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Physiology
UWORLD Round 1 2021 Part 2
Question | Answer |
---|---|
Decreased T4 and increased TSH. Dx? | Primary hypothyroidism |
How is T3 is mainly made? | Produced by conversion from T4 in peripheral tissues |
How are the serum thyroid hormone levels in patients with Primary hypothyroidism? | Serum levels widely fluctuate due to its short half-life and can often be within the normal range |
What does NAGMA stands for? | Non-anion gap Metabolic Acidosis |
What is the pathogenesis of Nonanion gap Metabolic acidosis? | Results from the loss of bicarbonate (HCO3-), leading to a relative increase in H+ |
What are the most common causes of Nonanion gap Metabolic Acidosis? | 1. Severe diarrhea 2. RTA 3. Excessive saline infusion |
What is the pathogenesis of Anion gap Metabolic acidosis? | Accumulation of unmeasured acidic compounds |
What are some important causes of Anion gap Metabolic acidosis? | 1. Lactic acidosis 2. DKA 3. Renal Failure (uremia) 4. Methanol, ethylene glycol 5. Salicylate toxicity |
How is NAGMA often referred as? | Hyperchloremic acidosis |
Hyperchloremic acidosis is also known as: | Non-Anion gap Metabolic Acidosis |
A person with severe and recurrent diarrhea is most likely to develop anion or nonanion gap metabolic acidosis? | Non-Anion gap Metabolic Acidosis |
Why is nonanion gap metabolic acidosis referred as hyperchloremic acidosis? | Due to the decrease in serum bicarbonate is compensated by an increase in serum chloride to maintain electronegative balance |
How is the electronegative balance maintained in cases of diarrhea, which causes the loss or decrease of large amounts of serum bicarbonate? | Increase of serum chloride |
What is the main cause of Primary Nocturnal enuresis? | Brain maturational delay in the development of bladder control |
What is the result of a brain maturation delay in bladder control? | Primary Nocturnal enuresis |
What are some causes of Primary Nocturnal enuresis? | 1. Brain maturational delay in bladder control development (MCC) 2. Increase nocturnal urine output 3. Decreased bladder capacity |
What is the major stimulator of "respiration"? | PaCO2 |
What happens even with a slight or minor decrease in PaCO2? | Stimulates the central chemoreceptors and triggers increased respiration |
Which is the major respiratory stimulant, PaCO2 or PaO2? | PaCO2 |
What is possible explanation to the increased respiratory drive seen in COPD patients? | PaCO2 response is blunted, which causes hypoxemia to be the main respiratory stimulant |
Which chemoreceptors are responsible to sense PaCO2, central or peripheral? | Central chemoreceptors |
Which chemoreceptors sense preferible changes in PaO2, central or peripheral? | Peripheral chemoreceptors |
How are peripheral chemoreceptors suppressed? | Oxygen administration |
Where are peripheral chemoreceptors found? | Carotid and Aortic bodies |
Which part (node or muscle) has the slowest cardiac action potential conduction speed? | AV node |
Which fibers have the fastest conduction speed? | Purkinje fibers system |
Increasing order of cardiac action potential conduction speed | AV node < Ventricular muscle < Atrial muscle < Purkinje system |
What deficiencies are seen with a Vegan diet? | Calcium and vitamin D |
What is prevented with Calcium and vitamin D supplementation in a Vegan diet? | Osteoporosis and bone fractures |
What water soluble vitamin is seen to be deficiency with a strict vegan diet? | Cobalamin |
Where in the lung are ventilation and perfusion the highest? | Base |
Where in the lung are ventilation and perfusion the lowest? | Apex |
How does V/Q ratio increase along the lung? | Apex is largest and as it goes to the base it decreased |
Where in the lung V/Q is the highest? | Apex |
What causes Atrial Flutter? | Large reentrant circuit that traverses the cavotricuspid isthmus of the right atrium |
How is atrial flutter treated? | Radiofrequency ablation targeted to the cavotricuspid isthmus of the right atrium |
From where does AFIB originate? | Pulmonary vein ostia and/or catheter ablation of pulmonary vein trigger sites |
What is the role of ATP in skeletal muscle contraction? | ATP binding to myosin causes release of the myosin head from its binding site on the actin filament |
What is the result of the binding of ATP to myosin in skeletal muscle contraction? | Release of the myosin head from its binding site on the actin filament |
What causes unilateral Renal Artery Stenosis? | Hypoperfusion and activation of the RAAS |
What are actions or causes of Angiotensin II? | Arteriolar vasoconstriction and increases aldosterone and ADH synthesis |
What common action creates a high demand for ATP? | Intense exercise |
What is the primary source of ATP at the beginning of intense exercise? | Phosphocreatine shuttle |
What is the function of Phosphocreatine shuttle? | It is the main source of ATP at the beginning of intense exercise |
How long does the Phosphocreatine shuttle serves as the main source of ATP in exercise? | Around the first 10 seconds |
Once the Phosphokinase shuttle activity is finished, what processes take charge in creation of ATP during exercise? | Anaerobic glycolysis, followed by Oxidative phosphorylation |
How is blood flow associated with vessel radius? | Blood flow is directly proportional to the vessel radius raised to the 4th power |
Resistance to blood flow is --> | Inversely proportional to the vessel radius raised to the 4th power |
Is resistance or blood flow is directly proportional to vessel radius to the 4th power? | Blood flow |
If flow is reduced by a factor of 16, it means the radius has been: | Reduced radius by 50% |
How are most particles lodged in the Bronchial tree cleared or removed? | Via proximal transport by Ciliated Epithelial cells |
What part of the respiratory anatomy removes particle via mucociliary clearance? | Bronchial tree |
How far along the bronchial tree do Mucus-secreting cells? | All the way down to the larger bronchioles |
The smaller bronchioles uses what cells are the ones that replace the Mucus-secreting cells in the larger bronchioles? | Club cells |
What is the level of phosphate in CKD patients? | Develop hyperphosphatemia due to decreased filtration of phosphate |
Is CKD characterized with hyperphosphatemia and hypophosphatemia? | Hyperphosphatemia |
How is hyperphosphatemia regulated in CKD patients? | Secretion of Fibroblast growth factor 23 (FGF23) which lowers plasma phosphate by reducing intestinal absorption and renal reabsorption of phosphate |
What condition is associated with secretion of FGF23? | Hyperphosphatemia in CKD |
How does FGF23 work? | Secreted by hyperphosphatemia, which causes: 1. Reduced intestinal absorption 2. Renal reabsorption of phosphate |
What is an useful early marker of abnormal phosphate metabolism in patients with CKD? | FGF23 levels |
What is the effect of GFR during pregnancy? | Increased GFR |
What is the end result of all the renal adaptations during pregnancy? | Trace urinary protein excretion (<300 mg/24 hours) is a normal finding in pregnancy |
What are the renal adaptations of pregnancy? | 1. Increased GFR 2. Greater basement membrane permeability 3. Decreasing tubuar resorption of filtered protein |
What are the hemodynamic results of a PDA? | 1. Increased LV preload and, 2. Decreased systemic vascular resistance |
What causes the increased preload in PDA? | Increased pulmonary venous return to the left atrium |
What causes the decreased SVR in PDA? | Continuous L-to-R shunt |
What is the hemodynamic result of the continuous L-to-R shunt in PDA? | Decrease in SVR |
The lower SVR in PDA translates into a decreased ____________. | Afterload |
What does a combination of increased Preload and decreased Afterload result in? | Increase in Left-ventricular Cardiac Output |
What are the causes of Pleural effusion? | 1. Increased rate of fluid inflow from nearby vasculature, or, 2. Decreased rate of fluid outflow through the parietal fluid lymphatics |
What is the cause of Ascites in patients with hepatic cirrhosis? | Develop due to hemodynamic changes related to Portal hypertension |
What causes the activation of RAAS by Splanchnic vasodilation? | Splanchnic vasodilation decreased Splanchnic vascular resistance and lowers effective arterial blood volume, which activates RAAS and promotes sodium and water retention |
Hypoalbuminemia causes: | Low oncotic pressure |
What is a common cause of Hypoalbuminemia? | Liver disease |
A low oncotic pressure leads to: | Reduction of fluid reabsorption from the interstitium |
What are two causes of Pleural effusions? | Transudative and Exudative |
What are two causes of Transudative pleural effusions? | 1. Increased hydrostatic pressure gradient 2. Decreased oncotic pressure gradient |
What is the simple definition of Hydrostatic pressure ? | Fluid going out of vessel into pleural space |
What condition is associated with increased hydrostatic pressure gradient causing Transudative pleural effusions? | Heart failure |
What is an example of a condition that leads to a decrease in oncotic pressure? | Nephrotic syndrome |
What does it mean to have a decreased oncotic pressure gradient? | Decrease in plasma proteins |
What are the main causes of Exudative pleural effusions? | 1. Increased vascular permeability 2. Lymphatic obstruction |
What causes an increase in vascular permeability leading to exudative pleural effusion? | Walls of the vessels destroy or damaged |
What condition can lead to exudative pleural effusion due to increased vascular permeability? | Infection |
A person with a pleural malignancy will most likely form what kind of pleural effusion? | Exudative pleural effusion |
Which is the only type of pleural effusion due to a decrease in outflow? | Exudative pleural effusion due to lymphatic obstruction |
What is a common cause of High Output heart failure? | Markedly decreased systemic vascular resistance that leads to increased venous return and increased cardiac output |
Why does decompensated HF failure is a resultant of increased cardiac output? | The left ventricle is unable to keep up with the increased venous return in prolonged or chronic state, leading to a decompensated HF |
What are some adverse effects of excessive anabolic steroids? | Acne, gynecomastia, azoospermia, decreased testicular size, and increased aggression |
How are testosterone levels with use of anabolic steroids? | Normal or slightly elevated serum levels |
What is the effect of endogenous testosterone production and spermatogenesis with excessive anabolic steroid ingestion? | Decreased |
What is the MCC of secondary Hyperthyroidism? | TSH-secreting pituitary adenoma |
TSH-secreting pituitary adenoma is the MCC of: | Secondary Hyperthyroidism |
In addition to regular primary hyperthyroid symptoms, what other features are seen in Secondary hyperthyroidism? | Elevated TSH causes generalized hypertrophy of the thyroid gland (diffuse goiter) |
How are the levels of all three, TSH, T3, and T4, in secondary hyperthyroidism? | All three are elevated |
What procedure increases the risk of developing a Hypogonadal state? | Bilateral orchiectomy |
Why does a bilateral orchiectomy causes a hypogonadal state? | Extragonadal andronges sources are inadequate to replace the loss of testosterone |
What are the physical effects of loss of testosterone? | Decreased lean body weight, increased subcutaneous fat, and decreased bone density |
What is the effect of low testosterone in the prostate? | Low testosterone lead to a significant decrease in prostate volume |
What two compounds have the lowest Tubular fluid concentration as they travel along the proximal tubule length? | Glucose and amino acids |
Which electrolytes have an approximate Tubular fluid concentration of 1.0 along the length of the Proximal tubule? | Sodium and Potassium |
Which has a higher tubular fluid concentration as it travels the length of the Proximal tubule, Creatinine or Urea? | Creatine |