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341 Cards in this Set
- Front
- Back
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How do you calculate LDL cholesterol?
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LDL = Total - HDL - (trig/5)
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Which lipoprotein disorder has eruptive xanthomas?
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Type 1 (also Type 5)
I.e. familial chylomicronemia syndrome |
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Which lipoprotein disorder has tendon xanthomas?
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Type IIa
I.e. familial hypercholesterolemia |
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Which lipoprotein disorder has palmar xanthomas?
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Type III
I.e. familial dysbetalipoproteinemia |
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Which lipoprotein is increased in familial chylomicronemia (type 1)?
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Chylomicrons
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Which lipoprotein is increased in familial hypercholesterolemia (type IIa)?
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LDL
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Which two lipoprotein disorders are NOT associated with xanthomas?
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Type IIb - familial combined hyperlipidemia
Type IV - familial hypertriglyceridemia |
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Which lipoprotein is increased in familial combined hyperlipidemia (type IIb)?
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LDL + VLDL
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Which lipoprotein is increased in familial dysbetalipoproteinemia (type III)?
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Chylomicron remnants
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Which lipoprotein is increased in familial hypertriglyceridema (type IV)?
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VLDL
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Which is the only lipoprotein disorder that has NORMAL triglyceride levels?
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Type IIa - familial hypercholesterolemia
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Which lipoprotein disorder may cause pancreatitis?
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Type 1 - familial chylomicronemia syndrome
Also, Type 5 |
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Which lipoprotein disorder will NOT cause either pancreatitis or coronary artery disease?
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Type IV - familial hypertriglyceridemia
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What is the defect in type 1 familial chylomicronemia syndrome?
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A defective lipoprotein lipase and/or ApoCII
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What is the defect in type IIa familial hypercholesterolemia?
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Defective LDL receptor
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What is the defect in type III familial dysbetalipoproteinemia?
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Deficiency of ApoE
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What are secondary causes of dyslipoproteinemias (7)?
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1. High fat diet/obesity
2. EtOH abuse 3. Diabetes mellitus 4. HYPOthyroidism 5. NephrOtic syndrome 6. Chronic renal failure 7. Drugs |
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Which apo-protein does HDL contain?
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ApoA1
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What are some causes of a DECREASED HDL level?
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1. Smoking
2. Obesity 3. Sedentary life style 4. Insulin resistance 5. Chronic inflammatory diseases 6. Familial hypoalphalipoproteinemia |
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What are the "high risk" ages for a male and female regarding hyperlipidemia?
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> 45 y/o for men
> 55 y/o for women |
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What is the diagnostic criteria for diabetes mellitus on the basis of: symptoms and a plasma glucose of > 200 mg/dL?
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1. Polyuria + polydipsia + weight loss
2. On two separate occasions 3. @ random (any time, no relation to food) |
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What is the diagnostic criteria for diabetes mellitus on the basis of: fasting plasma glucose?
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1. FPG of > 126 mg/dL
2. On two separate occasions 3. Fasting = no caloric intake for 8 hours |
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What is the diagnostic criteria for diabetes mellitus on the basis of: 2-hour plasma glucose on an oral GTT?
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1. 2-hour PG of > 200 mg/dL
2. On two separate occasions |
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What is impaired glucose tolerance?
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Fasting --> 100 to 126 mg/dL
Non-fasting --> 140 to 200 mg/dL |
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What is the significance of impaired glucose tolerance (i.e. what would you tell someone with an impaired glucose tolerance)?
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They have a 25% chance of progressing to DM over the next 3-5 years
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What is the pathophysiology of Type 1A DM?
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Antibodies against islet cells, insulin, and glutamate decarboxylase
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What is the pathophysiology of Type 1B DM?
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Idiopathic destruction of beta cells
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What is the level of twin concordance in Type 1 DM?
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LESS than 50%!!
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What is the pathophysiology of Type 2 DM?
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1. Insulin resistance
2. Decreased insulin production 3. Increased glucagon levels |
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What lipid levels are a risk factor for Type 2 DM?
Which sex has a higher risk of developing Type 2 DM? |
HDL < 35 mg/dL, or trigs > 250 mg/dL
Females are at a greater risk |
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Which cells do not require insulin for glucose entry, and thus are at risk for sorbitol-mediated swelling?
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1. Retina (retinopathy)
2. Neurons (neuropathy) 3. Kidney (nephropathy) |
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How does non-enzymatic glycosylation cause damage?
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Glycosylation --> increased collagen and matrix --> thicker basement membranes --> organ damage
The thicker basement membranes are more impermeable to O2 |
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What are 6 complications of DM?
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1. Vasculopathy (micro and macro)
2. Nephropathy 3. Retinopathy 4. Neuropathy 5. Joint/connective tissue 6. Periodontal disease #5 and #6 cannot be helped via glucose control |
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What does ghrelin, secreted from the hypothalamus, do to the pituitary?
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Increases GH secretion
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What is the action of somatostatin on the anterior pituitary?
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Decreases:
GH, TSH, ADH |
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What is the action of GnRH on the anterior pituitary?
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Increases:
FSH, LH, GH |
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What is the action of TRH on the anterior pituitary?
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Increases:
TSH, Prolactin, GH |
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What hypothalamic hormones increase GH secretion (4)?
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TRH, GnRH, GHRH, Ghrelin
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What is the treatment for ACTH deficiency from hypopituitarism?
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Glucocorticoids +/- mineralocorticoids
Glucocorticoids are more important!! |
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What is the treatment for prolactin deficiency from hypopituitarism?
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No treatment needed!
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What would the serum prolactin level be in a prolactinoma?
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> 250 ng/mL
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What would the serum GH level be in gigantism/acromegaly?
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> 1 ng/mL
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In which pituitary tumor are drugs the first-line therapy?
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Prolactinoma
All others have surgery as a 1st line therapy |
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How is calcium carried in the blood?
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45% ionized
45% on albumin 10% on other anions |
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How does the binding of calcium to protein change with acid-base status?
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Acidosis decreases binding (more positive charges)
Alkalosis increases binding (causes a hypocalcemia) |
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What is a normal 'serum calcium'?
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8.5 - 10.5 mg/dL
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What are the actions of PTH on bone, kidneys, and intestines?
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1. Release
2. Reabsorption 3. Absorption |
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What are the actions of vitamin D on bone, kidneys, and intestines?
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1. Release (high levels), deposition (low levels)
2. Decreased excretion 3. Absorption |
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What are the actions of calcitonin on bone, kidneys, and intestines?
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1. Incorporation of Ca2+
2. Ca2+ excretion 3. No action on small bowel |
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How can PTH lead to bone formation?
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INTERMITTENT PEAKS of PTH can cause bone formation
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What are symptoms of HYPERcalcemia?
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1. Altered mental status
2. Anorexia, constipation 3. Positive heart inotropy, digitalis toxicity 4. Nephrogenic diabetes insipidus 5. Decreased GFR 6. Renal stones/calcifications |
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Which medications can cause HYPERcalcemia?
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1. Thiazides
2. Lithium 3. Vitamin A 4. Vitamin D 5. Aminophylline (bronchodilator) |
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Which non-endocrine, non-malignancy diseases can cause HYPERcalcemia?
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Granulomatous diseases (sarcoidosis, TB, fungal)
They are associated with an extra-renal production of vitamin D |
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What is the MCC of primary hyperparathyroidism?
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Single parathyroid adenoma
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What are serum electrolyte and hormone levels in primary hyperparathyroidism?
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High = Ca+, Cl-, PTH, alk phos
Low = phosphate, bicarb |
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What is seen in the urine in primary hyperparathyroidism?
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High Ca2+, high phosphate, high cAMP
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What is the MCC of secondary hyperparathyroidism?
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Renal failure
Malabsorption can also cause it |
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How can you diagnose secondary hyperparathyroidism?
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1. High serum PTH w/ low or nml Ca2+
2. High serum phosphorus 3. Low vitamin D |
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How can you diagnose tertiary hyperparathyroidism?
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A high serum PTH with high serum Ca2+
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What is the treatment for 2ndary or 3ary hyperparathyroidism?
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1. Ca2+ supplements
2. Vitamin D (calcitrol); must be the 1-25 OH type! |
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What are the REQUIRED tests to evaluate hypercalcemia?
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1. Serum Ca2+
2. PTH levels 3. 24 hour urinary Ca2+ |
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What are symptoms of HYPOcalcemia?
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1. Tetany, parasthesias, seizures
2. Decreased mental status 3. Cataracts 4. Dental hypoplasia 5. HYPOtension 6. CHF |
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How can drug interactions cause HYPOcalcemia?
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Drugs that induce P450 will increase active vitamin D metabolism
(phenytoin, phenobarbital, carbamazepine, isoniazid, theophylline, rifampin) |
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What is the typical daily intake of iodine, and how much of it is used by the thyroid?
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Intake = 250 ug/day
Thyroid use = 50 ug/day |
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What two things increase thyroid hormone regulation?
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1. TSH
2. Iodine deficiency (causes an enhanced response to TSH) |
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What decreases thyroid hormone regulation?
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Iodine excess
This reduces organification, and decreases secretion of thyroid hormones |
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What is the Wolff-Chaikoff effect?
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A reduced organification of iodine caused by iodine excess
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How is hypothalamic TRH release regulated (i.e. what increases and decreases it)?
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Increased by catecholamines
Decreased by T4/T3 and somatostatin |
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How is pituitary TSH release regulated (ii.e. what increases and decreases it)?
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Increased by TRH from hypothalamus
Decreased by T3, dopamine, and glucocorticoids |
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Why would you order a radioactive iodine uptake test?
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To determine the etiology of a patient's hyperthyroidism
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Pt. has hyperthyroidism + high radioactive iodine uptake; what is the differential?
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Graves, Hashimotos, Plummer syndrome, thyroid adenoma, exogenous TSH
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Pt. has hyperthyroidism + low radioactive iodine uptake; what is the differential?
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Subacute thyroiditis, exogenous thyroid hormone
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What are the 'general' clinical manifestations of hyperthyroidism?
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Weakness and fatigue; NO muscle cramps
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What are the 'reproductive' manifestations of hyperthyroidism?
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Oligo- or amenorrhea, infertility, gynecomastia
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What are the lab readings in hyperthyroidism (4)?
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1) Anemia
2) Low cholesterol 3) High alk phos 4) High Ca2+ |
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What are causes of hyperthyroidism that are associated with a low radioactive iodine uptake (2)?
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Subacute (de Quervain's) thyroiditis, lymphocytic thyroiditis
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What are two pathognomonic findings in Graves disease?
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1) Ophthalmopathy
2) Pretibial myxedema |
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What is the Jod Basedow phenomenon?
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Hyperthyroidism after giving iodine to deficient patients
These pts had subclinical hyperthyroidism/Graves |
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What are 'general' clinical manifestations of hypothyroidism?
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Weakness + fatigue + muscle cramps
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What are 'reproductive' clinical manifestations of hypothyroidism?
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Oligo- or amenorrhea, infertility, galactorrhea
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What are lab findings in hypothyroidism (4)?
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1) Anemia
2) High CPK 3) High chol. and TG 4) Low Na+ |
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What three diseases are associated with Graves disease?
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1) Myasthenia gravis
2) Vitiligo 3) Idiopathic thrombocytopenic purpura |
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Which three drugs can cause iatrogenic hypothyroidism?
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1) Lithium
2) Aminoglutethimide 3) Amiodarone (has lots of iodine in it) |
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What are the most and 2nd most common targets of the autoantibody in Hashimoto's thyroiditis?
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Antibody to thyroperoxidase (90%)
Antibody to thyroglobulin (70%) |
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Which three diseases are associated with Hashimoto's thyroiditis?
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1) Addison disease
2) Pernicious anemia 3) Diabetes mellitus |
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If administering thyroxine therapy, what is the maintenance dose?
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50 to 175 ug/day
LESS if the pt is older or has CAD |
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What two things should you watch out for when administering thyroxine therapy?
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1) Addisonian crisis
2) Angina |
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What are laboratory findings in Cushing syndrome (5)?
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1) Glucose intolerance or diabetes
2) Hypokalemic metabolic alkalosis 3) Hypercalcuria + hypercalcemia 4) Polycythemia 5) Decreased lymphocytes and eosinophils |
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What is the MCC of Cushing syndrome?
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Pituitary adenoma (68%)
I.e. Cushing disease |
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What is the MCC of ectopic ACTH Cushing syndrome?
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Small cell CA
Can also see it in carcinoids |
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What is the MCC of adrenal ACTH Cushing syndrome?
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Adrenal adenoma
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What is the MCC of ACTH-independent Cushing syndrome?
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Exogenous steroids
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What are the two steps in diagnosing Cushing syndrome?
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1) Establish a glucocorticoid excess
2) Establish the source |
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What is a positive result for Cushings in a 24-hr urinary free cortisol collection?
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If > 3X normal
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In an overnight Dex-suppression test, what serum cortisol level can rule out a diagnosis of Cushings?
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Serum cortisol < 1.8 ug/dL
This level can also be used to rule out Cushings in a 2-day Dex-suppression test |
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In a 2-day Dex-suppression test, what urine cortisol level can rule out a diagnosis of Cushings?
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Urine cortisol < 10 ug/day
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If a pt has excess cortisol and high ACTH levels, but a pituitary MRI is negative, what is the next diagnostic step?
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Perform a petrosal sinus samplling
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If a pt has excess cortisol and high ACTH levels, but a petrosal sampling does not show high ACTH, what is the next diagnostic step?
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Perform a chest CT to look for small cell carcinoma
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If a pt has excess cortisol but low serum ACTH, what is the next diagnostic step?
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Perform an imaging test of the adrenals to look for an adenoma
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What drugs can decrease ACTH to treat Cushings (3)?
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1) Bromocriptine
2) Cyproheptadine 3) Valproic acid |
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What drugs can decrease cortisol to treat Cushings (3)?
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1) Ketoconazole
2) Metyrapone 3) Aminoglutethimide |
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Which drug can block the effect of cortisol to treat Cushings?
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RU-486 (mifepristone)
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Is the airspace enlargement seen in emphysema proximal or distal to the terminal bronchiole?
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DISTAL
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What is the clinical diagnosis used for chronic bronchitis?
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1) A productive cough...
2) Lasting most days for 3 months... 3) For two consecutive years |
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When would you suspect a1-antitrypsin deficiency in a pt. with emphysema (5)?
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1) Age < 45 y/o
2) Nonsmoker 3) Emphysema is basilar, not apical 4) Unexplained family hx 5) Has idiopathic cirrhosis |
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What is Hoover's sign in COPD? What other hyperinflation sign can you see in COPD?
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A paradoxical inward movement of the ribcage during inspiration
Can also see an increase in the chest AP diameter |
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How does smoking cause COPD?
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1) Activation of macrophages and PMNs, which cause inflammation --> bronchitis
2) Proteases are released AND anti-proteases are inhibited, which causes ECM injury --> emphysema |
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What is the criteria for "reversibility" in asthma?
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If after giving bronchodilators:
FEV1 increases > 12% and/or by 200mL |
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What are the two common symptoms in asthma?
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1) Coughing
2) Chest tightness |
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What causes the early response in asthma?
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Mast cell degranulation (histamine, LTNs, PGs, PAF)
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What causes the late response in asthma?
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Eosinophil release of LTNs and cytokines
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What are some diseases associated with pulmonary fibrosis (5)?
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1) Connective tissue disease (RA, scleroderma, polymyositis)
2) Sarcoidosis 3) Pneumoconiosis 4) Hypersensitivity pneumonitis 5) Langerhans cell histiocytosis |
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What are three drugs that can cause pulmonary fibrosis?
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1) Bleomycin
2) Amiodarone 3) Cyclophosphamide |
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What are four manifestations of pulmonary fibrosis, other than dyspnea?
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1) Rapid shallow breathing
2) Inspiratory crackles (sounds like Velcro) 3) Clubbing of the fingers 4) Right heart failure (seen later) |
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How does bronchitis contribute to obstructive lung disease?
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Increases mucus in the airways
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How does asthma contribute to obstructive lung disease?
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Causes smooth muscle constriction
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How does emphysema contribute to obstructive lung disease?
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Causes airway collapse
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What three focal lung diseases can cause restrictive lung disease?
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1) Tumor
2) Pneumonia (or pul. edema) 3) Atelectasis |
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What are extra-pulmonary causes of restrictive lung disease (4)?
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1) Obesity
2) Kyphoscoliosis 3) Neuromuscular disease 4) Pleural effusion |
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Compared to healthy, what are the values for FVC and FEV1 in a pt with restrictive lung disease
|
FVC and FEV1 are slightly DECREASED!
They both depend on the total amt of air inspired, so... |
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What changes are seen in expiratory Vmax in obstructive and restrictive lung disease?
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Obstructive --> decreased Vmax
Restrictive --> preserved Vmax |
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What are the definitions for hypoxemic and hypercapnic respiratory failure?
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Hypoxemic --> PaO2 less than 50mmHg
Hypercapnic --> PaCO2 more than 50mmHg |
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What are the two steps in evaluating a pt. presenting in respiratory distress?
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1) Decide if pt has respiratory failure
2) Determine the mechanism of respiratory failure |
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What will hypoventilatory respiratory failure ACUTELY cause (2)?
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1) Acidosis
2) Pulmonary HTN (low O2 causes vasoconstriction) |
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What are two endocrine/metabolic etiologies of hypoventilatory respiratory failure?
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1) HYPOthyroidism
2) Metabolic alkalosis |
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What are three structural etiologies of hypoventilatory respiratory failure?
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1) COPD
2) Kyphoscoliosis 3) Obesity |
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What are five consequences of acute CO2 retention?
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1) Acidosis
2) Cerebral vasodilation 3) Pulmonary HTN 4) CO2 narcosis 5) Hypoxemia |
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Of the three main mechanisms of respiratory failure, which one is most common?
|
V/Q mismatch
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What is the ideal V/Q ratio?
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0.8
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What are four etiologies of pulmonary shunt respiratory failure?
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1) Atelactasis
2) Edema 3) Consolidation 4) ARDS |
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Pulmonary shunt respiratory failure causes what two things (just like V/Q mismatch)?
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1) Hypoxemia
2) HYPOcapnia |
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How can you differentiate shunts from V/Q mismatch?
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Give pt. increased inspired O2
If there is no increase in PaO2, pt has a shunt |
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Under what condition will respiratory failure occur in a person with decreased diffusion capacity?
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Exercise
Blood moves faster, so any diffusion limitation results in hypoxemia |
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What are the O2, CO2, and A-a gradient in a pt with exercise-induced hypoxemia (decreased diffusion capacity)?
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HYPOxemia, HYPOcapnia, HIGH A-a gradient
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What are the two things you determine when evaluating a pt with respiratory failure?
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1) What is the PaCO2?
2) What is the A-a gradient? |
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What is a normal A-a gradient? How do you calculate it?
|
10 to 15 mmHg
147 - (PaCO2 * 1.2) |
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What is the A-a gradient in hypoventilation?
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Normal
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What is the A-a gradient in V/Q mismatch?
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Increased
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What is the A-a gradient in a shunt?
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Increased
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What is the treatment for hypoventilation respiratory failure?
|
Controlled increased FIO2
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What is the target PaO2 in treatment of all kinds of respiratory failure?
|
Target PaO2 = 50-60 mmHg
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What is the treatment for V/Q mismatch?
|
Oxygen
Mechanical ventilation if needed |
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What is the treatment for pulmonary shunts?
|
Positive end-expiratory pressure or mechanical ventilation
Also bronchodilators, antibiotics, treat the CHF |
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What are three reasons for the paradoxical worsening of CO2 with O2 therapy?
|
1) Loss of ventilatory drive
2) Reversal of hypoxic pulmonary vasoconstriction 3) Haldane effect |
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In ACUTE respiratory acidosis, how does pH change with PCO2?
|
pH decreases 0.08 units for every 10mmHg increase of PCO2
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In CHRONIC respiratory acidosis, how does pH change with PCO2?
|
pH decreases 0.03 units for every 10mmHg increase of PCO2
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In ACUTE respiratory acidosis, how does HCO3 change with PCO2?
|
HCO3 increases 1 meq/L for every 10mmHg increase of PCO2
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In CHRONIC respiratory acidosis, how does HCO3 change with PCO2?
|
HCO3 increases 3.5 meq/L for every 10mmHg increase of PCO2
|
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In ACUTE respiratory alkalosis, how does pH change with PCO2?
|
pH increases 0.08 units for every 10mmHg decrease in PCO2
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In ACUTE respiratory alkalosis, how does HCO3 change with PCO2?
|
HCO3 decreases 2 meq/L for every 10mmHg decrease in PCO2
|
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In CHRONIC respiratory alkalosis, how does pH change with PCO2?
|
pH is usually normal!
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In CHRONIC respiratory alkalosis, how does HCO3 change with PCO2?
|
HCO3 decreases 5.0 meq/L for every 10mmHg decrease in PCO2
|
|
|
lopermide HCl
|
Gastrointestinal Agents
Brand: Imodium Use: antidiarrheal |
|
|
What are four things seen in the clinical presentation of ARDS?
|
1) Acute onset
2) Bilateral pulmonary infiltrates 3) PaO2/FIO2 ratio < 200 4) PCWP < 18 mmHg (normal!) |
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What are the two ventilatory treatments for ARDS?
|
1) Positive end-expiratory pressure
2) Low tidal volumes |
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What is the pathologic cause of dyspnea?
|
A discrepancy b/w the drive to breath and the level of ventilation achieved
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Pulmonary edema, pulmonary hemorrhage, pleural effusion, and pneumonia are causes of acute or chronic dyspnea?
|
ACUTE
|
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Interstitial fibrosis, effusions, anemia, and tracheal stenosis are causes of acute or chronic dyspnea?
|
CHRONIC
|
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Histamine, serotonin, and acidosis do what to vascular resistance?
|
INCREASE it
|
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What is the normal pressure and vascular resistance in the pulmonary circulation?
|
Pressure = 25/15
Resistance = 2.6 torr/L/min |
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What is the MCC of pulmonary HTN?
|
Left heart failure
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What explains an increased P2 (increased splitting) seen in pulmonary HTN?
|
Increased pulmonary artery pressure
|
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What explains a right ventricular S4 heart sound in pulmonary HTN?
|
Right ventricular hypertrophy
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What explains a right ventricle S3 heart sound in pulmonary HTN?
|
Right heart failure
|
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What are 5 treatments for pulmonary HTN?
|
1) Prostacyclins
2) Endothelin antagonists 3) Phosphodiesterase inhibitors 4) Anticoagulation 5) Oxygen |
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Epoprostenol, treprosternol, and iloprost are what types of treatment for pulmonary HTN?
|
Prostacyclins
|
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Bosentan is what kind of treatment for pulmonary HTN?
|
Endothelin antagonist
|
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Sildenafil is what kind of treatment for pulmonary HTN?
|
Phosphodiesterase inhibitor
|
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What is the pathophysiology of pulmonary embolism (3 reasons)?
|
1) Release of platelet factors (serotonin, thromboxane A2)
2) Decreased alveolar perfusion 3) Loss of surfactant |
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What are five symptoms of a pulmonary embolism?
|
1) Dyspnea
2) Pleuritic chest pain and rub 3) Cough 4) Hemoptysis 5) Syncope |
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Which kidney disease poses a risk factor for DVT/pulmonary embolism?
|
NephrOtic syndrome
|
|
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What are four techniques used to diagnose a pulmonary embolism?
|
1) V/Q scan
2) Spiral CT angiogram 3) Pulmonary angiogram 4) Lower extremity US |
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Which two techniques to diagnose pulmonary embolism you can NOT perform in a pt with renal failure?
|
Spiral CT angiogram and pulmonary angiogram
|
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What is the gold standard in diagnosing pulmonary embolism?
|
Pulmonary angiogram
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Which technique for diagnosing pulmonary embolism you can NOT do in a pregnant pt?
|
V/Q scan
|
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Which technique for diagnosing pulmonary embolism is a proxy to start anticoagulation?
|
Lower extremity ultrasound
|
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Which three neurotransmitters are involved in sleep?
|
GABA, serotonin, and adeosine
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|
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Which sleep stage is regenerative?
|
Stage 3 and 4
|
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Which sleep stage has fast theta waves?
|
Stage 1
|
|
|
Which sleep stage has 12-14 Hz bursts and a double negative wave?
|
Stage 2
12-14 Hz bursts = sleep spindles Double negative waves = K complexes |
|
|
How much of total sleep does REM comprise?
|
20%
|
|
|
Are pts with sleep apnea moving during the nighttime symptoms?
|
Possibly; flailing of limbs is a nighttime symptom of sleep apnea
|
|
|
Which sex has a higher prevalence of sleep apnea?
|
Males
|
|
|
What four things might you find on physical exam with a pt with sleep apnea?
|
1) Short fat neck
2) Obesity 3) Upper airway narrowing (large tonsils, enlarged uvula, long soft palate 4) Micrognathia/retrognathia |
|
|
What frequency of apneas is considered "not normal"?
|
At least 5 to 10 per hour = not normal
|
|
|
What are acute clinicopathologic effects of sleep apnea?
|
Brady/tachyarrhythmias
Due to the autonomic tone |
|
|
What are chronic clinicopathologic effects of sleep apnea?
|
Systemic HTN, pulmonary HTN, CHF
Myocardial infarction, Stroke, Hypercapnic respiratory failure |
|
|
What is a ventilatory therapy for obstructive sleep apnea?
|
CPAP (continuous positive airway pressure)
|
|
|
What are the four manifestations of narcolepsy?
|
1) Cataplexy
2) HypnaGOgic hallucinations 3) Sleep paralysis 4) Sleep attacks during the day |
|
|
What is cataplexy?
|
Bilateral loss of muscle tone after STRONG EMOTION
|
|
|
What are the Multiple Sleep Latency Criteria for narcolepsy (3)?
|
1) A mean sleep latency of < 8 minutes
2) > 2 sleep onset REM periods during naps 3) No other apparent cause, such as sleep deprivation |
|
|
What is the pathophysiological explanation for narcolepsy?
|
A loss of the orexin-producing NEURONS
Orexin normally promotes wakefulness and suppresses sleep/REM |
|
|
What fluid could you sample to evaluate a pt with cataplexy?
|
CSF; orexin levels may be decreased
|
|
|
What are behavioral treatments for narcolepsy (3)?
|
1) Structural sleep schedule with naps
2) Avoid heavy meals 3) Physical activity during the day |
|
|
What are pharmacological therapies for sleep attacks in narcolepsy (4)?
|
1) Modafinil
2) Methylphenidate 3) Dex-amphetamine 4) Gamma hydroxybutyrate |
|
|
What are pharmacological therapies for cataplexy in narcolepsy?
|
1) Re-uptake inhibitors (clomipramine, venlafaxine, fluoxetine)
2) Gamma hydroxybutyrate |
|
|
Lesions in the basal ganglia produce which three symptoms?
|
1) Bradykinesia
2) Lead pipe rigidity 3) Cog-wheel rigidity (rigidity w/ tremor; seen in parkinsons) |
|
|
What are symptoms seen in an UMN lesion?
|
1) Hemiparesis
2) Hyperreflexia 3) Unilateral clasp-knife spasticity 4) Babinki's sign 5) Possible spontaneous spasms 6) External rotation of LE and internal rotation of UE |
|
|
Will a lesion of the internal capsule cause cranial nerve symptoms?
|
NO!
|
|
|
Will a lesion of the brainstem cause cranial nerve symptoms?
|
YES!
|
|
|
What are symptoms seen in a LMN lesion?
|
1) Weakness
2) Muscle atrophy 3) Fasciculations and fibrillations 4) Decreased/absent reflexes 5) Flaccidity 6) Cramping |
|
|
What is decorticate rigidity and where is the lesion?
|
Flexion of arms and extension of legs
Lesion is in the upper midbrain, which removes inhibition of the red nucleus |
|
|
What is decerebrate rigidity and where is the lesion?
|
Extension of BOTH arms and legs
Lesion is in the upper pons (below red nucleus), which destroys the rubrospinal tract |
|
|
What cord levels are tested with the biceps, triceps, patellar, and ankle deep tendon reflexes?
|
Biceps = C6
Triceps = C7 Patellar = L4 Ankle = S1 |
|
|
Which lesions, UMN or LMN, will you see fasciculations?
|
LMN
|
|
|
Which peripheral neuropathy, toxic or ischemia, will have symmetric symptoms?
|
Toxic!
|
|
|
Which peripheral neuropathy, toxic or ischemia, will have asymmetric symptoms?
|
Ischemic!
|
|
|
Which kind of fibers are damaged first in peripheral neuropathy of toxic etiology?
|
Longest fibers are damaged first
|
|
|
What are some etiologies of toxic peripheral neuropathy (4)?
|
1) Alcohol
2) Diabetes mellitus 3) Lead 4) Paraneoplastic syndromes |
|
|
What is the etiology of Guillain-Barre syndrome (3)?
|
1) C. jejuni infection
2) Other infections 3) Post-vaccinations |
|
|
What are 4 clinical manifestations of Guillain-Barre syndrome?
|
1) ASCENDING weakness
2) Peripheral SENSORY loss 3) Loss of REFLEXES 4) Increased CSF protein, but not increased cells (albumino-cytological dissociation) |
|
|
Which neuropathy, peroneal nerve or lateral femoral cutaneous nerve of the thigh, has NO motor involvement?
|
Lateral femoral cutaneous nerve of the thigh
|
|
|
Which neuropathy, peroneal nerve or median nerve, has NO sensory involvement?
|
Peroneal nerve
|
|
|
What is a plexopathy? What can cause it?
|
A disorder affecting a network of nerves, blood vessels, or lymphatics usually due to localized trauma or compression
|
|
|
Where are common locations for plexopathies (3)?
|
Cervical, brachial, lumbosacral
|
|
|
What are Ca2+, K+, and glucose levels in muscle motor weakness?
|
High Ca2+, low K+, low glucose
|
|
|
Which illness, peripheral neuropathies or muscle motor weakness, will affect proximal muscles more?
|
Muscle motor weakness (such as MG or LE)
|
|
|
Which illness, peripheral neuropathies or muscle motor weakness, will affect distal muscles more?
|
Peripheral neuropathies
|
|
|
Describe the reflexes seen in muscle motor weakness
|
They are preserved!
|
|
|
Describe the sensory loss in muscle motor weakness
|
There is none!
|
|
|
What is the definition of ataxia?
|
Incoordination of movement due to inappropriate integration within the motor system that is NOT due to weakness
|
|
|
Does ataxia get worse in darkness/eyes closed?
|
YES!
|
|
|
What are the three causes of ataxia (which provide the basis of the Romberg test)?
|
1) Proprioceptive defect
2) Vestibular defect 3) Cerebellar defect Need 2 of the 3 working to not have ataxia |
|
|
What is atasia?
|
Inability to maintain normal sitting/standing posture
|
|
|
What does a positive Romberg test show?
|
Defect in PROPRIOCEPTION
|
|
|
What is dysmetria? What test can you perform to measure it?
|
Inaccurate targeting of movement
Test via finger-to-nose |
|
|
What is dysynergia?
|
Loss of postural maintenance (can't coordinate various body segments)
|
|
|
What are some chronic causes of cerebellar dysfunction?
|
1) Hereditary spinal ataxia
2) Tumor 3) EtOH degeneration 4) Multiple sclerosis |
|
|
If a pt's dopamine>ACh, what kind of movement disorder could they have?
|
HYPERkinetic
|
|
|
If a pt's ACh>dopamine, what kind of movement disorder could they have?
|
HYPOkinetic
|
|
|
What are four etiologies of a resting (pill-rolling) tremor?
|
1) Parkinsons
2) Heavy metal toxicity 3) MPTP (meperidine) 4) Midbrain stroke |
|
|
What are two etiologies of an intention tremor?
|
1) Cerebellar disease (EtOH, trauma, stroke, tumor, MS)
2) Midbrain stroke |
|
|
How are the treatments for intention tremor vs resting tremor vs postural tremor?
|
Resting tremor Rx = dopamine agonists
Intention tremor Rx = physical therapy Postural tremor Rx = B-blockers, EtOH, primidone |
|
|
What are two etiologies of a postural tremor?
|
1) Exaggerated physiologic tremor (catecholamine excess)
2) Essential tremor (unknown cause) |
|
|
What are the four frequencies seen in the four tremor types?
|
Resting = 4 to 6 Hz
Intention = 3 to 4 Hz Postural exaggerated = 10 to 12 Hz Postural essential = 4 to 10 Hz |
|
|
What is the pathophysiology of chorea (2)?
|
1) Dopamine excess in the straitum (loss of ACh)
2) Estrogen effect (mild) |
|
|
Which diseases are associated with chorea (6)?
|
1) Huntington
2) Rheumatic fever 3) Cerebral palsy 4) Pregnancy 5) Wilson's 6) Drugs = OCPs, neuroleptics, levodopa, stimulants, anticonvulsants, antiepileptics |
|
|
What is the Rx for chorea?
|
Dopamine antagonists
|
|
|
What are dystonias?
|
Sustained, involuntary contractures
|
|
|
What are two treatments for dystonia?
|
1) Anticholinergics
2) Botox |
|
|
Which chromosome is affected in Huntington's?
|
Defect in chromosome 4, which encodes for the huntington protein
|
|
|
Which two types of cells are degenerated in Huntington's?
|
Cholinergic + GABA-ergic cells in the basal ganglia
|
|
|
What are the clinical manifestations of tardive dyskinesia (2)?
|
1) Orofacial repetitive movements
2) Limb and trunk involuntary movements |
|
|
What is the pathogenesis of tardive dyskinesia?
|
1) Chronic (>6 weeks) exposure to anti-psychotics (dopamine antagonist)
2) This makes hypersensitive striatal dopamine receptors |
|
|
What are two treatments for tardive dyskinesia?
|
1) Stop the neuroleptic
2) Reserpine to deplete dopamine |
|
|
Is hemiballismus unilateral or bilateral?
|
UNILATERAL...that's why it's called hemi
|
|
|
What is the pathophysiology of hemiballismus?
|
A stroke in the subthalamic nucleus
|
|
|
What is the Rx for hemiballismus?
|
Dopamine antagonists
|
|
|
What could be a possible etiology for tics/tourettes?
|
Dopamine excess causing disinhibition of the limbic system
|
|
|
What three adjectives describes tics?
|
1) Brief
2) Stereotypic 3) Suppressible |
|
|
What is an Rx for tics?
|
Dopamine antagonists, but you can also wait it out
|
|
|
What are the four classical characteristics of Parkinsonism?
|
1) Bradykinesia
2) Resting tremor (usually unilateral) 3) Cogwheel rigidity 4) Loss of postural reflexes |
|
|
What is a non-pharmacologic therapy for Parkinsons?
|
Deep brain stimulation of the subthalamic nucleus
|
|
|
What are pharmacologic therapies for Parkinsons?
|
1) Dopamine agonists
2) Amantadine (blocks DA re-uptake) 3) COMT inhibitors 4) Selegeline |
|
|
What is the symptomatic difference b/w myasthenia gravis and Lambert-Eaton?
|
MG = "gets worse as the day goes on"
LE = "gets better as the day goes on" |
|
|
What kind of antibody is found in myasthenia gravis?
|
Anti-muscle-specific tyrosine kinase antibody
|
|
|
What is destroyed in myasthenia gravis?
|
Post-synaptic NM junction nicotinic ACh receptors
|
|
|
Which muscles are most seen affected in myasthenia gravis (3)?
|
1) Eye lids
2) Proximal muscles 3) Diaphragm |
|
|
What is seen concurrently with the myasthenia gravis 15% of the time?
|
Thymoma
|
|
|
What will the EMG show with myasthenia gravis?
|
DECREASE in action potentials with repetitive stimulation
|
|
|
What are therapies for myasthenia gravis (6)?
|
1) Long-acting ACh-esterase inhibitors
2) Steroids 3) Cytotoxics 4) Thymectomy 5) Plasmapheresis 6) IVIG |
|
|
What is the target of the antibodies in Lambert-Eaton syndrome?
|
P/Q-type presynaptic voltage-gated Ca2+ channels
|
|
|
Which muscles are most affected by Lambert-Eaton syndrome?
|
Proximal muscles (legs > arms)
|
|
|
What is seen concurrently with Lambert-Eaton 50-60% of the time?
|
Small cell carcinoma
|
|
|
What will the EMG show with Lambert-Eaton syndrome?
|
INCREASE in action potentials with repetitive stimulation
|
|
|
What are therapies for Lambert-Eaton syndrome (4)?
|
1) Treat underlying cancer
2) Plasma exchange +/- IVIG 3) 3,4-diaminopyridine (DAP) increases release of ACh 4) Prednisone, azathioprine |
|
|
How is myotonic dystrophy inherited?
|
Autosomal dominant
|
|
|
How is the DM1 loci affected in myotonic dystrophy?
|
CTG trinucleotide repeats cause abnormal RNA to accumulate in the nucleus
|
|
|
How is the DM2 loci affected in myotonic dystrophy?
|
CCTG tetranucleotide repeats cause abnormal RNA to accumulate in the nucleus
|
|
|
In myotonic dystrophy, which three other gene products are affected by the abnormal RNA?
|
1) Muscle Cl- channel (causes myotonia)
2) Insulin receptor (causes hyperinsulinemia) 3) Cardiac troponin T (causes arrhythmias and LV abnormalities) |
|
|
Which muscles are affected in myotonic dystrophy DM1 (2)?
|
1) Facial muscles
2) DISTAL limb muscles DM2 has weakness in the proximal muscles |
|
|
What are therapies for myotonic dystrophy (2)?
|
1) Symptomatic treatment
2) Membrane stabilizers (mexiletine, phenytoin) |
|
|
How is Duchenne muscular dystrophy inherited?
|
X-linked recessive
|
|
|
What is the avg time course of Duchenne muscular dystrophy?
|
1) Onset @ 2 to 3 years
2) Wheelchair @ teens 3) Death @ 20s |
|
|
What are clinical manifestations of Duchennne muscular dystrophy?
|
1) PROXIMAL muscle weakness
2) Calf pseudohypertrophy 3) CHF, arrhythmias 4) Elevated CPK |
|
|
What drug can slow down the progression of Duchenne muscular dystrophy?
|
Prednisone
|
|
|
What is the pathophysiology of polymyositis/dermatomyositis?
|
T-cell mediated muscle injury with secondary Ab formation
|
|
|
Which disease is associated with Gottron's papules and heliotrope eyelids?
|
Dermatomyositis
|
|
|
What are therapies for polymyositis/dermatomyositis (4)?
|
1) Steroids
2) Cytotoxics 3) Plasmapheresis 4) IVIG |
|
|
What are clinical findings of polymyositis/dermatomyositis (3)?
|
1) SYMMETRIC PROXIMAL muscle weakness
2) PAIN 3) Elevated plasma muscle enzymes |
|
|
What are the MacDonald's criteria for multiple sclerosis (2)?
|
1) Young age
2) Two separate neurologic regions |
|
|
What will MRI imaging show on a pt with multiple sclerosis?
|
MRI plaques
|
|
|
What are three abnormal findings in the CSF of a pt with multiple sclerosis?
|
1) IgG
2) Myelin basic protein 3) Oligoclonal banding All three are signs of central myelin degradation! |
|
|
What are the four criteria needed for a stroke?
|
1) Acute, sudden onset
2) Neurological deficit 3) Decreased cerebral blood flow due to a vascular disease 4) Fits a vascular territory |
|
|
What is the most common stroke type?
|
Ischemic @ 70%
(Hemorrhagic strokes are seen 25% of the time) |
|
|
Which type of stroke has the higher risk of death? Which type of stroke has the worse post-stroke state?
|
1) Hemorrhagic = higher risk of death
2) Ischemic has worse post-stroke state b/c the neurons are dead |
|
|
Which perfusion rate in brain ischemia is still considered reversible injury?
|
50 cc of blood per 100g of tissue
|
|
|
Which perfusion rate in brain ischemia is considered irreversible injury?
|
20 cc of blood per 100g of tissue
|
|
|
What is seen in irreversible injury vs reversible injury in brain ischemia?
|
Ca2+ influx, which activates intracellular phospholipases and proteases that cause cellular destruction
|
|
|
Which type of seizures are more common, motor or sensory?
|
Motor
|
|
|
What is the chance for a seizure based on location in the brain?
|
Temporal > frontal > occipital > parietal
|
|
|
What three things will a seizure NEVER involve?
|
1) Nuclei
2) White matter 3) Cerebellum |
|
|
What is the progression of a generalized tonic-clonic seizure in 5 steps?
|
1) Aura
2) Tonic 3) Clonic 4) Relaxation 5) Paralysis |
|
|
What is the most common type of seizure?
|
Generalized tonic-clonic seizure
|
|
|
Which type of seizure has an altered consciousness, as well as sensory findings (i.e. smelling gas)?
|
Complex partial seizure
|
|
|
What is always seen in generalized seizures?
|
Loss of consciousness!
|
|
|
What are the six different types of generalized seizures?
|
1) Generalized tonic-clonic
2) Absence 3) Myoclonic 4) Clonic 5) Tonic 6) Atonic |
|
|
What are two markers of epileptiform foci in an EEG reading?
|
1) Spike (70 msec) +/- wave
2) Sharp waves (70 to 200 msec) |
|
|
What are two drugs of abuse that predispose to seizures?
|
1) Cocaine
2) Alcohol |
|
|
What are two medications that can predispose to seizures?
|
1) Beta-lactams
2) Lidocaine |
|
|
What are two definitions for status epilepticus?
|
1) A single seizure lasting over 30 minutes
2) Two or more seizures w/o recovery of consciouness in between |
|
|
What are consequences of status epilepticus (2)?
|
1) Neuronal damage in 30 minutes
2) Death occurs in 5 to 25% of cases |
|
|
What are treatments in status epilepticus (3)?
|
1) Protect airway and ventilation
2) IV anti-convulsants 3) General anesthetics |
|
|
In epileptogenesis, what two substances can block inhibitor GABA receptors?
|
1) Beta-lactams
2) Picrotoxin |
|
|
What is a Jacksonian seizure?
|
A progressive motor seizure
|
|
|
What is reflex epilepsy?
|
A sensory trigger of a seizure
|
|
|
What is "kindling"?
|
Recurrent stimulation that then causes a seizure
|
|
|
Which two anticonvulsants act by blocking the glutamate receptor?
|
1) Lamotrigine
2) Topiramate |
|
|
How does the anticonvulsant zonisamide act?
|
Suppresses the Na+ channel
|
|
|
What is the unstable trigeminovascular reflex in the pathogenesis of migraines?
|
1) Antidromic stimulation of CN5
2) Release of substance P and calcitonin gene-related peptide 3) Pain and vasodilation |
|
|
How is serotonin related to migraines?
|
Serotonin has anti-migraine effects; levels of serotonin are decreased during an attack
Suppresses neurogenic inflammation, CN5 excitability, and is a vasoconstrictor |
|
|
What are two drug types that can treat a migraine attack?
|
1) NSAIDs
2) Triptans (serotonin agonists) |
|
|
What are three drug types that can prevent a migraine attack?
|
1) Anti-HTNs
2) Anti-depressants 3) Anti-convulsants |
|
|
How are triptans administered to treat a migraine attack?
|
All are PO
Only sumatriptan can be given via nasal spray |
|
|
Which headaches are more common in men? In women?
|
Men = cluster headaches
Women = migraines |
|
|
What are clinical manifestations of a cluster headache?
|
1) Rapid onset located behind the eyes
2) May see an ipsilateral red eye, runny nose, Horner's syndrome 3) Pt prefers to stay active rather than lie down 4) Sensitivity to alcohol |
|
|
What are the two pathophysiological explanations for cluster headaches?
|
1) Vasodilation of the carotid in the cavernous sinus
2) Hyperactivity of the PNS |
|
|
What are three therapies for an event of cluster headaches?
|
1) Oxygen
2) Ergots 3) Triptans |
|
|
What are four therapies to prevent cluster headaches?
|
1) Verapamil
2) Prednisone 3) Lithium 4) Ergots |
|
|
What are characteristics of tension headaches?
|
1) Most common type of headaches
2) Bilateral 3) Pt commonly has a multidrug Rx history |
|
|
What meds can cause a chronic daily headache (5)?
|
1) NSAIDs
2) Narcotics 3) Barbiturates 4) Benzos 5) Caffiene |
|
|
What are symptoms seen in a headache due to temporal arteritis?
|
1) Elevated ESR (> 50)
2) Vision loss 3) Fever 4) Anemia |
|
|
What are three causes of a low pressure headache?
|
1) Lumbar puncture
2) Trauma 3) Surgery A reduction in CSF causes the brain to sag into the cranial fossa... |
|
|
What causes the headache of pseudotumor cerebri?
|
Inadequate clearance of CSF
Seen mainly in obese women 20 to 44 y/o |
|
|
Which type of memory is the toughest to lose? Which type is easiest to lose?
|
Toughest = procedural
Easiest = episodic In between is semantic memory |
|
|
What word describes the role of the hippocampus in memories? What is it NOT involved in regarding memory?
|
Gatekeeper
Is NOT involved in storage or retrieval |
|
|
What is the circuit of Papez?
|
Hippocampus -> fornix -> mamillary bodies -> mammillothalamic tract -> thalamus -> cingulate gyrus -> hippocampus
|
|
|
What system is required for forming new memories?
|
Limbic system
Utilizes the Papez circuit |
|
|
What is the basic pathophysioology of Alzheimer's Disease (not plaques or tangles)?
|
Idiopathic loss of cholinergic neurons in the CNS
|
|
|
What type of drug may be effective in treating Alzheimers?
|
Anticholinesterases
|
|
|
What is transient global amnesia?
|
A sudden onset of ANTEGRADE amnesia that lasts a few hours
Pt recovers; no treatment needed |
|
|
What does the HIV gene Gag encode?
|
P24 core protein
|
|
|
What does the HIV gene Pol encode?
|
Protease and reverse transcriptase
|
|
|
What does the HIV gene Env encode?
|
gp120, gp41
|
|
|
What is the probability of HIV transmission of a needlestick?
|
0.3 - 0.4%
|
|
|
What is the probably of HIV transmission from mother to infant? On Zidovudine?
|
26%
8% |
|
|
What event carries the highest probability of HIV transmission above all else?
|
Blood transfusions; 95% chance
Sexual contact is only as high as 3%! |
|
|
What is the most common risk factor for HIV transmission among males?
|
MSM
|
|
|
What is the most common risk factor for HIV transmission among females?
|
High-risk heterosexual contact
|
|
|
Which ethnicity in the US has the highest prevalence of AIDS?
|
African americans
|
|
|
What are the AIDS-defining illnesses other than PCP, Kaposi sarcoma, and CNS toxoplasmosis?
|
1) Esophageal candidiasis
2) Cryptosporidiosis 3) Reactivation HSV 4) Cryptococcus meningitis 5) TB 6) CMV retinitis |
