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216 Cards in this Set
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What does glucose in the urine indicate about the plasma levels of glucose?
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Since any glucose in the urine is reabsorbed up to 200-300 mg/dL, any glucose in the urine indicates that the blood sugar is greater than 200-300.
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What is the definition of clearance in renal physiology?
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Clearance is the amount of something removed in a certain amount of time. By convention, 24 hours is often used. Can also consider clearance as the volume of blood plasma (per unit time) needed to supply the amount of solute that appears in the urine.
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If the clearance of a solute X is greater than the GFR, is their net reabsorption of secretion of solute x?
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Clearance>GFR --> secretion
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If the clearance of a solute X is less than the GFR, is their net reabsorption of secretion of solute x?
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Clearance<GFR --> reabsorption
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Can you accurately measure the GFR outside of steady state?
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No; creatinine is used as a proxy for GFR, but it is only useful in steady state.
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How does the BUN/Cr ratio change in dehydration conditions?
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The BUN/Cr ratio increases during dehydration. Urea is actively absorbed in the renal tubules. In dehydration, flow through the tubules is slow, and the tubules have more time to act on the fluid (i.e., reabsorb more urea), so relatively more urea is absorbed and creatinine is secreted, causing an increase in BUN/Cr
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What's the difference beteen azotemia and uremia?
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Azotemia is high BUN, whereas uremia is high BUN with symptoms of renal failure (e.g., anorexia, nausea, weight loss, confusion).
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Which of the following is not a systemic manifestation of acute renal failure (ARF)?
A) Hypokalemia B) Metabolic acidosis C) Hypophosphatemia D) Anemia |
A and C are incorrect, Hyperkalemia and Hyperphosphatemia occur in ARF
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What is the definition of prerenal failure?
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Prerenal failure is defined as a decrease in the GFR due to decreased renal perfusion that can be restored with increased renal perfusion and is not associated with structural damage of the kidney.
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Which of the following is not a cause of prerenal failure?
A) CHF B) Glomerulonephritis C) Dehydration D) Sepsis |
B) Glomerulonephritis is a cause of intrinsic renal failure
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Why do you have a high BUN/Cr ratio in prerenal failure?
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When there’s a decreased blood flow to the kidney, the kidney reabsorbs more urea at the glomerulus, while Cr is not reabsorbed, and hence you have a greater BUN/Cr ratio.
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What percentage FeNa (fractiona excretion of sodium) would expect in someone with prerenal failure?
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<1%
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What is the definition of postrenal failure?
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Post renal failure refers to obstruction anywhere in the urinary tract causing renal failure.
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What are common causes of postrenal failure (i.e. what can cause the obstruction)?
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Enlarged prostate
Stones Obstructed catheter |
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What group/syndrome is generally the most common inpatient cause of AKI vs outpatient?
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Inpatient – intrinsic renal failure (specifically, acute tubular necrosis)
Outpatient – Prerenal failure |
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What is the definition of intrinsic renal failure?
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Intrinsic renal failure occurs when one or more components of the kidney are damaged. These components are: glomeruli, blood vessels, tubules, and the interstitium.
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What is the most common cause of AKI in developing nations versus industrialized nations?
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Hypovolemic shock from diarrhea in developing nations
Bypass cardiac surgery in industrialized nations |
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What urine abnormality is the hallmark of acute tubular necrosis (ATN)?
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Brown granular casts
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What is the definition of chronic kidney disease?
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Chronic kidney disease (CKD) is defined as kidney damage for > 3 months resulting in pathologic and/or functional abnormalities. Often results in a decreased GFR (<60 cc/min).
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In the U.S., what are the 2 top causes of chronic kidney disease (CKD)?
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Hypertension and Diabetes Mellitus
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What are the most common complications of chronic kidney disease (CKD)?
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Most common complications of CKD:
1. HTN from salt and H2O retention 2. Anemia from lack of EPO synthesized by kidneys 3. Secondary hyperparathyroidism from Ca++/Phosphorus/vit D dysregulation 4. Malnutrition from GI disturbances |
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What is hyperfiltration?
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After the initial injury, the remaining functioning nephrons need to increase solute excretion/per nephron to maintain solute level and GFR.
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Are patients with chronic kidney disease at risk for hypo or hypernatremia?
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Trick question. They’re at risk for both, because they lose their ability to both concentrate and dilute urine.
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What factors can worsen hyperfiltration?
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Hyperglycemia
Obesity High protein diet |
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What is a medical treatment to slow the process of hyperfiltration?
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ACE inhibitors dilate the efferent arteriole and decrease intraglomerular blood pressure, thus slowing the process of hyperfiltration.
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Why does secondary hyperparathyroidism occur in patients with chronic kidney disease (CKD)?
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With decreased GFR, serum phosphorus gets elevated, you get less vit D, because you can’t hydroxylate it. This leads to decreased calcium which causes the parathyroid to secrete PTH, causing secondary hyperparathyroidism. Secondary parathyroidism is adaptive as it increases Ca++ release from bone and stimulates urinary phosphate excretion.
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At what point do you consider renal replacement in chronic kidney disease?
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Renal replacement is indicated when the GFR is <10-15cc/min and has uremic symptoms or when a patient has an acute indication
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What are the main characteristics of nephritic disease?
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Hematuria
HTN Azotemia Variable proteinuria Edema |
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What are the main characteristics of nephrotic disease?
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Proteinuria > 3.0 g/day
Hypoalbuminemia Edema Hypercholesterolemia |
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What are risk factors for kidney disease progression?
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Elevated creatinine
High proteinuria HTN Scarring/damage on biopsy |
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Post Infectious Glomerular nephropathy and IgA nephropathy are similar in that they typically present after an infection. What differs between the two in terms of the timing of presentation?
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Post Infectious Glomerular nephropathy occurs 1-3 weeks after the infection, whereas IgA nephropathy occurs almost immediately after the infection/cold (1-2 days).
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An 18 yo smoker (gas station attendant) presents with shortness of breath. He is hypoxic, and CXR shows bilateral infiltrates. He has a cough that is blood tinged. Laboratory results show anemia and an elevated creatinine. Urinalysis shows blood and protein present in the urine. What illness does he probably have?
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Goodpasture's syndrome (Anti-GBM disease)
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What is the pathogenesis of Goodpasture's syndrome?
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Goodpasture's syndrome (Anti-GBM disease) is a pulmonary-renal syndrome caused by autoantibodies that bind to type IV collagen found in the glomerular basement membrane and the lung. It’s usually found in young males.
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What is the clinical range of microalbuminuria in a spot collection or a 24 hour urine collection?
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30-300 mcg/mg creatinine for spot collection
30-300 mg for 24 hour collection 20-200 mcg/min for timed collection |
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Which demographic most commonly gets IgA nephropathy?
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Asian males (especially Japanese)
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If a patient has asthma, eosinophilia, blood and protein noticed on routine exam and uncontrolled wheezing on their lung exam, what disease do they probably have?
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Churg-Strauss
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Passage of albumin through the glomerular filtration system should be about 15%, but it’s not. Why is that?
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Albumin is negatively charged in the circulation.
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Nephrotic patients, especially those with membranous nephropathy, are prone to developing intravascular clots. What can cause this?
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Urinary loss of anticoagulant proteins like protein S (AT III could also be a culprit)
Hemoconcentration from fluid extravasation Increased production of certain clotting factors When ambient albumin concentration is decreased, platelets become hyperaggregable |
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What is the upper limit of normal proteinuria?
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60 mg/M^2 body surface area per day or 100 mg/day
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Why do you get hyperlipidemia and hypercholesterolemia in nephrotic syndrome?
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The loss of albumin and protein causes increased synthesis of protein by the liver and consequent synthesis of lipids and cholesterol, which accumulate in the blood.
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What morphological feature is the hallmark for minimal change disease (MCD)?
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Fused processes is the hallmark for minimal change disease
Diagnosed via electron microscopy Most common cause of nephrotic syndrome in children |
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What causes the fusion of foot processes in minimal change disease (MCD)?
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Loss of negative charge.
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What is the pathogenesis of Alport syndrome?
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Alport syndrome is an X-linked disorder with defective type IV collagen (especially affecting the alpha 5 domain—also, alpha 3 and 4 are not detected, but they’re normal) in the glomerular basement membrane. They also have a deficiency of prolyl hydroxylase.
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If a diabetic patient presents with microalbuminuria, what form of treatment would you use?
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Can put on ACE inhibitors to reduce the pressure to protect the kidneys
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What tool provides the ultimate diagnosis of amyloidosis?
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Electron Microscopy (EM)
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What are morphological findings on electron microscopy for post-streptococcal (or post-infectious) glomerulonephritis?
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Large dark subepithelial humps on electron microscopy
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Can you describe where immune complexes deposit for diffuse proliferative versus membranous glomerulopathy in lupus?
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Membranous: subepithelial and mesangial
Diffuse proliferative: subendothelial and mesangial |
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What differentiates Lupus Membranous Nephropathy from Idiopathic Membranous Nephropathy?
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Idiopathic Membranous Nephropathy: subepithelial deposits and NO deposits in mesangial matrix
Lupus Membranous Nephropathy: subepithelial deposits AND deposits in mesangial matrix |
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In one scenario of immune complex deposition and immune response activation, a non-intrinsic foreign tissue antigen implants itself in the glomerular capillary, evokes an immune response, and subsequently the circulating antibody binds to the already implanted antigen. What disease/syndrome is this characteristic of?
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Poststreptococcal glomerulonephritis.
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What is the mechanism of action of local anesthetics?
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Local anesthetics block the Na+ channel and hence the action potential (they block the Na+ channel more than the K+ channel).
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Which form, the charged, or un charged form, of local anesthetics is responsible for the blockage of nerve conduction?
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It is the charged/cationic form of the local anesthetic that is responsible for the blockage of nerve conduction, blocking the sodium channel from the axoplasmic side of the membrane.
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What is the effect of raising the pH on the potency of local anesthetics? What is a clinical example of such an action?
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Raising an external pH increases the uncharged lipid-soluble form which accumulates more inside the axoplasm, increasing the charged form as well. This produces more Na channel blocking and hence increases the potency of the local anesthetic.
This could be accomplished clinically with the use of sodium bicarbonate to alkalize the local anesthetic solution, which maximizes the uncharged lipid-soluble form. |
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How does inflammation affect the potency of local anesthetics?
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Inflammation causes tissue acidosis and decreases the pH, decreasing the anesthetic concentration inside the axoplasm and reducing the potency of the anesthetic.
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What is the site of action of local anesthetics?
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Local anesthetics act on the alpha subunit of the sodium channel, which is a pore-forming membrane protein.
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What is use-dependent block?
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Use dependent block refers to the fact that the blocking potency of local anesthetics is enhanced by repetitive stimulation, which opens the channel. Thus, repetitive nerve activity that potentiates conduction block by local anesthetics is called use-dependent block. (i.e. Repetitive depolarization enhances the sodium channel blocking action by lidocaine.)
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What is frequency-dependent block?
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Increasing the frequency of the repetitive activity enhances the degree of use dependent block and is called frequency-dependent block.
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What’s the difference between ester and amide types of local anesthetics in terms of how they are metabolized?
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The difference between ester and amide types of local anesthetics lies in how they are metabolized. Ester-type local anesthetics are rapidly hydrolyzed by plasma pseudocholinesterase (butrylcholinesterase), whereas amide-type local anesthetics are metabolized in the liver by P450 enzymes.
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How does cocaine produce its euphoric effect?
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Cocaine inhibits the re-uptake of dopamine. (Other inhibitors of uptake: tricyclic antidepressants, methylphenidate).
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Do ester type or amide type local anesthetics cause allergic reactions more often? What molecule is responsible?
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Allergic reactions occur more often with ester-type local anesthetics and are extremely rare with amide local anesthetics. The culprit for allergic reactions is due to derivatives of p-aminobenzoic acid, a metabolite of the ester type local anesthetics.
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How does tetrodotoxin enact its toxic effect?
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Tetrodotoxin, from the puffer fish, blocks voltage-gated Na channels from the axoplasmic side of the excitable membranes in nerves and skeletal muscles (but not the cardiac Na channels). TTX prevents initiation of rapid Na-dependent action potentials in nerve and muscle (there are pre and post-junctional voltage-gated Na+ channels).
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What is the function of SNARES in neurotransmission?
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SNARES are responsible for priming the vesicles (i.e. making the vesicle fusion competent) and are thus essential for neurotransmitter release. SNARES have Ca++ sensors called synaptogamins intimately attached to them, awaiting an increase in intracellular calcium. When Ca++ binds the calcium sensors, you get a primed release of vesicle neurotransmitter contents.
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What terminates the synaptic action of ACh in normal physiologic conductions at the neuromuscular junction?
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Enzymes called cholinesterases are present in the plasma on membranes or within the cytoplasm of many types of cells. They catalyze the hydrolysis of ACh to choline and aceticacid.
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Can you describe the pre and postsynaptic events that induce an action potential at the nerve terminal for skeletal muscle?
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Presynaptic events:
The action potential causes the voltage-gated Ca++ channel to have an influx of Ca++ (down its concentration gradient) Then Ca++ binds to the Ca++ sensor which causes the release of vesicles Postsynaptic events: ACh binds to its receptor, opening a non-selective channel which causes the influx of Na+ which causes the EPP if it reaches a threshold, which causes an AP via the voltage-gated Na+ channel (tetrodotoxin-sensitive) It’s terminated by acetylcholinesterase which hydrolyzes ACh |
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What is hemicholinium, and what does it do?
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Hemicholinium inhibits choline uptake, which reduces the quantity of ACh present in the presynaptic nerve terminal, causing a miniature EPP due to less ACh release. When neuromuscular junctions are paralyzed by hemicholinium, MEPPs are extremely small.
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What is the pathogenesis of myasthenia gravis?
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Myasthenia gravis is characterized by a reduced number of nicotinic ACh receptors due to autoimmune attack of the receptors by circulating antibodies.
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How does botulinum toxin work?
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Botulinum toxins work on a SNARE called SNAP-25
It cleaves a small portion of SNAP-25 and reduces Ca++ sensitivity release, which inhibits secretion of ACh |
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Which agents/disorders reduce the EPP amplitudes without changing the MEPP amplitudes by blocking the entry of Ca++ ions via Ca++ channels in response to membrane depolarization?
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Mg++ and all other impermeant polyvalent cations (e.g., Co++, Mn++, Cd++, La+++, etc.)
Aminoglycoside antibiotics (e.g., neomycin, kanamycin, amikasin, gentamicin, tobramycin) Lambert-Eaton Myasthenic Syndrome (LEMS) -- reduced number of Ca++ channels in the nerve ending |
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How does the black widow spider venom cause its harm?
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It’s thought that the active ingredient of the venom, alpha-latrotoxin, causes asynchronous vesicular exocytosis and MEPPs due predominantly to the formation of cation channels in the nerve ending after binding of latrotoxin to either of its two receptors.
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How can you tell a prejunctional defect in neurotransmitter release from post junctional?
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In prejunctional defects, the EPP amplitude is decreased without a change in MEPP amplitudes, i.e. the defect is due to a decrease in evoked ACh release. There is a decrease in the number of ACh quanta and hence the amount of ACh released. This is a common phenomenon.
In a postjunctional defect, you will see a decrease in the MEPPs. This is pathognomonic for a postjunctional defect. |
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Can you describe phase I/phase II block?
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Nicotinic agents like ACh or succinylcholine depolarize muscle fibers at the end plate and produce trains of APs followed by twitches. After this burst of APs, the end-plate region of muscle becomes refractory to any form of stimulus. Transmission is thus blocked by depolarization, which is called phase I block.
| In phase II block, the depolarizing drug is still present, and the end-plate becomes less sensitive to the action of the depolarizing drug over time. The membrane has returned to its resting, polarized level despite the depolarizing drug, but neuromuscular communication is still blocked. |
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What are the underlying mechanisms for phase I/phase II block?
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Phase I:
a) the presence of depolarizing drug prevents ACh released from nerve terminals from interacting with the receptor and b) the depolarizing drug has pushed the nicotinic receptors towards the equilibrium potential (E ACh) where current flow cannot occur | Phase II a) The drug is still occupying the receptor site, preventing neutrally-released ACh from reaching the nicotinic receptor b) the nicotinic receptor is in a desensitized conformation and cannot be activated to produce an ionic current |
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What is the mechanism of action of tubocurarine?
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Tubocurarine blocks transmission at nAChRs by reducing the sensitivity of the end plate to ACh. It combines with the same receptors as ACh (thus making them unavailable to ACh released from the nerve ending), but cannot activate the conductance channel. It is a competitive inhibitor that could be overcome by excess amounts of ACh.
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What does the “curonium” suffix denote? What about “curium?”
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Curonium: Steroid
Curium: benzylisoquinolinium structure |
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Why isn’t tubocurarine used anymore?
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It causes histamine release.
It also causes ganglionic block at certain doses. |
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What is an important side effect of pancuronium?
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Pancuronium blocks vagal tone and hence causes tachycardia.
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Does vecuronium cause any cardiovascular effects?
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No; it has no cardiovascular effects! It's also primarily removed by the liver and is thus useful for patients with renal failure.
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What is malignant hyperthermia and how does it occur?
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Malignant hyperthermia is an instance of sustained muscle contraction and heat generation due to a flood of Ca++ released by certain agents (e.g., succinylcholine). Succinylcholine binds to ryanodine receptors in the T tubules and causes the release of Ca++.
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What class of blocker is succinylcholine?
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Succinylcholine is a depolarizing blocker.
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How would you treat malignant hyperthermia?
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You can provide dantrolene, which blocks the release of Ca++ from the sarcoplasmic reticulum.
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What receptors do postsynaptic parasympathetic fibers act on?
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Postsynaptic parasympathetic fibers release ACh to stimulate muscarinic receptors.
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Can you describe the actions of epinephrine on blood vessels of skeletal muscle and the liver?
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Epinephrine vasodilates skeletal muscle and liver blood vessels
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What branch of the autonomic system regulates sweating?
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Sweating is an example where sympathetic cholinergic secretions come into play (i.e. the preganglionic is ACh and postganglionic is also ACh as opposed to norepi).
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What aspect of the autonomic system is the major determinant of blood pressure?
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Sympathetic tone is the major autonomic determinant of blood pressure. Increased tonic firing of APs in sympathetic nerves causes vasoconstriction, and decreased tonic firing of APs causes vasodilation.
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Can you describe the barostatic reflex to an increase in blood pressure (BP)?
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An increase in BP is sensed by stretch receptors in the aortic arch and carotid sinus. This increases the firing of nerves IX and X. These nerves synapse in the Nucleus tractus solitaries and in turn stimulate the vagal nucleus. The stimulation of the vagus nerve (X) produces a slowing of the heart.
Thus the response of the heart to an increase in BP is a reflex bradycardia. |
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Can you describe the barostatic reflex to a decrease in blood pressure (BP)?
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The decreased BP is sensed by the aortic arch and carotid sinus. The subsequent decrease in firing of baroreceptor afferents reflexively increases the release of NE to a) increase vasomotor tone and b) increase the heart rate i.e. reflex tachycardia. If this reflex is impaired, you get orthostatic hypotension.
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What is the function and activation scheme for the I(funny) current?
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The If current is activated by hyperpolarization and is thus funny compared to most currents which are activated by depolarization. A non-selective cation channel is opened, letting mostly Na+, K+, and possibly some Ca++ ions move through the channel. The inward movement of Na+ causes a depolarizing current which generates the pacemaker potential of the SA node.
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What is the action/response of ACh on the blood vessels?
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You get smooth muscle relaxation and vasodilation mediated by nitric oxide increasing cyclic GMP.
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What is methacholine used for?
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Methacholine is used as a challenge test for asthma. It’s a non-selective muscarinic receptor agonist in the PNS that causes bronchoconstriction when inhaled in aerosolized form.
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What is Bethanechol used for?
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Bethanechol is an agonist specific for muscarinic receptors; it can be used to enact micturition or defecation (defecation in adynamic ileus patients).
| Contraindications: 1) i.v., i.m.; effect on heart could produce shock (effects are like ACh + neostigmine) (give sub Q or oral only) 2) asthmatics 3) hyperthyroid patients – susceptible to arrhythmias 4) peptic ulcers 5)intestinal or bladder obstruction |
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What can pilocarpine be used for?
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Pilocarpine is a tertiary amine and a muscarinic agonist.
1) Glaucoma therapy – by contracting the circular muscle fibers, pulls the iris towards the center of the eye and uncrowds the filtration angle 2) Sjrogen’s syndrome |
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What can be used to treat Sjrogen’s syndrome?
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You can use muscarinic agonists like Pilocarpine (used for dry mouth) and Cevimeline.
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Can you name the 3 inhibitory mechanisms of parasympathetic innervation at the SA node?
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1) ACh acts on muscarinic receptors to increase the conductance of a potassium channel, which hyperpolarizes the membrane and decreases heart rate
2) ACh inhibits the funny current, which is activated by hyperpolarization and generates the pacemaker potential 3) ACh inhibits L-type calcium currents |
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How do reversible ChE inhibitors (neostigmine, etc.) work?
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Stigmines anchor at anionic site of ChE and attach at esteratic site. The first attack by serine leaves a carbamylated enzyme, which reacts with water at a very slow rate.
Enzyme is tied up by carbamyl group sitting at the active site, prohibiting the hydrolysis of ACh. |
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Why does edrophonium have a weak, transient action in AChesterase inhibition (think about its mechanism of action)?
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Edrophonium doesn’t bind at the esteratic site; it binds to the anionic site of acetycholinesterase, and there’s no interaction with serine; thus it has weak, transient action.
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What is Diisopropylphosphorofluoridate (DFP), and how does it work?
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DFP is a specific irreversible cholinesterase inhibitor, and it phosphorylates the serine residue; the enzyme is stuck, and there’s no hydrolysis at all, and it takes 3-6 weeks to re-synthesize the enzyme. This is how insecticides and organophosphorus poisons work.
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How do you treat someone poisoned with nerve gas?
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You decontaminate the patient first.
Next you use large doses of atropine (competitive inhibitor of ACh at muscarinic receptors) to block excessive muscarinic activity. For skeletal muscle effects, you may need artificial respiration, but you may also use 2-PAM to block nicotinic effects. |
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What is atropine, and what are at least 3 uses of atropine?
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Atropine is a competitive inhibitor of ACh at muscarinic receptors. Thus, its effects are opposite to those of parasympathetic stimulation.
1) used to block decrease of heart rate during surgery 2) treats bed wetting in children by increasing bladder capacity 3) used to treat COPD and asthma |
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What is atropine's use in Parkinson’s disease?
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The balance of neuronal activity is shifted towards the ACh side, and atropine helps right that.
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What drug is on ER shelves to treat atropine toxicity, and what are other methods of treating atropine toxicity?
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Physostigmine is the drug on the shelves to treat atropine toxicity
Also… You could induce emesis with syrup of ipecac Gastric lavage Activated charcoal after gastric emptying |
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What is the use of scopolamine?
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Scopolamine is a muscarinic antagonist that stops emesis, and it’s used as a transdermal patch to prevent motion sickness.
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What are CNS effects of muscarinic receptor blockers?
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1) anti-emesis by targeting muscarinic receptors in the vestibular nucleus and the vomiting center
2) sedation by blocking muscarinic receptors in the cholinergic basal forebrain and mesopontine cholinergic nuclei associated with the reticular activating system 3) amnesia by blocking muscarinic receptors in the septo-hippocampal projection |
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Which drugs would ophthalmologists use to block muscarinic receptors?
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Cyclopentolate (for children)
Tropicamide (for older patients) |
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Why is tiotropium superior to ipratropium?
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There are presynaptic muscarinic receptors that are blocked by ipratropium, but blocking the presynaptic inhibitory receptors stimulates ACh release, which defeats the bronchodilatory effect that you desire with ipratropium.
Tiotropium only blocks the postsynaptic receptors and hence has the bronchodilatory effect. |
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What is trimethaphan, and what are its uses and mechanism of action?
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Trimethaphan is a ganglionic blocker that blocks autonomic innervation at the site of the preganglionic nerve synapse; thus it can inhibit both parasympathetic and sympathetic action. It’s used to treat hypertensive crisis, dissecting aortic aneurysm, and pulmonary edema. It can also be used to reduce bleeding during neurosurgery.
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When is adrenergic uptake 2 important?
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It becomes more important and predominant when the distance between the nerve and the receptor becomes greater than usual (which is 40-50 nm).
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What are the metabolites of catecholamines in the CNS and PNS?
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Peripheral – VMA (used to detect the presence of a pheo)
Central – MHPG |
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Can you describe the intermediates and synthesis progression for catecholamines?
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Tyrosine->Dopa->Dopamine->Norepinephrine->Epinephrine
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What are the effects of loop vs. thiazide diuretics in terms of Ca++ reabsorption?
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Loop thiuretics block Ca++ reabsorption, but thiazide diuretics actually promote Ca++ reabsorption
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What is the function of calcimimetics?
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Calcimimetics bind to the transmembrane domain of the Ca++ receptor.
Calcimimetics thus decrease PTH secretion, mRNA expression and synthesis. They also decrease parathyroid cell proliferation. |
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Why is it important to get the 24 hour urinary excretion of Ca++ in patients with high PTH?
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The high PTH may be due to FHH rather than hyperparathyroidism. Patients with FHH will not have hypercalciuria, although patients with hyperparathyroidism will have hypercalciuria. If you send patients with FHH to have their thyroid removed, you can induce hypocalcemia.
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What is FGF23, and what is its physiologic function?
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FGF23 is a hormone made in the bone that has its major action on the kidney. As phosphate increases, FGF23 increases and goes and acts on the kidney to increate phosphate excretion and decrease calcitriol synthesis.
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How does the action of PTH and FGF23 on the kidney differ?
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Although they both increase phosphate excretion, PTH increases calcitriol synthesis, while FGF23 decreases calcitriol synthesis. PTH also decreases Ca++ excretion.
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How does extraskeletal mineralization change for low bone turnover versus high bone turnover?
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Actually, in both low bone turnover and high bone turnover, you get high extraskeletal mineralization.
In high bone turnover, there is release of Ca++ from bone, which gets deposited into extraskeletal locations. In low turnover, the bone can’t buffer the Ca++ and phosphate circulating around, so you have no influx of those ions into the bone, and they deposit into tissue |
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Can you describe the 3 phases of the clinical course of acute tubular necrosis?
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Oliguric phase:
Decreased tubular function, increased BUN, increased K+, acidosis, fluid retention | Early Diuretic Phase: Increased urine output, increased fluid loss, decreased K+ | Late Diuretic Phase (recovery) Concentrating ability& BUN return to normal slowly |
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What are key differences between ischemic and nephrotoxic forms of acute tubular necrosis?
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Ischemic is usually pre-renal, characterized by pale kidneys, edema, patchy necrosis of proximal tubule, rupture of TBMs, casts in the distal tubules and collecting ducts. Pathogenesis for ATN in ischemic cases is due to decreased oxidative respiration and oxphos and corresponding depletion of ATP leading to endothelial dysnfunction and vasoconstriction.
| Nephrotoxic type is due to antibiotics or other toxins and characterized by diffuse necrosis of the middle segment of the proximal tubule. The pathogenesis for ATN in the nephrotoxic case is due to the formation of free O2 radicals, lipid peroxidation, cross linking of proteolipids and proteolysis. The tubular damage is reversible for ischemic but not for nephrotoxic. |
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In what type of illness do you get thyroidization of atrophic tubules?
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Chronic pyelonephritis
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What is the characteristic morphologic feature of drug-induced hypersensitivity nephritis?
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Interstitial edema and influx of eosinophils
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What is the pathogenesis of benign HTN, and how could you manage it?
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Benign HTN, or essential HTN, is due to an inability to excrete Na+ due to insensitivity of the kidney to blood pressure.
You also have defective Na+/Ca++ transport which increases one’s sensitivity to vasoconstriction. There’s also elevated neurohormonal release. It could be managed with a diuretic. |
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What are morphological features of the kidney in benign HTN?
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You get scarring and sclerosis and a granular appearance of the kidney. Morphological features are due to long standing damage to the kidneys.
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In what type of HTN do you see flea-bitten kidneys?
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Malignant HTN
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What hormone is secreted in large amounts by an ischemic kidney?
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Renin
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Which gene mutations are associated with which polycystic kidney disease (PKD)?
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Autosomal dominant PKD – polycystin 1 and 2
Autosomal recessive PKD – fibrocystin Medullary cystic complex disease – nephrocystin |
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In what disease do you get “chocolate cysts,” and how do they form?
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ADPKD: Sometimes the cyst presses on an intrarenal blood vessel so much that it ruptures, and the blood goes into the cystic cavity and becomes coagulated, and when you make a cut section, all you see is the clotted blood, which they call the chocolate cyst.
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A 22 year old Caucasian male was playing basketball and took a break to use the bathroom and found he had hematuria. What is the likely diagnosis?
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Adult polycystic kidney disease.
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This kidney disease is autosomal recessive in children, but autosomal dominant in adults and is characterized by salt wasting, polyuria, and is the most common genetic cause of childhood kidney failure. What is it?
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Medullary cystic disease complex.
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This kidney disease is characterized by radial fusiform cysts, hepatic fibrosis, and bile duct proliferation. What is it?
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Autosomal Recessive form of Polycystic Kidney Disease
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What are the 3 postulated mechanism that are responsible for the formation of a cyst in ADPKD?
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1) altered cell matrix interactions
2) fluid formation 3) cell proliferation |
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Can you generally describe the actions of the 4 main adrenergic receptors (alpha 1, 2, beta 1,2)?
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Alpha 1 : smooth muscle contraction
Alpha 2 : inhibition of cellular function Beta 1 : cardiac stimulation Beta 2: smooth muscle relaxation |
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Which receptors do the following agonists stimulate: 1) norepinephrine 2) epinephrine 3) isoproterenol?
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1) Norepinephrine stimulates alpha and beta 1 receptors (NO beta 2)
2) Epinephrine stimulates alpha, beta 1 and beta 2 receptors 3) Isoproterenol stimulates beta 1 and beta 2 receptors (NO alpha) |
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What factor is the main determinant of diastolic blood pressure?
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Peripheral resistance is the main determinant of diastolic blood pressure.
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What is phenylephrine, and what is its clinical use?
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Phenylephrine is a selective alpha1 agonist, and it’s used as a nasal decongestant to “get the red out.” It has a vasoconstrictor mechanism.
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What are the imidazoline derivatives, and what are their clinical use?
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Imidazoline derivatives are selective agonists for postsynaptic alpha 1 receptors, but they are also agonists on alpha 2 receptors at higher doses.
Examples: Naphazoline Tetrahydrozoline – visine eye drops Oxymetazoline Xylometazoline They are long acting, as they are not substrates for MAO or COMT |
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What is midodrine, and what is its clinical use?
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Midodrine is a prodrug hydrolyzed to a selective alpha 1 receptor agonist called desglymidodrine.
It’s used to increase blood pressure in cases of severe liver or kidney disease. It’s also used to treat orthostatic hypotension, especially in patients with autonomic failure or diabetic autonomic neuropathy. |
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How does the activation of alpha 2 receptors in the hypothalamus or the medulla affect blood pressure?
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There’s tonic sympathetic innervation of beta 1 receptors at the heart and alpha 1 receptors on the blood vessels that increase the blood pressure. Activation of alpha 2 receptors in the hypothalamus or medulla inhibits this tonic sympathetic firing and reduces blood pressure.
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What is clonidine, and what is its clinical use?
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Clonidine is an alpha 2 receptor agonist and inhibits sympathetic outflow in the medulla and hypothalamus. This decreases sympathetic activity from the CNS to the periphery.
Clonidine can induce hypotension by reducing plasma concentrations of NE. It decreases cardiac output via decreased heart rate. It decreases vascular resistance. It’s thus used as an anti-hypertensive and is used in the clonidine suppression test to distinguish essential hypertension from a pheo. |
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What are apracolonidine and brimonidine, and what are they used for clinically?
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They are both alpha2 agonists, and they’re used to treat stubborn cases of glaucoma by inhibiting aqueous humor secretion.
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What is alpha-methyl dopa, and what is its clinical use?
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Alpha-methyl dopa is an alpha 2 agonist, and it’s used clinically as an antihypertensive for HTN during pregnancy.
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What are guanfacine and guanabenz, and what are they used for?
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Guanfacine and guanabenz are both alpha 2 agonists, and guanfacine is used for ADHD, and guanabenz is similar to clonidine.
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What is dobutamine, and what is it used for clinically?
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Dobutamine is a beta 1 receptor agonist, and it’s used to increase the force of cardiac contraction with minimal effect on the heart rate. It’s thus used in congestive heart failure or cardiogenic shock to increase cardiac output.
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What’s albuterol, and what is its clinical use?
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Albuterol is a beta 2 receptor agonist, and it’s used as a rescue inhaler with rapid onset and 4-6 hour duration.
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What is terbutaline, and what is its clinical use?
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Terbutaline is a beta 2 receptor agonist and the only drug in its category available for parenteral use. It’s used as a bronchodilator and is also useful for uterine relaxation during premature labor.
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What is ritodrine, and what is it used for clinically?
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Ritodrine is a beta 2 receptor agonist, and it’s used to prevent or delay premature labor.
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What are the long acting beta agonists (LABAs)?
|
Salmeterol – like albuterol (rescue inhaler for asthmatics), but longer acting
Formoterol – like salmeterol but slightly faster in onset |
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This molecule is found in cheese, beer, aged meats, herring, etc., enters the nerve ending by Uptake I and displaces NE, which goes and activates adrenergic receptors. What is it?
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Tyramine
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What are ephedrine derivatives (e.g, pseudoephedrine), and what are their clinical uses?
|
Ephedrine derivatives are mixed acting sympathomimetic amines. They have both alpha and beta effects like EPI, although less potent than EPI. Their beta 2 effect is strong.
They can be used clinically in OTC anti-asthma preparations for their beta 2 effect. They can also be used as a nasal decongestant for their alpha effect. Note: they can be abused as herbal ecstasy (Ma Huang). |
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Cardiogenic shock is a sequelae of a myocardial infarction in which there is a tremendous fall in cardiac output and arterial systolic pressure as well as reflex tachycardia, reflex venous constriction, and oliguria. What are the two drugs of choice to treat cardiogenic shock?
|
Dobutamine – increases cardiac output with minimal increase in heart rate.
Dopamine – low dose has a beta effect to increase cardiac output like dobutamine. It also has a direct vasodilator effect on specific D-1 dopamine receptors in renal and mesenteric vascular beds (relieves oliguria). (Higher doses have alpha effect.) |
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What drug is used at NU for the purpose of treating premature labor (relaxing the uterus via beta 2 agonist)?
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Terbutaline
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What is the main therapeutic use for phenoxybenzamine?
|
Phenoxybenzamine is an irreversible alpha receptor blocker (has a little selectivity for alpha 1), and it’s main therapeutic use is in the management of pheochromocytoma. In surgeries to remove pheos, you can have a release of catecholamines which can drastically increase BP, and blocking alpha receptors is a necessary step to prevent this occurrence.
It can also be used to treat sexual dysfunction. |
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What enzyme is responsible for the metabolism of beta blockers?
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CYP2D6
NOT CYP3A4 |
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What is the therapeutic use of labetalol?
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Labetalol is a 3rd generation beta blocker that blocks both alpha1 and beta1 receptors. It can be used to treat pheochromocytomas and hypertensive crises.
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What is phentolamine, and what is its clinical use?
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Phentolamine is an alpha receptor blocker, very good against circulating catecholamines.
It can be used to test for pheochromocytoma. It could also be used to treat sexual dysfunction. |
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What is prazosin, and what is its clinical use?
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Prazosin is an alpha 1 receptor blocker, and it’s used to decrease blood pressure without persistent tachycardia.
There are alpha 1 receptors in the bladder neck, prostate smooth muscle and urethra, so it’s also used to treat BPH. |
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Where are alpha1-A receptors located? Where are alpha1-B receptors located? What drugs target alpha1-A receptors?
|
Alpha1-A is present in prostate, bladder, and other places
Alpha1-B is present on blood vessels | Alpha1-A blockers: Tamsulosin – used to treat BPH Alfuzosin Silodosin |
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What is yohimbine, and what are clinical uses for it?
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Yohimbine is an alpha 2 receptor blocker—very selective. It is effective in treating importence.
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What is sildenafil, and what is its clinical use?
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Sildenafil is a selective inhibitor of phosphodiesterase type 5 (PDE5), and it prevents the breakdown of cyclic GMP, which thereby enhances vasodilation in the erectile tissues. It’s used to treat impotence.
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What is latanoprost, and what is its clinical use?
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Latanaprost is a PGF2alpha derivative that increases the outflow of aqueous humor by the uveal scleral route.
Important side effect: can produce irreversible darkening of the iris and eyelashes, which especially occurs in hazel eyed patients. |
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What is propranolol, and what is its clinical use?
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Propranolol is a Beta receptor blocker used to decrease HR, CO
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What is timolol, and what is its clinical use?
|
Timolol is a beta blocker and is used to inhibit the secretion of aqueous humor for the treatment of all forms of glaucoma.
(Secretion of aqueous humor is mediated by beta receptors in the ciliary body.) |
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Can you list the clinically important Beta 1 receptor blockers?
|
Metoprolol – strong as propranolol, effective for cardiac arrhythmias, HTN, angina, esp. in asthmatics
Atenolol – similar to metoprolol Betaxolol – may be used in place of timolol to treat glaucoma in patients with airway disease Esmolol – useful for very short duration; hydrolyzed by esterases |
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Can you list the clinically important Beta 2 receptor blockers?
|
Labetalol – used for pheos, HTN crises
Carvedilol – mild-moderate heart failure; for patients who do not have significant HTN or pulmonary congestion and are already being treated with an ACE inhibitor, a diuretic and digoxin |
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What is the definition of an effective osmole, and are Na+, K+, and urea effective osmoles?
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An effective osmole is a solute that can cause the movement of H2O, because it does not freely cross the plasma membrane.
Na+ and K+ are effective osmoles, but urea is not, since it can freely cross the plasma membrane. |
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What is the usual cause of hyponatremia?
|
Hyponatremia is usually due to water retention and not to electrolyte loss, since the kidneys have a good capacity to excrete free water. Therefore, hyponatremia is due to an inability to excrete free water by the kidneys.
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What are 3 factors that stimulate thirst?
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1) Increase in plasma osmolality
2) Decrease in ECF volume 3) ADH |
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Osmoreceptors are extremely sensitive, and only a 1% change in plasma osm is required for ADH response. Besides hypertonicity and decrease in effective circulating volume, what are other stimuli for ADH secretion?
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1) Nausea
2) Pain 3) Drugs |
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What are causes of hyponatremia with high osmolality?
|
1) Hyperglycemia
2) Mannitol infusion |
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What are causes of hypovolemic hyponatremia?
|
1) Skin loss of H2O
a) sweating b) burns 2) Renal loss a)thiazide diuretics b) osmotic diuresis 3) GI loss a) vomiting b) diarrhea |
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What are causes of hypervolemic hyponatremia (total body water is increased, but effective circulating volume is decreased)?
|
1) CHF
2) Cirrhosis 3) Nephrotic syndrome |
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What are causes of euvolemic hyponatremia?
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1) SIADH (most common cause)—could be lung cancer
2) Hypothyroidism 3) Adrenal insufficiency 4) Primary polydipsia |
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What is beer potomania?
|
Beer potomania is a hypo-osmolality syndrome due to massive consumption of beer, which is poor in solutes and electrolytes. The intake of solutes is necessary to excrete free water, but in the lack of proper solute intake, the amount of free water excretion can be severely limited. This can lead to dilution of the serum sodium and thus hyponatremia. Symptoms of hyponatremia include dizziness, muscular weakness, neurological impairment and seizures.
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If a patient is hyponatremic, and the urine osm is < 100 mOsm/kg, what is the likely diagnosis?
|
<100 mOsm/kg is the maximal volume of maximally dilute urine, indicating that there’s a primary polydipsia (e.g., psychogenic cause of hyponatremia) or reset osmostat.
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Why shouldn’t you raise the plasma Na+ more than 10mmol in the first 24 hours to treat hyponatremia?
|
You could get Osmotic demyelination syndrome (ODS) or Central Pontine Myelinolysis (CPM), which is a demyelinating disease in the brain causing flaccid paralysis, dysarthria, dysphagia due to rapid correction of serum sodium and the sudden osmotic shrinkage of brain cells that have adapted to hyponatremia.
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Why would you use a loop diuretic instead of a thiazide diuretic to treat hyponatremia?
|
Loop diuretics cause equal loss of Na+ and H2O, but thiazides cause a greater loss of Na than H2O, and can cause hyponatremia.
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What are some acquired causes of nephrogenic diabetes insipidus (NDI)?
|
Drugs – lithium
Hypercalcemia (inhibits ADH action in the kidney) Hypokalemia (inhibits ADH action) Pregnancy (synthesis of vasopressinase by placenta) |
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How do you differentiate CDI from NDI?
|
The water deprivation test
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|
What is the calculation for free water deficit?
|
Free H2O deficit= total body H2O * { (serum Na+ /140)-1}
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What is the C4d test, and what is it used for?
|
The C4d test is used to test for preformed Abs that can cause hyperacute rejection due to preformed Abs. C4d is a complement fragment that binds to the interstitial capillaries between the tubules, and if there’s a reaction with the interstitial capillaries, they label the patient as having an Ab-mediated rejection i.e. the pt has circulating Abs that are targeted to the graft
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|
What is tubulitis the hallmark of?
|
Acute cellular rejection
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|
In the context of kidney transplants, what could the vacuolization of the glomerulus possibly indicate?
|
It could indicate that the patient is over-drugged.
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|
What is the incidence of recurrence of membranoproliferative disease in transplant cases?
|
90%; that’s why they don’t give them kidneys.
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Which form of kidney transplant rejection is reversible, hyperacute, acute, or chronic?
|
Acute is reversible
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How does Hyperkalemia alter the membrane potential? How about hypokalemia?
|
Hyperkalemia - > less negative (depolarized)
Hypokalemia -> more negative (hyperpolarized) |
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|
What’s the first thing you give to treat hyperkalemia in a patient?
|
You give insulin to make the K+ go inside the cells.
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What are causes of hyperkalemia?
|
Inhibitors of Na+/K+ ATPase pump:
Beta adrenergic blockade Digitalis toxicity Acidosis | Other: Intense exercise (activation of K+ ATP channel) Hyperosmolality (water rich in K+ exits the cells due to osmolar effect) |
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What are the 2 most important determinants of cortical tubule secretion of K+?
|
Aldosterone
Na+ delivery and transport |
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|
What is the pathogenesis of Barterr’s syndrome?
|
see image
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|
Which is more important to the body, volume status or osmolality?
|
Volume status; when push comes to shove, the body will defend volume status (and therefore tissue perfusion) over osmolality.
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|
What is the definition of the effective arterial blood volume (EABV)?
|
EABV is the part of the extracellular fluid that is in the arterial system and is effectively perfusing the tissues.
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What is the effect of spironolactone on aldosterone?
|
Spironolactone blocks aldosterone.
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Where in the kidney does aldosterone work?
|
Aldosterone works on the principal cell of the collecting tubule.
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What is underfilling versus overfilling, and in which case would a diuretic be more helpful?
|
Underfilling is when the kidney doesn’t sense all the volume in the blood vessels and thinks the volume is low, so it retains extra salt and water over time.
Overfilling is inappropriate retention of salt and water, leading to increased plasma and interstitial volumes. A diuretic would be more helpful in the case of overfilling. In underfilling, removal of fluid may decrease perfusion, which can lead to greater retention of salt and water, while fluid removal is usually safe with overfilling. |
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|
What are the characteristics of each stage of diabetic nephropathy?
|
Stage 1: silent phase characterized by hyperfiltration/hyperfunction and hypertrophy
Stage 2: Incipient phase characterized by micoralbuminuria Stage 3: Overt phase characterized by proteinuria and renal insufficiency Stage 4: Advanced stage characterized by renal failure |
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|
How long does it take to see significant positive benefits of glycemic control for diabetic nephropathy?
|
10 years; you get more bang for your buck by controlling the blood pressure
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|
What’s the most important risk factor for the progressive decline in GFR in diabetes?
|
HTN (particularly arterial HTN) is the most important risk factor for the progressive decline in GFR in diabetes.
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|
What is the role of TGF-Beta in the pathogenesis of diabetic nephropathy?
|
TGF-beta is a cytokine that potently stimulates the production of ECM proteins, leading to excessive mesangial matrix expansion (i.e., glomerular sclerosis) and tubulointerstitial fibrosis.
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|
Which is better for treating diabetic nephropathy, ACE inhibitors or ARBs?
|
ARBs, at least for now, seem superior for treating diabetic nephropathy in type 2 diabetes than ACE inhibitors.
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|
What is this characteristic of?
|
Kimmelstiel-Wilson – nodular glomerulosclerosis (sign of stage 3 diabetic nephropathy)
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|
What is the mechanism of action of loop diuretics, and what are important side effects?
|
Loop diuretics (e.g., furosemide, torsemide, bumetanide) inhibit the Na+-K+-2Cl- symporter in the thick ascending limp of the loop of Henle.
Side effects: fluid and electrolyte imbalances like hypokalemia, volume depletion, ototoxicity, hyperuricemia, hyperglycemia, increased LDL and triglycerides. |
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How do thiazide diuretics work, and what are important side effects?
|
Thiazide diuretics inhibit the Na-Cl symporter in the distal convoluted tubule. They are excellent for treating high blood pressure and kidney stones, because they can cause an increase of calcium in the urine, as a greater amount of Ca++ is taken up into the cell via the channel.
Side effects: impotence, fluid and electrolyte imbalances, impaired glucose tolerance, and increased cholesterol |
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|
What is spironolactone, and what is its clinical use? What are possible side effects?
|
Spironolactone is a K+ sparing distal diuretic.
Side effects: could cause hyperkalemia, since more K+ is staying in the cell |
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|
What is amiloride, and what is it used for?
|
Amiloride works at the principal cell in the collecting tubule, blocking the Na+ channel and causing greater Na+ excretion. Same result as spironolactone, just a different mechanism.
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|
MAO and COMT mediated Phase I and Phase II metabolic reactions, respectively, and they break down catecholamines but are not the major terminators of the action of released NE. What is their main purpose?
|
They’re important in degrading ingested amines (e.g., tyramine in cheeses).
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|
What are uptake 1 and 2 in adrenergic neurotransmission?
|
Instead of hydrolysis, the synapse is terminated by uptake, which could either be:
Uptake 1) Into nerve terminal itself Uptake 2) Uptake into the non-neural effector cell |
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|
What is acetazolamide, and what is it used for?
|
Acetazolamide is a proximal tubule diuretic. It inhibits the activity of carbonic anhydrase, which promotes the aborption of bicarbonate at the proximal tubule. In the proximal tubule, Na+ absorption is coupled to bicarb absorption, so a carbonic anhydrase inhibitor will impair the absorption of sodium by interfering with the absorption of bicarb.
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|
What are high anion gap reasons for metabolic acidosis?
|
Methanol
Uremia (can cause both gap and non-gap) Diabetic Ketoacidosis Paraldehyde Idiopathic Lactic Ethylene Glycol Salicylates |
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|
What are non-gap reasons for metabolic acidosis?
|
Diarrhea
Uremia (gap and non gap), ureteral diversion (sigmoid diversion - urine goes in bowel) RTA (renal tubular acidosis) Hyperchloremic fluids (e.g., a lot of normal saline - controversial) Adrenal insufficiency Medications (e.g., carbonic anhydrous inhibitors - the proximal tubule diuretic) |
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|
Are local anesthetics reversible?
|
Yes
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|
What's the effect of an alkyl substitution on either an aromatic or terminal nitrogne of a local anesthetic?
|
Alkyl substitutions on either aromatic or terminal nitrogens enhance the potency and prolong the duration of action of local anesthetics, because they enhance hydrophobiity (lipid solubility).
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|
What is the form of the Henderson-Hasselbalch equation we learned for the local anesthetic lecture?
|
see image
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|
What would be the action on GI motility of an alpha2 inhibitor like phenoxybenzamine?
|
It would increase GI motility via disinhibition. Other alpha2 blockers include phentolamine and yohimbine.
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|
What's an example of an alpha 2 agonist, and what would be its action on aqueous humor secretion?
|
Clonidine; Alpha2 activation would inhibit the secretion of AH.
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|
What type of agents cause cycloplegia?
|
Anti-muscarinic agents (e.g., atropine, tropicamide, cyclopentolate) cause cycloplegia.
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|
What classes of agents could precipitate a narrow-angle glaucoma attack in an individual?
|
Alpha1 agonists or anti-muscarinics
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|
Can you describe the breakdown of body water in terms of the compartments?
|
see image
|
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|
What is the definition of oliguria?
|
Oliguria can be defined as urine output < 500mL
Anuria can be defined as urine output < 100 mL |
|
|
How do you define acute renal failure (ARF)?
|
ARF is a deterioration of renal function over hours to days ,resulting in the kidney's inability to: 1) excrete nitrogenous waste products (urea) 2) maintain fluid balance 3) maintain electrolyte balance.
| AF is observed clinically by a rise in serum creatinine of 0.5 mg/dL if the baseline < 2.5 mg/dL or of more than 20% if the baseline is > 2.5 mg/dL |
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|
In acute tubular necrosis (ATN), what will the urine sodium be (high, low, normal?)
|
With ATN, you expect high urine sodium, because the tubule cells aren’t working and can’t reabsorb the Na+
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