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38 Cards in this Set
- Front
- Back
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Difference between Partial and Generalized Seizures
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Partial Seizures involve only one area of the brain. Can generalize, but secondarily.
Generalized Seizures are due to diffuse high frequency neuronal firing. Multiple types. |
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Difference between Simple Partial Seizure and Complex Partial Seizure
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Change in Consciousness
Simple - No Change Complex - Change |
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Difference between Nephritic and Nephrotic Syndrome
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Nephritic Syndromes are associated with primarily with hematuria and RBC casts. Proteinuria<3.5g/day, azotemia are also present.
Nephrotic Syndrome is characterized by massive proteinuria (>3.5g/day) and edema. |
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Difference between Migraine and Cluster and Tension Headaches
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Migraines are unilateral and can be associated with phonophobia, photophobia, and aura (visual, sensory, speech disturbance). <72 hours. F>M
Tension Headaches are unilateral and are associated with periorbital pain and ipsilateral lacrimation, rhinorrhea, and Horner's syndrome. M>F Tension headache - bilateral steady pain >30 min. |
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Difference between Type I and Type II Diabetes
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Type I - Insulin-dependent Diabetes Mellitus. Due to ↓ PRODUCTION of INSULIN. Younger onset. More commonly ass'd with DKA due to loss of inhibitory effect on glucagon.
Type II - Non-Insulin Dependent Diabetes Mellitus - Due to ↓ SENSITIVITY to INSULIN (of insulin receptors). Older onset, associated with Obesity. |
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Difference between Treatment for Type I and Type II Diabetes
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Type I Treatment Paradigm - Low-sugar diet & Insulin
Type II Treatment Paradigm - Weight Loss (Diet & Exercise), Oral Hypoglycemics, and then Insulin-Replacement (if necessary) |
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Difference between Upper Motor Neuron signs and Lower Motor Neuron signs
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UMN: ↑ reflexes, ↑ Tone, + Babinski (↑going toe), spastic paralysis
LMN: ↓ reflexes, ↓ tone, (-) Babinski, atrophy, fasciculations **WEAKNESS is not diagnostic of either, it is present in BOTH |
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Horner's Syndrome Triad
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Ptosis, Miosis, Anhydrosis IPSILATERAL TO LESION
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Parasympathetics and Sympathetics Begin...
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In the HYPOTHALAMUS
NOT CN nuclei. |
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Path of Facial Nerve
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See charts... probably good to know
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Cranial Nerves that carry Parasympathetics and what ganglia they use
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See charts... good to know
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Difference between Endolymph and Perilymph in Ear
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Perilymph is like Extracellular fluid. Therefore high in Sodium
Endolymph is like Intracellular fluid. Therefore, high in potassium |
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Difference between Childhood and Adult 1° CNS tumors
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Childhood tumors - primarily INFRATENTORIAL
Adult tumors - Primarily SUPRATENTORIAL |
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Unhappy Triad
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1. MCL Damage
2. ACL Damage 3. Medial Meniscus Damage Common football injury (hit from side with leg extended) |
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ACL versus MCL
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Anterior and Posterior refer to attachment to tibia.
Anterior Drawer Sign = ACL damage Posterior Drawer Sign = PCL Damage |
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Hand Distortions
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Caused by LUMBRICAL FUNCTION.
Loss of lumbricals leads to claw hand All = Klumpke Medial (4th & 5th digits) = Ulnar Lateral (2nd & 3rd digits) = Median |
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Differences between Skeletal Muscle Contraction and Smooth Muscle Contraction
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Skeletal muscle contraction.
1. Nerve cell depolarized --> Ca influx --> NT Release 2. ACh binds to nicotinic receptor (↑Na) --> Muscle cell depolarization 3. T-tubules carry depolarization to sarcoplasmic reticulum 4. Depolarization causes conf. Δ in DHP receptor 5. DHP receptor coupled to Ryanodine receptor --> Ca release from Sarcoplasmic reticulum 6. Ca binds Troponin C on Actin --. Tropomyosin moves out of binding groove 7. Myosin head binds ATP --> release from actin --> head cocks toward + end --> ATP hydrolyzed --> Myosin binds actin --> release of ADP = POWERSTROKE Smooth Muscle Contraction: 1. Nerve cell depolarized --> Ca influx --> NT release 2. Depolarization of muscle cell 3. Voltage gated Ca channels open 4. Ca binds to CALMODULIN 5. Calmodulin activates MLCK (myosin light chain kinase) 6. Phosphorylated myosin and actin form cross bridges --> Contraction |
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Difference between Type I osteoporosis and Type II osteoporosis
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Type I is POSTMENOPAUSAL. ↓ estrogen --> ↓OPC --> ↑ RANK-RANKL interaction and ↑ osteoclast activation
Type II osteoporosis - Men and women >70 Senile Osteoporosis End result is same, pathophysiology is different. |
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Difference between Osteoarthritis and Rheumatoid Arthritis
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Osteoarthritis
Mechanical damage of articular cartilage due to normal wear and tear. Findings: Subchondral cysts/sclerosis, joint space narrowing, osteophytes ↑ risk with age and obesity Occupation can be hint since it is a disease associated with USE Symptoms: Worse with use; better with rest Rheumatoid Arthritis Autoimmune, inflammatory disorder Autoantibodies against Ig-G (Rheumatoid Factor). Association with HLA-DR4 Findings: rheumatoid nodules, ulnar deviation, subluxation, NO DIP INVOLVEMENT!! Sx: improve with use, worse in morning, SYMMETRIC, systemic symptoms (fever, fatigue, etc.) |
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Difference between Polymyositis and Dermatomyositis
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Dermatomyositis has dermatological findings such as malar rash, heliotropic rash, shawl and face rash
Increase risk of Malignancy! |
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Differences between NSAIDs, Acetominophen, and Aspirin
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NSAIDs
Drugs: Ibuprofen, Naproxen, Indomethacin, Ketorolac Toxicity: Renal Toxicity, Gastric Ulcers, Aplastic Anemia Aspirin Key Idea: essentially NSAIDs + Antiplatelet activity MOA: IRREVERSIBLY blocks COX-1 & 2. Uses: Dose dependent <300 = Antiplatelet activity 300-2400 = Antipyretic (fever) and analgesic (pain) >2400 = Anti-Inflammatory Toxicities: GI upset, Interstitial Nephritis, and Bleeding Acetominophen Key Idea: Acts only on CNS; inactivated in periphery (NO ANTI-INFLAMMATORY properties) Toxicity: Hepatic Necrosis. Acetominophen and metabolites deplete glutathione. Metabolite is directly toxic if not inactivated. (Tx: N-Acetylcysteine) |
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Important Distinctions in Conducting Zone of Lung versus Respiratory Zone
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Conducting Zone - Nose to Terminal Bronchioles. No gas exchange, walls contain smooth muscle. Cartilage in trachea and Bronchi only.
Respiratory Zone - Respiratory Bronchioles to Alveoli. Participates in Gas Exchange, NO GOBLET CELLS. **Pseudostratified Ciliated epithelium from Trachea to Respiratory Bronchioles** |
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Difference Between Type I and Type II Pneumocytes
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Type I - Squamous. 97% of alveolar surface. Thin, perfect for gas exchange.
Type II - clustered, cuboidal cells that secrete surfactant (dipalmitoyl phosphatidylcholine) to ↓ surface tension. ↑ during lung damage. |
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Process of diffusion
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O2 and CO2 diffuse across epithelium (Type I pneumocytes), basement membrane, and vascular endothelium down their concentration ∇. CO2 exits blood into alveoli and O2 exits alveoli into blood.
Therefore anything that damages epithelium, endothelium, increases thickness of cells, etc. can decrease diffusion. |
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Course of Lung Vasculature and Lymphatic Drainage
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Arteries and Bronchioles (Airways) run together. Each Broncopulmonary segment has a 3° bronchiole and 2 arteries in center.
Veins and lymphatics drain along the borders of the segment. |
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Location of Pulmonary Arteries in relation to Mainstem Bronchi
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RALS
Right - Anterior (Pulm. artery ANTERIOR to R. Mainstem Bronchus) Left - Superior (Left Pulm. Artery SUPERIOR to L. Mainstem Bronchus) |
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Difference between Obstructive and Restrictive Lung Disease
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Obstructive
↓ TLC ↓↓ FEV1 ↓ FVC FEV1/FVC <80% (sig. ↓) Air trapping --> ↑ pressure --> premature closure of bronchioles COPD (chronic bronchitis, emphysema (3 types), asthma, bronchiectasis Restrictive Lung Disease ↓ TLC ↓ FEV1 ↓ FVC ↑ FEV1/FVC (>80%) Poor respiratory effort due to muscular or structural defect or lung disease causing poor lung diffusion. |
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Key Principles of Anesthetics
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1. Drugs Must be LIPID SOLUBLE to cross into CNS
2. ↓ solubility in BLOOD = RAPID induction and recover 3. ↑ Solubility in LIPID = ↑ potency (1/MAC) ∴ ↓ MAC = ↑ Potency Ex: N2O has ↓ lipid and blood solubility so it has rapid onset and recovery, but ↓ potency (↑ MAC) Halothane has ↑ lipid and blood solubility, so it has slow onset and recovery, but ↑ potency (↓ MAC) |
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Type IB Antiarrhythmics
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Na+ Channel Blocker and ↑ K+ Channels (Faster Repolarization)
Works on Ischemic/Depolarized Ventricular Tissue. ***DRUG OF CHOICE POST MI VENTRICULAR ARRHYTHMIAS*** |
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Type IC Antiarrhythmics
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Na Channel Blocker (no effect on K+ Channels)
ONLY HEALTHY TISSUE **Antiarrhythmic of LAST RESORT for refractory VENTRICULAR Tachyarrhythmias.** Toxicity is Proarrhythmias, ↑↑↑ POST MI !! |
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Type II & Type IV Antiarrhythmics
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Beta Blockers & Ca Channel Blockers
Primarily Affect NODAL cells. Think NODAL ARRHYTHMIAS |
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Type III AntiArrhythmics
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Used when other Arrhythmics have FAILED.
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2° Messenger Systems
Gs receptor mechanism and receptors which use it |
Receptor --> Gs (GTP-->GDP) --> ↑ Adenylyl Cyclase --> ↑ cAMP --> ↑ Protein Kinase A --> ↑ Phosphorylation of Target Proteins
Receptors which use Gs: β1, β2, D1, H2, V2 |
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2° Messenger Systems
Gi receptor Mechanism and which receptors use it |
Receptor --> Gi (GTP-->GDP) --> ↓ Adenylyl Cyclase --> ↓ cAMP --> ↓ Protein Kinase A activity --> ↓ Phosphorylation of Target Proteins
Receptors which use Gi: α2, M2, D2 |
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2° Messenger Systems
Gq receptor mechanism and which receptors use it |
Receptor --> Gq (GTP-->GDP) --> PIP2 --> Phosphoplipase C --> DAG & IP2.
IP2--> ↑ Ca from SR DAG & Ca --> ↑ Protein Kinase C --> Target Protein Phosphorylation Receptors Which Use It: α1, M1, M3, H1, V1 |
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What is Inotropy and what is the cause of Δ in Inotropy?
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Inotropy is the contractility of the cardiac muscle.
Inotropy is determined by the intracellular concentration of Calcium. Receptor Effects: Increased by B1 receptor activation, Cardiac Glycosides (Digoxin/Digitalis) Decreased by M2 receptor activity, Beta Blockers, ↑ HR (↓ time for Ca to leave cell, so overall ↑ in Ca) |
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What is Chronotropy and what is the cause of Δ in Chronotropy?
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Chronotropy is the HR.
Chronotropy is determined by the rate of SA Node firing which is based off of the # of funny Na channels open. (↑ channels --> ↑ depolarizations --> ↑ HR) Receptor Effects: Increased by B1 receptor activity Decreased by M2 receptor activity, Beta Blockers, Type I Antiarrhythmics, |
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What is Dromotropy and what is the cause of Δ in Dromotropy?
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Dromotropy is the conduction velocity through the AV Node
Dromotropy is determined by the # of Ca channels open during depolarization and # of K channels open during repolarization of AV Node. Receptor/Drug Effects: Increased by B1 receptor activity (↑ Ca channels) Decreased by M2 receptor activity (↓ Ca Channels, ↑ K Channels), Ca Channel Blockers (Verapamil>Diltiazem), Beta Blockers |
