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489 Cards in this Set
- Front
- Back
Describe the pathway of an upper motor neuron. |
When a Neisseria gonorrhoeae infection spreads from the reproductive organs to the liver capsule resulting in acute perihepatitis
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What is the most likely organism to cause infection in patients with indwelling catheters or those with prosthetic joint replacements?
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Staphylococcus epidermidis: gram -, coagulase +, can form BIOFILMS on prosthetics
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What is it called when TB involves the vertebral bodies?
|
Pott's disease or tuberculous spondylitis
- osteomyelitis & arthritis in 2(+) vertebra |
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What are the 4 most popular typical antipsychotics?
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D2 dopamine receptor blockers:
1) Thioridazine 2) Haolperidol 3) Fluphenzaine 4) Chlorpromazine |
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What is the MOA of atypical antipsychotics?
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block 5-HT2 & dopamine receptors
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Why do patients with Chediak-Higashi disease sometimes present with partial albinism?
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This AR disease is characterised by a failure of phagolysosome formation
- melanosomes are derivatives of lysosomes & thus can be dysfunctional as well |
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To what type of infection are patients with chronic granulomatous disease most susceptible?
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Microbes that produce their own catalase (e.g. Staphylococcus & Candida)
- Due to NO NADPH oxidase - Dx: negative tetrazolium dye reduction |
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How do patients with selective IgA deficiency present?
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Sinus & Lung infections due to lack of enough functional IgA in mucous membranes
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What immunodeficiency presents with severe, recurrent bacterial, viral, protozoal, & fungal infections?
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SCIDs b/c of a defect in early stem-cell differentiation
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What is the product of the p53 gene?
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- a transcription factor that regulates apoptosis & prevents defective cells from undergoing division.
- mutation causes uncontrolled cell division |
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What are the products of the BCR1 (ch. 17) & BRCA2 (ch. 13) genes?
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DNA repair products
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What is the product of the APC gene (ch. 5)?
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Membrane cell adhesion products
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What drug is used to prevent chemo-induced nausea/vomiting and has the SE of headache & constipation?
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Ondansterol (5-HT antagonist)
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What is the MOA of metoclopramide?
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- Prokinetic agent that promotes GI motility
- Potent dopamine antagonist that enters the CNS & makes it antiemetic & SE of extrapyramidal (i.e. Parkinsonian-like adverse effects) |
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What is Trimethobenzamide used for?
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- Nausea & vomiting
- MOA = unknown - SE: headache, depression, muscle cramps, dizziness |
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What are the derivatives of the 1st aortic arch?
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Maxillary artery (part of it is derived from this arch)
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Define "hot T-Bone Steak"
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IL1 = fever (Hot)
IL2 = T lymphocyte stimulator IL3 = Bone marrow stimulator IL4 = IgE stimulation IL5 = IgA stimulation |
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What cancers is recombinate IL2 (adesleukin) used to trat?
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Renal cell & Metastatic melanoma
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What are the 3 pathologic stages in RDS?
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1: exudative stage with intra-alveolar hyaline membrane formation
2: proliferation stage with increase in type II pneumocytes & fibroblast 3: fibrotic stage with lung remodeling & fibrosis |
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What anti-hypertriglyceridemia drug is contraindicated in patients with cholesterol gallstones?
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Gemfibrozile b/c fibrates can increase the development of gallstones
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What antihypertensive drugs are most useful for patients with asthma?
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A BEAM: (selective B1-blockers)
- Acebutolol - Betaxolol - Esmolol - Metoprolol |
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What is the CD marker on all lymphocytes of thymic origin
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CD2 is on all helper T-cells, cytotoxic T-cells, & natural killer cells
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What lymphocytes have CD3?
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All CD4 & CD8 cells, but NOT natural killer cells
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What is the T-cell (TCR) receptor?
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alpha/beta heterodimer encoded by genes undergoing V(D)J recombination that is expressed by each clone of the T lymphocyte that gives it antigen binding specificity
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Why does prolonged diarrhea & vomiting cause hyponatremia (& t/f seizures)?
|
1st: Loss of solute & H20 loss
2nd: Hypovolemia induces secretion of ADH (conserves H2O without Na) 3rd: Hyponatremia -> neurologic dysfunction induced by cerebral edema |
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Why does metabolic alkalosis result in hypokalemia?
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More H2O & bicarb are delivered to the distal K-secretory site in the kidney & aldosterone is released = renal loss of potassium
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How does hyperkalemia present?
|
- Weakness progressing to flaccid paralysis
- Metabolic acidosis - Cardiac conduction disturbances by peaked T wave on ECG |
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What is the most common H. influenzae type to cause acute otitis media?
|
NTHi = Haemophilus influenzea nonencapsulated (nontypable):
- 75% of adults & children carry this bac in their nasopharynx - NB: Type B is covered by the childhood vaccine |
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What are the 3 most common causes of acute otitis media?
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1) Streptococcus pneumoniae (aerobic, gram + coccus)
2) Haemophilus influenzea (NTHi) 3) Moraxella catarrhalis (gram -, diplococci) |
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How does a Nocardia asteroides present in an immunocompromised patient?
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lung abscesses & cavitations
- late erosion of blood vessels and dissemination to brain: abscesses - gram +, filamentous, weakly acid-fast Rx: sulfonamides (dihydropteroate synthetase blockers = blocks nucleotide synthesis) |
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What is the MOA of amphotericin B?
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Antifungal that binds ergosterol & membrane pores in the outer membrane
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What fructose metabolism enzyme is missing in patients that experience severe hypoglycemia, vomiting, jaundice, & hemorrhage?
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Aldolase B
- No conversion of fructos-1-phosphate to glyceraldehydes & dihydoxyacetone phosphate - Result: intracellular trapping of fructose-1-phosphate |
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What vasculitis is associated with Hep B infection in 10% of cases?
|
Polyarteritis nodosa:
- NO lung involvement - Livedo reticularis: puplish discoloration skin rash - transmural infalmmation of s/m arteries -> fibrous, thickened vessel wall (each lesion is at a different age) - episodes last a few weeks to moths & <10% relapse |
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What diabetic drug causes GI adverse effects including abdominal cramps, diarrhead, & flatulence? & is contraindicated in cirrhosis & requires liver function monitoring?
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Acarbose: alpha-glucosidase inhibitior
- MOA: decreases hydrolysis & absorption of diaccharides & polysaccharides at the intestinal brush border - Reduces postprandial hyperglycemia |
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What patients cannot be prescribed metformin?
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those with renal insufficiency (b/c of the risk of lactic acidosis)
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Why were 1st generation thiazolidinediones (like troglitazone) taken off the market?
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- Extreme hepatotoxicity
- MOA: sensitizes the peripheral tissues to insulin's action |
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What is lacking in Factor V Leiden disorder?
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Mtation resulting in an arginine-to-glutamine substitution @ position 506 in factor V & is thus resistant to cleavage by protein C
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What should be ruled out in all patients >50 years old that complain of nonremitting, yet, tolerable, flank pain & hematuria without signs of infection?
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Malignancy
- check for renal cell: contrast-enhancing, solid renal mass arising from the renal cortex upon imaging |
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What is the antidote for methanol or ethylene glycol (antifreeze) tox?
|
Fomepizole
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What is the antidote for tricyclic antidepressant tox?
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NaHCO3
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What is the antidote for cyanide tox?
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Thiosulfate
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What are non-oncologic uses of methotrexate?
|
MOA: folic acid analog natimetabolite that inhibitis dihydrofolate reductase:
- Ectopic pregnancy - Psoriasis - Inflammatory bowel disease - Rheumatoid arthritis |
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Why are tetracyclines used in early rheumatoid arthritis?
|
Inhibit the activity of metalloproteinases that are involved in join destruction by the rheumatoid synovium
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What are non-oncologic uses for cyclophosphamide?
|
MOA: alkylating agent
- SLE immunosuppressant - MS - Autoimmune hemolytic anemia |
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What is the MOA of B-blockers?
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- Inhibit B-receptors & inhibit the G-proteins/cAMP mechanism
- Decreased cAMP & protein kinase A = decreased Na+ & Ca2+ current within the AV node - T/F decrease the slope of phase 4 & ) = suppression of abnormal pacemakers |
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Where are the nicotinic receptors of ACh?
|
Direct membrane receptor coupling to a Na+/K+ ion channel:
- ANS ganglia - Skeletal neuromuscular junctions - CNS |
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Where are the GABAa receptors that are directly coupled to Cl ion channels?
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CNA
|
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What receptors increase cAMP to activate protein kinase A to phosphorylate tissue specific substrate enzymes?
|
Gs:
- catecholamines (beta) - dopamine (D1) - glucagon - histamine (H2) - prostacycline - 5HT |
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What receptors decrease cAMP to down regulate protein kinase A & lower phosphorylate tissue specific substrate enzymes?
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Gi:
- Catecholamines (alpha 2) - ACh muscarineic (M2) - Dopamine (D2 subtypes) - Several opiod & 5HT subtypes |
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Which receptor systems activate phospholipase C to release IP3 & DAG from membrane PIP2 (IP3 then releases Ca2+ from the SR, which with DAG activates protein kinase C to phosphorylate tissue specific substrate enzymes?
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- ACh (M1 & M3)
- Norepinephrine (alpha 1) - Angiotension II - Several opioid & 5HT subtypes |
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What is the mechanism of vascular smooth muscle vasodilation?
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- Cyclic GMP is the 2nd messanger
- Facilitates dephosphorylation of myosin light chains to prevent their interaction with actin |
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How does Nitric oxide (NO) promote vasodilation?
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Released from endothelial cells by vasodilatiors (e.g. H1 & M3 agonists, or nitrates) to activate guanylyl cyclase to increase cGMP
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What receptors mediate the first steps in insulin & growth factor signaling?
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EGF: endothelial growth factor
PDGF: platelet derived growth factor ANF: atrial naturitic factor Recognition sites extracellularly + tyrosine kinase cytoplasmic domains that are dimerized upon ligand binding & result in tissue-specific substrate protein phosphorylation |
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What are Nn receptors?
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Nicotinic: PANS & SANS ganglia & adrenal medulla
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What are Nm receptors?
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Nicotinic: skeletal muscle motor endplate
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What are M receptors?
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Muscarinic: organs/tissues innervated by post-ganglionic nerves of the PANS & thermoregulatory sweat glands of SANS
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What are α & β receptors?
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Adrenoceptors: organs/tissues innervated by post-ganglionic nerves of SANS
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What receptors use ACh as a neurotransmitter?
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N & M receptors of innervated tissues:
- Nicotinic: skeletal muscle motor endplate - Muscarinic: organs/tissues innervated by post-ganglionic nerves of the PANS & thermoregulatory sweat glands of SANS |
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What receptors use NE as the neurotransmitter?
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Most adrenoceptors in innervated tissues
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What receptors use DA (dopamine) as the neurotransmitter?
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D1 receptors in renal vasculature
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What receptors use E (Epinephrine) as the neurotransmitter?
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- Adrenal medulla
- Activates most adrenoceptors whether or not the tissues are innervated |
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What receptors use 5HT, purines, & opioid peptides as the neurotransmitter?
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ENS & many ANS fibers in the GI tract
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What is the neural response to an increase in Bp?
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- Baroreceptor discharge
- Increase in PANS activity -> bradycardia - Decrease in SANS -> decrease in HR & decrease in contraction & decrease in vasoconstriction |
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What is the neural response to a decrease in Bp?
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- ANS neural feedback:
- decrease PANS outflwo & increased SANS -> increased CO & TPR |
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What is the hormonal response to decrease mean Bp (i.e. hypotension)?
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- Decrease in renal blood flow -> decrease in renal pressue
- Increase in renin release -> increase in angiotensins - Angiotensin II increases aldosterone release from the adrenal cotex - Retention of Na & H2O to increase blood volume - Increased venous return increases Co - Angiotension II also causes vasoconstriction to increase TPR |
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What is the target of indirect-acting cholinomimetics?
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AChE: the amjor mechanism of termination of ACh actions
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How does the Cholinergic neuroeffector junction work?
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ACh is synthesized via ChAT & accumulates in synaptic vesicles
- Excitation opens voltage-dependent Ca2+ channels and there is a Ca2+ INFLUX - ACh is released and activates post-junctional receptors |
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Where does Botulinum toxin act?
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Blocks ACh release at Cholinergic neuroeffector junctions
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Name the cholinomimetics that target postjunctional cholinergic receptors (direct-acting cholinomimetics)?
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- Nicotinic: Nicotine
- Muscarinic: bethanechol, methacholine, pilocarpine |
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Name the cholinoceptor antagonists that target postjunctional cholinergic receptors (direct-acting antagonists/blockers)?
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- Nicotinic (Nn): hexamethonium, mecamylamine
- Nicotinic (Nm): tubocurarine, atracurium, succinylcholine - Muscarinic: atropine, benztropine, glycopyrrolate, scopolamine |
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What are the Muscarinic receptors of the Eye?
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M3:
- Sphincter (contracts = miosis) - Ciliary muscle (contract = accomodation for near vision) |
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What are the Muscarinic receptors of the Heart?
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M2:
- SA node: decrease in HR: negative inotropy - AV node: decrease in conduction velocity |
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What are the Muscarinic receptors of the Lungs?
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M3:
- Bronchioles: contract/bronchospasm - Increased secretion |
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What are the Muscarinic receptors of the GI?
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M3: increased motility = cramps
M1: increased secreation M3: contraction = diarrhea |
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What are the Muscarinic receptors of the bladder?
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M3:
- Wall: contraction - Sphincter: relaxation |
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What does activation of M3 receptors generally do to sphincters?
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Relaxes them
EXCEPT lower Esophageal |
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What are the Muscarinic receptors of the glands?
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M3:
- increases secretation (sweat = thermoregulatory) - increases salivation - increases lacrimation |
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What are the Muscarinic receptors of the glands?
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M3:
- dilation VIA NO or EDRF (not innervation) |
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What are the Nicotinic receptors of the Adrenal medulla?
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Nn: secretion of E & NE
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What are the Nicotinic receptors of the Autonomic ganglia?
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Nn:
- Stimulation: effects depend on ANS innervation & dominance: - BV = SANS = vasoconstriction - GI = PANS = increased motility & secretions |
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What are the Nicotinic receptors of the Neuromuscular junction?
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Nm:
- Stimulation = twitch/hyperactivity |
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What is the mechanism of M1 & M3 receptors?
|
Cholinergic, Gq:
- Increase DAG & IP3 = increased intracellular Ca2+ |
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What is the mechanism of M2 receptors?
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Cholinergic, G1:
- Decreased adenylyl cyclase = decreased cAMP |
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What is the mechanism of Nn & Nm receptors?
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NO 2nd Messengers:
- Activation = opening of Na+/K+ channels |
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What is the activity, AChE hydrolysis, & clinical use for bethanechol?
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Direct-Acting Cholinomimetic
- Activity: M receptors - AChE hydorlysis: none - Rx: ileus (post-op/neurogenic), - urinary retention |
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What is the activity, AChE hydrolysis, & clinical use for methacholine?
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Direct-Acting Cholinomimetic
- Activity: M > N receptors - AChE hydorlysis: yes - Rx: bronchial hyper-reactivity |
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What is the activity, AChE hydrolysis, & clinical use for pilocarpine?
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Direct-Acting Cholinomimetic
- Activity: M receptors - AChE hydorlysis: none - Rx: glaucoma (topical), xerostomia |
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What is the action & clinical use of edrophonium?
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Indirect-acting Cholinomimetic:
- Action: short-acting - Use: Dx myasthenia from cholinergic crisis |
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What is the action & clinical use of physostigmine?
|
Indirect-acting Cholinomimetic:
- Action: tertiary amine (enters CNS), intermediate action - Use:glaucoma, antidote in atropine tox |
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What is the action & clinical use of neostigmine/pyridostigmine?
|
Indirect-acting Cholinomimetic:
- Action: quaternary amine (no CNS entry), intermediate action - Use: ileus, urinary retention, myasthenia, myasthenia, reversal of non-depolarizing NM blockers |
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What is the action & clinical use of donepezil, tacrine?
|
Indirect-acting Cholinomimetic:
- Action: lipid soluble (CNS entry) - Use: Rx = Alzheimer's disease |
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What is the action & clinical use of organophosphates?
|
Indirect-acting Cholinomimetic:
- Action: lipid-soluble, long-acting irreversibel inhibitors - Use: NONE (insecticides: malathion, parathion; NERVE GAS) |
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What are the symptoms of AChE inhibitor poisoning?
|
DUMBELS:
Diarrhea Urination Miosis Bronchoconstriction Excitiation (muscle & CNS) Lacrimation Salivation & Sweating |
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What is the management for AChE poisoning?
|
2 drugs, give together:
- Atropine (enters the CNS) - Pralidoxime (2-PAM) to regenrate phosphorylated AChE |
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What type of drug is atropine?
|
- Muscarinic receptor antagonist; PARASYMPATHOLYTICS
- Tertiary amine (enters the CNS) |
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What does atropine do?
|
"Dry as a bone; red as a beet, hot as a pistol, blind as a bat, mad as a hatter"
- Heart: low dose = decreases HR, moderate dose = increases HR - Decreases secretions (salivary, bronchiolar, sweat) - Mydriasis & cycloplegia - Hyperthermia with resulting vasodilation - Decreased GI motility - DELUSIONS & HALLUCINATIONS |
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How do you manage an atropine OD?
|
symptomatic +/- physostigmine
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What are the clinical uses of atropine?
|
Muscarinic receptor antagonist; PARASYMPATHOLYTIC:
- Antispasmodic - Antidiarrheal - Antisecretory - AChE inhibitor Overdose |
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What is the clinical use of tropicamide?
|
Muscarinic receptor antagonist; PARASYMPATHOLYTIC:
- Opthalmology (topical) |
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What is the clinical used of ipratropium?
|
Muscarinic receptor antagonist; PARASYMPATHOLYTIC:
- Ashtma & COPD (inhalational) - NO CNS entry |
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What is the clinical use of scopolamine?
|
Muscarinic receptor antagonist; PARASYMPATHOLYTIC:
- Antimotion sickness - SE: causes sedation & short-term memory block |
|
What is the clinical use of Glycopyrrolate?
|
- Antispasmodic
- Antisecretory - Anti-ulcer NO CNS entry |
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Where do ganglionic blocking agents act?
|
Competitive antagonists at the Nn rectpors in ANS ganglia
|
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What determines the effect of ganglionic blockers?
|
Blockers REDUCE dominate TONE
- PANS dominate in tissues with dual innervation (SA & AV nodes; pupil, GI/GU muscles & sphincters) = BLOCKER -> tachycardia, mydriasis, & muscle relaxation & sphincter closure - SANS dominate in vascular tone & sweat glands = BLOCKER -> vasodilation & reduced secretion |
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What are the 3 ganglionic blockers?
|
- Hexamethonium
- Mecamylamine - Trimethaphan |
|
What is the use of ganglionic blockers?
|
Shows whether a drug action is direct (e.g. on heart rate) or due to ANS reflex response (blocks reflex brady/tachycardia elicited by change in mean Bp)
|
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What happens when hexamethonium is given after phenylephrine is administered?
|
- Phenylephrine will cause vasocontriction
- Hexamethoium will block the reflex bradycardia |
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What happens when hexamethonium is given after a M-receptor activator is administered?
|
Nothing, the action is direct on the heart & not a reflex that Hexamethonium can block
|
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What are the general characteristics of a nondepolarizing NMJ blocker? List the 3 main drug examples
|
- Competitive antagonist of NM muscle endplate
- Reversible by AChE - E.G.: tubocurarine, atracurium, pancuronium |
|
What are the general characteristics of a depolarizing NMJ blocker?
|
- Agonist at NM receptors
- Initial fasciculation then paralysis through persistent membrane depolarization - NOT reversibel by AchE inhibitors - E.G. succinylcholine |
|
Explain the main steps of NE synthesis?
|
1) Tyrosine is converted to DOPA (dihydroxyphenylalanie) via tyrosine hydroxylase
2) DOPA is converted to dopamine (DA) via L-aromatic amino acid decarboxylase (DOPA decarboxylase) 3) DA is converted to NE via DA beta-hydroxylase & is taken up & stored in granules |
|
How does inactivation of NE via MAO occur?
|
Regulation/reduction in prejunctional levels in the mobile pool, but has NO effect on granular NE (i.e. already NE already stored in granules)
|
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Explain the mechanism of NE release?
|
1) Membrane excitation opens voltage-dependent Ca2+ channels
2) Ca2+ influx 3) NE released from granules into the neuroeffector junction 4) NE activates postjunctional receptors & effect depends on the alpha or beta adrenoceptor subtype |
|
What are the 4 ways that NE action can be terminated?
|
1) NE transporter system (reuptake)
2) Activation of prejunctional alpha2 adrenoceptors that are then feedback inhibitors 3) Diffusion from neuroeffector junction 4) Taken up by target cells & inactivated by COMT |
|
What are MOA of MAO inhibitors?
|
- Drugs: phenelzine, tranylcypromie
- Increase prejunctional NE Action: inhibits MAO A & B: - MAO A (in liver) = also metabolizes NE, 5HT, & tyramine - MAO B: mainly in Brain & metabolizes DA |
|
What drugs act on the mobile pool of NE (indirect acting sympathomimetics)?
|
Amphetamine, Ephedrine, Tyramine
- MOA: displaces NE & t/f enhances post-junctional actions |
|
What indirect sympathomimetic inhibits NE reuptake to increase postjunctional NE?
|
Cocaine
|
|
What adrenoreceptor drugs activate prejunctional alpha receptors to inhibit tyrosine hydroxylase & t/f NE release from synaptic vesicles?
|
- Clonidine
- Alpha methyldopa |
|
What drugs block the granular uptake of NE within neurons?
|
Reserpine: decreases prejunctional levels of NE available for release
|
|
What drugs block the release of NE from granules to decrease postjunctional actions of NE?
|
Guanethidine
|
|
What distinguishes typical viral meningitis from CNS invasion by HSV?
|
- CSF will show RBCs present due to necrosis of infected brain tissue & resultant cerebral hemorrhage
- Otherwise, the CSF findings will be viral: increased lymphocytes, normal/elevated protein, normallow glucose |
|
How can selective COX-2 inhibitors (like Celecoxib) cause renal failure?
|
- Inhibits prostaglandin synthesis
- If a patient becomes DEHYDRATED, they have no physiological mechanism to retain renal blood flow (vasodilation of the afferent & efferent arterioles) |
|
Where is the macula densa in the kidney?
|
portion of the thick ascending limb adjacent to the hilus of the glomerulus
|
|
What does inhibition of cycloxygenase-2 enzyme result in?
|
Decrease in production of:
- prostaglandins - thromboxane - prostacyclines (reduce platelet function) |
|
What does myxedema look like?
|
Nonpitting edema on the anterior surface of both legs with overlying skin that is dry & waxy & may have several diffuse, slightly pigmented papules
|
|
What is the MOA of propylthiouracil & methimazole?
|
Block tyrosine iodination (i.e. organification) & coupling
- Prophylthiouracil also decreases peripheral conversion of thyronine to triodothyonine Rx: hyperthyroidism (e.g. Grave's) |
|
What determines blood flow at the base of the lungs when a person is standing?
|
difference between arterial & venous pressure (arterial pressure is greatest & alveolar pressure is weakest)
|
|
In the middle lobes of the lung, what has the greatest pressure: arterial, alveolar or venous?
|
arterial > alveolar > venous
|
|
What is the treatment for nephrogenic diabetes insipidous?
|
Hydrochlorothiazide: inhibits reabsorption of Na from the H20-impermeable early distal convoluted tubule. Inhibits hyperdilution
|
|
How is the late distal convoluted tubule & collecting duct made amenable to H20 absorption?
|
Hypertonic intersitium enabled by the thick ascending limb: solute transport & deposition of ions into the medullary interstitial fluid
|
|
What organ clears the body of capsulated organisms?
|
spleen
|
|
Why does Wilson's cause extrapyramidal symptoms?
|
Basal ganglia degeneration
|
|
What lab results indicate Wilson's?
|
- Severe hepatic impairment -> hemolytic anemia
- Reduction in serum levels of cerulopasmin (copper carrier protein) |
|
What is the DOC for Wilson's
|
penicillamine
|
|
What disease is caused by the loss of debranching enzyme?
|
Cori's
- accumulation of glycogen in liver, heart, & skeletal muscle - S/S: (like Von Gierke's but milder) hyperlipidemia, fasting hypoglycemia, heaptomegaly |
|
Where does glucocerebroside accumulate in Gaucher's?
|
Monocytes & macrophages = enlarged histiocytes with "wrinkled tissue paper" appearance
|
|
Where does heparan sulfate & dermatan sulfate (mainly) accumulate in patients with Hurler's
|
Heart
Brain Liver |
|
What melena indicated?
|
Blood loss in the upper GI (lower GI blood loss = RED stools)
|
|
What is the most common cause of iron deficiency anemia in postmenopausal women?
|
Occult blood loss: usually from a GI source
|
|
What are the adrenoreceptors in the eye?
|
Alpha1:
- Radial (dilator) muscle: contraction/mydriasis |
|
What are the adrenoreceptors in the arterioles (skin/viscera)?
|
Alpha1:
- Contraction = increased PVR & afterload |
|
What are the adrenoreceptors in the veins?
|
Alpha1:
- Contraction = increased venous return & preload |
|
What are the adrenoreceptors in the bladder trigone & sphincter?
|
Alpha1:
- Contraction = urinary retention |
|
What are the adrenoreceptors in the male sex organs?
|
Alpha1
- Vas deferens contraction = ejaculation |
|
What are the adrenoreceptors in the liver?
|
Alpha1:
- increased glycogenolysis |
|
What are the adrenoreceptors in the prejuctional nerve terminals?
|
Alpha2:
- decreased transmitter release & NE synthesis |
|
What are the adrenoreceptors in the platelets?
|
Alpha2:
- aggregation |
|
What are the adrenoreceptors in the pancreas?
|
Alpha2:
- decreased insulin secretion (these are the dominate receptors) |
|
What are the adrenoreceptors in the heart?
|
Beta1:
- SA node = increased HR (+ chronotrophy) - AV node = increased conduction velocity (+ dromotropy) - Muscle = increased force of contration (+ inotrophy), conduction velocity, CO & O2 consumption - His-PUrkinje = increased automaticity & conduction velocity |
|
What are the adrenoreceptors in the kidney?
|
Beta1:
- Increased renin release |
|
Define each: chronotropy, dromotropy, inotropy
|
Chronotrophy: HR
Dromotrophy: conduction velocity Inotropy: force of contraction |
|
What are the adrenoreceptors in the blood vessels?
|
Beta2:
- Vasodilation -> decreased PVR, diastolic pressure, afterload |
|
What are the adrenoreceptors in the uterus?
|
Beta2: relaxation
|
|
What are the adrenoreceptors in the bronchioles?
|
Beta2: dilation
|
|
What are the adrenoreceptors in the skeletal muscle?
|
Beta2: increased glycogenolysis -> contractility (tremor)
|
|
What are the adrenoreceptors in the liver?
|
Beta2: increased glycogenolysis
|
|
What are the adrenoreceptors in the pancreas?
|
Beta2: increased insulin secretion
|
|
What is the dominace of adrenoceptor when drugs active on beta & alpha receptors are given at low & high doses?
|
Low: beta dominance
High: alpha dominance E.G. Epinephrine |
|
What type of adrenoceptors does dopamine activate?
|
D1 (peripheral) in renal, mesenteric, & coronary vasculature
- Result: VASODILATION - In Kidney = increased GFR, RBF, & Na+ excretion |
|
What type of receptor is alpha1?
|
- Adrenergic
- Gq coupled: increase in DAG & IP3 = increased intracellular Ca2+ |
|
What type of receptor is alpha2?
|
- Adrenergic
- Gi coupled: decreased adenylyl cyclase = decreased cAMP |
|
What type of receptor are beta2, beta1, and D1?
|
- Adrenergic
- Gs coupled: increased adenylyl cyclase = increased cAMP |
|
What is the action of alpha1 agonist drugs? Give 2 examples.
|
- MOA: increase Bp (& reflex bradycardia)
- Phenyleprine: decongestant (mydriasis w/o cyloplegia) - Methoxamine: Paroxysmal Atrial tachycardia + vagal reflex |
|
What is the action of alpha2 agonist drugs? Give 2 examples.
|
- MOA: CNS actions -> decreased vasomotor outflow & decrease in mean Bp
- Clonidine: abrupt D/C causes rebound HTN - Alpha methyldopa: pro-drug forming alpha-methyl NE |
|
What is the action of beta1&2 nonselective agonist drugs? Give 1 example.
|
- MOA: increase in HR, SV, CO (beta1) & decrease in PVR (beta2)
- increase in mean Bp = increase in pulse pressure & no reflex on heart - Rx: bronchospasm, heart block, bradyarrhythmias - SE: flushing, angina, arrhythmias - ISOPROTERENOL |
|
What is the action of beta1 > 2 nonselective agonist drugs? Give 1 example.
|
- MOA: increase in HR, SV, CO (beta1) & no change in PVR, GFR, or RBF
- Rx: acute CHF (tachyphylaxis) - DOBUTAMINE |
|
What are the 4 main selective beta2 agonists and what is the use of each?
|
Ashtma: metoproterenol, albuterol, terbutaline
Premature Labor: ritodrine |
|
What is the action of Norepinephrine used as a drug?
|
MOA: alpha1, apha2, beta1 agonist
- increased PVR = increase DIASTOLIC pressure - increased HR & SV = increased SYSTOLIC pressure & small increase in PP - increased mean BP w/ reflex bradycardia |
|
What is the action of Epinephrine used as a drug?
|
MOA: Alpha 1+2, beta 1+2 agonist
- LOW dose: beta dominance = increase in HR & small decrease in mean Bp - HIGH dose: alpha dominace = increase PVR & increase diastolic pressure = reflex bradycardia - bronchodilation & increased liver glycogenolysis, muscle glycogenolysis & glycolysis, increased FFA (activates lipase) - Rx: Anaphylaxis, cardiac arrest, adjunct to local anesthetics, glaucoma |
|
What is "epinephrine reversal"?
|
- The effect of using an alpha blocker after eliciting a hypertensive response with a HIGH does of epinephrine
- When alpha1 is blocked, then there is an unmasking of epinephrine's beta2 activation = HYPOtension |
|
What type of drug is amphetamine? What is its action & clinical use?
|
Indirect adrenoceptor agonist
- Releases NE from the mobile pool - Peripheral = sympathetic stimulation - CNS = release of both NE & DA Rx: ADHD, weight loss, narcolepsy |
|
What type of drug is amphetamine? What is its action & clinical use?
|
Indirect adrenoceptor agonist
- Releases NE from the mobile pool - Peripheral = sympathetic stimulation - CNS = release of both NE & DA Rx: decongestant (also pehnlypropanolamine) |
|
What type of drug is Dopamine? What is its action & clinical use?
|
LOW dose: D1 = increased renal/mesenteric blood flow -> increase RBF & GFR
MEDIUM dose: B1 = increased CO (+ inotropy) HIGH dose: A1 = vasoconstriction + increased systolic & diastolic Bp |
|
What is the action of alpha adrenoceptor antagonists?
|
- Decrease PVR & mean Bp -> tachycardia & H2O retention
- Marked reflex tachycardia if alpha2 receptors are blocked too (reduced feedback inhibition) |
|
Which alpha adrenoceptor antagonists are used to treat pheochromocytoma?
|
Phenotolamine & Phenoxybenzamine:
- Decrease PVR & mean Bp -> tachycardia & H2O retention - Marked reflex tachycardia if alpha2 receptors are blocked too (reduced feedback inhibition) |
|
What type of drug is Prazosin? What is its clinical use?
|
- Prototyle alpha1 selective blocker
- Less reflex tachycardia - 1st-dose syncopy = postural hypotension |
|
What drugs have the same MOA as prazosin?
|
doxazosin
terazosin amulosin All are alpha1 selective blockers: - decrease PVR & mean Bp -> (a bit of) tachycardia & H2O retention |
|
What is the MOA of beta adrenoceptor antagonists?
|
- Heart: decreased contractility, HR, CO, O2 demand & Bp
- Delayed hypoglycemis b/c reduced glycogenolysis - Decreased ciliary epithelial secretions = decreased IOP - SE: AV block & heart failure, bronchospasms in asthmatics |
|
What type of drug is propranolol? What are its SE?
|
- Prototype non-selective beta blocker
- Chronic used can lead to increased LDL-C & TGs |
|
What are the benefits & limitations of selective beta blockers?
|
- Benefits: safer in asthma, diabetes, & PVD
- LImits: less effects on vasculature, bronchioles, uterus, & metabolism E.G. acebutolol, atenolol, metoprolol |
|
What are the beta blockers with ISA?
|
ISA = intrinsic sympathomimetic activity
- have less bradycardia & minimal change in plasma lipids - acebutolol & pindolol |
|
Which beta-blockers have NO CNS entry? Which have a particularly long halflife?
|
- NO CNS entry: atenolol & nadolol
- Long HalfLIfe: cavedilol & nadolol |
|
Which beta blockers have combined alpha & beta blocking action?
|
Cavedilol
Labetalol |
|
Why should you taper doses when discontinuing beta blockers?
|
- B/C chronic use of beta blockers leads to receptor up-regulation
- T/F tapering reduces excess CV rebound of endogenous amines |
|
What is the action, ISA, sedation, effect on lipids, & clinical use for acebutolol?
|
Action: B1-selective
ISA: yes (less bradycardia & minimal change in plasma lipids ) Sedation: yes Lipids: NA Clinical Use: angina, HTN |
|
What is the action, ISA, sedation, effect on lipids, & clinical use for atenolol?
|
Action: B1-selective
ISA: no Sedation: no Lipids: INCREASED Clinical Use: angina, HTN |
|
What is the action, ISA, sedation, effect on lipids, & clinical use for esmolol?
|
Action: B1-selective
ISA: no Sedation: yes Lipids: no Clinical Use: antiarrhythmic (Class IV); 10 minute T1/2 |
|
What is the action, ISA, sedation, effect on lipids, & clinical use for labetalol?
|
Action: B non-selective + alpha1
ISA: no Sedation: yes Lipids: no Clinical Use: HTN & hypertensive crisis & pheochromocytoma |
|
What is the action, ISA, sedation, effect on lipids, & clinical use for metoprolol?
|
Action: B1-selective
ISA: no Sedation: yes Lipids: INCREASED Clinical Use: angina, HTN, post-MI antiarrhythmic |
|
What is the action, ISA, sedation, effect on lipids, & clinical use for pindolol?
|
Action: B non-selective
ISA: YES Sedation: yes Lipids: no Clinical Use: angina, HTN |
|
What is the action, ISA, sedation, effect on lipids, & clinical use for propranolol?
|
Action: B non-selective
ISA: no Sedation: YES Lipids: YES Clinical Use: angina, HTN, post-MI, migraine, tremor, performance anxiety, thyrotoxicosis |
|
What is the action, ISA, sedation, effect on lipids, & clinical use for timolol?
|
Action: B non-selective
ISA: no Sedation: YES Lipids: YES Clinical Use: HTN, migraine, glaucoma |
|
What beta blockers are linked with worsening blood lipids?
|
- atenolol
- metoprolol - protranolol - timolol |
|
Which beta blocker does not cause ANY sedation (there is only 1)?
|
atenolol
|
|
Which 4 beta blockers have no affect on blood lipids?
|
acebutolol
esmolol labetalol pindolol |
|
Which 2 beta blockers are used to treat migraine?
|
propranolol
timolol |
|
Which beta blocker is used to treat glaucoma?
|
timolol
|
|
Which 2 beta blockers are indicated as antiarrhythmics?
|
esmolol
metoprolol |
|
Which betablocker is used in hypertensive crises?
|
labetalol (b/c also a A1 blocker)
|
|
Which is the only beta blocker not used for HTN?
|
esmolol (short T1/2 = 10 minutes)
|
|
What is the PANS & SANS innervation of the SA & AV nodes
|
PANS = M2 (decreases phase 4 slope by decreasing cAMP)
SANS = B1 (increases phase 4 slope by increasing cAMP) |
|
What does activation of B1 heart receptors (& therefore an increase in cAMP) cause?
|
- Increase in upstroke velocity in pacemakers in Increasing I (C-L type)
- Decreasing action potential duration by Increasing Ik - Increases HR by increasing If, thus increasing slope of phase 4 |
|
What does activation of M2 heart receptors (& therefore an decrease in cAMP) cause?
|
- Decreases upstroke velocity in pacemakers in decreasing I (C-L type)
- Increases action potential duration by decreasing Ik - Decreases HR by decreasing If, thus increasing slope of phase 4 - Produces a K+ current (Ik/ACh), which slows diastolic depolarization & decreases HR |
|
What is the mechanism of Class IA antiarrhymics?
|
- Decreases Vmax: Blocks fast Na channels (decreases Ina) "state dependent"
- Increases ADP (action potential duration) & ERP (effective refractory period: block of K+ channels (decreased Ik, delayed rectifier current) |
|
What is the MOA of Quinidine?
|
Class IA (Na+ channel blocker)
- M-bock: increases HR & AV conduction - SE: nausea & vomiting, cinchonism, hypotension (due to alpha block), increased QRS & QT interval -> syncopy (torsades) Interactions: - increases digoxin tox - decreases effects of AChE inhibitors in myasthenia - hyperkalemia increases tox |
|
What is cinchonism?
|
SE of Quinidine: GI, tinnitus, ocular dysfunction, CNS excitation
|
|
What is the MOA of procainamide?
|
Class IA (Na+ channel blocker):
- Less M-block (less HR & AV conduction increase) - Cardiodepressant - Prolongs ADP b/c is metabolized via N-acetyltransferase (genotypic variation) to NAPA, that prolongs ADP - SE: SLE-like syndrome (30% of patients) more likely in slow acetylators, hemotox (throbocytopenia & agranulocytosis), CNS effects (dizziness, hallucinations, CV effects (torsades) |
|
What is "torsades de pointes"?
|
- ECG demonstrates a rapid, polymorphic, ventricular tachycardia with a characteristic twist of the QRS complex around the isoelectric baseline
- Can follow a prolonged QT intervals on ECG - Associated with a fall in arterial Bp, which can produce fainting - It can degenerate into ventricular fibrillation |
|
What are the characteristics of "Trosades de pointes"?
|
- Rotation of the heart's electrical axis by at least 180º
- Prolonged QT interval LQTS - Preceded by long and short RR-intervals - Triggered by an early premature ventricular contraction (R-on-T PVC) |
|
What is the treatment for "Torsades"?
|
- Withdrawal of the causitive agent (can be class IA or class III antiarrhythmics)
- Infusion of magnesium sulfate & antiarrhythmic drugs, & electrical therapy as needed Because of the polymorphic nature of torsades de pointes, synchronized cardioversion may not be possible, and the patient may require an unsynchronized shock (or defibrillation). [edit] |
|
What electrolyte imbalances predisposed to torsades?
|
- Diarrhea
- Hypomagnesemia - Hypokalemia T/F watch malnourished individuals & chronic alcoholics |
|
What are the signs of PCP (phycyclidine) use?
|
belligerance
impulsiveness fever psychomotor agitation vertical & horizontal nystagmus tachycardia ataxia homicidality psychosis delirium |
|
By what mechanism can PCP re-intoxicate a patient during withdrawal?
|
When the PCP, trapped in an ionized form in the acidic gastric lumen, is reabsorbed in the alkaline duodenum
- Check for normal or small pupils |
|
What is the post-cocaine "crash"?
|
Withdrawal: severe depression, hyper-somnolence, fatigue, malaise, & severe psychological craving
|
|
What are the 4 mature defense mechanisms?
|
- sublimation
- altruism - humor - suppression |
|
Which viruses are associated with hepatocellular carcinoma?
|
HBV & HCV
|
|
How are arbo & flaviruses transmitted?
|
mosquito bites:
- Arbo: Dengue fever - Flav: Yellow fever |
|
What is the main function of the Golgi complex?
|
to add oligosaccharides to proteins & lipds
|
|
What indicates that a protein is destined for the lysosomal pathway?
|
mannose-6-phosphate residuses
|
|
What are the 2 main enzymes in Peroxisomes?
|
1) Oxidases for catabolic pathways (e.g. beta oxidation of long-chain fatty acids)
2) Catalase to regulate H2O2 concentration to oxidize toxic substances |
|
What is the main function of SER (smooth ER)?
|
- Lipid biosynthesis
- Membrane synthesis/repair - Detox of metabolic by-products - NB: no ribosomes!! |
|
What is the main function of RER in the cell?
|
Initiates the processing of finalized protein products
NB: Contains ribosomes |
|
What should one do regarding the results of a study if the P value is greater than 0.05?
|
Accept the null hypothesis
|
|
What potential error are you making if you do NOT reject the null hypothesis?
|
Beta (type II) = 1-power
|
|
What type of error does a P value represent?
|
type I
- If P < 0.05, then there is less than a 5% chance that the null hypotheses was incorrectly rejected |
|
What is a type I error?
|
Incorrectly rejecting the null hypothesis: accepting a difference when none exists (i.e. the null is true)
|
|
What is a "CV wave"?
|
- When, dues to tricuspid regurgitation, blood flows backward into the atria during ventricular systole
- This pressure is transmitted back into the RA & jugular vein & results in the JVC pressure change: joining of the C & V wave |
|
What sections of the nephron are responsible for Na reaborption?
|
Proximal Convoluted Tubule: 67%
Thick Ascending Limb: 25% Late Distal Convoluted Tubule: 3% 1% = excreted (i.e. NOT reabsorbed) |
|
What type of tumors have tartrate-resistant acid phosphatase as a marker?
|
B lymphocyte neoplasms (e.g. hairy cell leukemia)
|
|
What cancers can be marked by CEA (carcinoembryonic antigen) in 70% of cases?
|
colorectal & pancreatic
|
|
What is the marker for hepatocellular carcinoma?
|
Increased levels of alpha fetoprotein
|
|
What type of tumor is marked by S-100?
|
melanomas
|
|
What type of tumor produces bombesin (a tumor marker)?
|
neuroblastomas
|
|
What is the pathogenesis of cor pulmonale?
|
dysfunction of the RV due to pulmonary hypertension in diseases affecting the lung or its vasculature
|
|
What can a chest X-ray showing basilar hyperlucency in a young patient indicate?
|
alpha1-antitrypsin deficiency
|
|
What maternal disease can put a child at risk for transposition of the great vessels?
|
Early fetal cyanosis due to maternal diabetes
|
|
What are congenital defects that can occur if a pregnant woman contracts rubella (caused by Rubivirus, a togavirus)
|
- PDA
- VSD - cataracts - deafness |
|
What infection can cause rapid death (within 3 weeks) in an AIDS patient who presents with neurological deficits of speech, memory, & coordination along with vision problems?
|
JC virus causing progressive multifocal leukoencephalopathy (PML)
- causes multiple areas of demyelination throughout the white matter of the CNS |
|
What is a common viral casue of temporal lobe encephalitis in HIV/AIDS patients?
|
Herpes simplex: rapid onset of fever & focal neurological deficits due to damage of the temporal lobe
- memory problems, personality changes, seizures |
|
What is a common cause of pneumonia in HIV patients with a CD4+ count below 200/mm3?
|
Pneumocystis jroveci
- Dx: X-ray picture of "ground glass" |
|
What is a common cause of encephalitis in patients with HIV/AIDS with a CD4+ cound below 100/mm3?
|
Toxoplasmosis
- S/S: seizures & headache - X-ray: ring-enhancing lesions with surrounding edema |
|
What is the cellular mechanism of a type IV hypersensitivity reaction?
|
- Initial exposure to antigen triggers differentiation of CD4+ T lymphocytes into T-helper type 1 lymphocytes
- Re-exposure = quick activation to secrete cytokines that mediate the local inflammation |
|
What are the 3 main mediators released in a type I hypersensitivity reaction?
|
- Histamine
- Leukotriene - Prostaglandin |
|
Describe the changes a female goes through during Tanner stages 1-5.
|
1: Elevation of the breast papilla only & no pubic hair
2: Small breast buds with elevation of breast & papille with sparse, straight, downy hair on the labila base 3: Enlargement of the breast & areola with a single contour & darker, coarse curled pubic hair 4: Projection of the areola & papilla with separate contous & adult-type public hair limited to the genital area 5: Mature breast & adult quantity/pattern of pubic hair that extends to the thighs |
|
When is organogesis?
|
Weeks 3-8
|
|
What are the findings of fetal alcohol syndrome?
|
1) pre & postnatal developmental retardation
2) microcephaly 3) facial abnormalities 4) limb dislocation 5) heart & lung fistulas MOA: inhibition of cell migration |
|
What fetal problems can occur if a mother takes chlorothiazide?
|
fetal thrombocytopenia & jaundice
|
|
What fetal problems can occur if a mother takes doxycycline?
|
Permanent tooth staining & enamel hypoplasia
Rx: Lyme disease & genital infections |
|
What fetal abnormalities are associated with lithium use?
|
Ebsteins & malformations of the great vessels
|
|
What fetal abnormalities are associated with Valproic acid use?
|
neural tube defects
cleft lip renal anomalies |
|
Which rash moves from the trunk outward? Which moves from the extremities and moves inward? (Choices: Rocky Mountain & Typhus)
|
Rickettsia prowazekii (epidemic typhus): trunk -> extremities
Rocky Mountain: extremities -> trunk |
|
What is the treatment for Kawasaki's?
|
IV IG & asprin
|
|
What are the physical exam findings in Kawasaki's?
|
Strawberry tongue
Lymphadenopathy Bright RED cracked lips Conjunctivities Swollen hands/feet |
|
What type of hematoma shows up as crescent-shaped on CT?
|
Subdural (usually bridging veins from cerebrum to dural sinuses in the elderly)
|
|
Where is the most common location of a Berry aneurysm?
|
Posterior communicating artery
|
|
What hematoma shows up as a biconvex disc on CT?
|
epidural: usually middle meningeal artery due to trauma
|
|
What type of hematoma usually shows no signs on CT?
|
intraparenchymal due to atherosclerosis & occlusion in hypertensive patients
|
|
What hormone is spironolactone similar to?
|
Progesterone
- T/F can cause gynecomastia & erectile dysfunction |
|
What are the 2 top causes of erosive gastritis?
|
H. pylori
NSAIDs |
|
What are the unique features of Zollinger-Ellison ulcers?
|
1) Unusual location: beyond the 1st part of the duodenum
2) Presense of MEN type I (tumors in the parathyroid, pancreas, & pituitary) |
|
What type of thalassemia is lethal in utero?
|
hydrops fetalis:
- no functional alpha chains are made - only Hb Bart's si made (y4 tetramer): poor O2 delivery to peripheral tissues |
|
What is Cooley's anemia?
|
- beta-thalassemia major (absence of both b-globin chains)
- S/S = severe hemolysis & ineffective erythropoiesis |
|
What results from absense of the four alpha-globin genes?
|
Hemoglobin H
- microcytic anemia & mild hemolyisis |
|
What microbial constituents do TLRs (toll-like receptors) recognize?
|
- LPS (lipid A, core sugar, + variable carb chain O antigen)
- flagellin - unmethylated CpG DNA |
|
What is the MOA of fluroquinolones?
|
- Drugs: Ciprofloxacin, Levofloxacin, Ofloxacin
- Inhibits DNA gyrase (topoisomerase II) that relaxes DNA supercoils |
|
What metabolic pathway produces 2,3 DPG (2,3-diphosphglycerate)?
|
- Anaerobic glycolysis
- 2,3-DPG causes a DECREASED hemoglobin affinity for O2 (= right shift of O2-hemoglobin dissociation curve) so that more O2 is unloaded to tissues |
|
What dopamine receptor antagonists are used as antipsychotics and cause galactorrhea?
|
D2 blockers: (typical antipsychotics)
- Chlorpromazine - Thioridazine - Haloperidol - Fluphenazine |
|
What is the MOA of amitriptyline?
|
TCA: prevents norepinephrine & serotonin reuptake from synaptic cleft
|
|
What drug is a dopamine analog?
|
Bromocriptine
- agonist at pituitary dopamine receptors & t/f prevents prolactin release - Rx: prolactin-secreting adenomas |
|
What is the MOA of fluoxetine?
|
- SSRI
- Rx: depression |
|
What is the MOA of Selegiline?
|
- MOA B inhibitor that prevents the breakdown of dopamine in the synaptic cleft
- Rx: Parkinson's |
|
What cellular defect results in Chediak-Higashi syndrome?
|
Microtubule polymerization = decreased phagocytosis
|
|
What is the MOA of cisplatin?
|
Alkylating agent" binds to guanine & forms inter/intra strand crosslinks
|
|
Which prevents microtubule formation and which inhibits their breakdown: paclitaxel or vincristine?
|
Paclitaxel: hyperstabilizes polymerized microtubules
Vincristine: prevents polymerization of microtubules |
|
What type of bacterial infection can present at crepitus after a penetrating wound?
|
Clostridium perfringens (gas-producing anaerobe)
Rx: clindamycin |
|
What 3 antibiotics are most associated with C. difficile overgrowth, destruction of the colon's normal fora & pseudomembranous colitis?
|
- Clindamycin
- Penicillin - Cephalosporin |
|
What antiviral is associated with ataxia, dissiness, & slurred speech?
|
Amantadine
|
|
What is the structure of a steroid hormone receptor?
|
- Zinc finger proteins: a polypeptide with a zinc atom bound to 4 cysteines
- Hormone binding region + a DNA binding region that activates gene transcription |
|
What are the 4 main actions of angiotension II?
|
- Arteriolar vasoconstriction
- Thirst sensation - Increased ADH & aldosterone secretion - Increased Na reabsorption |
|
What 5 tissues have angiotension II receptors?
|
Via angiotensin I neuropeptide receptor (Gq _> increase IP3 & DAG bia phospholipase C pathway):
- Vascular smooth muscle (vasoconstriction) - CNS (increased thirst) - Zona glomerulosa of adrenal cortex (aldosterone secretion) - Renal tubules (increased Na reabsorption) |
|
What type of receptors does ANP (atrial natriuretic peptide) work on?
|
GC (guanylate cyclase) receptors
- with intrinsic GC activity to produce cGMP - to catalyze protein kinase G to phosphorylate serine & threonine protein residues - Result: arteriole vasodilation |
|
Does insulin directly alter gene transcription?
|
No, its second messenger (MAP kinase) enters the nucleus to alter gene transcription:
- Insulin binds to a receptor tyrosine kinase to autophyosphyrlate tyrosine within the receptor - Intracellular proteins bind the the SH2 of this phosphotyrosine - This activates MAP kinase (mitogen-activated protein kinase) by covalent phosphorylation of tyrosine & threonine |
|
What are the 2 receptor-mediated actions of vasopressin (ADH)?
|
V1 receptors on arterioles:
- Activate Phospholipase C to liberate DAG & IP3 frome membrane lipids = vasoconstriction in SUPRAphysiologic doeses V2 on principal cells of cortical & medullary collecting ducts: - activates G proteins that in turn activate adenylate cyclase (which produces cAMP - cAMP activates protein kinase A - increased expression of AQUAPORIN H2O channels in the collecting duct |
|
What is the pathology of Lambert-Eaton disease?
|
Autoimmune antibodies against presynaptic voltage-gated Ca channels & reduced muscle use
- Result: reduced release of synaptic vesicles at prsynaptic terminal b/c no Ca influx |
|
When a muscle stimulation test shows initial unresponsiveness but response after repetitive stimulation, what does the patient likely have?
|
Lambert-Eaton: enough vesicles are released to cause activation on the postsynaptic acetylcholine receptor.
- vesicle release is impaired in this disease due to autoimmune attack of presynaptic votage-gated Ca channels - only enough vesicles are released for post synaptic activation after repetitive stimulation |
|
What are the results of a muscle stimulation test that indicate myasthenia gravis?
|
- Fatigability in the test
- b/c they have reduced amounts of acetylcholine receptors (due to autoimmune attack) to respond to the neurotransmitter release (& their is no pathology of release) |
|
What is the principle inhibitiory receptor of the CNS?
|
GABAa: inhibitory Cl channel
|
|
What diseases are associated with EBV infection?
|
- Endemic African Burkitt's lymphoma
- heterophil-POSITIVE mononucleosis - Oral hairy leukoplakia (HIV patients) - Hodgkin's & non-Hodgkin's lymphomas in immunocompromised patients - Nasopharyngeal carcinoma |
|
What infections are linked with Heterophil-negative mononucleosis?
|
- CMV
- acute HIV - Toxoplasmosis - Herpies types 6 & 7 |
|
What are noninfectious states are associated with hepatocellular carcinoma?
|
- Cirrhosis (2ndary to alcolol or crytogenic)
- Hemochromatosis - Aflatoxin ingestion - Alpha1-antitrypsin deficiency |
|
What are the risk factors for gastric carcinoma?
|
- H. pylori infection
- atrophic gastritis - postgastrectomy states - achlorhydria - pernicious anemia - Menetrier's disease - Adenomatous polyps |
|
What 3 carcinomas notoriously spread hematogenously?
|
- Hepatocellular
- Renal Cell - Follicular thyroid |
|
Where does HCC often metastese to?
|
Lung, portal vein, periportal nodes, brain, bones
|
|
How does Hodgkin's spread?
|
Continguous manner
|
|
How does ovarian & appendiceal cancers spread?
|
Pseudomyxoma peritonei: direct dissemination throughout the peritoneal cavity
- Diffuse collection of gelatinous materials in the abdomen, peritoneal surface & pelvis |
|
What direction is DNA synthesized?
|
5'-3' direction
|
|
What is the CD marker for pluripotent stem cells?
|
CD34: cells found in the
- umbilical cord, bone marrow, endothelial progenitors of blood vessels, mast cells and certain dendritic cells |
|
What is the CD marker for hematopoietic stem cells that can differentiate into erythroblasts & myeloblasts?
|
CD38
- Stimulated to differentiate by graulocyte colony-stimulating factor |
|
What is the marker of antigen-presenting cells?
|
B7 protein
|
|
What results in the loss of phosphatidylinosital glycan A?
|
- Episodic acute intravascular hemolysis = paroxysmal nocturnal hemoglobinuria
- this is required for the anchoring of decay-accelerating factor on the surface of RBCs, which BLOCKS compliment activation |
|
Which type of hemophilia is most common in Ashkenazi Jews?
|
C: Factor XI deficiency (AR)
|
|
What are the symptoms of Horner's syndrome?
|
Loss of sympathetic innervation to one side of the face:
1) Ptosis: eyelid drop 2) Hemi-Anhidrosis: lack of sweating 3) Miosis: pupil constriction |
|
What lung tumor is associated with Horner's?
|
Pancoast: apical tumor can compress the 1st & 2nd thoracic nerve roots & t/f block sympathetic innervation of the IPSILATERAL face
|
|
What nerve palsy leads to difficulty in lateral gaze?
|
Abducens nerve palsy (CN VI)
|
|
What nerve palsy/disruption can lead to drooping of the nasolabial fold?
|
Facial (CN VII)
|
|
What is the MOA of ganciclovir?
|
- Phosphorylated by viral protein kinases
- Acts as an analog to dGTP & competitively inhibits the incorporation of dGTP into viral DNA SE: myelosuppression & nephrotox (MUST monitor Px) |
|
What is the MOA of Enfurvirtide?
|
- Binds to the gp41 subunit of the HIV viral envelop
- prevents entry of the virus into the host cell Rx: HIV therapy |
|
What is the MOA of ritnovir?
|
Protease inhibitor: inhibits the cleavage of viral polyproteins
Rx: HIV SE: GI & paresthesias |
|
What is the MOA of oseltamivir?
|
- Inhibits viral neuraminidase & prevents release of viral progeny from infected cells
Rx: influenza |
|
What are the major side effects of Niacin treatment?
|
- facial flushing
- Gout - Impaired glucose tolerance |
|
What is the function of lipoprotein lipase?
|
- degradation of VLDL cholesterol
- up-regulated by fibrates |
|
Where are the BCRA1 & BCRA2 genes found?
|
BRCA1 = Ch. 17
BRCA2 = Ch. 13 Both are gumor suppressor genes and both alleles must be loss for the suppressive function to be lost |
|
When does rigor mortis set in?
|
3-4 hours after death
- ATP is depleted & without it, myosin cannot be released from the contraction complex - Muscles are frozen in a contracted in a contracted state |
|
What is the mechanism of muscle relaxation after rigor mortis?
|
- 72 hours after death, enzymes are released (due to a drop in pH) & these hydrolyze the myosin-actin complex
- Result: muscle relaxation |
|
What are the histological markers of diabetic nephropathy?
|
- Increase in mesangial matrix by marked nodular accumulations (Kimmelsteil-Wilson nodules)
- Diffuse glomerulosclerosis |
|
What is the pathogenesis of membranoproliferative glomerulonephritis?
|
- Autoimmune disease of the young (8-30 years old)
- HISTO: mesangial proliferation, thickening of peripheral capillary walls by subENDOthelial depositis & mesangial interposition into capillary wall (= TRAM-TRACK) |
|
What is the pathogenesis of rapidly progressive (crescentic) glomerulonephritis?
|
extensive capillary damage:
- accumulation of cells & fibrinous changes in Bowman's space = "crescent" on biopsy |
|
What is the pathogenesis of focal segmental glomerulosclerosis?
|
Nephrotic disease
- young, hypertensive, Black men with risk factors: obesity & HIV - Injury to podocytes leads to mesangial, endothelia, & epithelial cells & later shrinkage/collapse of glomerular capillaries -> SCLEROSIS (focal & segmental pattern) - Hyaline casts on urinalysis |
|
What causes cleft lip?
|
- failure of the maxillary prominence to fuse with the medial nasal prominence
- can be unilateral or bilateral |
|
What is the marker for active viral replication of Hep B & likely transmissibility?
|
HBeAg (detectable 2-4 months after exposure): marker of the virus core
|
|
What Hep B marker indicates low trasmissibility?
|
HBeAb (detectable 5 months post exposure or 1 month after detection of HBeAg)
|
|
What Hep B marker shows former carriers or immunization?
|
HBsAb (provides immunity)
|
|
What Hep B marker indicates chronic disease?
|
IgG HBcAb
|
|
What Hep B marker indicates recent disease?
|
IgM HBcAb
|
|
What is gastroschisis?
|
- Congenital abdominal wall defect: herniation of abdominal organs not covered by a membrane as they are in an omphalocele
- Complication of a patent urachus |
|
What embryological structure becomes the median umbilical ligament?
|
urachus (a remnant of the allantosis)
|
|
What are the 2 main drug types that are oxidative and cause oxidative stress (jaundice) in patients with G6PD deficiency?
|
- Sulfa drugs (e.g. trimethoprim-sulfamethoxazole)
- Antimalarials |
|
What are the symptoms of HYPERcalcemia?
|
- Constipation
- Poly -uria/dipsia - HYPOreflexia - Lethargy |
|
What diuretic drugs are useful to treat HYPERcalcemia?
|
Loop Diuretics (Furosemide):
- Block Na+/K-/2Cl- transporter in thick ascending loop of Henle - Blocks both Na & Ca reabsorption |
|
What diuretic class is useful to treat idiopathic hypercalciuria?
|
Thiazides (hydrochlorothiazide):
- Inhibits Na/Cl cotransporter in the distal tubule - Decreases Na reabsorption & increases Ca reabsorption |
|
What are Auer rodes?
|
Fused lysosomal granules
- Cytoplasmic inclusions in myelocytic precursor cells - Indicative of acute promyelocytic leukemai (M3 variant of AML) |
|
What happens if there is a sudden release of Auer rods due to rapid treatment of acute promyelocytic leukemia?
|
- DIC & fatal hemorrhage
- Histo: Helmet-shaped cells & Schistocytes |
|
What are schistocytes and when are they often found?
|
- irregular or fragmented RBCs
- result from attempts to squeeze through the fibrin meshwork of small vessel thrombi (e.g. in DIC) |
|
What are acanthocytes (aka "spur cells)?
|
- Spiny RBCs
- Aassociated with abetalipoproteinemia & severe liver disease |
|
What are Burr cells (aka echinocytes)?
|
- Abnormal RBCs with short, blunt projections around the periphery
- Found in: hemolytic-uremic syndrome, pyruvate kinase deficiency, ureamia... |
|
What are teardrop cells?
|
Abnormal RBCs seen in myeloid metaplasia with myelofibrosis
|
|
How do hormones produced in the liver enter the systemic circulation (i.e. by which vessel)?
|
Hepatic Vein to the IVC
|
|
What vessel carries O2-rich blood to the liver?
|
Hepatic artery
|
|
Describe the vessel flow through the hypophyseal portal system.
|
- Blood supplied by the hypophyseal artery goes through the capillary bed supplying the hypothalamic nuclei (which secretes tropin-releasing hormones that affect the anterior pituitary)
- Then blood passes through the capillary bed that supplies the anterior pituitary |
|
What vessel delivers blood from the GI track to the liver?
|
Portal vein
|
|
What vessel provides venous drainage from the kidneys to the IVC?
|
Renal veins
|
|
What does dermatitis herpetiformis look like? What disease does it indicate?
|
- multiple, nonblanching, purpuric, grouped lesions located on the upper & lower extremities
- Celiac disease (gluten-sensitive enteropathy) due to gladin allergy & cross-reactivity of antibodies to the small intestine villi |
|
What is the histological picture of Celiac disease?
|
- Lymphocytic infiltrate into the epithelial layer
- Atrophic & blunted vili |
|
When does Celiac disease present?
|
After the introduction of cereals into the diet
|
|
What is the histological picture in lactose intolerance?
|
BENIGN mucosa
|
|
What is the pathogenesis of Whipple's disease?
|
Tropheryma whippelii (rod-shaped bacili) invade macrophages:
- Distended macrophages block lymphatic blockage & lipid deposition - S/S: arthropathy, diarrhea, & weight loss |
|
Which presents with relapsing blood diarrhea, Chrohn's or Ulcerative colitis?
|
UC, along with mucus, abdominal pain, & cramps
|
|
What inhibitor of peptidoglycan synthesis is only used in topical form?
|
Bacitracin
- MOA: prevents transfer of mucopeptides into the bacterial cell wall - Rx: gram-, gram+ bac via a mild skin cut |
|
What is the primary secretory product in 55% of cases of multiple myeloma?
|
IgG
|
|
What uncommon form of lymphoma results in plasma cells that secrete monoclonal IgM paraproteins?
|
Waldenstrom's macrogloulinemia
|
|
What is the function of histamine?
|
- To promote vasodilation
- To promote leukocyte estravsation |
|
What do these S&S indicate: chorea, fever, polyarthritis, valvular damage?
|
Rheumatic heart disease
- can cause congestive heart failure due to mitral &/or aortic valve damage - Histo: Aschoff bodies = noncaseating granulomas with multinucleated giant cells |
|
What histological finding is common in elderly patients with aoritic stenosis?
|
degenerative calcification
|
|
What histological finding is associated with mitral valve prolapse?
|
myxoid degeneration
|
|
What is "contraction alkalosis"?
|
- When there is rapid loss of bicarb-free fluids (e.g. stomach contents, urine) = increase in plasma [bicarb]
- Body response: stimulation of the renin-angiotension-aldosterone system: 1) angiotension-mediated increase in H+ secretion via the antiporter in the proximal tubule 2) aldosterone-triggered influx of Na & H2O with an efflux of K & H+ in the distal tubule RESULT = metabolic alkalosis |
|
What is the parentral rout of transmission?
|
- Sexual activity
- Blood transfusions - Transplacental (Think: HIV) |
|
What immune system deficiency most often leads to a susceptibility to Neisseria infection?
|
Complement component deficiency
|
|
What are 1/2 of viral cases of myocarditis caused by?
|
Coxsackie B (icosahedral, Picornaviridae)
|
|
What sign of hypoglycemia do beta-blockers mask?
|
tachycardia
|
|
What happens when the tubule & glomerular basement membranes are nonenzymatically glycosylated?
|
Diabetic neptropathy:
- increase permeability to proteins - cytokin release causes glomerular hypertrophy - HISTO: diffuse mesangial expansion in the glomeruli & later nodular glomerulosclerosis (Kimmelsteil-Wilson nodules) |
|
What features characterize nodular glomerulosclerosis?
|
- Increased cellularity
- Mesangial matrix deposition - Hyaline masses & thickening of the lamina densa Diabetic nephropathy |
|
What is the histological picture of lupus nephropathy?
|
- wire-loop glomeruli
- subendothelial basement membrane deposits |
|
What is the most common cause of abruptio placentae?
|
Rupture of defective maternal vessels in the decidua basalis
- RF: hypertension, cocaine use, smoking, uterine fibroids, advanced age, sudden uterine decompression, premature rupture of the membranes, & bleeding diathesis |
|
What causes Placenta accretia?
|
placental villi attach directly to the myometrium due to a defect in the decidua basalis layer
- @ delivery, there is incomplete separation of the placenta - can cause severe postpartum hemorrhage |
|
Define labor.
|
Regular uterine contractions that result in cervical change
|
|
Define preterm labor.
|
Labor that occurs between 20 & 37 weeks of gestation.
|
|
What are the components of prokarytoic ribosomes?
|
Large (50S) subunit
- 5S rRNA molecule + 23S rRNA molecule Small (30S) subunit - 15S rRNA molecule All rRNA are bound to & protected by the ribonucleoprotein component of the ribosome |
|
What is the best treatment for "thyroid storm"?
|
1st: primary stabilization = propranolol
2nd: propylthiouracil or methimazole to inhibit endogenous synthesis of thyroxine |
|
Which is better during thryotoxicosis & thyroid storm: aspirin or acetaminophen?
|
Aceaminophin: antipyretic
NOT asprin b/c it displaces throxine from thyroid-binding globulin & worsens symptoms |
|
What are the earliest visible manifestations of endometriosis?
|
Whitish peritoneal plaques
|
|
When whitish periotneal plaques are found along the uterosacral ligament, where is the endometriosis?
|
- pelvic cul-de-sac
- complications = adhesions to bowel can cause obstruction |
|
Why does a metabolic acidosis often result in hyperkalemia?
|
- Increased H+ ions are used to balance Cl- in the urine
- This prevents K+ secretion by the H+/K+ exhcanger in the distal tubule Rx: loop diuretic (e.g. furosemide) to increase Na & K excretion in the loop of Henle |
|
What is the most common of inherited aplasic anemia?
|
Fanconi's anemia = defective DNA repair
- radial ray abnormalities can result in abnormal or absent radii or thumbs - Other signs: kidney malformations, hypogonadism, microcephaly, high fetal hemoglobin |
|
What is Diamond-Blackfan anemia?
|
Congential RBC aplasia caused by primary failure of erythroid progenitor cells in the bone marrow
|
|
What is lacking in alkaptonuria patients?
|
homogentisic oxidase
= no effective tyrosine degradation (homogentisic acid to maleylacetoacetic acid) - homogentisic acid builds up in urine - when urine is exposed to alkali or O2 = DARK BLACK - S/S = usually benign or presents with arthritis |
|
What enzyme is lacking in Maple syrup urine disease?
|
alpha-ketoacid dehydrogenase, which catabolizes branched amino acids (valine, leucine, isoleucine)
|
|
What is cystinuria?
|
- a defect of amino acid (cystine) transport in the renal tubules
- can result in cystine stone formation |
|
What are the symptoms of homocystinuria?
|
- Mental retardation
- Spinal abnormalities (kyphosis, Marfanoid habitus) - Atherosclerosis - Lens subluxation MO: defect in conversion of methionine to cysteine - 3rd decade of life = thromboembolic events increase |
|
What is the treatment for primary syphilis?
|
benzathine penicillin G (long-acting): 1, intramuscular dose
|
|
What is the treatment fo Chlamydia or Haemophilus ducreyi?
|
Azithromycin (1 oral dose)
|
|
What is the most common fetal neoplasm?
|
sacrococcygeal teratoma (multiple tissue types = remnant of the primitive streak)
|
|
What are the 2 types of MSUD (maple syrup urine disease)?
|
Intermittent: presents during times of catabolism (e.g. after infections)
Classical: ketonuria 48 hrs to 1 week after birth |
|
What CSF finding is found in 80-90% of MS (multiple sclerosis) patients?
|
Increased Ig levels: reflects presence of intrathecal humoral immune activation
|
|
What CSF finding is the hallmark of Guillain-Barre syndrome?
|
albuminocytologic dissociation: greatly increased protein concentration with only a modest increase in cell count
- MOA: acute demyelination of peripheral nerves (acute ascending paralysis) after a viral infection or gastroente ritis from C. jejuni infection |
|
What is the mechanism of basal ganglia destruction in Huntington's
|
- gutamate toxicity of the ganglia in the caudate & putamen
- gliosis & neuronal depletion result in a loss of motor inhibition = chorea & athetoid movements |
|
What causes neurofibrillary tangles?
|
- Hyperphosphorylated tau protein
- Characteristic of Alzheimer's disease |
|
What is the treatment for phenylketonuria?
|
Dietary
- Avoid phenylalanine - Suppliment tyrosine (b/c the phenylalanine cannot be converted to tyrosine) |
|
What is the most common cause of pneumonia in malnourished, debilitated, or alcoholic patients?
|
Klebsiella pneumoniae (gram -, rod)
- X-ray: diffuse infiltrates (NOT lobular) |
|
What three "drugs" have zero-order elimination?
|
1) ethanol
2) phenytoin 3) high-dose asprin |
|
What is lateral medullary syndrome (aka posterior inferior cerebellar artery (PICA) syndrome or Wallenberg's syndrome)?
|
A Stroke Syndrome:
- Symptoms: numbness of the ipsilateral face & contralateral limbs, diplopia, dysarthria, & ipsilateral Horner's - Cause: disruption of PICA - blood supply to dorsolateral quadrant of medulla, including nucleus ambiguus & inferior surface of the cerebellum |
|
What happens when the posterior inferior cerebellar artery (PICA) is infarcted?
|
Lateral medullary syndrome due to dorsolateral quadrant disfunction:
- Tract of CN V = facial pain - Vestibular nuclei = dysequilibrium - Nucleus ambiguus = palate problems & hoarse voice - Spinothalamic tract = contralateral pain & temperature loss - Descending sympathetic fibers = ipsilateral Horner's |
|
What is the 2nd most common brainstem stroke syndrome?
|
Ischemia to the Anterior inferior cerebellar artery:
- Caudal lateral pontine tementum (including spinal tegmental tract of CNV) - Inferior surface of the cerebellum - Symptoms: ipsilateral deafness (labyrinthine artery to cochlea & vestibular apparatus), ipsilateral facial weakness, ataxia |
|
What is damaged in a lacunar stroke?
|
Lateral striate arteries (penetrating branches of the MCA):
- internal capsule, caudate nucleus, putamen, & globus pallidus |
|
What structures are damaged in a symptomatic internal carotid artery occlusion?
|
- lateral geniculate body
- globus pallidus - posterior limb of the internal capsule |
|
Which results in tetany: HYPO or HYPER calcemia?
|
Hypocalcemia (remember DiGeorge's symptoms)
|
|
What types of infections are you prone to if you have a T lymphocyte deficiency?
|
Viral & Fungal
|
|
What organism causes Hemolytic-uremic syndrome & what lab values characterize this problem?
|
- E. coli O157:H7 (gram - , rod, lactose-fermenting)
- Low platelet count, anemia, renal failure (e.g. uremia) |
|
What are the symptoms of rheumatic fever?
|
- Fever
- Migratory polyarthritis - Carditis - Can follow a Group A strep pharyngitis |
|
What are the signs of bacterial endocarditis?
|
- Fever
- New Murmur - Janeway lesions - Nail bed hemorrhages |
|
What is the most common cause of acute & subacute endocarditis?
|
- Acute: Staph aureus (10-20? of endocarditis)
- SubAcute: viridans strep (usually attacks previously-damaged valves); causes 50-60% of endocarditis |
|
Where does Pemphigus vulgaris attack?
|
Pathogenic antibodies are directed against dsmoglein-3, a cell-cell adhesion protein expressed by epidermal keratinocytes
- Result: intraepidermal acantholysis with sparing of the basal layer - Nikolsky's Sign: flaccid epidermal bullae that easily slough off leaving large denuded areas of skin (prone to infection) Rx: steroids |
|
What is lacking in patients with essential fructosuria?
|
BENIGN frutosuria b/c fructose does not enter cells & does not deplete cellular phosphate
- fructokinase: converts frutose to fructose-1-phosphate |
|
What is deficient in patients with hereditary fructose intolerance?
|
Aldolase B (aka fructos-1.6-bisphosphate aldolase): converts fructose-1-phosphate to dihydroxyacetone-phosphate
- fructose-1-phosphate accumulates in cell - Presentation: jaundice, hepatomegaly, vomiting, lethargy, convulsions, & hypoglycemia after ingesting fructose Rx: AVOID fructose & sucrose (glucose + fructose) |
|
What dietary recommendation is made for patients with McArdle's?
|
High protein + creatinine
|
|
What is the action of endogenous opioid peptides on the GI?
|
- Stimulate smooth muscle contraction
- Inhibit intestinal secretion of fluids & electrolytes (Morphine has these properties as well) |
|
What is the relationship between prevalence and the PPV of a test?
|
As disease prevalence decreases, the probability of a positive being a true positive decreases
|
|
Rank infectious agent types in order of increasing susceptibility to chemical sterilants.
|
Least to Most:
1) prions 2) spores 3) Myocbacteria 4) Nonenveloped viruses 5) Fungi 6) Gram+ bacteria 7) Gram- bacteria 8) Enveloped viruses |
|
What genetic disease results in skin that readily breaks & forms blisters with minor trauma?
|
Epidermolysis bullosa
- Caused by a mutation in either keratin 14 or 5 in basal epithelial cells |
|
What is the classical triad of Pott's disease?
|
- Spinal Pain
- Kyphosis (compromised vertebra) - Neurologic signs (radicular pain to cord compression & paralysis) |
|
For what systemic infection is amphotericin the DOC?
|
Disseminated mycoses:
- blastomycosis - cryptococcus - histoplasmosis |
|
What is the most common cause of a paraspinal abscess?
|
Staphylococcus aureus
Rx: IV vancomycin |
|
What lab findings indicate Paget's disease of bone?
|
Elevated Alkaline Phosphatase + normal micronutrient levels
|
|
what are 4 typical uses of sulfa drugs, like trimethoprim?
|
1) UTI
2) Nocardiosis 3) Toxoplasmosis 4) Prophylaxis for recurrent otitis media |
|
What sulfa drug perscription should be combined with folic acid supplementation?
|
Timethoprim
Why? To reduce megaloblastic anemia, leukopenia, & granulocytopenia |
|
What property of quinolones (like Gatifloxacin) makes them particularly useful for treating UTIs?
|
Concentrated in the urine
MOA: inhibit DNA gyrase during bacterial replication & growth |
|
What drug class is toxic to cartilage?
|
fluoroquinolones: can lead to tendinitis & tendon rupture
- e.g. gatifloxacin |
|
What 5 main problems are macrolides (e.g. erythromycin) used to treat?
|
1) Gram+
2) Legionnaire's 3) Syphilis 4) Mycobacterial pneumonia 5) Corynebacterial infections (e.g. diptheria) |
|
What broad-spectrum antibiotic is particularly effective for meningitis?
|
chloamphenicol
SE: aplastic anemia & gray baby syndrome |
|
What are two genetic/anatomical risk factors for testicular cancer?
|
- Klinefelter's (47, XXY): usually will be extragonadal, nonseminamatous testicular cancer
- Cryptorchidism |
|
What 2 cell types kill target cells through the release of preformed granules?
|
1) NK cells: perforin & granzymes
2) CD8+ |
|
What drug causes increased vessel permeability and subsequent edema in the face, lips, mouth, and subglottic tissue?
|
ACE inhibitors:
- block the 2ndary action of ACE on the degradation of bradykinin - High levels of bradykinin produce these symptoms |
|
What are the 2 main functions of prostacyclin?
|
Produced by vascular endothelial cells from PGH2:
1) prevents platelet aggregation 2) potent vasodiation |
|
What causes watery, foul-smelling stool with leukocytosis following antibiotic treatment?
|
C. difficile superinfection
Rx: metronidazole |
|
What are the pseduomembranes of C. difficile psuedomembranous colitis?
|
inflammatory exudates on the injured mucosa due to the to protein exotoxins (A & B) of C. difficile
|
|
How does S. aureus cause food poisoning?
|
heat-labile & heat-stable exotoxin secretion
|
|
What is the virulence factor of Clostridium perfringens?
|
produces lecithinase that breaks down cell membrane lecithin (& produces gas-bubbles)
|
|
How does Yersinia enterocolitica cause mesenteric adenitis?
|
invades Peyer's patches of the gut (& 2ndary fever & diarrhea)
|
|
What is the inhibitor (regulator) of phosophofructokinase & t/f of the rate-limiting step of glycolysis?
|
citrate (from the Krebs Cycle)
|
|
What regulates the Krebs cycle by providing negative feedback to pyruvate dehydrogenase?
|
Acetyl-coenzyme A (produced from pyruvate by pyruvate dehydrogenase)
|
|
What amino acids carries amino groups from the muscle to the liver?
|
alanine (can also be convered to pyruvate to be used in the Krebs cycle & can also inhibit pyruvate kinase)
|
|
What enzyme produces glucose-6-phosphate in the 1st step of glycolysis?
|
1) In all tissues: hexokinase
2) Liver ONLY: glucokinase |
|
Which antidiarrheal is an opiate analog & derivative of haloperidol?
|
Loperamide: binds GI opiate receptors & inhibits bowel motility
|
|
How does aluminum chloride decrease GI motility?
|
Osmotic & Ionic effects
|
|
How does Bismuth subsalicylate work?
|
- Binds to the ulcer base & provides physical protection
- Also allows HCO3- secretion to reestablish the pH gradient in the mucous layer |
|
What is the MOA of Kaolin?
|
An absorbent that binds toxic compounds from the GI wall & promotes their excretion
|
|
What is the use of a beta-blocker in patients with chronic liver disease?
|
Treats their portal hypertension
|
|
Why do loop diuretics cause a loss of potassium?
|
B/C loops block Na absorption in the thick ascending loop of Henle, the nephron attempts to absorb more Na in the distal tubule & collecting duct. In the collecting duct:
1) K+ & H+ are exchanged by the intercalated cells 2) Na & H2O are absorbed by principle cells & K+ is secreted |
|
How should salmonella gastroenteritis be managed?
|
1) Treat dehydration with fluid & electrolyte replacement
2) Give antibiotics if there is evidence of bacteremia or focal infection. Otherwise, antibiotic treatment will increase rates of relapse |
|
What are the most common risk factors for ectopic pregnancy?
|
1) PID
2) prior appendicitis 3) endometriosis 4) prior abdominal surgery |
|
List the 5 stages of neutrophil development.
|
1) Promyelocytes (with primary granules)
2) Myelocytes (with 2ndary granules) 3) Metamyelocytes (with more prominent indented nuclei) 4) Band (stab) cells (horseshoe-shaped, but not yet lobulated) 5) Mature neutrophils (with clearly lobulated nuclei) |
|
What is internuclear opthalmoplegia?
|
1) ispsilateral medial rectus palsy on attempted lateral conjugate gaze away from the lesion
2) monocular horizonal nystagmus in the contralateral abducting eye 3) Preserved convergence Cause: damage to the ipsilateral medial longitudinal fasciculus: the connection between the abduct & oculomtor nerve, where their actions become UNLINKED - PEDS: CNS infection or MS - Adults: vascular disease |
|
What does CN III innervate?
|
All extraocular muscles, except the lateral rectus (CN VI) & superior oblique (CN IV)
- Lesion: affected eye looks "down & out" when at rest (abducted & depressed) |
|
What 3 diseases can cause Argyll Roberson pupil?
|
1) Neurosyphilis
2) Diabetes 3) SLE Pupillary light-near dissociation: absent miotic reaction to light with preserved accommodation |
|
What is Marcus Gunn pupil and what causes it?
|
Relative afferent pupillary defect
Cause: lesion in the afferent limb of the pupillary light reflex - MS: retrobulbar neuritis |
|
What histological change in the CNS is often found in SIDS autopsies?
|
Astrogliosis: nonspecific response to injury to the brain stem & cerebellum
- Hypertrophy of astrocytes - Increase in glial fibrillary acidic protein immunostaining |
|
What are the histo findings in muscle tissue of patients that suffer from ALS (amyotrophic lateral sclerosis)?
|
- Fiber type grouping consistent with reinnervation
- Small angular fibers consistent with deinervation & neurogenic atrophy |
|
What are the physical exam findings in a child with Kawasaki's?
|
- Fever
- Conjunctivitis - Erythema in the oral mucosa - Cervical lymphadenopathy |
|
What is the typical clinical presentation of a patient with Buerger's?
|
Patient (20-40 years, heavy smoker)
- Intermittent claudication - Superficial nodular phlebitis - Cold Sensitivity |
|
What are the physical findings in a patient with PAN (polyarteritis nodosa)?
|
- Cotton-wool spots on the retina
- Microaneurysms - Palpable purpure on the skin (+ history of Hep B) |
|
What is the histo hallmark of PAN (polyarteritis nodosa)?
|
transmural inflammation of the arterial walls in kidneys, PNS, & GI tract
LAB: + perinuclear anti-neutrophilic cytoplasmic antibody (against myeloperoxidase) |
|
What is the histo characterization of Wegener's?
|
Necrotizing granulomas in the lung & upper airways + glomerulonephritis
LAB: + anti-neurophilic cytoplasmic antiboby |
|
What is the treatment for Lyme disease?
|
oral doxycycline
|
|
What are the classical symptoms of Cooley's anemia?
|
severe beta-thalassemia:
- Hemolytic anemia - Hepatosplenomegaly - "Chipmunk facies" due to extramedullary hematopoiesis in facial bones) LAB: increased HbF & HBA2 (neither require B chains), absense of HbA1 shows that there is NO beta chains RIP: cardiac failure 2ndary to hemochromatosis |
|
Which Thalassemia confers a mild protective effect against Plasmodium falciparum malaria?
|
Beta Thalassemia minor (heterozygous defect): b/c of shortened lifespan of RBCs
LAB: decreased HBA1 |
|
What is the geographical distribution of thalassemias?
|
beta: Mediterranean
alpha: Asia / Africa |
|
What is Kartagener's syndrome?
|
AR disease with this Triad:
1) Chronic sinusitis (& otitis media) 2) Bronchiectasis (chronic bronchitis & recurrent pneumonia) 3) Situs inversus Patho: poorly functioning dynein arms on all cilia in the body Presentation: unremitting asthma & sinus pressure headaches |
|
What are the functions of actins in cells?
|
Composition: multiple globular G-actin subunits
- Tracts for myosins: cell motility, vesicular transport, or muscle contraction |
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What are the cellular functions of myosins?
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Composition: ATP-driven dimeric molecular motor proteins
- Move along actin filaments for vesicular transport, cell motility, & muscle contraction |
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What is glyburide's MOA as a type II diabetic drug?
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Sulfonylurea: stimulates release of endogenous insulin to reduce blood sugar levels
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What class of drugs increase target cell sensitivity to insulin & decrease hepatic gluconeogenesis?
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Thiazolidinedines:
- Glitazone - Rosiglitazone - Pioglitazone |
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What drugs inhibit the intestinal brush boarder enzyme alpha-glucosidase?
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alpha-Glucosidase inhibitors (acarbose)
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What is the inherited form of hyperammonemia that presents with mental retardation, seizures, and finally death?
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- Ornithine transcarboamolyase
- Normal enzyme function: combines carbamoyl phosphate & ornithine to make citrulline in the urea cycle |
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What storage disease presents with generalized hypotonia, muscle weakness, & hypertrophic cardiomegaly?
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Pompe's (absent lysosomal alpha-1,4 glucosidase)
LAB: significantly elevated serum creatinine kinase |
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What enzyme defect presents with vomiting, diarrhea, failure to thrive & hypotonia within the 1st few days of life?
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galactose 1-phosphate uridyltransferase galactosemia
- galactose 1-phosphate is toxic to renal, hepatic, & neuronal cells Rx: galactose restriction. NB: patients may STILL have developmental delay, ataxia, & apraxia |
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What are the 2 effects of an aldose B dysfunction?
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No splitting of fructos-1-phosphate:
1) Inhibition of glucose production 2) Depletion of adenosine triphosphate |
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What enzyme deficiency presents with angiokeratomas, hypohidrosis, corneal & lenticular opacities, acroparesthesias, and vescular disease of the kidney, heart & brain?
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Fabry's: mutations in alpha-galactosidase A gene -> accumulation of ceramide trihexoside
Rx: enzyme replacement therapy |
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What foods should patients with hereditary fructose intolerance avoid?
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fructose, sucrose, sorbitol
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What are the typical clinical symptoms of ureteral or bladder calculus?
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- Sharp, intermittent, excruciating pain in the lower back, abdomen, or testicular region
+ Fever, nausea, vomiting, & hematuria |
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In a woman with symptoms of acute appendicitis, what hormone should be measured?
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Rule out ectopic pregnancy wiwht a beta-hCG level test
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What is Meniere's disease?
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IDIOPATHIC DISEASE WITH:
- Episodes of vertigo lasting for a period of hourse with associated fluctuation - Progressive low-frequency sensorineural hearing loss - Aural fullness or pressure (tinnitus) Cause: increase in the volume of the endolyphatic system (hydrops) 2ndary to malfunction of the endolymphatic system, which is responsible for the filtration/excretion of endolymoph in the membranous labyrinth of the inner ear |
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What causes BPPV (benign paroxysmal positional vertigo)?
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Freely moving crystals of Ca-carbonate within the semicircular canals cause seconds of vertigo & nystagmus
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What parts of the inner ear react to acceleration & deceleration of the head?
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utricle & saccule
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What lesion results in impairment in the high-frequency range of hearing & problems with speech discrimination?
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Cranial Nerve VIII (vestibulocochlear)
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What 3 conditions are associated with elevated beta-human chorionic gonadotropin levels?
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1) Pregnancy
2) Choriocarcinoma 3) Complete hydatidiform mole |
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What 2 diseases are associated with P-ANCA elevation?
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1) Microscopic polyangiitis
2) Churg-Strauss syndrome: allergic rhinitis, asthma, & eosinophilia |
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Which gyrus is the primary motor cotex?
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precentral: top = feet, bottem = face
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What is the UMN innervation of the face?
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- Upper 1/3: bilateral
- Bottom 2/3: contralateral primary motor cortex |
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What is the lateral collateral ligament complex?
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Ankle joint ligment complex that protects from inversion stress:
1) anterior talofibular ligament 2) calcaneofibular ligament 3) posterior talofibular ligament |
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What prevents eversion stress on the ankle?
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deltoid ligament
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What ligament is most commonly affected in ankle sprains?
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anterior talofibular ligament (usually protects against inversion stresses)
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What hormone acts on the hypothalamic thermregulatory center & slightly elevates basal body temp after ovulation?
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progesterone
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What is given as "rescue therapy" due to cyclophosphamide induced hemorrhagic cycstitis due to the accumulation of toxic metabolites in the urine?
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Mensa: converts some of the toxic metabolites (e.g. acrolein) into as less toxic form to be secreted in the urine
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What are the clinical signs of a pineoblastoma?
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- headache
- drowsiness &/or vivid dreams due to excessive melatonin production, which regulates sleep-wake cycles MRI: contrast-enhancing pineal mass located between the thalamic bodies |
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What is the classical sign of a craniopharyngioma?
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visual disturbances b/c this pituitary stalk tumor compresses the optic chiasm
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What are the 2 classical signs of a pituitary adenoma?
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- hyperprolactinemia
- bitemporal hemianopia (compresses the optic chiasm) |
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How does initial ICP present?
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headache, nausea, vomiting
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What are the 2 mechanisms of iron absorption?
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1) Heme-associated iron is taken up by heme transporter in the luminal plasma membrane of the duodenal epithelial cell.
2) Free ferric iron ions are converted to ferrous iron ions by a cytochrome B enzyme on the luminal plasma membrane of the duodenal epithelial cell. Ferrous iron ions are taken up by the DMT channel. W/in the cell, iron is transferred to mucosal ferritin & then shuttled to transferrin in the plasma |
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What glycogen storage disease occurs in adolescence?
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McArdle's
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What disease is a mild form of vonGierke's?
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- Cori's: deficiency in alpha-1,6-glucosidase (glycogen debranching enzyme)
- With NORMAL blood lactate levels! |