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Patho Exam 4
Patho Exam 4 - Piteti
| Question | Answer |
|---|---|
| Define tidal volume | Tidal Volume (TV) is the volume of air moved in and out of the respiratory tract (breathed) during each ventilatory cycle. |
| Vital capacity? | Vital capacity (VC) is the maximal volume of air that can be forcibly exhaled after a maximal inspiration. VC = TV + IRV + ERV |
| Person A has a FVC of 5 liters and a FEV1 of 3 liters whereas person B has a FVC of 4 liters and a FEV1 of 3 liters. What are their FEV1/FVC ratios?Which one most likely smokes cigarettes? | Person A: 3/5 x 100 = 60% Person B: 3/4 x 100 = 75% The normal ratio between the FEV1 and FVC (FEV1/FVC) is 70-75%. |
| Given the following locations in the lungs, which would have the highest P02 and which would have the lowest: trachea, bronchi, and alveoli? Why? | The trachea has the highest and the alveoli have the lowest. The tracheal air is 100% saturated but by the time it reaches the bronchioles (dead space) and then the alveoli the air is missed with stale outgoing air and the PO2 drops from 150mm Hg in the t |
| Oxygen saturation of arterial blood is mainly determined by what? | CaO2 = Hb (gm/dl) x 1.34 ml O2/gm Hb x SaO2 (Partial Pressure of Arterial Oxygen) |
| A person has a hemoglobin content of 14 gms/dl and a SaO2 of 80. What is the oxygen carrying capacity of this person’s blood? | CaO2 = 14 gm/dl x 1.34 ml O2/gm Hb x .80 CaO2 = 15.01 ml/100mL blood |
| What relationship is represented by the oxyhemoglobin dissociation curve? | This curve describes the relationship between available oxygen and amount of oxygen carried by hemoglobin. |
| What range of the oxyhemoglobin dissociation curve (i.e. PO2) represents PAO2? | The part of the oxygen hemoglobin dissociation curve at or above a PO2 of 60 mm Hg-100mm Hg represents PAO2 |
| When considering %oxyhemoglobin oxygen saturation, what is unique about this range? | No matter where you are in this range you will be at the same amount of saturation (90%) |
| What range of the oxygemoglobin dissociation curve (PO2) represents the tissue PO2 that surrounds systemic capillary beds? | PO2 < 40 mm Hg Represents PO2 in Capillary Beds |
| What is unique about this range? | As the PO2 decreases in the capillary bed the amount of oxygen released is directly related to saturation. (Supply and Demand) |
| Blood, with an Hb content of 14 gms/dl, enters a capillary bed with a PO2 of 93 mm Hg & leaves the capillary bed at a PO2 of 40. mm Hg. Using the graph on pg 28, estimate %oxygen saturation of blood entering and leaving the capillary bed at the given PO2 | 14 x 1.34 x .97 = 18.2 14. 1.34 x .76 = 14.3 |
| Then, from the formula of page 23, determine CaO2 of blood entering and then again leaving the capillary. How much O2, in gms/dl, was “unloaded” in the capillary bed | 18.2 – 14.3 = 3.9 ml/100ml |
| In what direction (right or left) does increasing temperature in the capillary bed shift the oxyhemoglobin dissociation curve? Decreasing temperature? | right, left |
| What affect does this have on the unloading of oxygen into that capillary? | If you shift to the right you release more oxygen, if you shift to the left you decrease the oxygen released |
| In what direction (right or left) does increasing 2,3-DPG in the RBC shift the oxyhemoglobin dissociation curve? | To the right |
| What two developments would cause a person’s RBCs to increase its concentration of 2,3-DPG? | Going to high altitudes or pulmonary lung disease (COPD) |
| What are the components of the Ventilation/Perfusion ratio? | V/Q V = alveolar ventilation (coming into the lung) Q = pulmonary capillary blood (going to the lung) Normal ratio is 0.8-1.0 |
| What effect would shunting have on the V/Q ratio, thus oxygenation of the blood? | It will shift the dissociation curve to the left decreasing it. |
| What condition will cause shunting? | Bronchitis and asthma |
| What effect would a dead space have on the V/Q ratio and thus oxygenation of blood? | It would lower oxygenation of blood due to the increasing of the VQ ration, because in a dead space there is wasted ventilation. |
| What diseases would cause dead space? | ARDS and Thromboembolus |
| What is the rhythmicity center and what two types of neurons are found within it? | The area of the brain that controls breathing, I and E nuerons |
| Where is the apneustic centre? | The Pons |
| What is the function? | To stimulate the I neurons in the medulla oblongata that results in inspiration |
| Where is the pneumotaxic centre and what is its function? | Situated in the pons, seems to antagonize the apneustic centre, inhibiting respiration |
| Name and give the locations of the three areas in the brain that control respiration | There are three areas in the brain stem that control respiration: two areas in the pons (apneustic and pneumotaxic centers) and one area in the medulla (rhythmicity center) |
| How do the I and E neurons in the rhythmicity center work to produce a rhythmic pattern? | I neurons stimulate spinal motor neurons that innervate the respiratory muscles producing Inspiration E neurons inhibit the I neurons and thus produce expiration by relaxation of the respiratory muscles |
| What controls voluntary or “conscious” breathing? | Cerebral Cortex “controls” Brain stem breathing center (Talking, singing) |
| What controls Involuntary or “Reflexive” breathing? | Central and Peripheral Chemoreceptors (Very sensitive to PaCO2) |
| Where are the central chemoreceptors located?How are they stimulated?Is it CO2 or H+ that directly stimulate these receptors? | Ventral portion of the medulla oblongata (floor of the 4th Ventricle). Indirectly by a rise in CO2. H+ |
| Where are the peripheral chemoreceptors located? What directly stimulates these receptors? What effect does PO2 have on peripheral chemoreceptors? | Coratid Sinus in Ascending Aorta. Increase in CO2 and H+. As the PO2 decreases, there is an increase in CO2 and H+ |
| What anatomical areas of the lungs are usually involved in atelectasis? Is intrapleural negative pressure lost? | Lobules. Pressure is not lost |
| What is obstructive (resorptive) atelectasis in terms of causes? | Caused principally by excessive secretions (e.g. mucous plugs) and is therefore most often found in bronchial asthma, chronic bronchitis and postoperative states |
| What is non-obstructive (compression) atelectasis in terms of causes? | Results whenever the pleural cavity is partially or completely filled by fluid (e.g. pleural diffusion due to left ventricle heart failure) or blood (due to trauma) |
| What roles do the pores of Kohn and canals of Lambert play in postoperative obstructive atelectasis? | These anatomical structures can alleviate postoperative atelectasis with deep inhalation followed by forceful expiration. Allow for collateral airway ventilation |
| Why does obstructive atelectasis often occur as a complication of abdominal surgery? | Breathing generally becomes shallower because of pain induced by the breathing, & the muscles beneath the lungs may be weakened. This prevents the patient from coughing or performing strong exhalations of air. Therefore, mucus plugs can result. |
| Is atelectasis reversible? | Yes |
| What are the consequences of chronic atelectasis on the airways? | Damage and increased risk of development of bacterial infections due to damage of the ciliated epithelium |
| What is pneumothorax in terms of:a) intraplural pressure differences with barometric pressure; and b) breech in either visceral pleura or parietal pleura. | Intraplural pressure drops to 0mm Hg, there is total lung collapse Is the presence of air or gas in the pleural space caused by a rupture in either the visceral pleural or parietal pleura or both |
| What is Atelectasis in terms of:a) intraplural pressure differences with barometric pressure; and b) breech in either visceral pleura or parietal pleura. | Intraplural Pressure: Remains -5mm Hg |
| In an open pneumothorax, what occurs when the hole becomes greater than 0.75 times the size of the trachea? | Air enters the hole (i.e. less resistance) rather than the trachea |
| What affect does this have on oxygenation and ventilation in both lungs? | Results in inadequate oxygenation and ventilation, and a progressive build-up of air in the pleural space, reducing oxygenation in the good areas of the lung and the other healthy lung |
| How should this be managed? | Field management involves place an occlusive dressing, such as the Ascherman Chest Seal, over the wound in order to insure that all air exchange in the patient involves the uninvolved lung. Or a chest drain |
| How does a tension pneumothorax differ from an open pneumothorax in terms of air pressure within the affected hemithorax? | See Answer on Pathology of the Lungs, #5 |
| If not treated, a tension pneumothorax will result in cardiovascular collapse from a combination of mechanical and hypoxic effects. What is the cause of the mechanical affect? | The mechanical effects manifest as kinking or compression of the superior and inferior vena cava because the mediastinum deviates as the intrathoracic pressure increases (Same answer as above) |
| The hypoxic affect of tension pneumothorax? | Hypoxia leads to increased pulmonary vascular resistance via vasoconstriction (called “hypoxic pulmonary vasoconstriction”), decreasing cardiac output and worsening metabolic acidosis secondary to decrease oxygen delivery to the periphery |
| What is the cause of a spontaneous pneumothorax? | This is caused by the spontaneous rupture of blebs (blister-like formations) on the visceral pleura that pops |
| In ARDS, what is meant by “refractory to oxygen treatment”? Non-cardiogenic edema? | The patient’s hypoxemia does not improve even when given pure oxygen. The edema is not secondary to left ventricular failure |
| Distinguish between ARDS and respiratory distress syndrome (RDS) of the new born. | ARDS is commonly caused by the diffuse damage to the alveolar capillary wall, triggering the release of inflammatory mediators by epithelial cells. RDS of the neonate is a deficiency in pulmonary surfactant. |
| What are four conditions that can cause ARDS? | Systemic sepsis, severe traumatic injury, multiple transfussion, those that have nearly drowned |
| No matter the cause of ARDS, alveolar capillary wall damage is thought to be produced by? | The production of the inflammatory mediators, which causes an accumulation of fluid and a hyaline membrane forms |
| What is the significance of the formation of the hyaline membrane in ARDS? | The alveolar hyaline membrane acts as if you lined the air sacs with cellophane, which would prevent the movement of oxygen and carbon dioxide across the alveolar-capillary membrane. Once this forms prognosis is not good |
| What does the acronym PEEP stand for and how is it used in ARDS? | Positive End Expiratory Pressure (PEEP) is a ventilator modality whereby a constant positive pressure is applied to the lungs during the expiratory phase of the respiratory cycle. PEEP will stabilize and recruit alveoli units. |
| What is a frequent undesired effect of PEEP? What is the cause of this undesired affect? | The most frequent undesired effect associated with the administration of PEEP is a reduction in the cardiac output. This is due to impeded venous return to the heart as a result of increased intrathoracic pressures. |
| When considering chronic obstructive pulmonary disease (COPD), what two lung diseases (both separate and together) usually cause this condition? What is the primary risk factor for COPD? For a person living in Los Angeles who does not smoke? | Chronic bronchitis and emphysema. Smoking. Air pollution |
| Define chronic bronchitis. Hyper secretion of mucus in the large and small airways is due to the hyperplasia of what specific cells? What types of cells are found in abundance in the interstitium of the lungs? | Chronic bronchitis is defined as a persistent productive cough for at least 3 consecutive months (usually winter) in at least 2 consecutive years. Goblets cells. Inflammatory Cells |
| What does the Reid Index actually measure? Why is this not of diagnostic use? | The ratio of the thickness of the mucous gland layer (b to c) to the thickness of the wall between the epithelium and cartilage (a to d) is known as the Reid Index. RI = bc/ad It is not of diagnostic use since it requires a dissection of the airway |
| Why does the reid index have post mortem value? | It has value post mortem evaluations and for research. You can determine a relationship between the RI and sudden infant death syndrome or SIDS.  ratios in persons who do not smoke but live in cities vs persons who do not smoke who live in rural areas |
| When comparing bronchitis/bronchiolitis and emphysema, what anatomical areas of the respiratory airways are most affected by bronchitis? Emphysema? | Trachea and the primary, secondary, and tertiary bronchi. Alveolar Walls |
| In emphysema, constant irritation of the lobules by cigarette smoke causes the accumulation of what inflammatory cell? As a result, what enzyme accumulates in the walls of the alveoli, alveoli ducts, and respiratory alveoli? | Neutrophils, Elastase |
| What is the effect of this process on the molecule elastin and therefore the walls of the airways? | Elastase dissolves the elastin fibers in the alveolar and respiratory bronchiole walls, resulting in destruction of these walls |
| When comparing “pink puffer” to “blue bloaters”, which one is mostly seen in COPD patients suffering primarily from emphysema? From chronic bronchitis? | “Pink puffers”, “Blue bloaters” |
| What are the threefold consequences of emphysema? | Reduced capillary perfusion, loss of elastic recoil, and the respiratory bronchioles suffer the same consequences |
| How does a person with consequences of empheysema try to compensate? | Hyperventilation, intense focus on breathing |
| What are the typical symptoms of a “pink puffer”? | -thin, barrel chest & reddish complexion. -little or no cough/ expectorant (airways clear of mucus secretion) -Breathing assisted by pursed lips & use of accessory respiratory muscles to “push” the air out; they may adopt the tripod sitting position |
| Explain the cause of “blue”, in “blue bloaters”. | The term "blue bloater" is derived from the bluish color of the lips and skin commonly seen in patients suffering from COPD due to chronic bronchitis. A blue bloater experiences cyanosis due to a decrease in sufficient amounts of oxygen due to a shunt |
| What causes hypoxic pulmonary vasoconstriction in blue bloaters? | A decrease in PAO2 (i.e., from 100 mm Hg to 40 mm Hg) caused by COPD constricts the arterioles perfusing the alveoli |
| Over time, what two pathological developments occur to pulmonary arteries that contribute to pulmonary arterial hypertension? | Chronic vasoconstriction, muscularization, thickening of the walls of the arteries |
| How is pulmonary arterial hypertension defined? | Defined as a mean pulmonary arterial blood pressure of greater than 25 mm Hg |
| Define Cor Pulmonale | Chronic system hypertension results in left ventricular failure, so too does chronic pulmonary hypertension results in right ventricular failure |
| What is the forward effect of cor pulmonale? | reduced cardiac output and poor oxygenation of blood in the lungs reduces the amount of o2 that is reaches the rest of the body (systemically), which results in cyanosis & the bluish color. Because of this, the person becomes sedentary, & increases weight |
| What is the backward effect of cor pulmonale? | Systemic edema, thus ankles and legs are swollen and distention of the jugular vein is seen during inspiration |
| How would you distinguish between a blue bloater patient and a patient with CHF. | One crude bedside test for distinguishing COPD from CHF is peak expiratory flow. If patients blow only 150-200 mL or less, they are probably having a COPD exacerbation; higher flows indicate a probable CHF exacerbation |
| What are the two components of Dr. Pitetti’s definition of asthma? | -an inflammatory disorder of the airways -with bronchial obstruction and hyper-responsiveness of the airways being a consequence of such inflammation |
| Why extrinsic asthma is also called atopic asthma? | The term “atopic” means caused by a hereditary predisposition toward developing certain hypersensitivity reactions, in this case, asthma. However, the development of atopic asthma in an individual has both genetic & environmental components. |
| The development of atopic asthma in an individual has both genetic and environment components. What are the genetic? | Genetic research currently implicates at least two key genes in the predisposition to asthma and IgE production |
| The development of atopic asthma in an individual has both genetic and environment components. What are the environmental? | actual expression of asthmatic symptoms in an individual requires the initial sensitization to an environmental allergen -correlates w/ childhood sensitization to inhaled house-dust mite allergen -Also cat dander, cockroach, and grass pollen |
| Whether it is extrinsic or intrinsic asthma, what is the key cell in the immediate or early phase? What role does this cell play in the late phase of asthma? | Mast Cells. If the mast cells continue to degranulate and attracts eosinophils |
| What is the key cell in the late phase of asthma? Which of these cells is responsible for the long-term bronchial inflammation and chronic symptoms of asthma? | Eosinophils, Eosinophils |
| What is the major affect (i.e., target) of inhaled corticosteroids? | Brochodilation of the airways |
| What four ways do intrinsic asthma differs from atopic asthma? |  Non-seasonal, non-allergic (i.e., negative skin test)  serum IgE is normal;  patients tend to be over 40 years old  chronic and persistent rather than episodic |
| What are four similarities in the immunopathology of intrinsic atopic and non-atopic asthma? |  infiltration and activation of mast cells;  Infiltration and activation of eosinophils  IgE production in airways (not high in serum);  Two phase responses: early and late phase |
| How is the peak flow meter used in diagnosing and treating asthma? | A peak flow meter is a portable, inexpensive, hand-held device used to measure how air flows from your lungs in one "fast blast." In other words, the Meter measures your ability to push air out of your lungs |
| What are the 5 types of treatment for asthma? |  Identification of the precipitating cause  Beta-2 agonist  inhaled corticosteroids  Cromolyn sodium, a “mast cell stabilizer” reduces amount of inflammatory mast cell releases  Theophylline relaxes the muscles surrounding the air passages |
| In bacterial pneumonia, what causes lobules to fill with fluid and thus restrict oxygenation? | Inflammation reaction, Increased amounts in T-cells, NK, macrophages, neutrophils, etc. |
| In bacterial pneumonia, what 3 factors determine the virulence of infection? |  Virulence of the infecting organism  Status of the local defenses  Overall health of the patient |
| What are the extrinsic factors that cause pneumonia? | Exposure to a causative agent usually through inhalation of infectious aerosols from droplets dispensed by the sneezing and coughing from a nearby infected individual |
| What are the intrinsic factors that cause pneumonia? | -Loss of protective upper airway reflexes - Local lung pathologies |
| How is pneumonia classified according to anatomical distribution? | Look at questions #39 Pathology of the lungs |
| What categories is viral pneumonia divided into? In which one is influenza type A and respiratory syncytial virus (RSV) found? | Primary Manifestation and Multisystemic Manifestation. Primary Manifestation |
| Besides humans, what other types of animals can type A influenza infect? | Influenza A viruses are found in many different species of animals other than man, including wild birds (ie, ducks, geese), chickens, and pigs—animals that man lives in close proximity. |
| How is influenza typically transmitted? | Transmitted from infected individuals through the air by coughs or sneezes, creating aerosols containing the virus |
| Most common vaccinations against influenza is trivalent—what does that mean? | Trivalent influenza vaccine contains purified and inactivated material from three viral strains. Typically this vaccine includes material from two influenza A virus subtypes and one influenza B virus strain. |
| Why is a vaccine formulated for one year usually become ineffective in the following year? | A vaccine formulated for one year may be ineffective in the following year, since the influenza virus changes rapidly over time and different strains become dominant |
| When considering the influenza virus, what is hemagglutinin (HA), where is it located and what is its function? | is an antigenic glycoprotein (i.e. it stimulates the immune system) and is responsible for binding the virus to the cell that is being infected. It facilitates viral entry into the target cell. |
| When considering the influenza virus, what is neuraminidase (NA),where is it located and what is its function? | Facilitates viral release from Target Cell and infect other cells |
| Explain how neuraminidase inhibitors prevent the spread of influenza. | Prevent the cleavage of Sialic acid (slows the infection and “keeps it hooked”) so that the immune system can stop the virus from spreading |
| A. Common cause of deaths in young, healthy patients who contract either the H5N1 (bird flu) or H1N1 (swine flu) due to a strong immune system response—What is this strong immune response called? | Cytokine Storm |
| Dr. P. always receives his influenza vaccination every fall. Explain why, if an antigenic drift takes place during that flu season, Dr. P will not be protected against this new strain. | Look at #53 Pathology of the lungs |
| In antigenic drift, to what surface protein did the point mutation occur? How does this differ from antigenic shift (include the process of genetic re-assortment)? | Hemagglutinin. The combination of two different types of virus entering the cell within the animal cell and re-assortment of genes occur and a brand new virus is made |
| What is the major cause of lower respiratory tract infection during infancy and childhood? What time of the year does it usually occur? Does natural infection produce immunity? | Human Respiratory Syncytial Virus. Winter. No, it does not induce protective immunity |
| Why is this virus called human respiratory syncytial virus? | The RSV attaches to cells of respiratory tract. Infected cells undergo necrosis (i.e., lytic cycle), also syncytia form through fusion which also results in cell death. |
| What are symptoms of RSV? | Hoarseness (barky cough – condition called “croup”, which the swelling of the vocal cords within the larynx to have seal like voice), cough and stridor upon inspiration |
| How is TB transmitted? | Transmission can only occur from people with active—not latent—TB. When people suffering from active pulmonary TB coughs, sneeze, speak, kiss, or spit, they expel infectious aerosol droplets 0.5 to 5 μm in diameter. |
| Using the terms “immunocompetent” and “compromised immune system”, differentiate between primary TB, progressive primary TB, and post primary (reactivation) TB. | Look at #57 of Pathology of the Lungs |
| Upon primary infection, M. Tuberculosis is engulfed by what types of macrophages? | NaĂŻve alveolar macrophages |
| Why and how is the tuberculosis bacilli allowed to use these macrophages to multiply? | Look at #58 in Pathology of the Lungs for answer |
| In the initial phase of TB, explain the key role played by the TH1 lymphocytes in “activating” the immunocompetent individual (i.e., what cells are being activated)? | Arrays of cytokines are then released by the TH1 which (a) activate monocytes into macrophages “specific” to M. tuberculosis (i.e., possess hydrolytic enzymes that can kill the bacillus once phagocytized) and (b) activates CD-8 cytotoxic killer cells. |
| Explain the formation of granulomas in terms of Location of the TH1 lymphocytes | Form a ring of cells that form the boundary of the granulomas |
| Explain the formation of granulomas in terms of definition, Location, and function of “epitheliod macrophages” | In the cytoplasm that release an enzyme to kill the TB |
| Explain the formation of granulomas in terms of Definition and location of “giant cells” | Cytoplasmic mass that form an ring or U shape, usually fused together with some macrophages |
| Explain the formation of granulomas in terms of location and causes of central necrosis or “crème cheese” | Formation of soft material resembling cream cheese due to destruction of normal tissues by released enzymes used to kill TB |
| At what two separate sites does the granuloma formation response occur? | One is the site of entry; usually the periphery of the lung (which is called the Ghon focus) and the other is within the draining lymph nodes |
| Distinguish between “Ghon focus” and “Ghon Complex”. |  site of entry, usually the periphery of the lung (which is called the Ghon focus)  The early Ghon focus together with the lymph node lesion constitute the Ghon Complex |
| Whether progressive primary TB or reactivation TB, how does miliary TB develop? | From the few granulomas that formed during primary TB, the bacilli will begin to disseminate into the surrounding lungs tissue |
| How can miliary TB spread to other organs? | Miliary tuberculosis can erode into a pulmonary vein. Once the bacteria reach the left side of the heart and enter the systemic circulation and seed organs such as the liver and spleen |
| How does cavitation TB occur (i.e., relationship between cavitation TB and tuberculosis bronchopneumonia)? | Look at #63 in Pathology of the Lungs for answer |
| At what point in the progression of TB (i.e., Ghon complex, miliary TB, cavitation TB) is the TB patient at the highest risk of contaminating other persons? Why? | The risk of spread of infection to non-infected persons from individuals with cavitary tuberculosis is very high. |
| What is the genetics of cystic fibrosis (CF) (i.e., how do seemingly healthy parents pass it on to their child)? | Autosomal recessive trait |
| Explain the difference in outcome between a normal CFTR channel and a mutant CFTR channel. | Normal CFTR Channel: Moves chloride ions to the outside of cell and water follows Mutant CFTR Channel: does not move chloride ions causing buildup of sticky mucous |
| What major glands (systems) are affected the CF? | Airways, sweat glands, liver, pancreas, small intestine, testes |
| What is a commonality with all these glands/systems in CF (i.e., what are they called)? | These secretory products must travel the ductal system to be released at their proper location. When the ducts become plugged with sticky mucous, the necessary secretory products cannot be released. Disease of the Exocrine glands |
| What are the two common methodologies for identifying newborns with CF? |  the quantitative sweat chloride test, or "sweat test", which measures the amount of salt in the sweat - . For newborns, an immunoreactive trypsinogen test (IRT) may be used instead. Involves drawing blood & analyzing it for trypsinogen. |
| What has allowed the survival rate of person’s born with CF to improve from 2yrs in 1950 to 36.8 years in 2006? |  proactive treatment of airway infection  good nutrition and an active lifestyle |
| What are the two main causes of lung damage in CF? |  chronic bacterial infections, especially Pseudomonas aeruginosa  thickened, viscous mucus layer in the airway |
| Define the acronym TOBI and what organism does it target? | TOBI (Tobramycin Inhalation Solution) that is commonly used for persons over 6 years with CF and who have Pseudomonas aeruginosa in their lungs |
| What role in the treatment of CP do the following play: nubulizer; ThAIR Vest; and acapella®? | Nubulizer: the mist contains the TOBI to help loosen secretions ThAIR Vest: chest physical therapy to dislodge sputum and encourage its expectoration Acapella: helps to mobilize pulmonary secretions |
| The hormones epinephrine, tetraiodothyronine (T4) is derived from what molecule? | Tyrosine |
| The hormone melatonin is derived from what molecule? | Tryptophan |
| What is the function of melatonin in humans? | It is a hormone that is important in our circadian cycle in terms of controlling our “awake” and “sleep” patterns |
| Why are antidiuretic hormone and insulin considered a polypeptide? | They are hormones composed of chains of small (less than 100) amino acids |
| Follicle stimulating hormone (FSH) and luteinizing hormone (LH) are glycoproteins. How do glycoproteins differ from polypeptides? | These are long polypeptides (containing more than 100 amino acids) on which is attached one or more carbohydrate group |
| Cortisol and Aldosterone are derived from what type of molecule? | Cholesterol |
| What is Rathke’s pouch and what portion of the pituitary does it form? | The anterior pituitary is derived from a pouch of epithelial tissue (Rathke’s pouch) that migrates upward from the embryonic mouth |
| Embryonically, how does the posterior pituitary form? | The posterior pituitary is formed from a downward growth of the brain |
| What are the two hormones released in the Posterior Pituitary? |  Oxytocin  ADH |
| The six hormones produced by the Anterior Pituitary? |  TSH  ACTH  FSH  LH  Growth Hormone (GH)  Prolactin (PRL) |
| Why are anterior hormones are called “tropic” hormones (3 characteristics)? | Trophic hormones (Trophic = food)  high concentrations cause their target organs to hypertrophy (ie, grow)  low levels cause their target hormones to atrophy  Trophic has been conventionally shortened to tropic or tropin |
| What would happen to the size of the thyroid gland due to hypersecretion of the anterior hormone, thyroid stimulating hormone (TSH)? | It would cause the thyroid gland to grow |
| Where do the following hormones originate and what are their functions: growth hormone releasing hormone (GHRH) and somatostatin inhibitory hormone? | Both of the hormones originate from the hypothalamus (GHRH): A peptide that stimulates the synthesis and secretion of GH from the pituitary (SIH): A peptide that inhibits the release of GH from the pituitary |
| What tissue is DIRECTLY stimulated by GH and what is it’s affect? | Fat Cells (Triglycerides) and it stimulates lipolysis |
| Define lipolysis. | The breakdown of triglycerides into fatty acids and the release of fatty acids into the blood |
| Indirect effects of GH are mediated primarily through what factor? Where is this factor produced? What are the main target tissues of this factor (four answers)? | Insulin-like growth factor (IGF-1), Liver, Muscle, bone, cartilage and the liver |
| What effect does insulin-like growth factor (IGF-1) have on the liver (include the term glycogenolysis)? | Promotes glycogenolysis and release of glucose into the blood by the liver cells |
| What effect does insulin-like growth factor (IGF-1) have on the Muscle, bone, cartilage (three answers)? | Stimulate chondrocytes resulting in bone growth, promotes muscle growth by stimulating the amino acid uptake and protein synthesis in muscle and other tissues |
| Define benign somatotroph adenoma and its relationship to pituitary gigantism. | Benign somatotroph adenomas grow very slowly, so that for many years the only effects is excessive growth hormone, causing excessive growth and extreme height |
| What are the two common diagnostic techniques used in determining pituitary gigantism? | Measurement of insulin-like growth factor 1 in the blood, or CT or MRI scans of head identifying pituitary tumor |
| Define acromegaly. | Is a hormonal disorder that results when the pituitary gland produces excess growth hormone (hGH) in adulthood. |
| Why doesn't acromegaly result in gigantism (include epiphyseal plate and scare)? | Does not result in gigantism because epiphyseal plate in the femur and tibia have already stopped growing in adulthood causing the bones to grow in width and not length turning the plates into scares |
| What is the most common cause of acromegaly? | Most commonly it is a benign hGH producing tumor derived from a distinct type of cells (somatotrophs) and called pituitary adenoma |
| What is the cause and proportionality of achondroplasia? | Dbone growth with normal growth hormone production, mutations in the gene for fibroblast growth receptor-3(FGFR3), inhibited proliferation of chondrocytes in growth plate cartilage. Individuals with achondroplasia grow up with un-proportional limbs |
| What is the cause and proportionality of Pituitary Dwarfism? | Pituitary dwarfism is caused by a failure to produce sufficient amounts of GH, and is called proportional dwarfism because the body parts are proportional (unlike achondroplasia) but small. |
| What is the most common cause of "little people"? | Achondroplasia |
| What controls thyroid stimulating hormone (TSH) secretion from the anterior pituitary? | Hypothalamus |
| What is the target organ of TSH? | Pituitary Glad |
| What effect does high blood levels of T3 and T4 have on the release of thyroid releasing hormone (TRH) from the hypothalamus? | High levels of T3 and T4 inhibit the release of TRH and TSH |
| What term is used describing this relationship? | Negative Feedback Loop |
| What controls adrenal corticotropic hormone (ACTH) secretion from the anterior pituitary? | CRF – Cortisol Releasing Factors |
| What is the target organ of ACTH? | Adrenal Cortex |
| What hormone is under direct or active control of ACTH? | Cortisol and androgens |
| Why is the release of aldosterone said to be under “permissive” control of ACTH? | ACTH keeps the cells in the adrenal cortex that make aldosterone healthy, but the release of aldosterone from these cells are controlled by the RAAS |
| What controls the release follicle stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary? | Hypothalamus through the gonadotropin-releasing hormone (GnRH) |
| In females, what is the target cell of FSH? | Graafian follicles |
| What hormone does FSH stimulate to release from Graafian follicles? | Estradiol/ Estrogen |
| In females, what is the target tissue of LH following ovulation? | Corpus Luteum |
| What hormone does LH stimulate to release from the corpus luteum? | Progesterone |
| In males, what is the target cell for FSH? | Sertoli Cells |
| What effect does FSH have on sertoli cells? | Stimulates the Sertoli cells to produce and place testosterone receptors on their cell membrane |
| What is the function of sertoli cells? | To “mentor” spermatogenesis and the production and release of sperm into the lumen of the seminiferous tubules |
| In males, what is the target cell of LH? | Leydig Cells |
| Where is the leydig cells located? | Located within the connective tissue in the seminiferous tubules within the testes |
| What effect does LH have on leydig cells (i.e., what hormone is released)? | Testosterone |
| What is the target cell of testosterone? | Sertoli cells |
| What two major roles does prolactin play in milk production? |  Induces lobuloalveolar growth  Stimulates lactogenesis |
| What controls the release of prolactin in terms of the hypophyseal-pituitary axis? | Dopamine plays an inhibitory role and that is released from the hypothalamus |
| What Stimulatory factor play a positive control over prolactin? | Dopamine, stimulation of the child suckling suppresses DA inhibition, allowing for prolactin release, plus abrupt drop in estrogen and progesterone following delivery |
| What area (i.e., nucleus) of the hypothalamus releases oxytocin? | Paraventricular nuclei |
| What role does oxytocin play in facilitating birth? | Oxytocin causes uterine contractions |
| How does oxytocin work with prolactin in breastfeeding? | Oxytocin acts at the mammary glands, causing milk to be 'let down' into a collecting chamber, from where it can be extracted by sucking at the nipple |
| Why is oxytocin called the “cuddle hormone”? | In the brain, oxytocin is involved in social recognition and bonding, and might be involved in the formation of trust between people (i.e., the “cuddle hormone”) |
| What area (i.e., nucleus) of the hypothalamus is sensitive to dehydration (i.e, increase in osmolality)? | Supraoptic Nuclei |
| What hormone (there are two names for it) is released in response to high osmolality? | Antidiuretic hormone (ADH) also called vasopressin |
| What is the target organ of ADH and what effect does it have on the target organ? | Kidney, increases reabsorption of water, decreases loss of water into the urine |
| Where are releasing and inhibiting hormones made, released, and how do they find their way to the anterior pituitary. | For the answer look at #4 in Endocrine System Guide Questions |
| Know the releasing and inhibiting hormones and their function | (TRH); stimulates TSH (CRH): stimulates the secretion of ACTH -(GnRH): stimulates the secretion of FSH and LH (PIH): controls the release of prolactin (GHRH): stimulates growth hormone secretion Somatostatin: inhibits growth hormone secretion. |
| What are the three functional categories of corticosteroids and give an example of each. | (Salt) Mineral corticoids: Aldosterone which regulates Na & K (Sugar) Glucocorticoids: cortisol, regulates the metabolism of glucose, fats,& proteins during “starvation” (Sex) Sex Steroids: mostly weak androgens (testosterone like) and estrogens. |
| What are the only two molecules used by the brain for energy? | Glucose and Ketones |
| During starvation, what effect does cortisol have on muscle to keep blood glucose high enough to feed the brain (include skeletal muscle, amino acids, and gluconeogenesis in your answer). | stimulates skeletal muscle to break down protein into amino acids & release the amino acids into the blood. The liver takes in the amino acids & through gluconeogenesis, converts them to glucose and releases the newly made glucose into the blood. |
| During starvation, explain “glucose sparing” and include lipolysis in your answer. |  Promoting lipolysis, which mobilizes free fatty acids into the blood thus making them a more available energy source  Promotes fatty acid use for energy by other cells of the body so there is less need for glucose as an energy source. |
| How does high levels of cortisol cause immunosuppression? | Cortisol may act as an anti-inflammatory agent, suppressing the immune system during times of physical and psychological stress |
| What causes Pituitary Cushing’s Syndrome? What hormone (s) is (are) released in excess? | Caused by an adenoma within the pituitary, Excess amounts of ACTH and therefore excess amounts of cortisol |
| What causes Adrenal Cushing’s Syndrome? What hormone (s) is (are) released in excess? | Caused by a adrenal cortex adenoma, Over secretion of cortisol, but also excess amounts of aldosterone and androgens |
| What causes Ectopic Cushing’s Syndrome? What hormone (s) is (are) released in excess? | Some benign or malignant tumors that arise outside the pituitary or adrenal gland can produce ACTH. Cortisol |
| What are the symptoms caused by redistribution of fat in Pituitary Cushing’s Syndrome and Ectopic Cushing’s Syndrome? | Redistribution of fat causing rounding of the face or “moon face”, abdominal obesity, and an accumulation of a fat pad between the shoulder blades referred to as “buffalo hump” |
| What are the symptoms caused by protein wasting in Pituitary Cushing’s Syndrome and Ectopic Cushing’s Syndrome? | Resulting in thinning and weakness of the extremities, and as a result of skin thinning, easy bruising, and abdominal striae |
| What are the symptoms caused by Adrenal Cushing’s Syndrome due to over secretion of excess aldosterone and androgens? |  muscle weakness due to potassium depletion and hypertension due to increase in blood volume (i.e., due to excess aldosterone)  excess body hair growth and menstrual irregularities in women (i.e., due to excess androgens) |
| What is the cause of most cases of Addison’s disease? | Most cases of Addison's disease (about 70%) are caused by an autoimmune disorder, in which there is a humoral response against the cells of the adrenal cortex |
| In Addison’s disease, what is the cause of reduce blood volume and hypotension?Craving for salty food?Loss of appetite and low blood sugar? | The kidneys are not able to regulate salt and water balance, causing reduced blood volume and hypotension. Because of salt loss, a craving for salty foods is common. Hyposecretion of Cortisol |
| In Addison’s disease, why is there an over secretion of ACTH? | The negative feedback process and low levels of cortisol causes the hypothalamus-pituitary axis to release more ACTH |
| What symptom is caused by over secretion of ACTH on melanocytes? | Hyperpigmentation of the skin |
| What events could lead to Addisionian crisis? | Stressful event, illness or an accident causing symptoms to become worse |
| If left untreated, what could be the outcome? |  sudden penetrating pain in the lower back, abdomen, or legs  severe vomiting and diarrhea  dehydration  low blood pressure  loss of consciousness Left untreated, an addisonian crisis can be fatal. |
| How is Addison’s disease treated? |  Cortisol is replaced orally with hydrocortisone tablets, a synthetic glucocorticoid, taken once or twice a day  Aldosterone is replaced with oral doses of a mineralocorticoid called fludrocortisone acetate (Florinef), which is taken once a day |
| What are the three hormones secreted by the thyroid gland? | Thyroxine (T4), triiodothyronine (T3), and calcitonin |
| Which hormone plays a role in regulating the body’s calcium? | Calcitonin |
| Which of the thyroid hormones, T3 or T4, activates the chromosomal receptor in its target cell and, therefore, is the most biologically active. | T3 |
| Where in the thyroid follicle is the glycoprotein, thyroglobulin, located? | Thyroglobulin |
| What are the target cells of thyroid hormones? | Essentially all the cells in the body are target cells of thyroid hormones |
| What two effects do thyroid hormones have on these cells? | stimulate the synthesis of protein once they have entered the cell nucleus (works with IGF-1). stimulating the activity of the cell's mitochondria (i.e, production of ATP). |
| How do the thyroid hormones control basal metabolic rate (BMR)(the answer is found in the answer question #54). | Another important function involves stimulating the activity of the cell's mitochondria (i.e, production of ATP-Energy). Energy needed for functioning of vital organs |
| According to the Harris-Benedict Equation, what four factors determine one’s BMR? | Males: 66 + (13.7 x W) + (5 x H) – (6.8 x A) Females: 655 + (9.6 x W) + (1.7 x H) – (4.7 x A) W = actual weight in kg (weight in lb/2.2 lb/ kg) H = height in cm (height in inches x 2.54 cm/in) A = age in years |
| What is the BMR of a 25 year old female who weighs 150 lbs and is 5’6” in height? | 150 lbs/2.2 lb/kg = 68 kg 5’6” = 66 inches x 2.54 cm = 168 cm = 655 + (9.6 x 68.2 kg) + (1.7 x 163) – (4.7 x 21) = 655 + 654.7 + 277.1 – 117.5 = 1460.3 |
| Explain the synergistic relationship between thyroid hormones and IGF-1. | There is a synergistic relationship between the thyroid hormone and insulin-like growth factor-1 (IGF-1). That is, both are needed for proper development of the central nervous system and for skeletal development |
| What is the primary cause of endemic cretinism (Congenital hypothyroidism) in non-industrial countries? How is it treated? | From a diet deficient in iodine, Iodine replacement |
| What is the primary cause of congenital hypothyroidism in industrial countries? | - fetus’s thyroid system fails to develop correctly. Sometimes the gland does not descend fully into the proper place. In other instances the gland is underdeveloped. In rare cases, the thyroid may fail to produce or release the thyroid hormone properly |
| How is congenital hypothyroidism identified? | a heel stick test (blood is drawn from the heel of the foot) within a few hours of birth. This test is often referred to as the PKU test, because it also covers phenylketonuria (PKU) along with the screening for congenital hypothyroidism |
| How is congenital hypothyroidism treated? | It involves prescription thyroid replacement hormone treatment, in pill form, taken daily. The goal is for the newborn to have normal hormone levels within the first 4 weeks of life |
| Worldwide, what is the major cause of adult hypothyroidism? What is the treatment? | Is iodine deficiency as associated with endemic goiter, Dietary iodine replacement |
| In the United States, what is the major cause of adult hypothyroidism? What is the treatment? | Primary hypothyroidism (Hashimoto's thyroiditis & idiopathic myxedema). Secondary hypothyroidism (dysfunction of the pituitary or hypothalamus) accounts 4 the majority of the remainder of cases. Treatment is w/ T3/T4 supplementation or desiccated thyroid |
| An obese friend of yours complains that the reason for her adipose problem is “a thyroid condition” that seems to be “in the family.” what physical symptoms is she not showing that would suggest that her problem is not w/ her thyroid. | Look at #63 in Endorcrine System Guide Questions for answer |
| What is the name given to adult hyperthyroidism? | Graves Disease |
| What are the three acutely obvious physical conditions presented by graves disease? Name four other conditions would be identified through physical evaluations. | Ophthalmopathy, Diffuse goiter, pretibial myxedema. Rapid HR, weight loss, fatigue, irritability |
| Where the parathyroid glands located and what are are their approximate size? | Size of a grain of rice and are located on the back of the thyroid |
| What is the “job description” of the parathyroid gland? | If calcium ion concentrations in extracellular fluid fall below normal, bring them back within the normal range. |
| What are the four affects (three direct, one indirect) of the parathyroid hormone (PTH)? |  Mobilization of calcium from bone  Enhancing absorption of calcium from the small intestine  Suppression of calcium loss in urine: Another effect of parathyroid hormone on the kidney is to stimulate loss of phosphate ions in urine. |
| Name the cell in the parathyroid that releases PTH? | Chief Cells |
| What role does the calcium-sensor receptor play in the release of PTH? | Parathyroid hormone is released in response to low extracellular concentrations of free calcium |
| What is the most common cause of primary hyperparathyroidism? | Primary hyperparathyroidism is usually the result of a single benign adenoma |
| Why is it difficult for clinicians to identify patients with primary hyperparathyroidism (two answers)? | Most patients with primary hyperparathyroidism are asymptomatic or minimally symptomatic Because manifestations of hyperparathyroidism are subtle, the disease may run an occult (long lasting or recurring) course for years prior to detection |
| What are the typical symptoms of hypercalcemia (recall the mnemonic) and explain each? | "painful bones, renal stones, abdominal groans, and psychic moans," |
| What are the two common causes for secondary hyperparathyroidism? |  Chronic Renal Failure  Vitamin D deficiency |
| What are the three causes of hypocalcemia in chronic renal failure? |  There is no reabsorption of Calcium by the nephrons  Because the nephrons do not absorb the calcium there is no vitamin D activation  Because there is no vitamin D activation there is not reabsorption of calcium from the intestines |
| In chronic renal failure patients, how do you treat for renal osteodystrophy? |  Dietary phosphate restriction  Phosphate binders  Vitamin D supplementation |
| What demographic population in the US is at risk for Secondary hyperparathyroidism due to Vitamin D deficiency?What are the three reasons for this condition? | Common in the elderly, They are housebound, have a decrease in skin production, and have a restricted income |
| What are the three primary cells that make up the Islet’s of Langerhans and what hormones/proteins do they secrete? | Alpha cells = Glucagon Beta cells = Insulin and amylin Delta cells = somatostatin |
| In addition to the rise in blood glucose, what other four events stimulate the release of insulin? | Release stimulated by increase in blood concentrations levels of:  glucose levels,  Amino acids  Fatty acids Insulin release also stimulated by:  Gastrointestinal hormones (e.g., gastric inhibitory polypeptide)  Parasympathetic or Vagal action |
| Explain the four steps that occur in the beta cell release of insulin. | Look at #80 in Endocrine System Guide Questions for answer |
| Besides glucose, what other nutrients will stimulate this same response? | It can be generalized that the same process occurs in beta cells with the entrance of amino acids and fatty acids following a meal |
| What are the three target cells (i.e., tissues) of insulin and what are the actions of insulin at each tissue? | Liver, liver and fat, muscle |
| Why is Insulin called an “anabolic hormone”? | It breaks down smaller molecules into larger molecules |
| What are the cellular action of insulin at the target cell (include insulin receptors and GLUT4 in your answer). | Look at #82 in Endocrine System Guide Questions for answer |
| In the “Fed State”, what three factors inhibit the release of glucagon from the alpha cells? | Increases in insulin and amylin secretion from the beta cells and entrance of glucose into the alpha cell |
| In the “Fed State”, what three factors inhibit the release of glucagon from the alpha cells? | Increases in insulin and amylin secretion from the beta cells and entrance of glucose into the alpha cell |
| In the “Fasting State”, what three factors allow for the release of glucagon from the alpha cell? |  There is little to no release of insulin and amylin by the beta cells;  Removal of the inhibitory effect that glucose entry into the alpha cells has on the secretion of glucagon. |
| What effect does glucagon have on the liver’s glycogen (what is the term for this)? What effect does this have on blood sugar? | Stimulates the liver to break down glycogen to glucose (i.e., glycogenolysis), Increases blood sugar |
| What effect does glucagon have on the liver in terms of its handling of amino acids (what is the term for this)? What effects does this have on blood sugar? | Stimulates the liver to convert amino acids into glucose (i.e., gluconeogenesis), Increases blood sugar |
| What effect does glucagon have on fat cells (what is the term for this)? What is the fate of fatty acids in the liver (what is the term for this)? What effect does this have on blood levels of ketones? | Stimulates lipolysis and the fatty acids released are converted to ketones in the liver (ketogenesis), Increases Ketones |
| What are the three types of diabetes studied in this course? | Type 1, type 2 and gestational diabetes (or type 3, occurring during pregnancy), |
| Which type of diabetes is identified with autoimmune destruction of the beta cells? Insulin insensitivity? Pregnancy? | Type 1, type 2 and gestational diabetes (or type 3, occurring during pregnancy),Type 1,Type 2 and gestational diabetes , Gestational diabetes |
| What is the usual age range for the onset of type 1 diabetes? | 9-13 |
| When considering the time line of type 1 diabetes, what is meant by “silent Beta cell loss”? | For most individuals, and the autoimmune attack results in the “silent” β-cell loss” (i.e., “silent” because no symptoms have become apparent) until the point of symptomatic onset |
| In type 1 diabetes, what two conditions cause diuresis? | High blood glucose and ketone levels |
| What do the terms polyuria and polydipsia mean? | Polyuria (excessive production of urine) Polydipsia (excessive thirst) |
| In type 1 diabetes, what four symptoms are caused by Ketoacidosis? | Abdominal pains, vomiting, confusion, and hyperventilation |
| What are the three characteristics of type 2 diabetes? | Insulin resistance, relative insulin deficiency, and hyperglycemia |
| What are the two metabolic defects that characterize type 2 diabetes? | 1) A derangement of beta-cell secretion of insulin 2) An inability of peripheral tissues to respond to insulin (insulin resistance) |
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