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CPP Exam #4

Cpp Exam #4

by ajmariano, Mar. 2010

Subjects: com cpp medicine uic

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371 Cards in this Set

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	What is class I lipoprotein disorder? Name lipoprotein affected, the defect, effect on triglyceride, xanthomas produced, what problem it leads to, and an example of the disease.	Affects chylomicrons Defect in lipoprotein lipase and/or apoCII Increases TGs Xanthoma eruptions Leads to pancreatitis Example: Familial Chylomicronemia Syndrome (FCS)
	What is class IIa lipoprotein disorder? Name lipoprotein affected, the defect, effect on triglyceride, xanthomas produced, what problem it leads to, and an example of the disease.	Affects LDL Defect in LDL receptor Normal TGs Xanthomas on tendons Leads to coronary artery disease Example: Familial Hypercholesterolemia
	What is class IIb lipoprotein disorder? Name lipoprotein affected, the defect, effect on triglyceride, xanthomas	Affects LDL and VLDL Defect in ??? Increases TGs Xanthomas - NONE Leads to Coronary Artery Disease (CAD) Example: Familial combined hyperlipidemia (FCHL)
	What is class III lipoprotein disorder? Name lipoprotein affected, the defect, effect on triglyceride, xanthomas	Affects remnants Defect in apoE2 Increases TGs Xanthoma on palmar surfaces Leads to Coronary Artery Disease (CAD) Example: Familial Dysbetaliproteinemia
	What is class IV lipoprotein disorder? Name lipoprotein affected, the defect, effect on triglyceride, xanthomas	Affects VLDL Defect ??? Increases TGs Xanthomas - NONE Leads to NOTHING Example: Familial Hypertriglyceridemia
	What is class V lipoprotein disorder? Name lipoprotein affected, the defect, effect on triglyceride, xanthomas	Affects chylomicrons AND VLDL Defect in ??? Xanthoma eruption Leads to pancreatitis Example: Not listed
	What is the Friedwald formula?	LDL = Total Cholesterol - HDL - (TG/5)
	List the secondary causes of dyslipoproteinemia.	High fat diet Obesity EtOH abuse Diabetes Mellitus Hypothyroidism Nephrotic syndrome (!) Chronic renal failure Drugs
	What main lipoprotein is found in HDL? What is HDL's function?	Main lipoprotein: apoA1 Function: Scavanges cholesterol from vessel walls and brings it back to the liver for catabolism
	List the causes of decreased HDL.	Smoking Obesity Sedentary Lifestyle Insulin Resistance Chronic inflammatory disease Familial hypoalphalipoproteinemia
	What factors places a patient in a high risk for cardiovascular disease?	Past Medical History of: Coronary Artery Disease, Diabetes Mellitus, hypertension, hyperlipidemia Family History of Coronary Artery Disease Behaviors: Smoking Things you can't change: being a male of >45 y.o. OR a female >55 y.o.
	What are the TARGET lipid levels for high risk cardiovascular disease patients?	LDL < 100 mg/dL TG < 150 mg/dL HDL > 40 mg/dL
	What type of diabetes do most people in the U.S. suffer from?	Type II (80-90%)
	What are the causes of diabetes outside of autoimmune destruction of islet cells and insulin resistance?	Pregnancy Maturity Onset Diabetes of the Young Pancreatic insufficiency (EtOH, viral, drugs, infection) Endocrinopathy (Cushing's, Acromegaly, etc) Drug Induced
	What are the criteria to diagnose diabetes at random times?	At 2 random times (any time with no relation to meals)... 1) patient has a >= 200 mg/dL glucose level AND 2) symptoms of polyuria, polydipsia, and weight loss
	What are the criteria to diagnose diabetes while fasting?	1) Fasting for 8 hours 2) 2 samples of blood at different times 3) Glucose >= 126 mg/dL
	What are the criteria to diagnose diabetes during an oral glucose tolerance test (GTT)?	1) 2 hour plasma glucose level of 200 mg/dL. AND 2) Performed at 2 separate occasions
	What are the fasting and non-fasting glucose levels that classifies an individual as "Impaired Glucose Tolerance"?	Fasting: 100 mg/dL - 126 mg/dL Non-Fasting: 140 mg/dL - 200 mg/dL
	What is the risk of developing DM in a patient that has Impaired Glucose Tolerance?	25%
	What is the pathophysiology of type 1 diabetes?	1) Antibody induced destruction of beta islet cells, insulin and glutamic acid decarboxylases. 2) Surgical Removal of gland 3) Fibrocalcific/fibrocalculus pancreatic disease Results in hyperglycemia, weight loss, ketoacidosis (breakdown of protein for energy --> ketoacids!), and the 3 polys.
	What is the pathophysiology of type II diabetes mellitus?	Insulin Resistance (post-receptor cascade) Decreased insulin production/processing Increased glucagon levels
	What are the risk factors/markers for type II diabetes mellitus?	Things you can't control: Age >= 45, female, family hx/genetic Modifiable behaviors: sedentary lifestyle Current health: >= 20% above ideal BW, prior glucose intolerance or gestational DM, HTN, HDL <= 35 mg/dL or TRG >= 250% mg/dL, baby > 9 lbs at birth
	What are the two types of end-organ damage that can occur with patients with DM?	1) Advanced Glycosylation End-Products (chronic hyperglycemia --> glycosylation of serum/tissue proteins --> increased collagen and matrix --> thickened basement membranes --> organ damage) 2) Sorbitol Accumulation (xs intracellular glucose) --> converted to sorbitol via ALDOSE REDUCTASE --> increased osmolarity --> cell swelling and injury
	Which cells do not require insulin for glucose entry?	1) Retina 2) Neurons 3) Kidney
	What are the complications of DM?	Vasculopathy (micro AND macro) Nephropathy Neuropathy Retinopathy Joint/Connective tissue Peridontal Disease
	Which complications of DM decrease with tight control of glucose?	Vasculopathy Nephropathy* Neuropathy* Retinopathy* * These are tissues that do not need insulin to get glucose*
	What is the etiology of hypopituitarism?	Tumors, ischemia, genetic, vascular, infiltration, inflammation, iatrogenic, infection, trauma PRETTY MUCH EVERYTHING CAN CAUSE HYPOPITUITARISM
	What is the diagnosis of hypopituitarism?	Measure and compare basal hormone levels with target gland hormone levels.
	What is the therapy for hypopituitarism?	Depends on what hormone is reduced. If.... ACTH Def: glucocorticoids +/- mineralcorticoids TSH Def: Thyroxine FSH/LH def: Estrogen/Progesterone/Testosterone GHRH Def: hGH in children Prolactin Def: None Vasopressin def: DDAVP
	What is the most common pituitary secreting tumor and how do you treat it?	Prolactin; treat with dopamine analogues
	A patient has a pituitary tumor that does not secrete any hormone. How would you diagnose, describe the disease, and treat the patient?	Diagnosis - Hormone levels/MRI Disease - +/- hypopituitarism Therapy - Surgery, XRT, drugs
	A patient has a pituitary tumor that secretes prolactin. How would you diagnose, describe the disease, and treat the patient?	Diagnosis - Prolactin level >250 ng/mL Disease - Galactemia, infertility, or impotence Therapy - DRUGS, surgery, XRT
	A patient has a pituitary tumor that secretes GH. How would you diagnose, describe the disease, and treat the patient?	Diagnosis - GH level > 1ng/ml, IGF-1 Disease - Gigantism/acromegaly Therapy - Surgery, drugs, XRT
	A patient has a pituitary tumor that secretes ACTH. How would you diagnose, describe the disease, and treat the patient?	Diagnosis - Dexamethasone suppression test Disease - Cushing's disease Therapy - surgery, drugs, XRT
	A patient has a pituitary tumor that secretes TSH. How would you diagnose, describe the disease, and treat the patient?	Diagnosis - TSH/T4 levels Disease - Hyperthyroidism Therapy - Surgery, XRT/Drugs
	A patient has a pituitary tumor that secretes LH/FSH. How would you diagnose, describe the disease, and treat the patient?	Diagnosis - LH, FSH levels Disease - HYPOgonadism Therapy - surgery, XRT/Drugs
	A patient has a pituitary tumor that secretes Alpha-subunit of TSH/LH/FSH. How would you diagnose, describe the disease, and treat the patient?	Diagnosis - Removal (?) Disease - +/- hypopituitarism Therapy - Surgery
	What is the second most common hormone secreted by a tumor?	GH
	What are the long term consequences of gigantism/acromegaly?	Arthropathy Neuropathy Cardiomyopathy HTN Colon CA DM Sleep Apnea
	Does blood pH affect calcium binding?	Yes; Acidosis - increases binding, Alkalosis - decreases binding
	What is the distribution of calcium in blood?	Ionized - 45% Albumin - 45% On other anions - 10%
	What is the normal serum calcium range?	8.5 - 10.5 mg/dL
	What does PTH do in the bone, kidneys, and small bowel?	Bone - Release calcium Kidney - Reabsorb calcium Small Bowel - Absorb
	What does Vit D do in the bone, kidneys, and small bowel?	Bone - Hi --> release calcium; Low --> deposition Kidney - Decrease excretion Small Bowel - Absorption
	What does Calcitonin do in the bone, kidneys, and small bowel?	Bone - deposition of calcium Kidney - excretion of calcium Small Bowel - Nothing
	Other than calcium regulation, what else does PTH do?	1) Increase renal 1-hydroxylation of vitamin D 2) Increase renal excretion of phosphorous 3) Intermittent peaks lead to bone FORMATION
	What are the clinical manifestations of hypercalcemia?	1) Neuropsychiatric - Altered mental status 2) Gastrointestinal - Anorexia, n+v, constipation 3) Cardiovascular - short QT, increased contractility, digitalis toxicity 4) Renal - nephrogenic DI, decreased GFR, nephrocalcinosis, nephrolithiasis
	What are the causes of hypercalcemia? Think big categories and give examples.	1) Endocrine - hyperthyroidism, hyperparathyroidism, Addison's, Pheochromocytoma, familial hypocalcuric hypercalcemia 2) Malignancy - metastass, ectopic PTH/PTHrP, 1,25(OH)D 3) Granulamatous Diseases - sarcoidosis, TB, fungal 4) Miscellaneous causes - Immobilization, ACUTE RENAL FAILURE, milk-alkali syndrome, and medications.
	What medications can cause hypercalcemia?	Thiazides, lithium, vit A, vit D, aminophyline
	What are the biochemical features of primary hyperparathyroidism?	Serum: High Ca and Cl, low P and HCO3, high PTH, high alk phos Urine: High calcium, phosphorous, and cAMP
	What genes are associated with primary hyperparathyroidism?	MEN 1 - 95% hyperplasia + pancreatic and pituitary tumors MEN 2A - 50% hyperplasia + medullary CA thyroid and pheochromocytoma
	What is the prevalence of primary hyperparathyroidism?	1-2/1,000/yr > 60 y.o.
	What is the etiology of secondary hyperparathyroidism? Diagnosis? Therapy?	Etiology: Renal failure or malabsorption --> hypocalcemia --> increased PTH Diagnosis: High serum PTH w/ low or normal Ca, high phosphorous, low 25 or 1-25(OH)D3 Therapy: Calcium supplements; Calcitriol
	What is the etiology of tertiary hyperparathyroidism? Diagnosis? Therapy?	Etiology: Renal failure --> chronic hypocalcemia --> chronic increased PTH --> parathyroid hyperplasia Diagnosis: High serum PTH with high Ca Therapy: Calcium supplements, calcitriol, and surgery if severe or symptomatic
	How do serum PTH and serum calcium affected in primary, secondary, and tertiary hyperparathyroidism?	ALL - Elevated PTH Primary - elevated calcium Secondary - low/normal calcium Tertiary - elevated calcium
	What tests are required to evaluate hypercalcemia? Which tests do you run only if indicated?	Required - Serum Ca, PTH, 24h urine Ca Only if Indicated - PTHrP, Vit D levels, Vit A level, Li level
	How do you treat hypercalcemia?	Specific Therapy - treat underlying disorder Nonspecific Therapy - NS hydration, loop diuretics, bisphosphonates, calcitonin, glucocorticoids, gallium nitrate
	What are the neuromuscular symptoms of hypocalcemia?	Tetany Parasthesias Seizures Decreased MS
	What are the symptoms of hypocalcemia?	Neuromuscular sx Cataracts Dental hypoplasia Hypotension CHF
	What causes hypocalcemia?	1) Absence of PTH effect - hypoparathyroidism (idiopathic, post-surgery, hypomagnesemia) or receptor defect 2) Absence of Vit D effect - decreased intake/malabsorption, unable to hydroxylate, or increased Vit D metabolism by P450
	What can increase vitamin D metabolism and what is the consequence of it?	Drugs such as phenytoin, phenobarbitol, carbamazepine, isoniazid, theophylline, rifampin Results in HYPOcalcemia
	How much iodine does the thyroid use on a daily basis?	50 micrograms; 250 micrograms/d intake; xs is eliminated in urine
	T/F: A vast majority of thyroid hormone is freely found in plasma.	FALSE >90% of thyroid hormone is organified and bound to thyroglobulin via a tyrosine residue on the protein
	How are T3 and T4 formed?	Monoiodotyrosine and diiodotyrosine are enzymatically coupled to form T3 and T4.
	T/F: Thyroxine (T4) lasts longer than triiodothyronine (T3).	TRUE T4 has a T1/2 of 5-7d; T3 has a T1/2 of 1d
	T/F: Thyroxine (T4) has a greater activity than triiodothyronine (T3).	FALSE T3 is 10x more active than T4
	What increases thyroid hormone levels? What decreases it?	Increase: 1) TSH - increases I- uptake, digestion of thyroglobulin, and release of T4/T3 2) Iodine deficiency - enhanced response to TSH Decreased: 1) Iodine xs - reduces organification; decreases secretion of T4/T3
	What is Wolff-Chaikoff effect?	Reduction of organification of thyroid hormone due to iodine excess.
	What increases TRH levels? What decreases it?	Increase - catecholamines Decrease - T4/T3; somatostatin
	What increases TSH levels? What decreases it?	Increased - TRH Decrease - T3, dopamine, glucocorticoids
	What is the radioactive iodine uptake test used for?	1) Determines etiology of hyperthyroidism 2) Helps calculate dose of radioactive iodine ablative therapy 3) Evaluates suppressibility of thyroid
	What is the differential for a high radioactive iodine update result? How about a low uptake?	If high: Increased production = Grave's, Hashimoto, Plummer's, adenoma, TSH If low: Inflammatory release = subacute thyroiditis, exogenous thyroid hormone
	What are the clinical manifestations of hyperthyroidism in regard to the reproductive system?	Oligo-amenorrhea, infertility, gynecomastia
	What are the clinical manifestations of hyperthyroidism in regard to labs? Don't give specific levels.	Anemia, low cholesterol, high alk phos, high Ca
	What is the pathophysiology, classic clinical sign(s), labs and disease association of Graves' disease?	Pathophysiology: Autoantibody against TSH receptor leading to HYPERthyroidism Classical Sign(s): Opthalmopathy (exopthalmos) and pretibial myxedema Labs: High radioactive iodine uptake/T4, low TSH Associated Dz: Myasthenia Gravis (MG), vitiligo, and idiopathic thrombocytopenic purpura (ITP)
	What is the pathophysiology, classic clinical sign(s), labs and disease association of Plummer's disease?	Pathophysiology: Unclear but leads to HYPERthyroidism Classial Sign(s): Occurs in elderly Labs: High radioactive iodine uptake/T4, low TSH Associated Dz: Unknown
	What is the pathophysiology, classic clinical sign(s), labs and disease association of Subacute (de Quervain's) thyroiditis?	Pathophysiology: Viral infection induced destructive release of T4 --> HYPERthyroidism Classical Signs: PAIN, fever Labs: High ESR, low radioactive iodine uptake, increased T4, low TSH
	What is the pathophysiology, classic clinical sign(s), labs and disease association of lymphocytic thyroiditis?	Pathophysiology: ? variant of Hashimoto's or may be post-partum induced --> HYPERthyroidism Classical sign(s): Labs: Low radioactive iodine uptake, high T4, low TSH, and antithyroid antibodies in 50%
	What is Jod-Basedow phenomenon?	Hyperthyroidism after giving iodine to deficient patients
	What are the clinical/lab findings of a toxic adenoma?	Nodule > 3cm High radioactive iodine uptake High T4 Low TSH
	What are the clinical manifestations of hypothyroidism in regards to labs?	Anemia High CPK High Cholesterol and TGs Low Na
	What are the clinical manifestations of hypothyroidsm in regards to reproduction?	Oligo-amenorrhea Infertility Galactorrhea ** Both hyper/hypo-thyroidism will result in olig-amenorrhea or infertility
	What is the pathophysiology, classic clinical sign(s), labs and disease association of Hashimoto's thyroiditis?	Pathophysiology: Auto-antibodies to thyroperoxidase (90%) and thyroglobulin (70%) leading to HYPOthyroidism Classical sign(s): Labs: Associations: Addison's, PA, DM
	What are the etiologies of hypothyroidism?	Hashimoto's thyroiditis Iatrogenic - post surgery, RAI for hyperthyroidism, post-therapy for Hodkin's or head/neck CA. Drugs - Lithium, aminoglutethimide, amiodarone Miscellaneous - postpartum, burnt-out Graves', iodide xs, gland replaced, congenital absence or mutations Rare - Iodine deficiency, TSH blocking Ab
	What are the etiologies of hyperthyroidism?	Grave's Disease Plummer's Disease Subacute (de Quervain's) Thyroiditis Lymphocytic thyroiditis Toxic Adenoma Factitious Jod-Basedow phenomenon TSH/TRH secreting tumors
	What are side-effects to look out for when providing thyroxine therapy?	Addisonian crisis and Angina
	What are factors that will slow thyroxine therapy?	Elderly Severity Long-standing dz CAD
	What is the maintenance dose for thyroxine therapy?	50-175 micrograms/day (less if elderly)
	What do you measure in thyroxine therapy? When do you do it?	Measure TSH in 4-6 weeks
	What would you expect a patient with Cushing's syndrome to present with?	Weight gain, weak, fatigue Acne, hirsutism, bruising, poor healing Infertility, amenorrhea Emotional lability Fractures
	What are the classical physical findings of Cushing's Syndrome?	Truncal obesity Sub-cutaneous, temporal, and dorsal fat pads increased Moon Facies Plethora Striae Proximal Muscle weakness HTN
	What are the laboratory findings of a patient with Cushing's Syndrome?	Glucose intolerance or DM Hypokalemic metabolic alkalosis Hypercalcuria +/- hypercalcemia Polycythemia Decreased lymphocytes and eosinophils
	What are the etiologies of Cushing's syndrome that are ACTH DEPENDENT?	1) Pituitary tumor - ACTH secreting 2) Ectopic ACTH - lung small cell CA, carcinoid
	T/F: Pituitary tumors that secrete ACTH are suppressible by a high does of dexamethasone.	TRUE Ectopic ACTH is NOT suppressible.
	What are the etiologies of Cushing's syndrome that are ACTH INDEPENDENT?	1) Exogenous steroids 2) Adrenal sources - adenoma or carcinoma, Micronodular hyperplasia, Macronodular hyperplaia
	What is the most common cause of Cushing's syndrome?	Pituitary Tumor (68%) Ectopic ACTH (12%) Adrenal sources (=< 10%)
	In a patient with Cushing's syndrome, what are the two things you need to establish with diagnostic tests?	1) How much GC excess 2) Source
	What is the problem with just measuring serum cortisol in a patient with Cushing's syndrome to determine GC excess?	Many false (+)!
	Describe the 24h free cortisol test in regards to what it is used for, how it is performed and important lab values.	1) Used to determine GC excess in Cushing's 2) Measure 24h urine cortisol levels 2) If >3x normal = Cushing's
	Describe the overnight dexamethasone suppression test in regards to what it is used for, how it is performed, and factors that cause false (+).	1) Used to determine GC excess in Cushing's 2) Administer 1mg of dex at midnight --> measure AM cortisol 3) Serum cortisol < 1.8 ug/dl --> r/o Cushing's 4) False (+): Obesity, depression
	Describe the 2-Day dexamethasone supression in regards to what it is used for, how it is performed, and important lab values.	1) Determines GC excess in Cushing's 2) Administer 0.5 mg q6h x 8 3) Serum cortisol < 1.8 ug/dL --> r/o Cushing's OR Urine cortisol <10 ug/day --> r/o Cushing's
	How would you determine the source of excess ACTH in Cushing's Syndrome?	Get serum ACTH and levels will determine what imaging modality to use! - ACTH normal/high --> MRI pituitary or CT chest - ACTH Low - CT/MRI adrenals
	What are the surgical treatments for Cushing's?	- Adenectomy - Hypophysectomy - Adrenalectomy + XRT
	What are the medical treatments of Cushing's?	- Decrease ACTH: bromocriptine, cryproheptadine, valproate - Decrease Cortisol: ketoconazole, metyrapone, aminoglutethimide, and others - Block Cortisol Effect: RU456
	What are the big categories of treatment for Cushing's?	1) Surgery 2) Medical 3) XRT
	Define Emphysema.	Airspace enlargement distal to terminal bronchiole. Due to destruction of alveolar wall.
	Neurontin	Gabapentin
	Define chronic bronchitis.	- Cough and sputum - Most days for 3 months or symptoms for 2 consecutive years
	What are the risk factors of COPD?	1) Host dependent - Genetic (alpha-1 antitrypsin deficiency), airway hyperresponsiveness 2) Environmental - TOBACCO, Occupation, Pollution
	What does a deficiency of alpha-1 antitrypsin do and what disease does it cause?	Destroys neutrophil elastase that leads to COPD
	What are the consequences of COPD?	- Airway Inflammation - Increased airway resistance - Increased work of breathing - Hyperinflation - Impaired regional ventilation
	What is the pathophysiology of pulmonary HTN in patient's with COPD?	V/Q mismatch --> hypoxemia --> pulmonary HTN
	What is the pathophysiology of coughing/sputum production in a patient with COPD?	Airway inflammation --> increased mucus and protease activity --> cough and sputum
	What are the physical exam signs of COPD?	- Cough and sputum (airway inflammation) - Wheezing/rhonchi/pursed lip breathing (Increased airway resistance) - Labored breathing/weight loss (Increased work of breathing) - Hoover's sign, increased AP Diameter (Hyperinflation) - Pulmonary HTN (Impaired regional ventilation)
	What is the pathophysiology of smoking induced COPD?	Smoking leads to activation of macrophages/neutrophils --> inflammation (chronic bronchitis) AND Protease released --> injury to ECM --> Emphysema
	What cells mediate asthma?	Mast cells, eosinophils, T-Lymphocytes, macrophages, PMN's, epithelial cells
	What are the chemical mediators of asthma?	Histamine, PG, leukotriene, PAF, kinins
	What is pulsus paridoxicus?	Drop of SBP of >10 mmHg with inspiration.
	What is the dual response in asthma?	Early (5 min) due to mast cell release of histamine, LT, PG, PAF Late (4hr) due to eosinophil release of LT and cytokines
	What is the pathogenesis of pulmonary fibrosis?	Initial insult --> immune response --> alveolitis --> WBC/macrophage cytokine release --> injury to epithelial cells and alveolar basal lamina --> repair with fibrosis
	What are the associated diseases of patients with pulmonary fibrosis?	- Idiopathic (cryptogenic fibrosing alveolitis) - CTD: RA, scleroderma, PMS - Sarcoidosis - Occupational lung disease: silicosis, asbestosis - Hypersensitivity pneumonitis - Langerhans cell histiocytosis - Drugs (e.g. bleomycin, amiodarone, cyclophosphamide)
	What are the clinical manifestations of pulmonary fibrosis?	- Dyspnea - Rapid, shallow breathing - Inspiratory crackles (velcro sound) - Digital clubbing - Late right HF
	What are the indications for pulmonary function testing (PFT)?	- Assess SOB/DIB - Determine presence/degree of pulmonary disease - Determine pathophysiology of pulmonary disase - confirm presence of COPD - Assess course, prognosis, and response to therapy - Assess disability - Assess surgical risk
	What do pulmonary function tests determine?	1) Dynamic lung function - FEV1 and FVC, maximum voluntary ventilation 2) Static lung function - volumes and capacities 3) Gas exchange - diffusion capacity, arterial blood gases
	What are the PFT classifications of pulmonary diseases? Give examples of each classification.	1) Obstructive - chronic bronchitis, emphysema, asthma, acute bronchitis, bronchiectasis, bronchiolitis obliterans 2) Restrictive - Pulmonary fibrosis/edema/focal lung diseases/lung resection or Extra-pulmonary (obesity, kyphoscoliosis, neuromuscular disease, pleural effusion)
	What happens to FVC, FEV1, FEV1/FVC, Vmax, FEF50, and MMV in obstructive lung diseases?	ALL DECREASE
	What happens to FVC, FEV1, FEV1/FVC, Vmax, FEF50, and MMV in restrictive lung disease?	** Only FEV1/FVC can be high. All others will be decreased or normal.
	What happens to the lung volumes in restrictive diseases?	ALL DECREASE
	What happens to lung volumes in obstructive disease?	TLC - Normal or high VC - Decrease FRC - Increase RV - Increase DLco - Decrease
	What is the definition of respiratory failure?	Hypoxemic respiratory failure = PaO2 < 50 mmHg Hypercapnic respiratory failure = PaCO2 > 50 mmHg
	List the mechanisms of hypoxemia.	1) Hypoventilation 2) V/Q Mismatch 3) Shunt 4) Diffusion Limitation 5) Low inspired FIO2
	What is the pathophysiology of hypoventilatory respiratory failure?	Insufficient volume/frequency of respiration --> Increased PaCO2 --> Decrease in PaO2 --> Causing acidosis, pulmonary HTN
	What are the etiologies of hypoventilatory respiratory failure?	1) Any destructive CNS disease 2) Endocrine/metabolic: hypothyroidism, metabolic alkalosis 3) Neuromuscular: Lesions of anterior horn cells, peripheral nerves, motor end plate, muscle itself 4) Structural: COPD, kyphoscoliosis, obesity
	What are the consequences of acute CO2 retention?	- Acidosis --> impaired tissue metabolism - Cerbral Vasodilation --> cerebral edema - Pulmonary vasoconstriction --> Pulmonary HTN - CO2 necrosis --> lethargy/coma - Hypoxemia --> organ dysfunction
	What is the most common type of respiratory failure?	V/Q Mismatch respiratory failure; often with some hypoventilation
	What is the ideal V/Q ratio?	0.8 4 L/min alveolar ventilation and 5L/min cardiac output
	What happens when V/Q decreases?	1) Less air reaches alveoli per given amount of perfustion 2) Less exchange of O2 and CO2 3) Alveolar end-capillary PO2 drops and PCO2 increases 4) "Healthier" alveoli can compensate for CO2 but not O2 5) ABG shows low PaO2 and low PaCO2
	What happens when V/Q increases?	1) More air reaches alveoli per given amount of perfusion 2) More exchange of O2 and CO2 3) Alveolar end-capillary PO2 increases and PCO2 drops 4) O2 dissociation curve flat at high levels; can't compensate
	What kind of shunt is a pulmonary shunt? What is the V/Q ratio?	- Right to left shunt - V/Q is 0
	What are the etiologies of a pulmonary shunt?	- Atelectasis - Edema - Consolidation, - Acute Respiratory Distress Syndrome
	What is the pathophysiology of a pulmonary shunt?	Atelectasis/edema/consolidations/ARDS ---> venous blood is shunted from pulmonary into systemic arterial system w/o oxygenation --> hypoxemia and hypocapnia like V/Q mismatch
	In a patient with a V/Q of 0, what happens to the blood oxygen and carbon dioxide levels when you increase inspired O2?	NOTHING (think about it!)
	What are the clinical presentations of a decreased diffusion capacity?	- Usually secondary to alveolar/interstitial inflammation and fibrosis (e.g. interstitial lung disease) - Exercise intolerance (exercise induced hypoxemia) - Hypoxemia, hypocapnea, high A-a gradient
	What is the clinical approach to respiratory?	Obtain PaCO2 --> If normal or low, it excludes hypoventilation \| If elevated, calculate the A-a gradient --> If normal, hypoventilation is the sole cause of the respiratory failure \| if increased, there is a V/Q mismatch or shunt
	How do you calculate the PAO2?	147 - (PaCO2 x 1.2) Normal is 10-15 mmHg
	How do you interpret a high A-a gradient?	Poor gas exchange = V/Q mismatch/shunt/diffusion limitation
	How would you treat a high A-a gradient?	Give 100% gas. If PaO2 rises, then you have a V/Q mismatch. If PaO2 doesn't do anything, you have a shunt.
	How would you interpret a normal A-a gradient?	Hypoventilation or decreased FIO2
	What is the treatment of hypoventilation-induced respiratory failure?	Controlled increased of FIO2; target PaO2 = 50-60 mmHg Mechanical ventilation if needed
	What is the treatment of V/Q-induced respiratory failure?	100% Oxygen; target= 50-60mmHg Bronchodilators, antibiotics, Rx CHV
	What is the treatment of shunting-induced respiratory failure?	Positive End-expiratory pressure (PEEP) or mechanical ventilation Target PaO2 = 50-60 mmHg Target FIO2 < 60%
	What is the treatment of diffusion limitation-induced respiratory failure?	Oxygen, target PaO2 = 50-60 mmHg Treat underlying pulmonary disease
	Describe the paradoxical worsening of CO2 with O2 therapy?	- Loss of ventilatory drive - tolerance occurs to hypercapneic drive; no tolarance with hypoxic drive - Reversal of hypoxic pulmonary vasoconstriction - sends more blood to unventilated alveoli. Decreased ability to exchange CO2 - Haldane effect - O2 displaces CO2 from hemoglobin --> increases CO2 in blood

	How do you determine the type of acidosis?	High pCO2 = respiratory acidosis Low HCO3 = metabolic acidosis
	What are the lab characteristics of respiratory acute vs. compensated (chronic) acidosis?	1) Acute - pH decreases 0.08 pH untis / 10 mmHg PCO2 increase. HCO3 increases 1 meq/L / 10 mmHg PCO2 increase 2) Compensated - pH decreases 0.03 pH units / 10 mmHg PCO2 increase. HCO3 increases 3.5 meq/L / 10 mmHg PCO2 increase
	What are the lab characteristics of respiratory acute vs. compensated (chronic) alkalosis?	1) Acute - pH increase 0.08 pH untis / 10 mmHg PCO2 decrease. HCO3 decreases 2 meq/L / 10 mmHg PCO2 decrease 2) Compensated - pH usually normal. HCO3 decreases 5.0 meq/L / 10 mmHg PCO2 decrease
	What is the clinical presentation of acute respiratory distress syndrome?	Acute Onset Bilateral Pulmonary Infiltrates PaO2/FIO2 < 200 Pulmonary capillary wedge pressure (PCWP) < 18 mmHg
	Outline the pathophysiology of acute respiratory distress syndrome?	Acute lung injury --> inflammation --> alveolar edema --> decrease lung compliance --> alveolar collapse
	What are the causes of acute respiratory distress syndrome?	Sepsis, shock, trauma, aspiration, drugs, inhaled toxins, oxygen toxicity
	A patient has acute respiratory distress syndrome, how do you treat?	Treat underlying cause PEEP - recruits as many alveoli as possible for respiration Low tidal volumes - prevents over inflation that can cause secondary damage
	What is the pathophysiologic cause of dyspnea?	A discrepancy between the drive to breath and the level of ventilation achieved.
	What are the causes of acute dyspnea?	Pulmonary edema Asthma Chest wall injury Pneumothorax PE Pneumonia ARDS Pleural effusion Pulmonary hemorrhage
	What are the causes of chronic dyspnea?	COPD CHF Interstitial fibrosis Asthma Effusions Thromboembolic disease Pulmonary vascular disease Psychogenic dyspnea Anemia Tracheal stenosis Hypersensitivity disorders
	What is the normal pressure in pulmonary circulation?	25/15 mmHg
	What increases/decreases pulmonary vascular resistance?	Increases: Sympathetic tone, PGF2, thromboxane, angiotensin, histamine, serotonin, alveolar hypoxemia/hypercapnia, acidosis Decrease: parasympathetic tone, Ach, Beta2 agonists, bradykinin, PGE1/PGI2, NO
	List the etiologies of pulmonary HTN.	1) Increased left atrial pressure - CHF, mitral stenosis 2) Increased pulmonary flow - left to right shunt 3) Increased pulmonary vascular resistance - hypoxia causing vasoconstriction, obstruction (primary pulmonary HTN, PE), obliterative (emphysema, pulmonary fibrosis)
	What are the pathophysiological causes for these physical exam findings in a pt. with chronic pulmonary HTN? Increased P2, RV S4, RV S3, Increased JVP, Edema, hepatomegaly, fatigue and dyspnea	Increased P2: Increased pulmonary artery pressure RV S4: Right ventricular hypertrophy RV S3: Right heart failure Increased JVP: Right heart failure Edema/hepatomegaly/fatigue/dyspnea: Right heart failure
	What are the therapies for pulmonary HTN?	- Oxygen - Prostacyclins: epoprostenol, treprosternol, iloprost - Endothelin antagonists: bosentan - Phosphodiesterase inhibitors: sildenafil - Anticoagulation
	Describe the pathophysiology of a PE.	1) Release of platelet factors: serotonin and thromboxane --> vasoconstriction--> pulmonary HTN, RV dysfunction, chest pain, low bp, hypoxemia 2) Decreased Alveolar Perfusion: increased dead space (increased V/Q) --> hypoxemia and hypocapnia. Reflex bronchoconstriction --> wheezing 3) Loss of surfactant: atelectasias, alveolar edema and bleed --> SOB, crackles, chest pain. Decreased V/Q --> hypoxemia. Irritant and J receptor stimulation --> hyperventilation and SOB
	What are the symptoms of a PE?	- Dyspnea - Pleuritic chest pain - Cough - Hemoptysis - Syncope
	What are the risk factors for DVT/Pulmonary embolism? Please give examples of each.	1) Venous stasis: immobility, heart disease, pregnancy 2) Vein wall disease: prior DVT, pelvic, hip, leg fracture or surgery 3) Hypercoagulable states: malignancies, estrogen, nephrotic syndrome, protein C/S deficiencies, factor V leiden, homocysteinemia, prothrombin gene mutation, high factor levels, antiphospholipid Ab
	What is the gold standard to diagnosis PE and what is its disadvantage?	Pulmonary angiogram; cannot perform with renal failure (contrast media...think about it!)
	What is a ventilation/perfusion scan used for and what are its disadvantages?	Used for PE dx Disadvantages are it requires cooperation and cannot be done in pregnant women
	What is a spiral CT angiogram and what are its disadvantages?	Used for PE dx May miss small peripheral emboli Cannot use in renal failure
	What is a lower extremity ultrasound used for?	A proxy to start anticoagulation in suspected PE.
	What are the neurotransmitters present in the wakefulness state?	Glutamate (RAS) ACh NE DA Histamine Hypocretin
	What are the neurotransmitters present in the sleep state?	GABA Serotonin Adenosine
	How many minutes or hours is a sleep cycle?	90 - 120 minutes (1.5-2 hours)
	In which stage(s) of sleep do you spend the most time in? What are some characteristics of this stage?	Stage 2 - 40-50% of total sleep time EEG: slower and higher amplitude, sleep spindles (12-14 hz), k-complexes (double negative waves)
	What stage(s) is considered regenerative? What are characteristics of this stage?	Stage 3/4 - Deep sleep EEG: high amplitude, slow (1-3hz)
	You come into a patients room and you read a low voltage, high frequency printout on the EEG. On the EMG, you see the pt. is atonic. What stage of sleep is this pt. in?	REM - Stage 4! Low voltage, high frequency = looks like wakefulness but EMG is atonic.
	What are the daytime symptoms of obstructive sleep apnea?	- Tiredness upon awakening, morning HA, excessive sleepiness, loss of libido/impotence. - MVA, work accidents, school/work problems, social embarassment, marital problems, memory/concentration trouble, depression
	What are the risk factors of obstructive sleep apnea?	Age Obesity M>F 2:1 Upper airway obstruction Craniofacial anomalies Medications Alcohol Smoking Genetics
	What are some physical exam presentations of obstructive sleep apnea?	Short, fat neck Obesity Upper airway narrowing (large tonsils, enlarged uvula, long soft palate) Micrognathia/retrognathia
	What are the polymnographic findings of a person with obstructive sleep apnea?	- Apneas often >30 per hour; 5-10 considered NOT normal - Terminated by arousal - Often occur over 50% of sleep time - Decreased stage 3/4/REM
	What are the acute clinicopathologic effects of sleep apnea?	Brady/tachyarrhythmias
	What are the chronic clinicopathologic effects of sleep apnea?	Systemic HTN Pulmonary HTN CHF MI CVA Hypercapnic respiratory failure
	What is the therapy of obstructive sleep therapy?	- Discontinue meds/EtOH - Weight loss - Tennis ball on back (wtf?) - Nasal CPAP (mask over face that provides positive pressure air to push past obstruction) - Surgical correction: uvulopharyngoplatoplasty or tracheotomy
	What is narcolepsy and what do narcoleptics experience when it manifests?	Narcolepsy is due to sudden onset of REM sleep. Patients experience cataplexy, hypnagogic hallucinations, sleep paralysis, and sleep attacks.
	What are the multiple sleep latency criteria for narcolepsy?	- Mean sleep latency < 8 min. - > 2 sleep onset REM periods during naps - No other apparent cause, such as sleep deprivation
	What is the pathophysiology of narcolepsy?	- Defect in the prepro-orexin gene that codes for orexin-A, orexin-B, hypocretin-1, and hypocretin-2. - These proteins bind to ox1/ox2 receptors to promote wakefullness and supress sleep and REM
	What are the abnormalities in cataplexy?	- NO defect in prepro-orexin gene - Loss of orexin producing neurons - CSF orexins decreased
	What are the treatments for narcolepsy?	- Behavioral: structured sleep schedule with naps, avoiding heavy meals, physical activity during day - Pharmacological: for sleep attacks modafinil, methylphenidate, dex-amphetamine, gamma hydroxybutyrate. For cataplexy, clomipramine, fluoxetine, gamme hydroxybutyrate, venulfaxine - Psychosocial
	What two spinal tracts are responsible for pyramidal movements?	Corticospinal and corticobulbar tracts.
	Where do pyramidal movements originate from in the cortex?	Motor, premotor, and sensory cortex
	Which tracts modify pyramidal movements?	Reticulospinal, tectospinal, and vestibulospinal tracts.
	What is the effect of a lesion to the pyramidal motor system?	Upper motor neuron (central) paralysis.
	Where does the extrapyramidal motor system originate from?	Basal ganglia and cerebellum.
	T/F: The extrapyramidal motor system links directly to the pyramidal system.	FALSE Links INDIRECTLY to pyramidal system via thalamus and cortex
	In the extrapyramidal motor system, what does the basal ganglia do? How about the cerebellum?	- Basal ganglia: initiation and planning of movement - Cerebellum: monitors, smoothes, and terminates movements * No direct initiation of movements
	Lesions to the extrapyramidal motor system (basal ganglia and /or cerebellum) lead to what?	- Basal ganglia: bradykinesia, lead pipe rigidity - Cerebellum: ataxia
	List the physical presentations of upper motor neuron (central) weakness.	- Weakness (hemi-) - Hyperreflexia - Unilateral clasp - knife spasticity, "rigidity" - Babinski's sign - May see spontaneous spasms - Anatomic associations: LE (external rotation), UE (decreased arm swing, internal rotation when extended), Facial (spares forehead, eye wider, nasolabial fold flat)
	What are the normal anatomical movements of babinski's sign? What about abnormal?	- Normal: flexion of hip, knee, and dorsiflexion of ankle, dorsiflexion of toes. - Abnormal: "upgoing" toes
	Pt. presents with trouble with language, spatial attention, touch recognition, and vision. Where is the lesion localized?	Cerebral cortex
	Pt. comes in with equal UE/LE weakness. He has no other cranial nerve or cortical symptoms. Where is the lesion located?	Internal capsule
	Pt. presents with deafness in left ear, absent abduction of eyes, b/l facial paralysis, cannot swallow or elevate palette, and can't clench jaw. Where is the lesion located?	Brainstem
	Pt. comes into the ER with bowel, bladder, and sexual dysfunction. He also can not move or feel any stimuli in his legs upon PE. His H&N are not involved. Where is the lesion located?	Spinal Cord
	What are the physical characteristics of a lower motor neuron (peripheral) weakness?	- Weakness (lol) - Muscle atrophy - Fasciculations and fibrillations - Decreased/absent reflexes - Flaccidity (decreased tone) - Cramping
	Which nerves in the spinal cord are damaged in a LMN (peripheral) weakness?	Anterior horn cells to the muscle
	What is the pathophysiology of decorticate rigidity and its clinical presentation?	Pathophys: Lesion in upper midbrain --> disinhibition of red nucles Presentation: UE flexed, LE extended
	What is the pathophysiology of decerebrate rigidity and its clinical presentation?	Pathophys: Lesion in upper pons --> destruction of rubrospinal tract Presentation: UE extended, LE extended
	Compare and contrast the clinical presentation of decorticate and decerebrate rigidity.	Both show LE extension Decorticate rigidity: UE Flexed Decerebrate rigidity: UE Extended
	What are the causes of spinal cord lesions?	- Trauma - Ischemia - Bleed - Tumor - Demyelination - Infection
	Which spinal cord level do these areas correspond with? Subclavicular, nipples, umbilicus, anterior thong, and genitals	C4 - subclavicular T4 - nipples T10 - umbilicus T12 - anterior thong S2/3 - genitals
	What are the spinal cord levels for these deep tendon reflex landmarks: biceps, triceps, patellar, and ankle?	C6 - Biceps C7- Triceps L4 - Patellar S1 - Ankle
	Compare and contrast UMN and LMN weakness in the following areas: location, muscle size, reflexes, fasciculations, and tone.	- Location: UMN in Cortex --> SC, LMN in Ant. horn cell --> Muscle - Muscle Size: UMN is normal, LMN is atrophic - Reflexes: UMN is increased, LMN is decreased - Fasciculations: UMN is absent, LMN is present - Tone: UMN is "clasp-knife" spasticity, LMN is decreased/flaccid
	What is axonal degeneration and what are its etiologies?	Toxic injury to neurons that is symmetric and affect the longest fibers first. Etiologies: EtOH, DM, PB, paraneoplastic
	What is ischemic degeneration and its etiologies?	Loss of peripheral vascular or vaso nervorum blood supply that causes an asymmetric neuropathy. Etiologies: DM, pressure induced neuropathies, vasculitis
	What is demyelination and its etiolgies?	Immune mediated injury to myelinated fibers that leads to symmetric loss of motor, sensory, and DTRs. Etiologies: Guillain Barre syndrome
	Compare and contrast axonal degeneration, ischemic, and demylenation neuropathies in terms of their symmetry.	Symmetric: Axonal degeneration and demyelination neuropathy Asymmetric: Ischemic neuropathy
	Pt. comes in with ascending weakness, peripheral sensory loss, and loss of reflexes. A LP was ordered and it was found that the CSF had increased protein. What does this patient have?	Guillain-Barre syndrome
	What is the pathogenesis of Guillain-Barre?	Immunologic attack on peripheral myelinated fibers
	What are the causes of Guillen-Barre Syndrome?	Campylobacter jejuni, other infections, post-vaccianations
	Pt presents with weak triceps and DTR. The area between his thumb and 1st finger is numb. When asked to extend his wrist, he says he cannot. What affected nerve is causing his symptoms?	Radial
	Pt. comes in saying that he can't "feel his foot". Upon PE, the patient has no tactile/pain/vibratory sense and he cannot flex his foot. What affected nerve is causing his symptoms?	Peroneal nerve
	Pt. comes to your office complaining of pain/numbness in his thumb and first two fingers. On PE, you see that there is muscle wasting around his thumb. What affected nerve is causing his symptoms?	Median nerve
	At a BBQ party, a friend approaches you on crutches and states that she has been having pain/numbness on her lateral thigh. She states that she can't move her affected leg. What affected nerve is causing her symptoms?	Lateral femoral cutaneous nerve
	What are the causes, characteristics, and locations of plexopathies?	- Causes: Trauma, cancer, radiation therapy - Characteristics: Multiple roots, dermatomes, and myotomes - Locations: Cervical, brachial, lumbosacral
	What are the etiologies of muscle motor weakness?	- Inflammation: dermato/polymyositis, inclusion body myositis - Abnormal proteins: muscle dystrophies - Toxins - Metabolic: High Ca, low K/glucose, hyper/hypothyroid - Neurmuscular junction: Myasthenia gravis, Lambert-Eaton
	What are the clinical manifestations of muscle motor weakness?	- Proximal > distal muscle weakness (NOT neuropathy) - Muscle pain if inflammatory - No sensory loss - Preservation of reflexes
	A pt. comes into the ER falling over himself and altered speech. When you examine him, you notice that his balance is worse when he closes his eyes. His muscle strength is good. What is this clinical appearance called?	Ataxia
	What are the causes of ataxia?	- Proprioceptive defect - Vestibular defect - Cerebellar defect
	What is station? What are its components? How do you test it?	- Station is the ability to maintain an erect unsupported posture - Components: Muscle proprioceptions (spindle fibers), vestibular nuclei, cerebellum (glocculonodular node and vermis), and vision - Test with Romberg
	What are the functions of the cerebellum?	- Vestibular interaction: Posture, eye movements, which way is down - Frontal lobe: compares motor program with result - Muscle: coordinates agonists and antagonists
	What are the cerebellar dysfunctions?	- Ataxia - Dysmetria (diagnostic!): Inaccurate targeting of movement - Dysdiadochokinesia: abnormal rapid alternating movements - Dysynergia: Lack of coordination between various body segments; loss of postural maintenance - Nystagmus - Action/intention tremor (diagnostic!)
	What are the ACUTE causes of cerebellar dysfunction?	EtOH, drugs, stroke, infection, MS
	What are the CHRONIC causes of cerebellar dysfunction?	Hereditary spinal ataxias, tremors, EtOH degeneration, MS
	What makes up the striatum?	Caudate + putamen
	T/F: One of the characteristics of basal ganglia dysfunction is weakness.	FALSE
	What motor symptom do you see when there is a lesion in the substantia nigra?	Bradykinesia - slow movement
	What motor symptom do you have see when there is a lesion in the subthalamic nucleus?	Ballismus - a type of involuntary movement in which one violently flings or jerks a limb (or limbs) in an uncoordinated manner
	What happens to movement when there is more dopamine than acetylcholine? More acetylcholine than dopamine?	Dopa > Ach: Hyperkinetic movement Ach > Dopa: Hypokinetic movement
	What are the characteristics of a tremor?	- To-and-fro oscillations around a joint - Regular or irregular - Predictable and simple
	Pt. comes in complaining of tremors. On PE you notice that his tremor stops when you ask him to point to an object. What disease do you think he has?	Parkinsonisms - tremors get better with intentional action
	A patient comes in complaining of tremor. Upon PE, you see that his tremor gets worse when he points to an object. What disease do you think he has?	Cerebellar disease (midbrain stroke)
	A pt. comes in complaining of tremors. You notice that he struggles to sit up straight and that he tremors when trying to do so. What diseases are you thinking about?	- Exaggerated physiologic tremor (seen with increased sympathetic tone) - Essential tremor (seen with normal sympathetic tone)
	What are the etiologies of a resting tremor? How do you treat?	Etiologies - 1) Parkinsonisms - Parkinson's disease, heavy metal toxicity (Fe/Cu), Drug (MPTP) 2) Midbrain stroke Treatment - Dopamine agonists
	What are the etiologies of an intention tremor? What is the treatment?	Etiology - 1) Cerebellar disease: EtOH, trauma, stroke, tumor, degeneration, MS 2) Midbrain stroke Treatment: Physical therapy
	What physical examination techniques would you use to distinguish a postural tremor?	- Outstretched arms and fingers - Tongue protrustion
	What are the etiologies of a postural tremor? How do you treat?	Etiology - 1) Exaggerated physiologic tremor: Catecholamine xs (endocrine, drug induced, stress) 2) Essential tremor: cause unknown, 50% inherited Treatment: Beta blockers, EtOH (!), primidone
	List the tremor frequency for resting, intention, and both types of postural tremors.	Resting: 4-6 Hz Action: 3-4 Hz Exaggerated Physiologic: 10-12 Hz Essential: 4-10 Hz
	What is the pathophysiology of chorea?	- Dopamine xs in striatum (loss of Ach) - Estrogen effect (mild)
	What are the etiologies of chorea?	- Huntington's disease - Syndenham's chorea (acute rheumatic fever) - Cerebral palsy - Pregnancy, Wilson's disease - Drugs: OCP's neuroleptics, levodopa, stimulants, anticonvulsants, antiepleptics
	How do you treat chorea?	Dopamine antagonists
	What are dystonias?	- Sustained, involuntary contractures - Focal: Cervical (torticollis), fingers (writer's cramp), orbicularis oculi (blepharospasms) - Segmental: 2 or more body parts - Generalized
	What are the etiologies of dystonias?	- Often occupational, worse with stress - Some focal are hereditary - Generalized may be due to central lesions
	How do you treat dystonias?	- Anticholinergics - Botulinum toxin injections
	What is the pathophysiology of Huntington's disease?	Defective huntingtin protein (chromosome 4) --> degeneration of cholinergic and GABA-ergic cells in basal ganglia --> relative excess of dopamine
	What are the physical manifestations of Huntington's disease?	- Middle age onset - Chorea - Violent outbursts, psychosis, withdrawal
	How do you treat Huntington's disease?	- Dopamine antagonists - Genetic Screening
	What is the pathogenesis of Tardive dyskinesia?	Chronic (>6 weeks) exposure to dopamine antaganists --> hypersensitive striatal dopamine receptors
	What are the clinical manifestations of Tardive dyskinesia?	- Orofacial repetitive movements - Limb and trunk involuntary movements
	How do you treat Tardive dyskinesia?	- Discontinue neuroleptic - Reserpine
	What is hemiballismus? What is its pathophysiology? How do you treat?	- Violent, sudden, large amplitude, unilateral gyrations - Pathophysiology: Stroke in subthalamic nucleus - Tx: Dopamine antagonists, usually resolves in several months
	What are tics? What is the pathophysiology? How do you treat?	- Brief, sterotypic, supressible. May be vocalizations, swearing or gestures. Worse with stress. - Pathophysiology: Unclear, dopamine xs causing disinhibition of limbic system - Tx: Time, dopamine antagonists
	What are the classical characteristics of parkinsonism?	- Bradykinesia - Tremor (4-6 Hz, initially unilateral) - Cogwheel rigidity - Loss of postural reflexes
	What are the etiologies of Parkinsonisms?	- Death of dopaminergic neurons in substantia nigra - Dopamine antagonists
	What therapies are used to treat Parkinsonism?	- L-dopa, Dopamine agonists - Amantidine (blocks DA re-uptake) - COMT inhibitors - Selegeline (MOA inhibitor) - Deep brain stimulation of subthalamic nucleus
	Describe the pathophysiology of myasthenia gravis.	- Autoimmune destruction of nmj AchRs - Antibody binds and induces cell mediated attack --> accelerated loss of AchRs - Anti-muscle-specific tyrosine kinase antibody
	What are the clinical anifestations of myasthenia gravis?	- Weak: proximal muscles, eye lids and EOM, cranial nerves, diaphragm - 15% have a thyoma
	How do you diagnose myasthenia gravis?	- After administering acetylcholinesterase inhibitor, you see improvement - EMG: Decrement in action potentials with repetitive stimulation - Assay for anti-ach receptor antibodies (+ in 80-90%) - Assay for anti-muscle specific tyrosine kinase (+ in 5%)
	How do you treat a patient with myasthenia gravis?	Long acting Ach inhibitors, steroids, cytoxics, thymectomy, plasmapheresis, IVIG
	What is the pathophysiology of Lambert-Eaton Myasthenic Syndrome?	Antibodies against P/Q-type presynaptic voltage-gated calcium channels (50%-80%)
	What are the clinical manifestations of Lambert-Eaton Myasthenic Syndrome?	- Weak: proximal muscles, leg>arms, less common cranial nerves, and eye changes - Autonomic dysfunction - Worse in morning and improve throughout day - 50-60% have a cancer (small cell lung ca), others with autoimmune Ab - Symptoms hopefully predate the tumor discovery
	What is the diagnosis for Lambert-Eaton Myasthenic Syndrome?	- Improvement after Ach inhibitor challenge - EMG: INCREASE in action potentials with repetitive stimulation? - Assay for anti-voltage gated calcium channel (+) in 50-95%
	How do you treat Lambert-Eaton Myasthenic Syndrome?	- Treat underlying cancer - Plasma exchange +/- IVIG - 3,4 - diaminopyridine (DAP) increase release of Ach - Prednisone, azathioprine
	Pt. comes in with muscle weakness. You suspect an autoimmune process. You order an EMG and look at the results. What would you expect to see if he is suffering from Myasthenia Gravis?	- Decreased EMG - In Lambert-Eaton, it is INCREASED
	What are the etiologies of myotonic dystrophy?	- AD mutation - DM1: CTG trinucleotide repeats --> abnormal RNA - DM2: Expansion of CCTG tetranucleotide repeat --> Abnormal RNA
	What is the pathophysiology of myotonic dystrophy?	DM1/DM2 tri/tetra-nucleotide repeats --> abnormal RNA --> accumulation in nucleus --> alter expression of other genes such as: 1) Muscle Cl channel --> myotonia 2) Insulin receptor --> hyperinsulinemia 3) Cardiac troponin T --> arrhythmias and LV abnormalities
	What is the most common muscular dystrophy in Caucasians?	Myotonic dystrophy
	What are the clinical manifestations of myotonic dystrophy?	- Adolescent or early adult onset - Myotonia, weak/wasting face and distal limb muscles - Frontol balding (ment), cataracts, cardiomyopathy - Endocrinopathies (interfetility in women, hyperinsulinemia, testicular atrophy) - Low IQ/Dementia, sensitivity to sedatives - EMG: myopathic potentials
	How do you treat myotonic dystrophy?	- Treat symptoms - Membrane stabilizers (mexiletine, phenytoin, etc)
	What is the pathophysiology of Duchenne Muscular Dystrophy?	- Variable mutations of dystrophin gene at Xp21 locus (X-linked rec) - Dystrophin protects sarcolemmal membrane from degradation by intracelullar proteases, absence --> muscle necrosis, Ca influx
	What are the clinical manifestations of Duchenne Muscular Dystrophy?	- Male onset at 2-3 y.o., wheelchair in teens, death in 20s - Proximal weakness with calf pseudohypertrophy (fat/fibrosis/inflammation) - Protruberant abdomen, lumbar lordosis - Cardiac: CHF, arrhythmias - CPK elevated - EMG: myopathic small polyphasic potentials
	How do you treat Duchenne Muscular Dystrophy?	- Treat symptoms - Prednisone slows progression
	What is Gower's sign?	Due to muscle weakness, the patient has to use their arms to "walk" into an upright position.
	What is the pathophysiology of polymyositis/dermatomyositis?	- T-cell mediated muscle injury - Secondary Ab formation (Jo-1, Mi-2, SRP)
	What are the clinical findings of polymysitis/dermatomyositis?	- Symmetric proximal muscle weakness with pain - Elevated plasma muscle enzymes - Myopathic changes on electromyography - Characteristic muscle biopsy abnormalities and the absence of histopathologic signs of other myopathies
	What are the signs, etiology, and associations of dermatomyositis?	- Signs: Gottron's papules and heliotrope eyelids - Etiology: Humorally mediated vasculitis - Associations: Adult form associated with malignancies
	What is the therapy of polymyositis/dermatomyositis?	Steroids, cytotoxics, plasmapheresis, IVIG
	Describe the epidemiology of multiple sclerosis.	- F>M 2:1, W > B, less nearer the equator - 10x first relative increased risk - 30% twin concordance
	What is the pathophysiology of multiple sclerosis?	- Cell-mediated immune destruction of central myelin --> decreased axonal conduction --> axonal block
	What are some visual manifestations of multiple sclerosis?	- Optic neuritis - Diplopia, internuclear ophthalmoplegia
	What are some non-visual clinical presentations of multiple sclerosis?	- Focal weakness, parasthesias, ataxia - Deficits occur over many minutes to hours (not stroke!)
	What are the two time-courses of multiple sclerosis?	- Relapsing-remitting: 85% cases; <40 y.o.; long disease free intervals; can become progressive - Primary progressive: slow, constant progression
	How do you diagnose multiple sclerosis?	- Clinical: Young age; 2 separate neurologic regions - Imaging: Typical MRI plaques - CSF: Increased protein w/o increased WBCs; Abnormal proteins (IgG, myelin basic protein, oligoclonal banding) - Evoked responses: visual, brainstem, auditory, somatosensory
	What can mimic a stroke?	- Altered blood glucose - Mass lesions - Infection/inflammation - Trauma - MS - Post-ictal state
	What are the frequency of the different types of stroke?	- Ischemic: 70% - Hemorrhagic: 25% - Other (vasculitis/arterial dissection/cerebral venous thrombosis): 5%
	What happens in an ischemic infarction at 50cc blood/100g of tissue/minute?	Reversible injury! Anaerobic metabolism of glucose - Increased lactate production - Less efficient ATP production - Less efficient Na/K ATP pump - Na accumulates in cells --> water is drawn into cell
	What happens in an ischemic infarction at 20cc blood/100g of tissue/minute?	Irreversible injury! - Glutamate release and receptor activation - Ca influx - Activates intracellular phospholipases and proteases - Cellular destruction and inflammation - Edema peaks at 72h
	What are the risk factors to cardioembolic strokes?	- A-fib - Dilates cardiomyopathy - Mural Thrombus - Endocarditis - Patent foramen ovale
	What are the most probable locations of a seizure?	- Motor > sensory - Temporal > frontal > occipital > parietal
	Where are seizures NEVER found?	Nuclei, white matter, cerebellum
	What are the top 3 causes of seizures?	- Idiopathic (60%) - Vascular/stroke (15%) - Other (10%)
	What is the path a generalized seizure takes?	Thalamus --> cortex
	What ALWAYS happens in a generalized seizure?	Loss of consciousness
	What are the subtypes of a partial/focus seizure?	1) Simple (consciousness normal) 2) Complex (consciousness altered) 3) Secondary generalized (begins as partial --> generalized)
	How do you diagnose a seizure?	- HISTORY!: the seizures are always the exact same type. - EEG (sleep): 80-85% (+) x1, >90% with 2 - Image: look for structural cause
	What is the progression of a generalized, tonic-clonic seizure?	Aura --> tonic --> clonic --> relaxation --> paralysis
	What are some EEG markers of an epileptiform foci?	- Spike (70 msec) +/- wave - Sharp waves (70-200 msec)
	What are the predispositions to epilepsy?	- Birth injury - Trauma - Encephalitis/meningitis - Fever - Stroke - Drugs: Cocain, EtOH - Hereditary
	What are the exogenous causes of epilepsy?	- Sleep deprivation - Hypo/hyperglycemia - Hypo/hypernatremia - Medications: Beta-lactams, lidocaine
	What is the definition of status epilepticus?	- Single seizure > 30 minutes OR - >=2 seizures without full recovery of consciousness in between
	What are the consequences of status epilepticus?	- Neuronal damage after 30 min - Death in 5-25%
	How do you treat status epilepticus?	- Protect airway, ventilation - IV anti-convulsant: diazepam, midozalam, phenytoin, phenobarbitol, valproic acid - General anesthesia
	What is the function of GABA receptors? Describe what drugs potentiate and block these receptors.	Function: Inhibitory Potentiated: Benzodiazepines, barbituates Blocked: B-lactams, picrotoxin
	What is the function of Glutamate receptors?	Function: Excitatory
	What is the pathogenesis of seizures?	- Paroxysmal depolarization shift of membrane potential - Action potential bursts --> synchronous firing of neurons --> seizure activity with EEG spike
	What is a Jacksonian seizure?	Progressive motor seizure
	What is a reflex epilepsy?	Sensory trigger of seizure.
	What is kindling?	Recurrent stimulation causing seizures.
	What are the anticonvulsant mechanisms of action? Big categories.	- Increase GABA inhibition - Glutamate receptor blockade - Suppression of Na channel - Unknown: Valproate, Felbamate
	What is the epidemiology of migraine headaches?	10% of population F>M 3:1
	What is the pathophysiology of migraine headaches in relation to the trigeminal n.?	- Unstable trigeminovascular reflex --> antidromic stimulation of trigeminal n --> release of substance P and calcitonin gene-related peptide --> pain and vasodilation
	Describe the four ways Scripture grounds obedience to the moral law. Give at least one example from Scripture each.	A moral command may be justified by an appeal to the: 1.) proper authority of the source of the command (Lev 24:23..."Thus the people of the Lord did as the Lord commanded Moses") 2.) goodness of the divine character reflection in the divine command (Matt 5:48 "You therefore must be perfect as your heavenly Father is perfect.") 3.) created nature of the recipient of the command (Gen 9:5-6. "And for your lifeblood I will require a reckoning... from his fellow man I will require a reckoning for the life of man... for God made man in his own image") 4.) motivation of the recipient of the command (Ex 22:20 "I have brought you out of Egypt)
	Other than the unstable trigemino-vascular reflex and decreased serotonin, what other migraine headache pathophysiologies are there?	- Neurovascular inflammation --> cortical hyperexcitability - Spreading depression of Leao: (+) wave = aura
	How do you prevent migraines?	- Indications - Antihypertensives: Beta-blockers (!), calcium channel blockers - Antidepressants: TCA's (!) such as amitryptyline - Anticonvulsants
	How do you treat migraines?	- NSAIDs - Triptans: Serotonin agonists (-triptan)
	How do you define the classic migraine?	Migraine WITH aura At least 2 attacks with both of: - At least 3 of: fully reversible aura, 1 aura sx gradual over 4 mins or 2 in succession, aura not >60 min, HA during aura or within 60 in - No organic cause
	How do you define the common migraine?	Migraine WITHOUT aura At least 5 attacks with all of: - HA for 4-72h if untreated - HA with 2 of: unilateral, pulsating, mod-severe, increases by activity - During HA one of: N+v, photophobia/phonophobia - No organic cause
	What is common between the common migraine and the classic migraine?	HA and NO organic cause.
	What is the epidemiology of cluster headaches?	M > F 25-40 y.o.
	What are the clinical manifestations of a cluster headache?	- Rapid onset, UNILATERAL, eye or temple - Ipsilateral red eye, runny nose, +/- Horner's - Prefer to stay active (NOT migraine) - Sensitivity to EtOH - Lasts 1-3 hours, occurs in clusters over a period of weeks
	What is the pathophysiology of a cluster headache?	- Hypothalamic mediated vasodilation of the cavernous sinus portion of the carotid - Hyperactivity of PNS
	How do you treat a pt with cluster headaches?	- Abortive: O2, ergots, triptans - Prevention: verapamil, prednisone, lithium, ergots
	What is a tension-type headache?	- bilateral, pure pain with no other symptoms - Most common headache syndrome - common multidrug Rx history
	What is a chronic daily headache?	- Medication overuse and withdrawal - Examples: NSAIDs, narcotics, barbiturates, caffeine, benzodiazpines
	What is a subarachnoid headache?	- Worst HA ever - Altered consciousness - Stiff neck
	What is temporal arteritis?	- >50, ESR > 50, tender scalp, fever, anemia, vision loss
	What is pseudotumor cerebri?	- Idiopathic intracranial hypertension - Inadequate clearance of CSF produced - Obese women, 20-44, chronic daily HA, papilledema
	What causes a low pressure headache?	LP, trauma, surgery
	Rank the types of memory types from hardest to easiest to lose.	Procedural > Semantic > Episodic
	Rank the type of episodic memories from hardest to easiest to lose.	Remote > Recent > Immediate (Working memory)
	Describe the Circuit of Papez.	- Used for creation of memories - Hippocampus --> fornix --> mammillary bodies --> mamillothalamic tract --> thalamus --> cingulate gyrus --> hippocampus via cingulum
	T/F: The hippocampus is the gateway, storage, and retrieval system for memories.	FALSE It's only the gateway.
	What system is required for the formation of new memories?	Limbic system
	What are the three categories that cause memory loss?	- Failure to create: hippocampus/circuit of Papez lesion - Failure to store: Loss of neurons in Alzheimer's - Failure to retrieve: Alzheimer's
	What is the pathophysiology of Alzheimer's Disease?	- Idiopathic loss of cholinergic neurons in CNS - Plaques and tangles - Predominantly temporal and parietal
	How do you treat Alzheimer's disease?	Anticholinesterases
	Pt. comes into the ER with a head injury. He is confused and disoriented. Throughout your H&P, he keeps asking where he is even though you told him multiple times. What is this patient suffering from?	Transient global amnesia FYI: Pathophysiology is unclear and there is no tx.
	What are the 3 important viral genes and their products?	- Gag: P24 (core protein) - Pol: Protease (cleaves gag and pol), RT - Env: Gp 120, Gp 41
	What is the probability of HIV transmission in the following:Transfusion, Mother --> infant on ZDV, Needle sharing, needle stick	Transfusion: 95% Mother --> infant: 26% Needle Sharing: 0.7% Needlestick: 0.3-0.4%
	What is the probability of HIV transmission in F --> F sex.	Virtually 0. lol.
	Between men and women, which have a greater # of AIDS cases?	Men
	Between what ages are the most AIDS cases are diagnosed?	30-44; peaks between 35-39
	In AIDS, what is the most frequent method of transmission in males?	Male to male sexual contact (59%) followed by high-risk heterosexual contact (17%)
	In AIDS, what is the most frequent method of transmission in females?	High-risk heterosexual contact (73%) followed by injection druge use (24%)
	Over the past 25 years, compare and contrast the trend of getting AIDS from male-to-male sexual contact with high-risk heterosexual contact.	Male to male sexual contact is decreasing/plateau-ing while high-risk heterosexual contact is increasing
	List the estimated frequencies of persons living with AIDS by race/ethnicity.	Blacks > whites > hispanics > asian americans
	What is the clinical spectrum of HIV/AIDS?	Acute retroviral syndrome --> asymptomatic infection --> severe immunodeficiency and AIDS
	What latent infections reactivate in a patient with AIDS?	TB and VZV
	In an AIDS patient, a viral load of 100 corresponds with what CD4 count? What about a viral load of 100,000?	VL 100 = CD4 ~ 300 VL 100,000 = CD4 ~ 200
	What is the CD4 level in the AIDS surveillance case definition?	CD4 < 200 or 14%
	Which neoplasia are associated with AIDS?	- Invasive cervical ca - Kaposi's sarcoma - Lymphoma: high grade or primary CNS
	T/F: PTH only leads to bone resorption to increase serum calcium levels.	FALSE! With intermittent, high doses of PTH, bone formation will occur (counterintuitive). Tx option for people with osteoporosis.
	How do granulomatous diseases cause hypercalcemia?	Any disease that forms granulomas will have giant cells. These giant cells can 1-hydroxylate 25-VitD and cause high concentrations of this active form. Calcium is then used to wall off the disease. XS calcium can escape into serum and cause hypercalcemia.
	What is pseudohypoparathyroidism?	Absence of PTH receptor on tissue. Pt. has high PTH and low serum calcium.
	How does the radioactive iodine uptake differ between Grave's and infection induced hyperthyroidism?	Grave's = HIGH uptake Infection = Low uptake
	What is Jod Basedow phenomenon?	Hyperthyroidism after iodine is given to deficient patient. Clinicians use a lot of iodine as a diagnostic, so we can create this often.
	What lung volume, i.e. FVC, INCREASES in obstructive pulmonary diseases?	RV and TLC (or it can remain normal)

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