaked T waves 2. > 6 mM -.> P waves disappear, QRS widens 3. Ventricular arrhymtia -> fibrillation |
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Hyperkalemia - treatment (3)
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1. Immediate infusion of calcium gluconate (counteract the cardiotoxic effect by reducing the excitability of cardiomyocytes)
2. Infusion of hypertonic glucose (insulin -> ICV shift) 3. Sodium bicarbonate infusion (-> alkalosis -> ICV shift) (Calcium plays a role in the electrical potential in the microenvironment immediately adjacent to the cell membrane (the environment where voltage-gated ion channels are). Increasing the gradient with gluconate infusion effectively hyperpolarizes the ion channels (but not the entire cell) which has the effect of inactivating them and reducing the arrhythmogenic potential of hyperkalemia. <- studentdoctor.net) (Damjanov) |
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Concentration of H+ at pH 7.4
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40 nM
(Damjanov) |
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Carbonic acid - pK
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6.35
(Wikipedia) |
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Acute and chronic respiratory and metabolic acidosis and alkalosis - which are associated with different lab values in acute and chronic?
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Acute and chronic respiratory abnormalities have different lab values because it takes time for the kidneys to compensate
(Damjanov) |
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Henderson-Hasselbalch formula
a. Formula b. Normal ratio of bicarbonate to carbon dioxide |
a. Image
b. 20:1 (Damjanov) |
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Metabolic acidosis - 4 groups of causes
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1. Loss of bicarbonate
(GI tract (intestinal, pancreatic, biliary) -> diarrhea, vomiting)(Some forms of renal tubular acidosis) 2. Inability to excrete hydrogen ions (end-stage renal failure due to inability to form ammonia, hypoaldosteronism <- hyperkalemia in the kidneys inhibit ammonia synthesis) (Some forms of renal tubular acidosis) 3. Excessive production of endogenous acids (DKA, lactic acidosis <- hypoxia, liver (where it's metabolized\removed)) 4. Ingestion of fixed acids (salicylates, methanol, ethylene glycol. These can also cause lactic acidosis by damaging liver cells) (Damjanov) |
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Anion gap
a. Formula b. Normal value c. Used in d. Mnemonic |
a. Anion gap = Na + K - Cl - HCO3
b. 10-20 mM c. Determining cause of metabolic acidosis (Normal AG: loss of HCO3 in diarrhea, hypoaldosteronism, some proximal or distal renal tubular acidosis) (The loss of bicarbonate in such cases is compensated for with reactive hyperchloremia) d. 1. DEKALS (diabetic acidosis, ethylene glycol\antifreeze (-> oxalic\glycolic acid), kidney failure, alcohols (ethanol, methanol), lactic acidosis, salicylate poisoning) CUTE DIMPLES (cyanide, uremia, toluene, ethylene glycol, diabetic acidosis, isoniazid (first-line antituberculosis drug), methanol, paraldehyde\propylene glycol, lactic acidosis, ethanol, salicylates) (Damjanov) |
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Acidosis - signs
a. Cardiac b. Vascular c. Respiratory d. CNS |
a. Can reduce cardiac output (especially if pH is under 7.2)
b. Decreased sensitivity to catecholamines -> hypotension c. Kussmaul breathing (deep and rhythmic)(especially in ketoacidosis) d. Cerebral vasodilation with secondary intracranial pressure elevation (especially with respiratory acidosis due to simultaneous hypoxia) (Damjanov) |
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Causes of persistent metabolic alkalosis (3)
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1. Extracellular volume contraction
(↓GFR -> ↑Na reabsorption is followed by obligatory HCO3 reabsorption) (Infusion of normal saline can correct this by expanding ECV and replenishing Cl) 2. Potassium deficiency (excessive H secretion and enhanced HCO3 reabsorption, H is moved into cell) 3. Mineralocorticoid excess (increased reabsorption of Na on the expense of K and H) (Damjanov) |
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Respiratory acidosis - causes
a. CNS depression (5) b. Neuromuscular diseases involving respiratory muscles (5) c. Chest wall\pleural disorders (3) d. Airway obstruction (4) e. Alveolar capillary block (3) f. Impaired perfusion of lungs (2) |
a. CNS depression
1. Trauma 2. Intracranial hemorrhage 3. Infections 4. Severe hypoxia 5. Drugs (opiates, barbiturates, anesthetic agents) b. Neuromuscular diseases involving respiratory muscles 1. Myasthenia gravis 2. Muscular dystrophy 3. Amyotrophic lateral sclerosis 4. Guillain-Barre syndrome 5. Cervical spinal cord injury c. Chest wall\pleural disorders 1. Throacic deformities (kyphoscoliosis) 2. Pleural effusion 3. Pneumothorax) d. Airway obstruction 1. Foreign body aspiration 2. Drowning\strangulation 3. Asthma 4. Chronic bronchitis or bronchiolitis e. Alveolar capillary block 1. Chronic interstitial pneumonitis\pneumonia 2. Pulmonary edema 3. Emphysema f. Impaired perfusion of lungs 1. Massive pulmonary embolism 2. Cardiac arrest (Damjanov) |
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Respiratory alkalosis - symptoms
a. CNS b. PNS |
a. Cerebral vasoconstriction due to acute hypocapnia
b. Perioral and peripheral paresthesia due to a drop in ionized Ca (Acute respiratory alkalosis can also cause tetanic contractions by the same cause) (Damjanov) |
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Respiratory alkalosis - causes
a. Respiratory center stimulation (8) b. Hypoxic causes (5) c. Last cause? |
a. Respiratory center stimulation
1. Voluntary hyperventilation 2. Anxiety 3. Reflex hyperventilation <- ie pulmonary embolism 4. Fever and sepsis 5. Drugs - ie salicylate poisoning 6. Brain diseases - tumor, stroke, meningitis 7. Liver disease - ie hepatic failure 8. Pregnancy b. Hypoxemia due to 1. High altititude 2. Pneumonia 3. Right-to-left shunt heart 4. CO poisoning 5. Anemia c. Mechanical ventilation (Damjanov) |
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Calcium
a. Distribution of Ca stores in the body in % b. How many % is free ionized? bound to serum proteins? bound to anions (biacrbonate, phosphate, lactate, citrate)? c. 2 causes causing increased concentration of protein-bound calcium? |
a. 99% in bones the rest is divided between plasma, ECF, and ICF
(The ratio if intracellular to extracellular Ca is 1:10 000) b. 45-50% free, 40-45% bound to serum protein (most of it to albumin - 80%), 10-15% bound to anions c. 1. Dehydration -> increase protein concentration 2. Multiple myeloma (Damjanov) |
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Formula for adjusted unbound Ca aaccording to albumin levels
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Adjusted serum Ca = total Ca (mM) + 0.02(47- albumin (mM)
(Damjanov) |
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Hypocalcemia - causes
a. Spurious (3) b. Hypocalcemia associated with hyperphosphatemia (3) c. Hypocalcemia associated with hypophosphatemia (5) |
a.
1. Hypoalbuminemia -> pseudohypocalcemia 2. Alkalosis 3. Venipuncture with prolonged application of the tourniquet 4. Tubes mistakenly drawn in EDTA or oxalate (these have artificially low Ca concentration because these anticoagulants binds Ca) b. Hypocalcemia with hyperphosphatemia 1. Hypoparathyroidism (Congenital <- Di George syndrome, acquired <- neck surgery) 2.Chronic renal failure (hypocalcemia through hyperphosphatemia retention and inadequate hydroxylation of vitamin D) 3. Hypomagnesemia (Mg is essential for active PTH formation. See low levels of PTH and peripheral unresponsiveness) c. Hypocalcemia with hypophosphatemia 1. Inadequate intake of vitamin D (-> rickets in children) 2. Intestinal malabsorption (vitamin D is fat-soluble <- intestinal, biliary, pancreatic disorders) 3. Renal or liver disease due to failure of vitamin D hydroxylation (vitamin D-resistent rickets) 4. Drug-related - some anticonvulsants may alter the metabolism of vitamin D in the liver (Hypocalcemia of acute onset can be caused by acute pancreatic necrosis or pancreatitis due to chelating of Ca with free fatty acids in the gut due to decreased absorption and in the blood due to released pancreatic lipase) (Damjanov) (Damjanov) |
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Hypocalcemia - signs
a. Neuromuscular symptoms (3) b. What is Chvostek's sign? b. What is Trousseau's sign? c. Cardiac signs (2) d. Behavioral\CNS signs (2) |
a.
1. Numbness 2. Paresthesia 3. Muscle spasm and cramps (laryngeal stridor <- laryngospasm) b. Chvostek's sign is induction of facial spasm in hypocalcemia by pressure on the facial nerve (in parotid region) c. Trousseau's sign is induction of carpal spasm in hypocalcemic patients by applying and tightening a blood-pressure cuff for at least 2 minutes c. Cardiac signs 1. Arrhythmias 2. QT interval prolongation c. Behavioral\CNS changes 1. Nonspecific - lack of alertness 2. Convulsions and loss of consciousness (Damjanov) |
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Causes of hypercalcemia
a. Most common (2) |
a. Most common
1. Primary hyperparathyroidism (most often parathyroid adenoma, less often primary pararthyroid hyperplasia) (2ndary <- chronic renal disease) 2. Malignant tumor (Metastasis to bone, paraneoplastic syndromes (PTHrP <- squamous cell carcinoma of the lung), multiple myeloma and lymphoma (secrete IL-1 and TNF -> activate osteoclasts) (Less common causes: graunloma (ie sarcoidosis), hypervitaminosis D, hyperthyroidism, drugs (thiazide)) (Uncommon causes: Paget's disease, Adrenal failure, Milk-alkali syndrome, Lithium therapy, Hypermagnesemia, Immobilization) (Damjanov) |
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Causes of hypophosphatemia
a. Reduced absorption and intake (3) b. Increased loss or removal (4) c. Shift of phosphates from extracellular to intracellular space (2) |
a. Reduced absorption and intake
1. Chronic malnutrition 2. Chronic alcoholism 3. Abuse of phosphate-binding antacids (aluminium hydroxide) b. Increased loss or removal 1. Hyperparathyroidism 2. Vitamin D deficiency 3. Dialysis - hemo- or peritoneal dialysis c. Shift of phosphates from extracellular to intracellular space 1. Insulin and carbohydrate metabolism-related (P and K follow glucose into the cells. This can happen during infusion of glucose or insulin, during treatment of diabetic acidosis, during nutritional recovery after starvation, and after severe burns.) 2. Alkalosis (Same principle) (Damjanov) |
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Phosphorus
a. Amount in the body b. Distribution c. Concentration d. Important signs and symptoms of hypophosphatemia (2) |
a. 600 g
b. 85% in bones, 14% intracellular (as inorganic phosphate, bound to nucleotides, proteins, and lipids), and 1% in extracellular fluid. c. 0.7-1.4 mM d. Nonspecific 1. General muscle weakness -> respiratory insufficiency 2. Reduce 2,3-Diphosphoglycerate -> impair the red blood cells ability to release oxygen -> generalized hypoxia (Also fatigue, ECG changes, confusion which can progress to coma with convulsions) (Damjanov) |
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Hyperphosphatemia - causes
a. Pseudohyperphosphatemia (2) b. Increased uptake (2) c. Cell lysis (5) d. Diminished excretion (1) |
a. Pseudohyperphosphatemia
1. Hemolysis of blood 2. Multiple myeloma b. Increased uptake 1. Rectal phosphate enema 2. Intravenous phosphate c. Cell lysis 1. Tumor lysis syndrome (Under chemotherapy) 2. Rhabdomyolysis of skeletal muscles during strenuous effort 3. Crush injury 4. Heat stroke 5. Severe hemolytic anemia\transfusion reactions 6. Massive hepatic necrosis d. Diminished excretion 1. Renal failure (Most common cause) (Hyperphosphatemia reduce further the synthesis of vitamin D -> reduce serum Ca and cause secondary parathyroid hyperplasia) (Damjanov) |
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Hyperphosphatemia - effects, signs, and symptoms
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1. Hypocalcemia
(-> tetany, seizures, disturbances of cardiac rhythm) 2. Metastatic calcification (When the serum calcium x phosphorus products exceeds a critical value. Most dangerous in the kidneys, can impair the kidneys ability to excrete minerals and waste product and cause renal insufficiency.) (Calciphylaxis is a severe form of such calcification of skin, soft tissues, and vessels, associated with dermal ulcerations) (Damjanov) |
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Serum protein electrophoresis - name the 5 fractions and some examples of their members
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1. Albumin
(Usually 2\3 of the proteins - 2:1 albumin:globulins, 80% of oncotic pressure. Normally: hyperalbuminemia <- dehydration and hypoalbuminemia <- liver, kidney, or intestinal loss, its synthesis is depressed by IL-6) 2. Alpha-1 globulins a. Alpha-1-antitrypsin (Serine protease inhibitor, 90% -> decrease in this fraction in its deficiency syndrome) b. alpha-1-fetoprotein (AFP) (Major fetal protein, increased in patients with liver cell carcinoma and gonadal and extragonadal germ cell tumors, and in pregnant women who carry fetuses with Down's syndrome or neural tube anomalies and atresia of the GI tract) c. Alpha-1-acid glycoprotein d. Alpha-1-lipoprotein e. Antithrombin III f. Transcortin and TBG (thyroxine-binding globulin) 3. Alpha-2 globulins a. Alpha-2-macroglobulin (Protease inhibitor, 750 kD <- one of the largest proteins in the blood. Increased in nephrotic syndrome due to bigger loss of other smaller proteins and due to compensatory increase in production to maintain oncotic pressure when albumin is lost) b. Prothrombin c. Factor VIII d. Haptoglobin e. Ceruloplasmin (Copper-containing protein with ferroxidase activity, important for transport of iron and copper, decreased in Wilson's disease, acute phase protein) 4. Beta-globulins a. Transferrin (Its concentration correlates with the total-iron binding capacity (TIBC) of the serum.) b. C3 and C4 (Reduced in active autoimmune disorders such as SLE) c. Fibrinogen, F V, VII, IX, XI, XII, XIII d. C-reactive protein (CRP) e. Beta-2-microglobulin (The light-chain portion of the Class I Human leukocyte antigen (HLA) expressed on nucleated blood cells and cells forming many tissues. Increased in patients with B-cell lymphoma, leukemia and multiple myeloma.) 5. Gamma-globulins (IgG = 80%, hypogammoglobulinemia is a feature of primary (congenital) or secondary immunodeficiencies. Hypergammaglobulinemia may be polycolonal (<- infections, autoimmune disorders) or monoclonal as in multiple myeloma) (Under physiologic conditions in slight alkaline pH, alkaline is slightly negatively charged and therefore migrates fastest toward the anode.) (Damjanov) |
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Albumin - causes of hypoalbuminemia (8)
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Decreased intake or synthesis
1. Malnutrition 2. Chronic liver disease 3. Malabsorption syndrome 4. Cachexia of chronic disease Increased loss 5. Nephrotic syndrome 6. Protein losing enteropathy 7. Burns 8. Bleedinig (Serious hypoalbuminemia is often seen in pregnancy due to increased plasma volume.) (Damjanov) |
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Alpha-1-fetoprotein (AFP)
a. What b. Increased in .... (2) |
a. A major fetal protein that is prominent in the serum of fetuses and infants.
b. Patients with 1. Some cancers - liver cell carcinoma and gonadal and extragonadal germ cell tumors 2. Women who carry fetuses with Down syndrome, neural tube anomalies, or atresia of the GI tract. (Damjanov) |
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Creatine kinase (CK)
a. What is an isoenzyme b. Its isoenzymes and their clinical applications |
a. One of a group of enzymes that catalyze the same reaction but may be differentiated by variations in physical properties.
(such as isoelectric point, electrophoretic mobility, kinetic parameters, or modes of regulation) b. 1. CK-MM -> marker for muscle injury 2. CK-MB -> used for MI, less used after troponins 3. CK-BB (Damjanov) |
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Acute-phase proteins
a. Which two proteins have the highest degree of elevation in inflammation |
C-reactive protein and Serum amyloid A.
(Alpha-1-antichymotrypsin (protease inhibitor), alpha-1-acid glycoprotein (tissue repair), ceruloplasmin, and transferrin are others that also are elevated, but to a less degree.) (Damjanov) |
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(Damjanov)
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Hyperlipidemia
a. Primary hyperlipidemia - what, examples (4) b. Secondary hyperlipidemia, what - examples (4) |
a. Primary hyperlipidemia
Genetic disorders. 1. Familial hypercholesterolemia (the most common monogenic defect related hyperlipidemia) 2. Familial combined hyperlipidemia (Most common primary hyperlipidemia, polygenic) b. Secondary hyperlipidemia Non-genetic. 1. Diabetes mellitus 2. Obesity 3. Alcoholism 4. Hypothyroidism (Damjanov) |
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Weight loss
a. Cachexia b. Marasmus and kwashiorkor b. Cachexia - effect on metabolism (4) |
a. Generalized weakness, weight loss, and wasting caused by cancer or other severe chronic diseases.
(Kakos: bad, hexos: condition) b. Marasmus and Kwashiorkor Both are protein-caloric malnutrition disorders. Kwashiorkor is associated more with protein deficiency and less with general caloric deficiency. (Kwashiorkor is characterized by edema with pot belly, depigmentation, loss of hair or change of hair color to red, bulky stool containing undigested food..) c. Cachexia - effect on metabolism 1. Increased basal metabolic rate (BMR) 2. Increased protein degradation (-> Increased BUN and creatinine, anemia, and hypoalbuminemia) 3. Reduced glucose utilization and increased gluconeogenesis -> hyperglycemia, insulin resistance, increased plasma lactate 4. Increased free fatty acids (Unsuppressed free fatty acid mobilization) (Proposed mechanisms of cachexia in cancer patients: obstruction of GI tract (stomach\esophagus, cancer of head of pancreas -> common bile duct), anorexia (some develop aversion to meat), early satiety (<- hyperglycemia? increased circulating amino acid and protein concentration), increased energy expenditure (tumor as parasite), cytokines released in response to tumor growth (TNF\Cachectin, IL-6 -> anorexia, hypermetabolism, muscle proteolysis, apoptosis), therapy (chemotherapy)) (Damjanov) |
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Fever
a. Definition - orally and rectally |
a. Orally - > 37.8 C, Rectally > 38.2 C
("The older the colder" - older in older people, lower in the morning (37.2 C, max in the evening (37.7 C).) b. |
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Hypothalamic thermoregulatory area
a. Endogenous pyrogens (3 groups) b. Mechanism of endogenous pryrogens c. Causes of fever (7) |
a.
1. Interleukins - IL-1Beta, IL-6 2. TNF-alpha and beta 3. IFN-alpha, beta, gamma (<- Activated macrophages and to a lesser extent from activated T cells) b. Act on endothelial cells of the organum vasculosum laminae terminalis (OVLT) -> endothelial cells produce PGE2 -> diffuse into adjacent hypothalamus and raise the set point in the thermoregulatory center. (OVLT is a highly vascular part of the wall of the third ventricle) c. 1. Infectious diseases (Acute infection (ie. influenza), chronic infection (ie. tuberculosis, AIDS) 2. Autoimmune diseases (RA, SLE) 3. Thrombosis, hemorrhage, and infarction (MI, CVA, Thrombophlebitis of leg veins) 4. Gout 5. Metabolic disorders (Hyperthyroidism, alcoholic hepatitis) 6. Drug reaction 7. Neoplastic diseases (Especially lymphoma, renal cell carcinoma, and liver tumors (both primary and secondary)). (2-4 <- pyrogens released from inflammatory cells infiltrating organs affected by autoimmune disease, tissue necrosis or crystalline arthropathy.) (Fever of unknown origin (FOU): > 38.3 C and > 3 weeks, for which the cause can not be found after 1 week of intense investigation. 80-90% is infectious or neoplastic.) (Damjanov) |
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Spinal cord
a. describe the elements of the vertebra surrounding the spinal cord from the vertebral body and posteriorly b. What is the different with the meninges in the spinal cord compared to the cranial cavity c. The two most common sites for disc herniations d. What is a synonym for the dura in the spinal cord |
a. Pedicle -> Transverse process -> Lamina -> Spinous process
b. 1. Epidural fat (Between the dura and the periosteum, in the cranial cavity the periosteal layer of the dura is tightly adherent to the periosteum) 2. Batson's plexus (Valveless meshwork of epidural veins) c. L4-L5 and L5-S1 (Combined they account for 98% of disc herniations causing pain) (Next most common place is in the cervical region.) d. The thecal ('capsule') sac. (Mixed) |
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Spinal cord
a. why is the nerve root involved in both cervical and lumbosacral hernations usually the one corresponding to the lower of the adjacent two vertebrae (L4-L5 disc herniation -> L5 radiculopathy) b. What are the different types of disc herniations, and what do they impinge upon |
a.
1. Posterolateral disc herniations in the lumbosacral spine usually impinge on nerve roots on their way to exit (in the lateral recess of the spinal canal) beneath the next lower vertebral bone, which correspond to the number of the nerve root involved. (L4-L5 disc herniation -> compress L5 nerve root which exit below L5) (Lumbar and sacral (all except cervical) nerve roots exit below the correspondingly numbered vertebral bone.) 2. Cervical discs are usually constrained by the posterior longitudinal ligament so they herniate laterally toward the nerve root which is the same number as the lower vertebra because C1-C7 exit above the same numbered vertebral bone. c. 1. Posterolateral disc herniations Usually impinge on nerve roots on their way to exit beneath the next lower vertebral bone, which corresponds to the number of the nerve root involved. 2. far lateral disc herniation Impinge on the next nerve root. (L5-S1 disc herniation -> S1 radiculopathy) 3. Central disc herniation Cauda equina -> impinge on nerve roots lower than the level of herniation Above L1 -> compress the spinal cord (Blumenfeld) |
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Dermatomes
a. C5 - area of representation b. C6 - area of representation c. C7 - area of representation d. C8 - area of representation e. T1 - area of representation f. Which fiber type and sensory modality is the most sensitive to test for dermatomal sensory loss |
a. C5 - area of representation
Shoulder b. C6 - area of representation Lateral arm, first two digits c. C7 - area of representation Middle digit d. C8 - area of representation Fourth and fifth digit e. T1 - area of representation Medial forearm and distal medial arm f. Often less overlap for smaller fibers. These can be tested by pinprick sensation. (Blumenfeld) |
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Neuropathy
a. Neuropathy b. Locations of neuropathies - name for focal, multifocal, and generalized neuropathy c. Important causes of neuropathy (7) |
a. General term for nerve disorder.
b. Focal - mononeuropathy Multifocal - mononeuropathy multiplex Generalized - polyneuropathy c. Important causes of neuropathy 1. Diabetic neuropathy Infectious 2. Lyme disease 3. Viral - HIV, CMV, VZV, HBV 4. Toxins 5. Malnutrition 6. Immune disorders - Guillain-Barre syndrome\Acute inflammatory demyelinating polyneuropathy (AIDP) (1-2 weeks after viral disease, most often by campylobacter jejuni enteritis, HIV) (Stronger motor involvement than sensory, areflexia, progressive weakness, symptoms peak 1-3 weeks after onset, 80% have near full recovery) 7. Hereditary neuropathies - Charcot-Marie-Tooth disease 8. Mechanical causes - traction, compression, laceration, or entrapment (Blumenfeld) |
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Diabetic Neuropathy
a. Mechanisms b. What is the most common pattern c. Which nerves are most often affected by mononeuropathies d. Onset and progression |
a.
1. Compromise of microvascular supply 2. Oxidative stress (Autoimmunity, neurotrophic and biochemical disturbances) b. Distal symmetrical polyneuropathy, which results in a characteristic glove and stocking pattern of sensory loss. c. 1. CN III 2. Femoral nerve 3. Sciatic nerve d. Often fairly sudden. Often partial or complete recovery over the course of weeks to months after onset. (Sensorimotor deficits can be accompanied by painful paresthesias in the nerve distributions.) (Blumenfeld) |
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Neuropathies
a. Mechanical causes (4) b. Mild mechanical disruption cause, severe mechanical disruption cause c. Long-term complications of severe mechanical disruptions |
a. Extrinsic compression, traction (pulling), laceration (tearing off), and entrapment.
b. Mild -> neurapraxia (a-, praxia: action) - temporary impairment of nerve conduction that resolves within hours to weeks. Severe disruption -> interruption of axons -> Wallerian degeneration - degeneration of axon and myelin (Axonal regeneration can occur at about 1 mm\day) c. 1. Incomplete or aberrant reinnervation 2. Complex regional pain syndrome (Type 1\Reflex sympathetic dystrophy - most common, follows an injury without specific nerve damage) (Type 2\Causalgia (Kausis: burning), follow damage to a specific nerve) (Both: local burning pain, edema, sweating) (Dystrophy - progressive changes that may result from defective nutrition of a tissue or organ.) (Painful paresthesias are treated with anticonvulsants, Serotonin-Norepinephrine reuptake inhibitors, and tricyclic antidepressants.) (Blumenfeld) |
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Guillain-Barre syndrome
a. Synonym b. Pathogenesis c. Signs and symptoms (2) d. Diagnosis (3) e. Treatment (2) |
a. Acute inflammatory demyelinating polyneuropathy (AIDM)
b. Autoimmune-mediated demyelination of peripheral nerves 1-2 weeks following viral infection. (HIV and Campylobacter jejuni enteritis have a strong association) c. 1. Progressive LMN-lesion signs (Motor involvement is most affected) 2. tingling distal paresthesias (Symptoms peak 1-3 weeks after onset) d. 1. Typical clinical presentations 2. CSF demonstrating elevated protein without a significantly elevated white blood cell count 3. EMG\Nerve conduction studies compatible with demyelination e. 1. Plasmapheresis (Aphairesis: withdrawal, removal of whole blood from the body) 2. Intravenous immunoglobulin therapy (80% have a complete or near-complete recovery) (Blumenfeld) |
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Myasthenia gravis
a. Can be accompanied with b. Signs and symptoms (3) c. Diagnosis (8) d. Treatment (4) |
a. Other autoimmune disorders such as SLE, Hypothyroidism, RA, and vitiligo.
b. 1. Generalized, symmetrical, proximal weakness - trunk, diaphragm, and neck muscles 2. Extraocular muscles (15% of cases have weakness only in extraocular and eyelid muscles - Ocular myasthenia) 3. Weakness become more severe with repeated use of a muscle or during the course of a day c. 1. Clinical features 2. The Ice pack test (With patients that have ptosis, placing an ice pack over closed eyelids for 2 minutes improve symptoms, maybe for cold-induced inhibition of cholinesterase) 3. The tensilon test (Dramatically improved symptoms following administration of short-acting acetylcholinesterase inhibitor (Edrophonium)) 4. Characteristic decreased amplitude over 10% in compound motor action potential measurement with repetitive nerve stimulation (3 Hz) 5. Single-fiber EMG (90% sensitivity, not specific) 6. Anti-acetylcholine receptor antibodies (AchR-Ab) (+ in 85% of generalized myasthenia gravis, 50% of ocular myasthenia) 7. Muscle specific receptor tyrosine kinase antibodies (MuK-Ab) (50% of those with generalized myasthenia without findings on AchR-Ab have + serology for this test) 8. CT or MRI of chest (12% have thymona (tumor of thymus gland), many have thymic hyperplasia) d. 1. Immunosuppressive agents (Steroids, azathioprine, mycophenolate, cyclosporine) 2. Anticholinesterase (pyridostigmine - long acting (2h) 3. Thymectomy (In patients > 60 years, with or without thymoma, improve symptoms by unclear mechanism - reduced autoimmune response?) 4. Plasmapheresis or intravenous immune globulin in myasthenic crisis (Bimodal age-related onset - female 20-30 years, males 60-70s) (Blumenfeld) |
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Fever
a. How much does the BMR increase per centigrade b. Healthy individuals an tolerate temperature up to c. Signs and symptoms of fever (4) d. What are the most common causes of very high fever (> 41.5C) |
a. 10%
b. 40.5 C c. 1. Headache 2. Convulsions, especially in children 3. DIC (> 42.1 C, by damaging the endothelium of blood vessels) (Microvascular thrombosis -> ischemic tissue injury -> especially in the brain and the heart) 4. Heat stroke (Prolonged exposure to high environmental temperatures. the affected person has high fever, but does not sweat, indicating a failure of central thermoregulation) (Summer during heat waves in elderly and those who have been incapacitated by drugs or alcohol) d. Most often stroke or other intraranial lesions. (Rarely infectious) (Damjanov) |
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Pain
a. Besides nociceptors, which receptors can cause pain b. The three effects of pain nerve endings being stimulated |
a.
1. Mechanoreceptors - especially pacinian corpuscles in the intestines (-> Visceral, dull pain) (Found in the mesentery and the pancreas) b. 1. Transmit the signal 2. Release inflammatory mediators such as substance P (-> act on endothelia -> increase their permeability and cause them to secrete cytokines - neurogenic inflammation. These cytokines, like bradykinin from endothelial cells and histamine from mast cells act on the nociceptors to increase their responsiveness (peripheral sensitization). This is associated with hyperalgesia) 3. Axonal reflex causing a vascular response (The nerve impulses also travel efferently through interconnecting axons, provoking a vascular response) (Damjanov) |
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Pain - classification
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1. Organic pain
(Can be explained in terms of underlying pathology) a. Neuropathic (<- Injury to the peripheral sensory nerves or nerves in the spinal cord and brain) b. Nociceptive (From excessive or prolonged stimulation of peripheral nerve endings) I. Somatic pain (Sharp, severe, pricking, dermatomal distribution) II. Parietal pain (Same characteristics as somatic. Can be localized or diffuse, and can be referred) III. Visceral pain (<- nerve endings in internal organs. Poorly localized, most intensively felt in the midline of the thorax and abdomen. Often dull, but can also be colicky and cause a feeling described by the patients as gnawing or burning) 2. Psychogenic pain (Can not be explained by underlying pathology) (Ie. chronic headache and back pain) |
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Headache - epidemiology
a. How many percent of people experience headache from time to time b. .. once a month c. .. daily d. Are men or women affected most frequently |
a. 75%
b. 50% c. 5% d. Women (2x as frequent) (Damjanov) |
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Headaches - identify the headaches with the following localizations
a. Unilateral, prodromal symptoms, relieved by sleep b. Bilateral, headband distribution across the brow and top of the head c. Unilateral periorbital or temporal lancinating pain, relieved by sleep, associated with eye symptoms such as tearing, or stuffy nose |
a. Migraine headache
b. Tension headache c. Cluster headache (15 min-3 hours) (Refractory to standard treatment with analgesics) (Damjanov) |
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Migraine headache
a. How many % of women does it affect b. What is the proposed mechanism c. Types |
a. 10%
b. The attack is thought to result from initial vasospasm (ischemia -> aura) followed by a dilation of intracranial and extracranial arteries (hypertension -> headache) c. 1. Migraine with aura (Aura\Prodromal symptoms #1 - Scintillating scotoma #2 - Digitolingual paresthesia Even hemiparesis can occur) 2. Without aura (Characterized by throbbing pain) 3. Complicated migraine (Presence of neurologic symptoms even after the headache has ceased) (<- alcohol, monosodium glutamate (asian-food), estrogens, premenstrual period, after exposure to bright light, during changes in weather) (Damjanov) |
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Secondary headaches - causes
a. Systemic causes (5) b. Head and neck infection (3) c. Chronic diseases of unknown origin (4) d. Intracranial diseases (3) |
a. Systemic causes
1. Viral infection (ie. influenza) 2. Hypertension 3. Anemia 4. Alcohol 5. Drugs b. Head and neck infection 1. Acute upper respiratory infection 2. chronic sinusitis 3. Otitis media c. Chronic diseases of unknown origin 1. Giant cell (temporal) arteritis 2. Glaucoma 3. Temperomandibular joint disorders 4. Cervical spine disorders - arthritis, spondylosis d. Intracranial diseases 1. Tumors of the brain 2. Intraranial bleeding 3. Intracranial infection - brain abscesses, enephalitis, meningitis (+ dental caries and abscesses, muscular problems - tension, fibromyalgia (syndrome of chronic pain of musculoskeletal origin but uncertain cause), osseous - Paget's disease, metastases) (Intracranially pain can be elicited by traction, displacement, compression, or inflammation of pain-sensitive structures which are the dura at the base of the skull, arteries, venous sinuses and the major veins, and CN V, VII, IX, and X (the largest)) (Damjanov) |
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Causes of chest pain (8)
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1. Dermal pain
(Localized, visible, Herpes Zoster -> dermatomal) 2. Myalgia (<- trauma, hematoma, myositis, strain, relative ischemia due to excessive effort. Psychologic component) 3. Ostalgia (<- Mechanical injury due to compression or inflammation, metastases. Intense pain) 4. Posterior root pain (Neuropathic, <- compression <- deformities of the thorax, narrowing of the intervertebral foramen <- spondylosis. Sharp, accentuated by motion) 5. Pleural pain (<- sharp, knifelike pain. Accentuated by respiratory movements. Parietal pleura) 6. Esophageal pain (<- distention, peristaltic disturbance. Substernal. Heartburn from GERD) 7. Cardiac pain (Ischemic heart disease) 8. Pericardial pain (The parietal pericardium is only weakly innervated by pain fibers. Pericarditis -> pain, partly via reaction of adjacent structures in the mediastinum or the parietal pleura) |
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Abdominal pain - categories (6)
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1. Visceral pain
(<- vague & poorly localized, midline. Crampy, especially when resulting from spastic contraction, distention, or twisting of intestines) 2. Parietal (<- skin, subcutaneous tissue, muscle, parietal peritoneum. Steadier and more localized) 3. Referred pain (<- thorax, spine, lower extremities. Perceived as parietal superficial usually.) 4. Metabolic or toxic pain (Porphyria, diabetic acidosis, lead poisoning (-> colicky) 5. Neurogenic pain (Radicular pain, tabes dorsalis (chronic meningitis that constrict the sensory nerves entering the posterior columns) 6. Psychogenic pain (Damjanov) |
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Arthralgia - causes (7)
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Non-inflammatory
1. Trauma I. vessel, cartilage, or ligament injury (tear) II. Neurogenic arthropathy III. Postsurgical or prosthesis-related arthropathy IV. Hemarthrosis in hemophilia 2. Degenerative joint disease 3. Bone diseases I. Aseptic bone necrosis II. Tumor III. Osteoporosis Inflammatory 4. Infection (Chronic granulomatous, chronic suppurative (Lyme disease, GU-related, GI-related, viral (HCV, B19 parvovirus), acute suppurative) 5. Autoimmune - SLE, RA (RA: Heberden's nodes -> fusiform swelling of DIP joints, Bouchard's nodes -> --||-- PIP joints, ulnar deviation) 6. Crystal deposition - Gout, Pseudogout (Pseudogout - Calcium pyrophosphate crystals. Not urate crystals as in gout) 7. Uknown cause - psoriasis, Reiter's syndrome, fibromyalgia, chronic bursitis (Reiter's syndrome: Association of various inflammatory conditions) (Damjanov) |
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Hyperkinetic movements from loss of inhibitory basal ganglia nuclei, include short explanation
(Dyskinesia - hyperkinetic and hypokinetic variants) |
1. Tics - rapid involuntary, nonrhythmic movements - ie. eye blinkin, facial spasm
(Can be simple or complex and can be associated with pain, Tic Douloureux\Trigeminal neuralgia. Feature of Tourette's syndrome (AD). They have complex motor tics on the face (blink, frown, sniff) and phonic tics (throat-clearing, grunting, 50% have coprolalia (a compulsive urge to curse) (Copro: filth\feces, lalia: speech) 2. Tremor - rhythmic repetitive muscle contraction (Resting (Parkinsonism) or intentinal (Cerebellar, MS) (Physiological causes - cold, fatigue, some drugs (caffeine)) 3. Chorea - rapid involuntary jerky movements of hands, feet, and face, merging with the voluntary movements (Huntington's disease, rheumatic fever (Sydenham's chorea) 4. Athetosis - slow, writhing movements involving the muscles of the entire extremity (Corpus striatum (caudate, putamen), Cerebral palsy) 5. Myoclonus - sudden contraction of muscles (Physiologic when falling asleep) (Myoclonic epilepsy, Alzheimer's, Creutzfeldt-Jakob, end-stage renal disease) (Hiccup - diaphragmal) (Damjanov) |
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Hypokinetic dyskinesia
a. Associated structures (3) b. Causes (2) c. The movement disorders (5) (Dyskinesia - hyperkinetic and hypokinetic variants) |
a. The substantia nigra, Locus ceruleus, and related dopaminergic basal ganglia.
b. 1. Parkinson's disease (90%) 2. Secondary parkinson's disease I. Drugs (Interfere with the action of dopamine in the basal ganglia) II. Toxins - CO III. Hemorrhage, inflammation, tumor c. 1. General hypokinesia and loss of involuntary movements (Rigid and expressionless face, monotonous speech) 2. Resting tremor (4-6 Hz, start localized) 3. Bradykinesia (Slow voluntary movements, no muscle weakness) 4. Rigidity (Limbs resist passive movement -> bent flexed posture. Pill-rolling tremor of fingers) 5. Gait abnormalities (Need time to get up, shuffling and unsteady) (Damjanov) |
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The posterior columns are susceptible to which two conditions
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1. Tabes dorsalis caused by syphilis
2. Degeneration from vitamin B12 deficiency (-> loss of proprioception -> adversely affect gait) (Damjanov) |
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Syncope - causes
a. Cardiac syncope (4) b. Vasomotor syncope (3) c. Orthostatic\Postural hypotension causes (Subdivision of vasomotor syncope) (4) d. Cerebral syncope (3) e. Other causes (2) |
a. Cardiac syncope
1. Arrhythmia - tachy or brady 2. Valvular - congenital or acquired (Most often aortic stenosis) (Hypertrophic cardiomyopathy can cause subvalvular obstruction) 3. Pulmonary embolus 4. MI b. Vasomotor syncope 1. During swallowing (Stimulate vagus) 2. Carotid sinus syncope (compress) 3. Micturition syncope (Elderly men, bathroom during night, probably vasovagal) (Young women, increased vagal tone, inadequate sympathetic peripheral vascular control. <- stress, pain. Predromal - nausea, sweating, blurring of vision, tachycardia) c. Orthostatic\Postural hypotension causes 1. Idiopathic orthostatic hypotension (Elderly men) 2. Autonomic system dysfunction <- diabetes mellitus 3. Persons on adrenergic blockers 4. Blood loss - traumatic, anaphylaxis d. Cerebral syncope 1. Hypocapnia 2. TIA 3. Hypoglycemia e. Other causes 1. Hyperventilation syncope (hypocapnia, respiratory alkalosis) 2. Posttussive (end of cough) and postdefecation syncope (Decreased venous return due to Valsalva maneuver) (Damjanov) |
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Coma - functional causes
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End-stage organ failure
1. Hepatic 2. Renal 3. Adrenal 4. Thyroid Systemic metabolic disorders 5. Diabetes (hyperglycemia) 6. Mineral metabolism I. Hyponatremia II. Hypercalcemia 7. Acid-base metabolism 8. Sepsis 9. Drugs & Toxins (Alcohol, opiates, barbiturates, benzodiazepines, anticonvulsants) 10. Epilepsy (Damjanov) |
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Supratentorial mass lesions - signs related to the normal order of the affected structures
1. Diffuse cerebral cortical depression 2. Diffuse deep-hemispheric depression 3. Thalamic impairment 4. Pontine impairment 5. Medullary impairment |
1. Diffuse cerebral cortical depression
Respiration - sometimes hyperventilation Pupils Oculomotor reflexes Extremities - hypo- or hypertonic 2. Diffuse deep-hemispheric depression Respiration Sustained hyperventilation, Cheyne-Stokes Pupils Oculomotor reflexes Extremities hypertonic, decorticate posturing in response to strong stimuli 3. Thalamic impairment Respiration - Cheyne-Stokes, sustained hyperventilation Pupils - Small but reactive Oculomotor reflexes - CN III paresis (esp. medial rectus -> abducted) Extremities - decerebrate response to noxious stimuli 4. Pontine impairment Respiration - irregular, periods of apnea Pupils - unreactive Oculomotor reflexes - CN VI (+ III)\Complete ophthalmoplegia Extremities - flaccid quadriplegia, no decorticate or decerebrate responses 5. Medullary impairment Respiration - ataxic (irregular depth and pattern), prominent apneic periods Pupils - dilated and unreactive Extraocular reflexes - complete ophthalmoplegia Extremities - flaccid quadriplegia, no decorticate or decerebrate responses (Damjanov) |
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Edema
a. Generalized edema is called b. Edema in the peritoneum is called c. Edema in the pleural space is called d. The four general causes of edema |
a. Anasarca
b. Ascites (Askos: a bag) c. Pleural effusion d. 1. Increased venous back pressure (Occlusion (thrombi), heart failure) 2. Reduced oncotic plasma pressure (Cirrhosis, Nephrotic syndrome, protein-losing enteropathy) 3. Increased vascular permeability (Brain after trauma, burned skin) 4. Lymphatic obstruction (Tumors in the lymph nodes, postsurgical lymph node dissection, parasitic infections obstruction the lymphatics -> elephantiasis (of filiaris)) |
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Clinically important forms of bleeding.
Give the name of the different conditions |
Hemoptysis (ptysis - spitting). From lungs or bronchial tubes.
Hematemesis (emesis - vomiting) Melena (melas - black) - dark-colored, tarry stool, had time to be altered by intestinal juices. Hematochezia (chezia - to go to stools) - bloody stools Metrorrhagia (metra - uterus) - bleeding between periods Menorrhagia\Hypermenorrhea (men - month) - excessive\prolonged menses Petechia - minute hemorrhagic spots, not blanched by pressure Ecchymosis - > 3 mm, purplish Purpura - different types, varied presentation (Damjanov) |
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Skin changes
a. Secondary skin lesions b. Name the skin lesions in the picture |
a. Develop from primary lesions as they enlarge, become infected, or from scratching\mechanical irritation.
b. 1. Macule ('spot') 2. Papule ('pimple') 3. Nodule ('knot') 4. Vesicle ('bladder') 5. Pustule (elevation containing purulent material) (Damjanov) |
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Macule
a. Characteristics b. What are large macules called c. Types (4) |
a. Localized changes in skin color.
(macule - 'spot') b. Patches. c. 1. Brown hyperpigmentation (Freckles, Cafe au lait pigmentation in neurofibromatosis type 1) 2. Depigmentation (Localized = vitiligo (autoimmune), generalized = lack of pigment in albinism, this is not a macule) 3. Skin hemorrhage I. Petechiae - < 3 mm II. Purpura - 3-5 mm III. Ecchymoses - > 5 mm (Red (fresh) -> greenish\yellowish (Hb -> biliverdin\bilirubin) 4. Drug exanthemas ('eruption') (Drug reactions. Dilation in vessels of dermis -> localized erythema) (Damjanov) |
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Papule
a. Characteristics b. What are large papules called c. Types (7) |
a. Small (<- 1 cm in diameter) and elevated lesions.
b. Plaques. c. 1. Xanthoma (xantho: yellow) (<- lipid-filled macrophages in the dermis in hyperlipidemia) 2. Lichen planus papules (Immune-mediated disease, flat-topped & silvery white) 3. Warts (<- HPV) 4. Molluscum contagiosum (<- Poxvirus, centrally depressed area ('umbilication')) (Molluscum ('soft') - a disease marked by the occurrence of soft, rounded tumors in the skin) 5. Condyloma ('knob') latum (<- secondary syphilis, palms and intertriginous areas, 'copper-colored') 6. Nevus\Mole (<- accumulation of pigment-bearing cells, congenital or acquired) 7. Seborrheic keratosis (benign epithelial tumor, small and brown, <- sebaceous gland) (Damjanov) |
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1-6?
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1. Crust
(Clotted blood and cell debris. Typically it develops at the site of previous vesicles and bullae or postules. Crusts derived from plasma are yellow, from blood are red, and from pus are yellow or greenish) 2. Erosion (Superficial, partial loss of epidermis. Linear erosions caused by scratching are called excoriations (excoriate - to scratch.) Heals without scarring.) 3. Ulcer (Full thickness loss of epidermis extending into the dermis. Heals with scarring. 4. Fissure (Crack in the skin extending vertically into the dermis) 5. Scar (A residue of the healing of wounds and other deep skin lesions. Characterized by accumulation of connective tissue. Keloids (kele - tumor) are hypertrophic scars.) 6. Scale (Thickening of the skin from hyperproliferation of epidermis and inadequate desquamation of keratinocytes) (Damjanov) |
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Plaques
a. Characteristics b. Examples (4) |
a. Large papules. Circumscribed, elevated, superficial, > 1 cm in diameter
b. 1. Psoriasis (psora - the itch) Primary skin lesion. Multiple erythematous plaques covered by silvery scales. 2. Atopic (allergic) dermatitis Immune-mediated, spongiotic papules -> hyperplasia and thickening from scratching and secondary infections -- lichenification (Leathery induration and thickening of the skin with hyperkeratosis), ecqematous rash 3. Dermal infections Various fungal, tuberculosis of skin, leprosy 4. Idiopathic diseases ('Chronic nonspecific dermatitis') I. Sarcoidosis II. Granuloma annulare III. Erythema multiforme (Damjanov) |
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Nodule
a. Characteristics b. Examples (4) |
a. Solid mass, > 0.5 cm in diameter
b. 1. Benign tumors (Lipoma, schwannoma) 2. Primary or metastatic carcinoma (Often ulcerated or necrotic) 3. Rheumatoid nodule (Granulomas) (Granuloma - Term applied to nodular inflammatory lesions, usually small or granular, firm, persistent, and containing compactly grouped modified phagocytes such as epithelioid cells, giant cells, and other macrophages) 4. Erythema nodosum (Idiopathic, granulomatous inflammation of the dermis and subcutis) (Damjanov) |
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Vesicles and bullae
a. Characteristics b. Examples (6) |
a. Vesicle is a raised lesion filled with fluid, a large vesicle is called a bulla
b. Examples 1. Herpes simplex (Lips, herpes genitalis -> external genitalia) 2. Herpes zoster (Along peripheral nerves, cause dermatomal symptomes, <- activation of dormant varicella zoster herpesvirus in dorsal ganglia after a childhood infection) 3. Contact dermatitis (Type IV hypersensitivity reaction, ie poison ivy, 1-2 days post-exposure) 4. Bullous pemphigoid ('blister-like') (Type II autoimmune hypersensitivity disease, subepidermal bullae, antibodies to basement membrane components, groin-axilla-flexural areas) 5. Pemphigus vulgaris (Type II autoimmune disease, autoantibodies against desmosomal proteins, intrapeidermal vesicles) 6. Burns ((Grade I and II burns, transudation of fluid in between the damaged epidermal cells) (Damjanov) |
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Pustule
a. Characteristics b. Examples (3) |
a. Papule (circumscribed\confined, solid elevation) that contains pus (a fluid product of inflammation).
b. Examples 1. Folliculitis (Bacterial infection of hair follicles) 2. Impetigo (Staphylococcus aureus, face of children) 3. Acne (Chronic infection, <- propionebacterium acnes, hair follicles and adjacent sebaceous glands) (Damjanov) |
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Disease
a. Etiology b. Pathogenesis c. Pathology d. Pathyophysiology e. Clinical features |
a. Etiology
Cause b. Pathogenesis How did it develop. c. Pathology The anatomical changes a disease produces. d. Pathyophysiology The functional consequences of the disease. e. Clinical features Signs and symptoms. (Damjanov) |
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Systemic diseases - the eight classes with one example each
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Systemic diseases
1. Genetic diseases - hereditary hemochromatosis 2. Metabolic diseases - gout 3. Toxic diseases - alcoholism 4. Circulatory diseases - shock 5. Infectious diseases - AIDS 6. Immune diseases - SLE 7. Neoplastic diseases - lung carcinoma (Damjanov) |
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Iron uptake
a. Mechanism b. Regulation of iron levels |
a. Uptake
Fe2+ is taken up by enterocytes in the duodenum via DMT-1 (divalent metal transporter) and then stored as ferritin or exported by ferroportin. b. 1. High iron levels in the liver -> increased hepcidin production -> inhibition of DMT-1 and ferroportin in enterocytes and macrophages 2. Transferrin sensors on precursor crypt cells cause a cascade leading to iron-absorptive enterocytes (DMT-1 and ferroportin positive) via HFE (-> hemochromatosis) in response to low saturation (Damjanov) |
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Hemochromatosis
a. Mechanism of tissue injury b. Which organs are affected |
a.
1. Excessive hemosiderin aggregation 2. Excess iron -> free radicals -> I. Inactivation of enzymes (Oxidative phosphorylation, transporters, synthesis) II. Fibrosis (Cell death -> repair) III. Carcinogenesis (From mutations caused by interaction of iron-generated free radicals and nucleic acids) b. Affected organs 1. Liver I. Fibrosis -> cirrhosis -> hepatomegaly, portal hypertension with splenomegaly, esophageal varices II. Liver cell carcinoma (Affect liver in 95% of cases) 2. Skin I. Brown hyperpigmentation - bronzing (Dermal macrophage hemosiderin accumulation, increased melanin) (90% of patients) 3. Endocrine glands I. Pancreas -> Diabetes (65% of patients) II. Thyroid -> hypothyroidism III. Testicles -> testicular atrophy 4. Joints Deposition -> synovial calcification -> secondary changes in adjacent bone (35% of patients) (2nd and 3rd MCP joints first) 5. Heart Deposits in myocardium -> Cardiopathy I. Pump failure II. Dilatation III. Conduction abnormalities (15%) (Damjanov) |
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Hemochromatosis - diagnostic tests (6)
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1. ↑Total plasma iron - > 200 ug\dL
(Normal 50-170 ug\dL \ 9-30 uM) (Elevated in chronic alcoholics) 2. ↑Transferrin saturation - > 50% (Normal - 35%) (Negative acute-phase protein -> lower in inflammatory conditions -> ↑saturation) 3. Serum ferritin - > 1000 ug\dL (Normal < 200 ug\dL) (Increased after hepatocellular necrosis) 4. ↑Urinary iron excretion (5-10 x higher than normal, normal is < 2 mg\day) 5. Liver biospy with Prussian blue stain (Can also measure biochemically) (Denser on CT\MRI) 6. Genetic testing (Damjanov) |
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Gout - mechanism of acute arthritis
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(Damjanov)
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Alcoholism
a. Acute intoxication\Drunkenness b. Alcohol abuse c. Alcohol dependence |
a. Acute intoxication\Drunkenness
Psychological and somatic consequences of alcohol. CNS depression -> 1. Sedation and drowsiness 2. Loss of motor coordination 3. Delirium 4. LOC -> lethal coma b. Alcohol abuse A repetitive pattern (> 1 month) of drinking that continues even though it has adverse effects in one or more of the following five spheres 1. Marital 2. Social 3. Legal 4. Occupational 5. Physical And he\she don't meet the criteria for alcohol dependence. c. Alcohol dependence Uncontrollable alcohol intake asscoiated with tolerance to the effects of alcohol and symptomatic withdrawal when alcohol is not available. (9 criteria - 1. The individual drinks more than he\she means to, often. 2. The individual is unsuccessful at cutting down. 3. Much time is spent thinking abut getting a drink, or when the next drink will be taken. 4. There are frequent ill effects from drinking, such as absence from work, or being drunk or hung over at work. 5. The individual gives up important nondrinking activities. 6. The individual continues to drink even though it causes problems in family or with health. 7. A tolerance for alcohol has developed. 8. The individual has physical withdrawal symptoms. 9. The individual takes substances to relieve withdrawal symptoms.) (Damjanov) |
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Alcohol metabolism
a. How, where in the hepatocytes (3) b. What is the effects of an incresaed ratio of NADH\NAD |
a. Metabolism
1. Alcohol dehydrogenase in the cytosol (The most important involved liver enzyme) 2. P450 cytochrome CYP2E in the SER of the microsomal fraction 3. Catalase in peroxisomes (1-2 reduce NAD in the reaction) Acetaldehyde is a toxic metabolite that is oxidized further to acetyl CoA by aldehyde dehydrogenase. Also using NAD. b. An increased ratio of NADH\NAD+ 1. inhibits the NAD+-dependent oxidation of lactate to pyruvate -> I. Lactic acidosis II. Lack of pyruvate -> hypoglycemia (Further exacerbated by poor nutritional intake in alcoholics) 2. Inhibit beta oxidation and enhance triglyceride formation -> fatty change in liver cells -> alcoholic steatohpatitis -> cirrhosis (Thus, the liver damage is from accumulation of toxic products and metabolic disturbances.) (Damjanov) |
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Alcoholism
a. Alcohol withdrawal syndrome b. Delirium |
a. Alcohol withdrawal syndrome
Symptoms varies from mild tremulousness, to deilirium tremens, seizures, and even death. (Delirium tremens (tremo - to tremble) a severe, sometimes fatal, form of delirium due to alcoholic withdrawal following a period of sustained intoxication.) (Occurs during the first 24 hours. Accompanied by physical signs as facial flushing, tachycardia, irritability) b. Delirium (deliro - to be crazy) An altered state of consciousness, consisting of confusion, disorientation, disordered thinking and memory, defective perception (illusions and hallucinations), prominent hyperactivity, agitation and autonomic nervous system overactivity; caused by a number of toxic, structural, and metabolic disorders. (Damjanov, Stedman) |
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The most common clinical consequences of chronic alcohol abuse
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Nervous system
1. Wernicke's encephalopathy (Confusion, ophthalmoplegia (paralysis of one or more of the ocular muscles), nystagmus, ataxia, peripheral sensory-motor neuropathy) 2. Peripheral neuropathy (Motor and sensory: weakness, pain, paresthesia, loss of touch, position, vibration, deep tendon reflexes) 3. Korsakoff's psychosis (Amnesia, inability to learn, tendency for confabulation) Heart 3. Cardiomyopathy (<- Toxic effects of alcohol on cardiac myocytes, thiamine deficiency (beri-beri heart). 4. Holiday heart (Acute overindulgence -> arrhythmia or bouts of tachycardia) 5. Rhabdomyolysis (-> progressive weakness and wasting. Renal tubular necrosis from obstruction of renal tubules with cytoplasmic detritus from rhabdomyolysis) 6. Steatohepatitis -> cirrhosis 7. Gout (From additional production and decreased excretion) 8. Acute and chronic pancreatitis 9. Acute gastritis 10. Testicular atrophy and loss of libido 11. Osteoporosis 12. anemia 13. Decreased resistance to infections (The symptomatology is a mixture of direct toxic effects and various deficiencies indirectly or directly related to it.) (Damjanov) |
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The most common clinical consequences of chronic alcohol abuse
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Nervous system
1. Wernicke's encephalopathy (Confusion, ophthalmoplegia (paralysis of one or more of the ocular muscles), nystagmus, ataxia, peripheral sensory-motor neuropathy) 2. Peripheral neuropathy (Motor and sensory: weakness, pain, paresthesia, loss of touch, position, vibration, deep tendon reflexes) 3. Korsakoff's psychosis (Amnesia, inability to learn, tendency for confabulation) Heart 3. Cardiomyopathy (<- Toxic effects of alcohol on cardiac myocytes, thiamine deficiency (beri-beri heart). 4. Holiday heart (Acute overindulgence -> arrhythmia or bouts of tachycardia) 5. Rhabdomyolysis (-> progressive weakness and wasting. Renal tubular necrosis from obstruction of renal tubules with cytoplasmic detritus from rhabdomyolysis) 6. Steatohepatitis -> cirrhosis 7. Gout (From additional production and decreased excretion) 8. Acute and chronic pancreatitis 9. Acute gastritis 10. Testicular atrophy and loss of libido 11. Osteoporosis 12. anemia 13. Decreased resistance to infections (The symptomatology is a mixture of direct toxic effects and various deficiencies indirectly or directly related to it.) (Damjanov) |
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Shock
a. Association with endothelium b. Important manifestations of shock seen in moribund patients (6) |
a. Hypoperfusion -> ischemia of endothelial cells in terminal microvasculature ->
I. Decreased capacity to react to physiological stimuli II. Increased permability -> edema III. Disseminated intravascular coagulation (DIC) + hypotension -> significant ischemia in parenchymal organs b. Manifestations 1. DIC Can see microvascular thrombi in many organs) 2. Diffuse alveolar damage caused by ARDS (Edematous lungs with widespread deposits of fibrin along the alveolar lining - hyaline membrane. -> Tachypnea and dyspnea. Unresponsive to oxygen therapy) 3. Renal tubular necrosis (Oliguria -> anuria, azotemia) 4. Centrolobular necrosis of the lievr (Increased serum AST and ALT, increased prothrombin time) 5. Ischemic necroses in the myocardium (-> Pump failure) 6. Edema and focal ischemic changes in the brain (Comatose patients in the last stages) (Damjanov) |
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Shock - characteristics of
a. Mild shock b. Moderate shock c. Advanced shock |
a. Mild shock
1. In distress but conscious 2. Hypotension and tachycardia 3. Tachypnea and mild dyspnea 4. Slightly reduced urine output b. Moderate shock 1. Confused and restless 2. Pronounced hypotension 3. Oliguria 4. Respiratory distress - need oxygen 5. Lactic acidosis c. Advanced shock 1. Multiple organ failure 2. Agitated, apathetic, or comatose 3. Severe hypotension - often unmeasurable 4. ARDS I. Tachycardia II. Hypoxemia III. Require ventilation treatment 5. Renal failure I. Oliguria -> anuria II. Azotemia 6. DIC 7. Increased liver function tests (Damjanov) |
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AIDS
a. AIDS b. HIV - category, predilection for infecting c. Prognosis of HIV infected persons in 10 years |
a. The final stage of infection with HIV.
b. Lentivirus from the family Retroviridae. Predilection for infecting CD4 helper T cells and monocyte\macrophages. c. Prognosis of HIV infected persons in 10 years 1. 50% develop AIDS 2. 30% develop a milder form of immunodeficiency 3. 20% remain asymptomatic. (Damjanov) |
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AIDS
a. The groups most at risk for contracting HIV in decreasing order b. Antibodies - which, when are they detectable by ELISA c. Antigens, other substance - which, when are they detectable |
a. The groups most at risk for contracting HIV at decreasing order
1. Infants of HIV infected mothers (>90%) 2. Sexual partners of infected persons 3. IV drug abusers 4. Recipients of multiple blood transfusions - ie. hemophiliacs (1:675 000 chance) 5. Health care providers (Needle pricks have a 0.3% of transmitting HIV in an infected person) b. Antibodies I. Antibodies to HIV-related antigen gp 120 II. After 4-12 weeks (window period) c. Antigens I. p24 antigen and viral RNA II. Immediately (Damjanov) |
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HIV infection
a. The three stages b. Acute retroviral syndrome c. Acute infection phase\Acute retroviral syndrome - duration d. Acute infection phase\Acute retroviral syndrome - symptoms |
a. The three stages
1. Acute infection phase - acute retroviral syndrome 2. Latency phase 3. AIDS b. Acute infection phase\Acute retroviral syndrome Set of symptoms that develop in 40-70% of all acutely infected persons. c. 4-8 weeks d. Acute infection phase\Acute retroviral syndrome - symptoms 1. Fatigue (95%, <- cytokine release from infected macrophages) 2. Fever (--||--) 3. Sore throat 4. Lymphadenopathy (3-4: 75%, <- hyperplasia of lymphoid follicles in the tonsils and other lymphoid organs) 5. Myalgia (60%) 6. Rash on the trunk or face (50%, <- immune complexes formed to viral antigens or pro-inflammatory cytokines) 7. Headache (35%, <- aseptic meningitis) (Damjanov) |
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HIV infection
a. The three stages b. The latency phase - duration c. The latency phase - CD4 count d. The latency phase - symptoms |
a. The three stages
1. Acute infection phase - acute retroviral syndrome 2. Latency phase 3. AIDS b. Varies, 80% develop immunodeficiency within 10 years. c. Typically > 200 cells\uL d. Symptoms 1. Lymphadenopathy (30-60%, at least two groups of lymph nodes outside the inguinal area, <- hyperplasia of lymphoid follicles) 2. Mucocutaneous infections (5-10%, genital or oral herpesvirus, varicella-zoster infection, hairy leukoplakia) 3. Skin diseases (Seborrheic dermatitis) 4. Bacterial pneumonia (Streptococcus pneumoniae, 4x risk over the general population) (Damjanov) |
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AIDS
a. Definition b. CNS involvements (4) c. Respiratory system involvements (3) |
a. Aids
I. CD4 count < 200 cells\uL II. AIDS-defining opportunistic infection (Usually develop within 4-10 years after infection) b. CNS involvements 1. HIV encephalopathy I. Dementia II. Low-pressure hydrocephalus 2. Aseptic meningitis (Most common in the seroconversion phase) 3. Opportunistic infections I. Toxoplasma gondii - localized encephalitis II. CMV - widespread encephalitis III. Virus, Fungi (cryptococcus neoformans), and bacteria (mycobacterium tuberculosis) can cause tuberculosis 4. Peripheral neuropathy I. HIV itself II. Opportunistic infections - CMV, herpes simplex virus, herpes zoster virus III. Side effect of drugs b. Respiratory system involvements 1. Pneumocystis carinii\jirovecii (One of the most common AIDS-defining infections) 2. Mycobacterium tuberculosis 3. Candida albicans (fungi) (Damjanov) |
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Systemic lupus erythematosus
a. Typical victims b. Etiology |
a. Women (9 x than males) and child-bearing years.
b. Etiology 1. Genetic predisposition I. Racial and ethnic differences (3-4x in black than in white women) II. High concordance in monozygotic twins (50%) III. Linage to certain histocompatibility antigens - HLA-DR2, 3 -> 3x risk IV. Genetic deficiencies of the complement system 2. Hormonal factors I. Affect women in child-bearing age II. Lower increased risk in females before puberty (4:1) III. Decrease after menopause IV. Female sex hormones from pregnancy or oral contraceptives can precipitate the disease 3. Environmental factors I. UV light - especially skin rashes (-> Keratinocytes secrete cytokines -> local inflammation, (in)directly alter vessel permeability of dermal capillaries) II. Viruses (Not found a pathogen yet, increased incidence of autobodies in lab technicians working with the specimens) III. Drugs (Chlorpromazine, hydralazine, isoniazid, methyl-dopa -> drug-induced lupus, disappear when discontinuing the drug therapy) (Damjanov) |
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SLE
a. What is the antibodies produced against b. How does the antibodies exert its tissue-damaging effect |
a. DNA, RNA, cell surface proteins, phospholipids...
(Presume the problem is related to helper or suppressor T cells) b. 1. Formation of immune complexes I. By reacting with cell components that have leaked into the blood from damaged\dead cells II. Deposit in many organs - typically at sites of ultrafiltration - glomerular basement membranes, serosa, synovia, chrod plexus, choroids of the eye II. Deposits in skin at epidermal-dermal junction III. Activation of complements which binds to the deposited immune complexes leads to inflammation in these sites. IV. Removal of complement is defective in these patients 2. Cytotoxic antibodies I. Antibodies vs specific cell surface molecules II. Cause cell death by complement-mediated mechanisms or by facilitating cell destruction by macrophages III. -> Hemolytic anemia, thrombocytopenia, leukopenia, vasculitis (endothelial injury) (Damjanov) |
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SLE - diagnostic criteria
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a. Diagnostic criteria
SLE if > 4 criteria are found 1. Arthritis 2. Renal disease 3. ANA (Positive) 4. Serositis - pleurisy, pericarditis 5. Hematologic disorders 6. Photosensitivity 7. Oral\Nasopharyngeal ulcers 8. Immunologic disorders 9. Neurologic disorders 10. Malar rash 11. Discoid rash (A RASH POINts MD) (American college of rheumatology) |
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