Discussion in 'NEET 2013 All india Exam' started by Guest, Jan 25, 2010.

  1. yunus.

    yunus. Guest

    Tonic-clonic seizures (TCS) are the most common type of seizure encountered in childhood, adolescence, and adulthood. The manifestations of generalized TCS can be divided into several phases beginning with vague prodromal symptoms that may occur hours to days before the actual convulsion. Common premonitory symptoms include headache, mood change, anxiety, irritability, lethargy, changes in appetite, dizziness, and lightheadedness. The tonic phase may be preceded by a series of brief, bilateral muscle contractions lasting a few seconds. The tonic phase begins with brief flexion of the trunk, accompanied by upward deviation of the eyes, mydriasis, and a characteristic vocalization as contraction of abdominal muscles produces forced expiration across a spasmodic glottis. This process is followed by a period of generalized extension lasting 10 to 15 seconds. With evolution of the clonic phase, tonic contractions alternate with periods of muscle atonia of gradually increasing duration until contractions cease. The seizure terminates with a final generalized tonic spasm. Loss of consciousness and autonomic alterations occur during the tonic and clonic phases. Secondarily, generalized seizures may be preceded by focal or lateralized clinical behaviors such as involuntary jerking of an extremity or head version before the onset of bilateral motor manifestations. Similarly, focal weakness of an extremity during the postictal state (Todd's paralysis) indicates seizure origin from the contralateral hemisphere. TCS commonly produce hypocarbia, owing to a combined respiratory alkalosis and lactic acidosis, transient hyperglycemia, mild cerebrospinal fluid (CSF) pleocytosis, and elevated serum prolactin. The immediate postictal state is characterized by coma that is gradually replaced by a confusional state. Once consciousness is regained, lethargy, myalgia, and headache are often reported. Most TCS are less than 1 minute in duration. Potential complications include oral and head trauma, vertebral body stress fractures, aspiration pneumonia, pulmonary edema, and death.

    what are postictal features
    aphasia, todds paresis, confusion

    what imaging should you do for seizure
    MRI of the brain: with and without contrast – look for structural abnormality
    PET scan of the brain – look for functional abnormality
    CT of the brain – look for intracranial hemorrhage

    do you have to have an abnormal eeg to have a seizure
    nope fifty percent have normal eeg
    better results if done within 24 hours

    what is epilepsy
    Epilepsy is the condition of recurrent (two or more) spontaneous (unprovoked) epileptic seizures
    persist abnorm brain fxn that allows abnormal neuron firing

    who does epilepsy occur most in
    young kids and elderly

    how do u get epilepsy
    inherited or aquired through trauma, stroke, birth defect, infxn

    what is the most comon generalized seizure disorder in adults!!
    when is its onset
    juvenile myoclonic epilepsy
    12-18 years of age
    assoc with mutations in several genes

    what dz is this: frequent myoclonic seizures typically after awakening,mostly in arm, no impair consciousness may progress to generalized tonic clonic
    Juvenile myoclonic ep
  2. yunus.

    yunus. Guest

    Temporal lobe epilepsies are a group of medical disorders in which humans and animals experience recurrent epileptic seizures arising from one or both temporal lobes of the brain. Two main types are internationally recognized according to the International League Against Epilepsy. Simple Partial Seizures (SPS) involve small areas of the temporal lobe such as the amygdala or the hippocampus. The term "simple" means that consciousness is not altered. In temporal lobe epilepsy SPS usually only cause sensations. These sensations may be mnestic such as déjà vu (a feeling of familiarity), jamais vu (a feeling of unfamiliarity), a specific single or set of memories, or amnesia. The sensations may be auditory such as a sound or tune, gustatory such as a taste, or olfactory such as a smell that is not physically present. Sensations can also be visual, involve feelings on the skin or in the internal organs.

    * Medial temporal lobe epilepsy (MTLE) arises in the hippocampus, parahippocampal gyrus and amygdala which are located in the inner aspect of the temporal lobe.
    * Lateral temporal lobe epilepsy (LTLE) arises in the neocortex on the outer surface of the temporal lobe of the brain.

    what happens if MT seizures spread outside the temp lobe
    motor symptoms of the contralateral hand, arm, or leg occur
    Dystonic posturing if coming from Basal ganglia, and Clonus if coming from primary motor complex

    what can occur if MT seizure happens during sleep
    secondary generalization

    what happens postictally after MT seizure
    The patient is often confused and amnestic for the ictal event
    post ictal localization: aphasia, hemiparesis, nose wiping with hand ipsilat to ictal side
  3. yunus.

    yunus. Guest

    Different Types of Synapses

    The human nervous system uses a number of different neurotransmitter and neuroreceptors, and they don’t all work in the same way. We can group synapses into 5 types:

    1. Excitatory Ion Channel Synapses.

    These synapses have neuroreceptors that are sodium channels. When the channels open, positive ions flow in, causing a local depolarisation and making an action potential more likely. Typical neurotransmitters are acetylcholine, glutamate or aspartate.

    2. Inhibitory Ion Channel Synapses.

    These synapses have neuroreceptors that are chloride channels. When the channels open, negative ions flow in causing a local hyperpolarisation and making an action potential less likely. So with these synapses an impulse in one neurone can inhibit an impulse in the next. Typical neurotransmitters are glycine or GABA.

    3. Non Channel Synapses.

    These synapses have neuroreceptors that are not channels at all, but instead are membrane-bound enzymes. When activated by the neurotransmitter, they catalyse the production of a “messenger chemical” inside the cell, which in turn can affect many aspects of the cell’s metabolism. In particular they can alter the number and sensitivity of the ion channel receptors in the same cell. These synapses are involved in slow and long-lasting responses like learning and memory. Typical neurotransmitters are adrenaline, noradrenaline (NB adrenaline is called epinephrine in America), dopamine, serotonin, endorphin, angiotensin, and acetylcholine.

    4. Neuromuscular Junctions.

    These are the synapses formed between motor neurones and muscle cells. They always use the neurotransmitter acetylcholine, and are always excitatory. . Motor neurones also form specialised synapses with secretory cells.

    5. Electrical Synapses.

    In these synapses the membranes of the two cells actually touch, and they share proteins. This allows the action potential to pass directly from one membrane to the next. They are very fast, but are quite rare, found only in the heart and the eye.
  4. jain.

    jain. Guest

    What's excitation?
    - Energy absorbed that raises an electron in an atom to a higher level without ejection of the electron

    What's ionization?
    - Radiation that has enough energy to release 1 or more electrons from an atom

    Alpha particle
    - Positively charged particle emitted from nucleus during radioactive decay, BIG, very ionizing, easily stopped

    Beta particle
    - Negative charged electron emitted from nucleus during radioactive decay, SMALL, stopped by plastic

    Gamma radiation
    - Very high energy photons, very dangerous, need lead to be stopped.

    Ionization of water forms:
    - H2O ion radical + e-, that can generate free radicals, ions, and molecular species
  5. jain.

    jain. Guest

    Due to their relatively large mass, protons have little lateral side scatter in the tissue; the beam does not broaden much, stays focused on the tumor shape and delivers small dose side-effects to surrounding tissue. All protons of a given energy have a certain range; very few protons penetrate beyond that distance.[4] Furthermore, the dose delivered to tissue is maximum just over the last few millimeters of the particle’s range; this maximum is called the Bragg peak.[5]

    To treat tumors at greater depths, the proton accelerator must produce a beam with higher energy, typically given in eV or electron volts. Tumors closer to the surface of the body are treated using protons with lower energy. The accelerators used for proton therapy typically produce protons with energies in the range of 70 to 250 MeV (Mega electron Volts: million electron Volts). By adjusting the energy of the protons during application of treatment, the cell damage due to the proton beam is maximized within the tumor itself. Tissues closer to the surface of the body than the tumor receive reduced radiation, and therefore reduced damage. Tissues deeper within the body receive very few protons so that the dosage becomes immeasurably small.[4]

    What are the direct and indirect effects of radiation?
    - Direct effect: radiation interacts directly with target molecule to eject electron
    - Indirect effect: Ionization of water forms free radicals that attack target molecule

    Steps to get from absorption of radiation to biological effect
    - Absorption of radiation
    - Ionization/excitation
    - Chemical lesion
    - Enzymatic repair or fixation of damage
    - Biological effect
  6. kim.

    kim. Guest

    What is the official name of the VHL gene?

    The official name of this gene is “von Hippel-Lindau tumor suppressor.”

    VHL is the gene's official symbol. The VHL gene is also known by other names, listed below.
    What is the normal function of the VHL gene?

    The VHL gene is a tumor suppressor gene, which means it prevents cells from growing and dividing too rapidly or in an uncontrolled way. The VHL gene provides instructions for making a protein that functions as part of a complex (a group of proteins that work together) called the VCB-CUL2 complex. This complex targets other proteins to be broken down (degraded) by the cell when they are no longer needed. Protein degradation is a normal process that removes damaged or unnecessary proteins and helps maintain the normal functions of cells.

    The VCB-CUL2 complex targets large proteins, particularly a protein called hypoxia-inducible factor (HIF), to be broken down within cells. HIF controls several important genes involved in cell division and the formation of new blood vessels.

    The VHL protein likely plays a role in other cellular functions, including the regulation of other genes and control of cell division. This protein is also involved in the formation of the extracellular matrix, which is an intricate lattice that forms in the spaces between cells and provides structural support to tissues.
  7. kim.

    kim. Guest

    Steps to get from absorption of radiation to biological effect
    - Absorption of radiation
    - Ionization/excitation
    - Chemical lesion
    - Enzymatic repair or fixation of damage
    - Biological effect

    Radiation dose to kill cell on cytoplasm and nucleus
    - Cytoplasm - > 250 Gy
    - Nucleus - 2 Gy (mitosis)

    Cell that can divide indefinitely
    Clonogenic cell

    How do you construct an in vitro survival curve?
    - Plate X number of cells, irradiate with increasing amount, then count colonies left, calculate plate efficiency and surviving fraction (mean number of colonis after dose per dish/mean number of cells plated per dish x PE=plating efficiency)

    Densely ionizing particles need ______ dose to kill. Name one of this particles.
    - Low, alpha particle.

    RT is delivered primarily with high-energy photons (gamma rays and x-rays) and charged particles (electrons and protons). The distinction between gamma rays and x-rays lies in their origin; gamma rays originate from excited and unstable nuclei, whereas x-rays are produced by electron energy transitions within the atom or through the deceleration of high-kinetic energy electrons (bremsstrahlung). Gamma rays are typically produced by radioactive sources used in brachytherapy , whereas x-rays are generated by linear accelerators and are used in external beam RT. Within a linear accelerator, a narrow beam of electrons is accelerated to nearly the speed of light before striking a tungsten target. As the electrons decelerate, they emit bremsstrahlung radiation (x-rays) with a spectrum ranging from zero to their maximum kinetic energy. Beam quality is often expressed as the highest-energy photons produced in kVp (kilovolts peak) or MV (megavolts). Therapeutic beam energies range from 50 kVp to 25 MV or greater. In this energy range, the relevant interactions of photons with matter include the photoelectric effect, Compton effect, and pair production.
  8. kim.

    kim. Guest

    If you give dose in fractions then at the end you need ______ dose to kill cells
    - More

    A single dose doesn't allow:
    - Repair

    Name the three types of radiation damage, describe them.
    - Lethal (irreversible and irreparable)
    - Potentially lethal (can be modified by environment using delay to repair)
    - Sublethal (can be repaired within 24 hrs)

    What does shift of the dose-surviving curve to the right up mean?
  9. kim.

    kim. Guest

    What happen if there is proliferation of cells at low dose rate?
    The curve moves up where there is little effect on cells.

    Normal tissue response IMPORTANT, divided in:
    - Acute responding tissues - express injury after weeks.
    - Late responding tissues - express injury after months or years

    4 R's of biology
    - Repair
    - Repopulation
    - Reassortment or Redistribution
    - Reoxygenation

    Why is fractionation of dose good for normal tissues?
    - Because give time to Repair by sublethal damage repair so Repopulation can occur if treatment long enough
  10. yunus.

    yunus. Guest

    ● The Diagnostic and Statistical Manual of Mental Disorders,
    Fourth Edition, Text Revision (DSM-IV-TR) specifies that the
    diagnosis of attention deficit/hyperactivity disorder (ADHD)
    cannot be made if the symptoms occur in a child with
    autism. However, symptoms of attention deficit and hyperactivity
    are a common problem in children with autism, which
    points toward some neuropathophysiological characteristics
    shared between these two groups of neurodevelopmental
    ● The frontostriatal model of developmental dysfunction links
    autism and ADHD by virtue of shared neural circuitry and
    predicts that the two disorders are likely to share common
    heritability factors. In addition, both disorders share a
    number of neurotransmitters, including dopamine,
    noradrenaline, acetylcholine, γ-amino butyric acid, and
    ● Children with autism have an increased risk of suffering tic
    disorder or Gilles de la Tourette syndrome, with the tics
    becoming more prevalent during times of stress and anxiety,
    such as a change in school placement.
    ● Epilepsy occurs in approximately 20% of young people with
    autism, emerging most commonly in early childhood or
    during adolescence and more frequently in children with
    more severe levels of intellectual disability.
    ● Standardized neuropsychological tests have demonstrated
    that the profile of autism is characterized primarily by
    deficiencies in cognitive flexibility and planning, whereas
    the neuropsychological profile of ADHD is characterized
    predominately by inhibitory deficits and problems with
    sustained attention.
    ● The management of autism relies on a multimodal program
    of structured and targeted behavioral and educational
    interventions supplemented, when indicated, by
    ● Effective medications are available for the treatment of
    ADHD but should be prescribed in the setting of a comprehensive
    educational and behavioral management program.
  11. yunus.

    yunus. Guest

    The Kaplan–Meier estimator (named after Edward L. Kaplan and Paul Meier), also known as the product limit estimator, estimates the survival function from life-time data. In medical research, it might be used to measure the fraction of patients living for a certain amount of time after treatment. An economist might measure the length of time people remain unemployed after a job loss. An engineer might measure the time until failure of machine parts. An ecologist may use it to estimate how long fleshy fruits remain on plants before they are removed by frugivores.

    There are two approaches to computing survival curves from life tables: the actuarial method and the Kaplan–Meier or product-limited method. Using the actuarial method, the time axis is divided into equal intervals, such as months or years, and survival is calculated at each interval by dividing the number surviving at each time period by the original number of participants. An alternative is to use the Kaplan–Meier or product-limit method of calculating the survival function. Although it is laborious to calculate, the principle behind it is simple. Each time the defined time interval has passed, the number surviving to the end of that period is calculated as a proportion of the number who had survived to the start of that period. The proportion for any one time period is multiplied by the proportions of all preceding time periods. If there are no censored data points, the actuarial and Kaplan–Meier method produce the same results, but when there are many censored points the Kaplan–Meier is the most appropriate method because the censored individuals are taken into account. The Kaplan–Meier method has the advantage over the actuarial method that it can produce a mean value of survival time for comparing groups of participants.
  12. kim.

    kim. Guest

    The usual logistic regression analysis takes place in stages. First, it determines whether there is a relationship between the outcome and the predictor(s); if there is not, there is no point proceeding. Assuming there is a relationship between a set of predictors and the dependent variable, the analysis determines whether this relationship can be simplified by reducing the number of predictors without decreasing the predictive value of the model. It can also show the best set of predictors from those included, and one can use the results to predict the outcome for new participants. There are two less common types of analysis, probit and multinomial. Probit analysis is similar to logistic regression except that it assumes a normal distribution underlies the dependent variable. It is frequently used in medical science. Multinomial regression is used when the dependent variable is categorical but not dichotomous; in other words, it has more than two categories. For example, salary may be categorised as high, medium, low. If the dependent variable has more than two categories, one alternative technique for analysing the data is discriminant analysis. In discriminant analysis the dependent variable needs to be categorical, the independent variables have to be continuous, and it is assumed that the relationship between the two is linear. The researcher attempts to determine membership of the groups of the dependent variable on the basis of one or a number of independent variables.
  13. kim.

    kim. Guest

    Cushing syndrome is the eponym used to describe the clinical findings and symptoms related to overexposure to glucocorticoids. Currently, the most common cause of Cushing syndrome is due to exogenous or iatrogenic hypercorticism. The term Cushing syndrome also includes cases of hypercortisolism secondary to functional tumors of the adrenal cortex. To be distinguished from the latter, the designation Cushing disease includes cases of hypercortisolism due to over production of ACTH as a result of either pituitary overproduction or ectopic ACTH production. Tumors associated with ectopic ACTH production most commonly occur in men and are seen in cases of small cell carcinoma of the lung, bronchial carcinoid, and medullary thyroid carcinoma (MTC). Patients with the loss of diurnal variation of ACTH and cortisol secretion have sustained increased levels of cortisol and present with the following symptoms: weight gain, psychological disturbances, decreased libido, hyperglycemia, hypertension, and a constellation of skin findings

    • The clinical signs and symptoms of Cushing syndrome and adrenal insufficiency include a constellation of findings that can involve most major organ systems of the body, including the skin.
    • There are no specific clinical manifestations of Cushing syndrome or adrenal insufficiency which are pathognomonic for these conditions, thus making the diagnosis a challenge.
    • Cutaneous manifestations of hypercortisolism include: facial redness (plethora), epidermal atrophy, acne, purpura, hirsutism, and striae distensae.
  14. kim.

    kim. Guest

    Cushing syndrome
    In patients with hypercorticism, the patient’s skin can appear atrophic, paper-thin, and translucent. Histologically, there is thinning of the epidermis, loss of the normal rete dermoepidermal junction pattern, and loss of the ground substance between collagen and elastin in the dermis resulting in a disorganized appearance of the dermal fibers. These changes are secondary to glucocorticoidrelated inhibition of type I and type III collagen synthesis and reduced hyaluronic acid content of the skin. With the loss of dermal support and decreased elasticity, ecchymoses or purpura from minor trauma are more common in areas like the arms and legs. The plethoric appearance of skin is related to dilatation of weakened vessel walls in an already thin epidermis. Cutis marmorata and purplish mottling of the lower extremities can also be seen in the setting of hypercorticism because of decreased vascular tone. Striae are characteristic in the setting of glucocorticoid excess, and are typically large, broad, and located on the trunk and extremities. In comparison to the usual striae seen in pregnancy and obesity, the striae in hypercorticism are deep, broad, and purple-colored because of dermal tearing and the translucency of the skin.

    • Hyperpigmentation is a feature of adrenocorticotropic hormone (ACTH)-dependent Cushing disease, while it is not a feature of Cushing syndrome due to primary adrenal hypercortisolism.
  15. divakar.

    divakar. Guest

    Which of the following are characteristics of
    A. fumigatus?
    A. A. fumigatus can only grow at low temperatures.
    FALSE: it is thermotolerant and grows at temperatures ranging from 15∞C to 55∞C.
    B. Its natural habitat is soil.
    TRUE: it grows on organic debris, decaying vegetation, and bird excreta.
    C. A. fumigatus produces large spores.
    FALSE: it produces small conidia that are easily airborne.
    D. Aspergillus is a filamentous fungus with branching hyphae.
    TRUE: Aspergillus hyphae are 3–5 mm in diameter and form dichotomous branches.
    E. Wounds are the main port of entry of A. fumigatus.
    FALSE: conidia are inhaled and the respiratory tract is the main port of entry.
  16. divakar.

    divakar. Guest

    A 30 yo woman has dry cough, SOB=Shortness of breath, pleurtic chest pain and subsequently develops fever, chills and bloody cough. Prior to all symptoms she had recieved cytotoxic chemotherapy for leukemia and developed neutrapenia. what infection might she now have?
    Aspergillus fumigatus

    What would be seen on a PE if someone had A fumigatus?
    fever, tachycardia, tachypnea, B/L rales over lungs

    A CT scan shows small pulmonary nodules that have a hazy rim with gound-glass attenuation. What is the sign called and what organism is in seen with?
    1) halo sign
    2) A fumigatus

    What filamentous fungi or mold presents like A fumigatus?

    What else is A fumigatus known as?
    invasive pulmonary aspergillosis

    What stain would be used to see A fumigatus? How would it look undermicroscope?
    1) silver stain
    2) acute angle branching hyphae

    What is the most common mold that causes human diseases?
    A fumigatus

    A. fumigatus
    Bronchoalveolar macrophages sense A. fumigatus through pathogenassociated
    membrane patterns (PAMPs) on the conidia via their Tolllike
    receptors TLR2 and TLR4, followed by engulfment and phagocytosis.
    Inhaled conidia via galactomannan bind some soluble receptors such as
    pentraxin-3 and lung surfactant protein D. This enhances phagocytosis
    and inflammatory responses. Phagosomes containing conidia fuse with
    endosomes followed by activation of NADPH oxidase-dependent
    killing. Nonoxidative mechanisms are also essential for the digestion of
    phagocytosed conidia by macrophages. Swelling of the conidia inside the
    macrophage appears to be a prerequisite for fungal killing. Conidial
    swelling inside macrophages or in the bronchoalveolar space alters cell
    wall composition and exposes fungal b-glucan. This further triggers fungicidal
    responses via mammalian b-glucan receptor dectin-1. However, the
    killing is delayed and quite slow and a total distruction of inhaled conidia
    by alveolar macrophages has never been reported. A. fumigatus is often
    able to block phagocytosis by producing hydrophobic pigments – melanins
    such as conidial dihydroxynaphthalene-melanin. Melanins are expressed
    on the conidial surface and protect the pathogen by quenching reactive
    oxygen species (ROS).
  17. divakar.

    divakar. Guest

    What is the most common mold that causes human diseases?
    A fumigatus

    What is the classic morphology of A fumigatus?
    thin hyphae that branch at V shaped 45 degree angle

    Does A fumigatus have different forms?
    no it is not dimorphic

    In tissue how is A fumigatus distinguished from other molds?
    it can't be

    what is A fumigatus associated with in nature?
    it is ubiquitous in nature and found with decaying vegetation

    How is A fumigatus acquired?
    breathing airborne conidia (spores)

    What are conidia?
    spores of A fumigatus

    What is the major risk factor for A fumigatus?
    cytotoxic drugs that cause neutropenia

    Can A fumigatus be transmitted person to person?:

    Incidence is a measure of the risk of developing some new condition within a specified period of time. Although sometimes loosely expressed simply as the number of new cases during some time period, it is better expressed as a proportion or a rate[1] with a denominator.
    Incidence proportion (also known as cumulative incidence) is the number of new cases within a specified time period divided by the size of the population initially at risk. For example, if a population initially contains 1,000 non-diseased persons and 28 develop a condition over two years of observation, the incidence proportion is 28 cases per 1,000 persons, i.e. 2.8%.

    Incidence rate
    It's a measure of the risk. Number of new events/number of persons exposed to risk

    Prevalence rate
    It's a measure of the extent. All cases of a disease/total population at risk

    Relationship between incidence and prevalence
    Prevalence = Incidence X Duration

    What happens to incidence and prevalence if: New effective treatment is initiated
    Prevalence decreases

    What happens to incidence and prevalence if: New effective vaccine gains widespread use
    Both incidence and prevalence decrease

    What happens to incidence and prevalence if: Number of persons dying from the condition increases
    Prevalence decreases

    What happens to incidence and prevalence if: Additional research funds are added
    No change in either incidence nor prevalence

    What happens to incidence and prevalence if: Behavioral risk factors are reduced in the poulation
    Both incidence and prevalence decrease
  18. divakar.

    divakar. Guest

    The number needed to treat (NNT) is an epidemiological measure used in assessing the effectiveness of a health-care intervention, typically a treatment with medication. The NNT is the number of patients who need to be treated in order to prevent one additional bad outcome (i.e. the number of patients that need to be treated for one to benefit compared with a control in a clinical trial). It is defined as the inverse of the absolute risk reduction. It was described in 1988.[1] The ideal NNT is 1, where everyone improves with treatment and no-one improves with control. The higher the NNT, the less effective is the treatment.[2]

    Variants are sometimes used for more specialized purposes. One example is number needed to vaccinate.[3][4][5]

    NNT values are time-specific. For example, if a study ran for 5 years and it was found that the NNT was 100 during this 5 year period, in one year the NNT would have to be multiplied by 5 to correctly assume the right NNT for only the one year period (in the example the one year NNT would be 500) [6]

    What happens to incidence and prevalence if: Contacts between infected and noninfected persons are reduced
    Both incidence and prevalence decrease

    What happens to incidence and prevalence if: Recovery from the disease is more rapid
    Prevalence decreases

    What happens to incidence and prevalence if: Long-term survival rates for the disease increase
    Prevalence increases

    Morbidity rate
    Rate of disease in a population at risk. Both incident and prevalent cases.

    Mortality rate
    Rate of death in a population at risk. Incident cases only.

    Attack rate
    A type of incidence in which the denominator is further reduced for some known exposure

    Point prevalence
    Prevalence at a specified point in time

    Period prevalence
    Prevalence during a span of time
  19. kim.

    kim. Guest

    Allergic bronchopulmonary aspergillosis (ABPA)
    The main allergic condition caused by A. fumigatus is ABPA, which develops as a result of a hypersensitivity reaction to A. fumigatus colonization of the tracheobronchial tree. Estimating the frequency of ABPA is difficult due to the lack of standard diagnostic criteria . It often appears not as a primary pathology, but as a complication of other chronic lung diseases such as atopic asthma, cystic fibrosis, and sinusitis. It occurs in approximately 0.5–2% of asthmatic patients (and in up to 15% of asthmatic patients sensitized to A. fumigatus) and in 7–35% of cystic fibrosis patients.

    Which of the following are the most frequent clinical presentations of ABPA?
    A. Severe joint pain.
    FALSE: not characteristic for ABPA.
    B. Wheezing, cough, fever, malaise, weight loss.
    TRUE: general symptoms characteristic for both ABPA and asthma patients.
    C. Skin rash.
    FALSE: not characteristic for ABPA.
    D. High levels of serum IgE.
    TRUE: characteristic for ABPA and asthma patients.
    E. Recurrent pneumonia.
    TRUE: additional clinical condition associated with ABPA.
  20. kim.

    kim. Guest

    Crude rate
    Measured rate for whole population

    Specific rate
    Measured rate for a subgroup of the population

    Standardized rate
    Adjustment to make groups equal on some factor

    Number needed to treat
    Inverse of incidence rate. Means that I would have to treat X number of people to prevent one case. 1/ARR; ARR = event rate in control group - event rate in treated group

    Crude mortality rate

    Cause-specific mortality rate
    Deaths from cause/population

    Cause-fatality rate
    Deaths from cause/number of people with the disease

    Proportionate mortality rate (PMR)
    Deaths from cause/all deaths

    The percentage of sick people for whom the test was positive: TP / TP + FN or a/a+c or 1-FN rate
  21. divakar.

    divakar. Guest

    G. lamblia, a flagellate protozoan, is the most common cause of outbreaks of waterborne diarrheal disease in the United States and is seen frequently in
    Rocky Mountain areas. Ingestion of cysts from contaminated water results
    in trophozoites in the duodenum and jejunum

    What are the presenting symptoms?
    1) sustained diarrhea >5/day
    2) nausea
    3) flatulence
    4) decrease appetite
    5) bloating

    How does the diarrhea initially present? how does it change?
    watery then greasy and foul

    What occurs on physical exam?
    distended and mildly tender abdomen

    On a chem seven what value is elevated?

    What are flatulence, foul smelling diarrhea primarily associated with?
    protozoal infection

    What is G. lamblia also known as?
    G. intestinalis, G. duodenalis

    How is giardia classified?
    intestinal flagellate

    What are its two primary forms?
    trophozoite and cyst
  22. kim.

    kim. Guest

    Clinical Features
    ● Acquired, possibly autoimmune disease with strong familial association
    ● Characterized by patches of pigment loss in skin
    ● Localized disease may show linear, segmental pattern
    ● Generalized vitiligo involves face, upper trunk, dorsa of hands, periorificial areas, and genitalia; scalp and eyelashes are not typically affected
    ● Stable patches of vitiligo are sharply demarcated and may be surrounded by a zone of hyperpigmentation; in active lesions, areas of total depigmentation may be surrounded by a zone of partial depigmentation and have a slight rim of erythema at the border

    Histopathology Vitiligo
    ● Low-power examination shows mostly unremarkable skin or mild superficial perivascular inflammation with scattered melanophages
    ● With silver stain, total absence of melanocytes is seen in well-established lesions and in the depigmented center of expanding lesions of vitiligo
    ● A few dopa-positive melanocytes may be seen in the hypopigmented areas; in the outer border of the patches, prominent melanocytes with long dendritic processes filled with melanin granules and a mild
    superficial perivascular inflammation are present
    ● Mild superficial perivascular and patchy lichenoid lymphocytic infiltrate and vacuolar alteration of the basal cell layer can be seen in normal-appearing skin adjacent to the vitiliginous patches

    ● Silver stains or the dopa reaction (Fontana-Masson) are used in demonstrating absence of melanocytes and melanin pigmentation
    ● Immunohistochemical stains for S-100 protein or pan-melanocytic marker may also be helpful in demonstrating melanocytes
  23. yunus.

    yunus. Guest

    Kidney Replacement Therapy
    Volume overload is generally recognized as an indication
    for KRT in AKF. Subjective criteria for the initiation
    of therapy include the impairment of cardiopulmonary
    function by pulmonary vascular congestion and
    the compromise of cutaneous integrity or wound healing
    by peripheral edema [45]. Objective and reproducible
    measurements, such as oxygen saturation,
    central venous pressure, pulmonary artery occlusion
    pressure, end-diastolic ventricular volume, or bioimpedance
    measurements, all have limitations in assessing
    volume status [38, 49]. More reliable parameters to determine volume status and volume responsiveness
    are dynamic measures such as inspiratory decrease in
    right atrial pressure, expiratory decrease in atrial systolic
    pressure, respiratory changes in pulse pressure,
    and respiratory changes in aortic blood velocity [49].
    Unfortunately, what constitutes “optimal volume statusâ€
    in a critically ill patient with AKF remains largely
    undefined. In addition, none of these measures has
    been studied rigorously as a parameter to guide the initiation
    of KRT.

    ›› In the absence of high-quality trials, no
    based criteria for the initiation of
    dialysis can be provided.
    ›› A serum potassium > 6.5 mEq/l and/or ECG
    changes is a generally accepted threshold to
    initiate dialysis.
    ›› Pulmonary edema and overt fluid overload are
    definite indications for kidney replacement
    therapy (KRT).
    ›› Oliguria (diuresis < 200 ml/12 h) or anuria
    (diuresis < 50 ml/12 h) after optimization of
    volume status are generally accepted indications
    to start KRT. It remains unclear whether
    an earlier start of KRT, triggered by a less pronounced
    or less prolonged decline of diuresis,
    is beneficial.
  24. yunus.

    yunus. Guest

    The presence of oliguria or anuria despite an “optimal”
    volume status is an accepted indication to start
    KRT [20, 33]. Oliguria is defined as a diuresis < 200
    ml/12 h and anuria as a diuresis < 50 ml/12 h [5]. In the
    perioperative period and intensive care unit (ICU) population,
    oliguria is often defined as an urinary flow rate
    of < 0.5 ml/kg/h [56]. The RIFLE criteria for urine output
    are a diuresis of < 0.5 ml/kg/h for 6 h, < 0.5 ml/
    kg/h for12 h, and < 0.3 ml/kg/h for 24 h or anuria to
    define class R (risk), class I (injury), and class F (failure)
    AKF, respectively [7]. Oligoanuria was the most
    common indication for KRT reported by clinicians in a
    questionnaire [50]. The presence of oligoanuria is generally
    associated with a subjective appreciation of
    more severe AKF. Some studies indeed found that the
    mortality rate of oliguric AKF was higher than that of
    nonoliguric AKF [2, 55], but patients with preserved
    diuresis had a lower APACHE II score and a higher
    creatinine clearance at inclusion

    ›› Oliguria (diuresis < 200 ml/12 h) or anuria
    (diuresis < 50 ml/12 h) after optimization of
    volume status are generally accepted indications
    to start KRT. It remains unclear whether
    an earlier start of KRT, triggered by a less pronounced
    or less prolonged decline of diuresis,
    is beneficial.
    ›› A trial of loop diuretics (furosemide 20 mg/h
    or bumetanide 1 mg/h) can be considered in
    volume-overloaded patients. Failure to
    increase diuresis to 0.5–1 ml/kg/h within a few
    hours should lead to prompt withdrawal of the
    diuretic and institution of dialytic support.
  25. yunus.

    yunus. Guest

    Uremic complications such as uremic encephalopathy,
    neuropathy, myopathy, and pericarditis require urgent
    initiation of KRT. Although traditionally mentioned as
    indications to start KRT, this extent of uremia is no
    longer seen in the current setting of AKI in ICU
    patients. Uremic symptoms, such as anorexia, nausea,
    vomiting, and pruritus are difficult to distinguish in
    critically ill patients, and therefore serum urea is used
    as a surrogate marker. Unfortunately, the optimal
    threshold for serum urea to initiate KRT is not known Based on historical trials [13, 17, 19, 20, 30, 47, 59], a
    threshold of 190 – 215 mg/dl (32–36 mmol/l) is commonly
    advised [21, 45, 46, 51].
    During the 1960s and 1970s, several retrospective
    studies supported “early†start of KRT, and the concept
    of prophylactic dialysis was introduced. In 1960,
    Teschan et al. reported an all-cause mortality of 30%
    in 15 oliguric patients who were dialyzed when urea
    reached 200 mg/dl (36 mmol/l), to keep it below 150
    mg/dl (25 mmol/l) [59]. There was no control group,
    but the authors reported that the results were better
    than their own earlier experience. In 1964, Easterling
    et al. reported a similar overall mortality of 36% in 45
    patients dialyzed to keep urea below 322 mg/dl
    (54 mmol/l) [17

    ›› A serum urea concentration of 190–215 mg/dl
    (32–36 mmol/l) is a commonly accepted
    threshold to initiate KRT. Whether earlier
    dialysis provides a survival advantage is
  26. Guest

    Guest Guest

    A 19 year old gang member is shot once with a 38 caliber revolver. The entry wound is in the left mid-clavicular line, two inches below the nipple. The bullet is lodged in the left paraspinal muscles. He is hemodynamically stable, but he is drunk and combative and physical exam is difficult to do.
    Management? Management:
    The point here is to remind you of the boundaries of the abdomen. Although this sounds like a chest wound, it is also abdominal. The belly begins at the nipple line. The chest does not end at the nipple line, though. Belly and chest are not stacked up like pancakes, they are separated by a dome. This fellow needs all the stuff for a penetrating chest wound (chest X-Ray, chest tube if needed), plus the exploratory lap
    A 27 year old intoxicated man smashes his car against a tree. He is tender over the left lower chest wall. Chest X-Ray shows fractures of the 8th, 9th and 10th ribs on the left. He has a blood pressure of 85 over 68 and a pulse rate of 128.
    Diagnostic test if stable?
    Diagnostic test if crashing? (2)
    Tx? Dx: Ruptured spleen

    Management if Stable: CT Scan
    (if he responds promptly to fluid administration, and does not require blood; further management in that case may well be continued observation with serial CT scans)

    Management if “crashing”: Peritoneal Lavage or Sonogram followed by (Tx)Exploratory Laparotomy
    A 27 year old intoxicated man smashes his car against a tree. He is tender over the left lower chest wall. Chest X-Ray shows fractures of the 8th, 9th and 10th ribs on the left. He has a blood pressure of 85 over 68 and a pulse rate of 128, which do not respond satisfactorily to fluid and blood administration. He has a positive peritoneal lavage and an exploratory laparotomy where a ruptured spleen is found and it is not salvagable.
    Further Management? Further Management:

    administration of Pneumovax and some would also Immunize for Hemophilus Influenza B and Meningococcus
    A 31 year old lady smashes her car against a wall. She has multiple injuries including upper and lower extremity fractures. Her blood pressure is 75 over 55, with a pulse rate of 110. On physical exam she has a tender abdomen, with guarding and rebound on all quadrants.
    Management? Dx: Blood (and possible feces) in the belly

    Management: Exploratory lap
    A 31 year old lady smashes her car against a wall. Her abdomen is tender with guarding and rebound tenderness present in all quadrants
    Management? Dx: Ruptured bowel

    Management: Exploratory lap, and repair of the injuries
    A patient involved in a high speed automobile collision has multiple injuries, including a pelvic fracture. On physical exam there is blood in the meatus.
    Dx? (2 possible)
    Diagnostic test? Dx: Bladder or Urethral injury
    (pelvic fracture plus blood in the meatus)

    Diagnostic test: Retrograde Urethrogram
    (because urethral injury would be compounded by insertion of a Foley catheter)
    A 19 year old male is involved in a severe automobile accident. Among many other injuries he has a pelvic fracture. He has blood in the meatus, scrotal hematoma and the sensation that he wants to urinate but can not do it. Rectal exam shows a “high riding prostate”.
    Diagnostic Test?
    Management? Dx: Posterior Urethral injury.

    Diagnostic test: Retrograde Urethrogram

    Suprapubic catheter
    (and the repair is delayed 6 months)
    A 19 year old male is involved in a motorcycle accident. Among many other injuries he has a pelvic fracture. He has blood in the meatus and scrotal hematoma. Retrograde urethrogram shows an anterior urethral injury.
    Management? Management: Anterior urethral injuries are repaired right away
    A patient involved in a high speed automobile collision has multiple injuries, including a pelvic fracture. Insertion of a Foley catheter shows that there is gross hematuria.
    Diagnostic test? Dx: Bladder injury
    (Presumably there was no blood in the meatus to warn against the insertion of an indwelling catheter, and since the latter was accomplished without problem, the urethra must be intact)

    Diagnostic test: Retrograde Cystogram
    A patient involved in a high speed automobile collision has multiple injuries, including rib fractures and abdominal contusions. Insertion of a Foley catheter shows that there is gross hematuria, and retrograde cystogram is normal.
    Diagnostic Test? Dx: Kidney injury
    (Lower injuries have been ruled out)

    Diagnostic test: CT scan

    (They will not ask you for fine-judgment surgical decisions, but the rule is that traumatic hematuria does not need surgery even if the kidney is smashed.
    They operate only if the renal pedicle is avulsed or the patient is exsanguinating)
    A 35 year old male is about to be discharged from the hospital where he was under observation for multiple blunt trauma sustained in a car wreck. It is then discovered that he has microscopic hematuria.
    Management? Management: Gross traumatic hematuria in the adult always has to be investigated
    A 4 year old falls from his tricycle. In the ensuing evaluation he is found to have microscopic hematuria.
    Management? Management: Microhematuria in kids needs to be investigated, as it often signifies congenital anomalies…particularly if the magnitude of the trauma does not justify the bleeding.
    Start with a Sonogram
    A 14 year old boy slides down a banister, not realizing that there is a big knob at the end of it. He smashes the scrotum and comes in to the E.R. with a scrotal hematoma the size of a grapefruit.
    What should be the physician's concern?
    Diagnostic test?
    Management? Concern: The issue in scrotal hematomas is whether the testicle is ruptured or not.

    Diagnostic test: Sonogram

    Management: If ruptured, surgery will be needed. If intact, only symptomatic treatment
    A 41 year old male presents to the E.R. reporting that he slipped in the shower and injured his penis. Exam reveals a large penile shaft hematoma with normal appearing glans.
    Tx? Dx: Fracture of the tunica albuginea
    (including the usual cover story given by the patient. These always happen during sexual intercourse with woman on top)

    Tx: this is one of the few urological emergencies.
    Surgical repair is needed
    You get a phone call from a frantic mother. Her 7 year old girl spilled Drano all over her arms and legs. You can hear the girl screaming in pain in the background.
    Management? Management:
    The point of this question is that chemical injuries – particularly alkalis-need copious, immediate, profuse irrigation.

    Instruct the mother to do so right at home with tap water, for at least 30 minutes before rushing the girl to the E.R
    While trying to hook up illegally to cable TV, an unfortunate man comes in contact with a high tension electrical power line. He has an entrance burn wound in the upper outer thigh and an exit burn lower down on the same side.
    What can occur from this event?
    Management of this? (3) Management: Extensive surgical Debridement
    (there is deep tissue destruction)

    What can occur? Myoglobinemia
    (leading to myoglobinuria and to Renal Failure)

    1. lots of IV fluids,
    2. Osmotic Diuretics (Mannitol),
    3. Alkalinization of the urine
    A man is rescued by firemen from a burning building. On admission it is noted that he has burns around the mouth and nose, and the inside of his mouth and throat look like the inside of a chimney.
    Diagnostic Test?
    Management? Dx: Inhalation burns

    Diagnostic test: Bronchoscopy

    Management: Respiratory support
    A patient has suffered third degree burns to both of his arms when his shirt caught on fire while lighting the back yard barbecue. The burned areas are dry, white, leatherly anesthetic, and circumferential all around arms and forearms.
    What is main problem?
    Management? (2) Problem: Circumferential burns
    (The leatherly eschar will not expand, while the are under the burn will develop massive edema, thus circulation will be cut off or in the case of circumferential burns of the chest, breathing will be compromised)

    Management: Compulsive monitoring of peripheral pulses and capillary filling.
    Escharotomies at the bedside at the first sign of compromised circulation
    A toddler is brought to the E.R. with burns on both of his buttocks. The areas are moist, have blisters and are exquisitely painful to touch. The story is that the kid accidentally pulled a pot of boiling water over himself.
    what type of burn?
    What should the physician question?
    Management? (2) Dx: Second degree burn
    (Note that in kids third degree is deep bright red, rather than white leatherly as in the adult)

    Question: How did it really happen? Burns in kids always bring up the possibility of child abuse, particularly if they have the distribution that you would expect if you grabbed the kid by arms and legs and dunked him in a pot of boiling water.

    Management: Silvadene cream.
    Possibly reporting to authorities for child abuse
    An adult male who weight “X” Kgs. Sustains second and third degree burns over ---whatever--- The burns will be depicted in a drawing, indicating what is second degree (moist, blisters, painful) and what is third degree (white, leatherly, anesthetic).
    What is the equation for proper fluid resuscitation management?
    What fluid and how much in first 8 hours? Management:
    4cc per Kg. of body weight per percentage of burned area
    (up to 50%)

    (if pt is 70kg and 18% burned, then 70x4x18)

    Fluid: Ringers Lactate

    (half of the calculated dose goes in during first 8 hours)
    A 42 year old lady drops her hot iron on her lap while doing the laundry. She comes in with the shape of the iron clearly delineated on her upper thigh. The area is white, dry, leatherly, anesthetic.
    Tx? Tx: Early excision and skin grafting
    (in very small third degree burns)
    A 22 year old gang leader comes to the E.R. with a small, 1 cm. deep sharp cut over the knuckle of the right middle finger. He says he cut himself with a screwdriver while fixing his car.
    Management? Dx: The description is classical for a human bite. No, nobody actually bit him, he did it by punching someone in the mouth...and getting cut with the teeth that were smashed by his fist. The imaginative cover story usually comes with this kind of lesion.

    Management: human bites are bacteriological the dirtiest that one can get. Rabies shots will not be needed, but surgical exploration by an orthopedic surgeon will be required.
    A 65 year old West Texas farmer of Swedish ancestry has an indolent, raised, waxy, 1.2 cm skin mass over the bridge of the nose that has been slowly growing over the past three years. There are no enlarged lymph nodes in the head and neck.
    Diagnostic Test?
    Tx? Dx: Basal cell carcinoma

    Diagnostic test: Full thickness biopsy at the edge of the lesion (punch or knife)

    Treatment: Surgical excision with clear margins, but conservative width
    A 71 year old West Texas farmer of Irish ancestry has a non-healing, indolent, punched out, clean looking 2 cm ulcer over the left temple, that has been slowly becoming larger over the past three years. There are no enlarged lymph nodes in the head and neck.
    Diagnostic Test?
    Tx? Dx: Basal cell carcinoma

    Diagnostic Test: Full thickness biopsy at the edge of the lesion (punch or knife)

    Tx: Surgical excision with clear margins, but conservative width
    A blond, blue eyed, 69 year old sailor has a non-healing, indolent 1.5 cm. ulcer on the lower lip, that has been present, and slowly enlarging for the past 8 months. He is a pipe smoker, and he has no other lesions or physical findings.
    Diagnostic Test?
    Tx? (2 possible) Dx: Squamous cell carcinoma

    Diagnostic test: Biopsy

    Treatment: Surgical resection with wider (about 1 cm) clear margins.
    Local radiation therapy is another option
  27. Guest

    Guest Guest

    A red headed 23 year old lady who worships the sun, and who happens to be full of freckles, consults you for a skin lesion on her shoulder that concerns her. She has a pigmented lesion that is asymmetrical, with irregular borders, of different colors within the lesion, and measuring 1.8 cms
    Diagnostic Test? Dx: Melanoma or Dysplastic Nevus

    Diagnostic test: full thickness biopsy at the edge of the lesion

    - margin free local excision if superficial melanoma
    (Clarks’ levels one or two, or under 0.75 mm)
    - wide local excision with 2 or 3 cm margin if deep melanoma
    A 35 year old blond, blue eyed man left his native Minnesota at age 18, and has been living the life as a crew member for a sailing yacht charter operation in the Caribbean. He has multiple nevi all over his body, but one of them has changed recently.
    Management? Dx: Melanoma

    (Change in a pigmented lesion is the other tip off to melanoma...It may be growth, or bleeding, or ulceration, or change in color)

    Management: Full-thickness biopsy at the edge of the lesion

    - margin free local excision if superficial melanoma
    (Clarks’ levels one or two, or under 0.75 mm)
    - wide local excision with 2 or 3 cm margin if deep
    A 44 year old man has unequivocal signs of multiple liver metastasis, but no primary tumor has been identified by multiple diagnostic studies of the abdomen and chest. The only abnormality in the physical exam is a missing toe, which he says was removed at the age of 18 for a black tumor under the toenail.
    Diagnostic Test for initial problem? Dx: Malignant Melanoma

    (the alternate version has a glass eye, and history of enucleation for a tumor. No self-respecting malignant tumor would have this time interval, but melanoma will)

    Diagnostic Test: full thickness biopsy at the edge of the lesion

    - margin free local excision if superficial melanoma
    (Clarks’ levels one or two, or under 0.75 mm)
    - wide local excision with 2 or 3 cm. margin if deep melanoma
    A 32 year old gentleman had a Clark’s level 5, 3.4 mm. Deep, melanoma removed from the middle of his back three years ago. He now has…(a tumor in a weird place, like his left ventricle, his duodenum, his ischiorectal area...anywhere!)
    Dx? Dx: Melanoma

    (The point of this vignette is that invasive has to be deep...metastasizes to all the usual places [lymph nodes plus liver-lung-brain-bone] but it is also the all-time-champion in going to weird places where few other tumors dare to go)
    An 18 year old lady has a firm, rubbery mass in the left breast that moves easily with palpation.
    Diagnostic Test?
    Imaging technique for young patient? Dx: Fibroadenoma

    Diagnostic Test: Tissue diagnosis...(choices in order)
    1. FNA; 2. Core Bx; 3. Excisional Bx

    (The only safe answer, even if the presentation favors benign disease, is to get tissue diagnosis)

    Sonogram is the only imaging technique suitable for the very young breast
    A 27 year old immigrant from Mexico has a 12 x 10 x 7 cm. mass in her left breast. It has been present for seven years, and slowly growing to its present size. The mass is firm, rubbery, completely movable, is not attached to chest wall or to overlying skin. There are no palpable axillary nodes.
    Diagnostic Test? Dx: Cystosarcoma Phyllodes

    (basically same presentation as Fibroadenoma, but >25yo)

    Diagnostic test: given the size best done with core or incisional biopsy

    (no need for axillary node dissection w/ phyllodes...mets is rare)
    A 35 year old lady has a ten year history of tenderness in both breasts, related to menstrual cycle, with multiple lumps on both breasts that seem to “come and go†at different times in the menstrual cycle. Now has a firm, round, 2 cm. mass that has not gone away for 6 weeks.
    Diagnostic Test? Dx: Fibrocystic disease

    Diagnostic test: Aspiration of the Cyst

    (tissue diagnosis [i.e: biopsy] becomes impractical when there are lumps every month)

    If the mass goes away and the fluid aspirated is clear, that’s all.
    If the fluid is bloody it goes to cytology.
    If the mass does not go away, or recurs she needs biopsy.
    (Answers that offer mammogram or sonogram in addition to the aspiration would be OK, but not as the only choice)
    A 34 year old lady has been having bloody discharge from the right nipple, on and off for several months. There are no palpable masses.
    Diagnostic Test?
    if test is inconclusive? Dx: Intraductal papilloma

    Diagnostic test: Mammogram
    (the way to detect breast cancer that is not palpable)

    (If negative, one may still wish to find an resect the intraductal papilloma to provide symptomatic relief. Resection can be guided by galactogram, or done as a retroareolar exploration)
    A 26 year old lactating mother has cracks in the nipple and develops a fluctuating, red, hot, tender mass in the breast, along with fever and leukocytosis.
    Management? Dx: Abscess

    (However, only lactating breasts are “entitled†to develop abscesses. On anybody else, a breast abscess is a cancer until proven otherwise.)

    Management: Incision and Drainage

    (if an option includes drainage with biopsy of the abscess wall, go for that one)
    A 49 year old has a firm 2cm mass in the right breast that has been present for 3 months.
    Management? Dx: This could be anything.

    (Age is the best determinant for Cancer of the breast. If she had been 72, you go for cancer. At 22, you favor benign. But they will not ask you what this is, they will ask what do you do.)

    Management: You have to have tissue. Core biopsy is OK, but if negative you don’t stop there. Only excisional biopsy will rule out cancer
    A 69 year old lady has a 4 cm hard mass in the right breast, with ill defined borders, movable from the chest wall but not movable within the breast. The skin overlying the mass is retracted an has an “orange peel†appearance…or the nipple became retracted six months ago.
    Diagnostic Test? Dx: Cancer of the Breast

    Diagnostic test: Core or Excisional Bx
    A 62 year old lady has an eczematoid lesion in the areola. It has been present for 3 months and it looks to her like “some kind of skin condition†that has not improved or gone away with a variety of lotions and ointments
    Diagnostic Test? Dx: Paget’s disease of the breast
    (which is a cancer under the areola)

    Management: Full thickness punch biopsy of the skin would be OK, but core biopsy or incisional biopsy of the tissue underneath would be OK also
    A 42 year old lady hits her breast with a broom handle while doing her housework. She noticed a lump in that area at the time, and one week later the lump is still there. She has a 3 cm hard mass deep inside the affected breast, and some superficial ecchymosis over the area
    Dx? Dx: Cancer, until proven otherwise

    (A classical trap for the unwary. Trauma often brings the area to the attention of the patient...but is not cause of the lump.)
    A 58 year old lady discovers a mass in her right axilla. She has a discreet, hard, movable, 2cm mass. Examination of her breast is negative, and she has not enlarged lymph nodes elsewhere
    Diagnostic Test? (2) Dx: Cancer, until proven otherwise

    (A tough one, but another potential presentation for cancer of the breast. In a younger patient you would think lymphoma. It could still be lymphoma on her.)

    Diagnostic test:
    1. Mammogram
    (we are now looking for an occult primary)
    2. Biopsy Node
    A 60 year old lady has a routine, screening mammogram. The radiologist reports an irregular area of increased density, with fine microcalcifications, that was not present two year ago on a previous mammogram
    Further Management? Dx: Cancer of the Breast

    Further management: Stereotactic Radiologically guided Core Biopsy

    (If unsatisfactory, the next move would be needle localized excisional biopsy)
    A 44 year old lady has a 2cm palpable mass in the upper outer quadrant of her right breast. A core biopsy shows infiltrating ductal carcinoma. The mass is freely movable and her breast is of normal, rather generous size. She has no palpable axillary nodes

    Tx? (2 steps) Tx:
    1. Segmental Resection (Lumpectomy) and axillary node dissection
    2. followed by Radiation Therapy to the remaining breast

    Axillary node dissection is to help determine the need for adjuvant systemic therapy
    A 62 year old lady has a 4 cm hard mass under the nipple and areola of her rather smallish left breast. A core biopsy has established a diagnosis of infiltrating ductal carcinoma. There are no palpable axillary nodes.

    Management? Management: Modified Radical Mastectomy

    (A Lumpectomy is an option only when the tumor is small [in absolute terms and in relation to the breast] and located where most of the breast can be spared.) A modified radical mastectomy is the choice here.

    Why go after the axillary nodes when they are not palpable?: Because palpation is notoriously inaccurate in determining the presence or absence of axillary metastasis.
    A 44 year old lady shows up in the Emergency Room because she is “bleeding from the breastâ€. Physical exam shows a huge, fungating, ulcerated mass occupying the entire right breast, and firmly attached to the chest wall. The patient maintains that the mass has been present for only “a few weeksâ€, but a relative indicates that it has been there at least two years, maybe longer.
    Diagnostic Test?
    Management? Dx: Advanced Cancer of the Breast

    Diagnostic Test: Core or an Incisional biopsy

    Management: currently inoperable, and incurable as well...but palliation can be offered.
    Chemotherapy is the first line of treatment.
    (In many cases the tumor will shrink enough to become operable)
    A 37 year old lady has a lumpectomy and axillary dissection for a 3cm infiltrating ductal carcinoma. The pathologist reports clear surgical margins and metastatic cancer in 4 out of 17 axillary nodes.

    Management? Management: Chemotherapy

    (Only very small tumors with negative nodes and very favorable histological pattern are “cured†with surgery alone. More extensive tumors need adjuvant systemic therapy, and the rule is that premenopausal women get chemotherapy and postmenopausal women get hormonal therapy.)
    A 66 year old lady has a modified radical mastectomy for infiltrating ductal carcinoma of the breast. The pathologist reports that tumor measures 4 cm. in diameter and that 7 out of 22 axillary node are positive for metastasis. The tumor is estrogen and progesterone receptor positive.

    Management? Management: Hormonal therapy

    (The agent used is Tamoxifen)
    A 44 year old lady complains bitterly of severe headaches that have been present for several weeks and have not responded to the usual over-the-counter headache remedies. She is two years post-op. from modified radical mastectomy for T3, N2, M0 cancer of the breast, and she had several courses of post-op chemotherapy which she eventually discontinued because of the side effects.
    Diagnostic Test? Dx: Brain mets (until proven otherwise)

    (Don’t get hung up on the TNM classification, if the numbers are not 1 for the tumor and zero for the nodes and mets, the tumor is bad.)

    Diagnostic Test: CT scan of the brain
    A 39 year old lady completed her last course of postoperative adjuvant chemotherapy for breast cancer six months ago. She comes to the clinic complaining of constant back pain for about 3 weeks. She is tender to palpation over two well circumscribed areas in the thoracic and lumbar spine.
    Diagnostic Test? Dx: Bone mets until proven otherwise

    Diagnostic test: Bone Scan
    (the most sensitive test for bone mets)

    If positive, X-Rays are needed to rule out benign reasons for the scan to “light upâ€.
    A young mother is visiting your office for routine medical care. She happens to have her 18 month old baby with her, and you happen to notice that one of the pupils of the baby is white, while the other one is black.
    Dx Differential? (2) Dx Diff: Retinoblastoma or Cataracts

    (An ophthalmological and potentially life-and-death emergency. A white pupil (leukocoria) at this age can be retinoblastoma. This kid needs to see the ophthalmologist not next week, but today or tomorrow. If it turns out to be something more innocent, like a cataract, the kid still needs it corrected to avoid amblyopia.)
    Your distant cousins that you have not seen for years visit you and brag about their beautiful baby with “huge, shiny eyesâ€. They show you a picture that indeed proves their assertion (or the exam booklet will have such a picture).
    Dx? Dx: Huge eyes in babies can be Congenital Glaucoma.

    (Tearing will indeed make them shine all the time. If undiagnosed, blindness will ensue.)
    A 53 year old lady is in the ER complaining of extremely severe frontal headache. The pain started about one hour ago, shortly after she left the movies where she watched a double feature. On further questioning, she reports seeing halos around the lights in the parking lot when leaving the theater. On physical exam the pupils are mid-dilated, do not react to light, the corneas are cloudy and with a greenish hue, and the eyes feel “hard as a rockâ€.
    Medicine Tx? (3 possible) Dx: Acute glaucoma

    (most are asymptomatic)

    Management: An ophthalmologist is needed stat

    1. Diamox
    2. Pilocarpine drops
    3. Mannitol
  28. divakar.

    divakar. Guest

    what is the typical approach to anemia?
    blood smear
    reticulocyte count

    what do you look for in peripheral blood to dx megaloblastic anemias?
    -oval macrocytes
    -severe anisocytosis (RBCs are of unequal size)
    -neutrophil hypersegmentation (>5 lobes

    pathophysiology of megaloblastic anemias
    difficulties with DNA synthesis (either by lack of folate or B12) causes impaired nuclear maturation --> and thus, larger sized RBCs that can't properly divide

    if an anemic pt answered "yes" to the question, "Do you eat lettuce?" what would you be able to rule out? what would you dx?
    rule out folate defieincy (bc vegetables are good source of folate). dx with B12 deficiency, instead!

    what are the 2 types of macrocytic anemias? give examples of each.
    megaloblastic: B12 and folate deficiency

    non-megaloblastic: sideroblastic, alcohol/lead, liver dz, hypothyroidism

    whole blood can be kept in fridge for ___ at ___degC
    35-42 days

    T/F: plasma in whole blood has coagulation factors
    false; only oncotic value

    administering 1 unit packed RBCs raises patients ___ by ___

    in case of volume loss, only give RBCs if loss is >___. if loss is >___, RBCs are required. in both cases also give saline, aka ___

    if Hb is >___ do not give RBCs. if Hb is <___ do give RBCs. In between it's not clear.

    T/F: platelet concentrate requires type match

    1 unit of platelets increases platelet count by ___

    platelets last in fridge for ___ and are kept at ___ degC
    5 days

    minimum allowed platelet count is ___ or ___ in acute bleeding
  29. Guest

    Guest Guest

    What is Thalassemia?
    - a group of inherited disorders that affect the RBCs
    -Hgb A is abnormal in thalassemia pts
    - alpha and beta types
    - severity depends on the # of genes affected

    What is the pathophysiology of Thalassemia?
    Hgb is made up of iron and a protein called globin. Four alpha-globin genes and two beta-globin genes are necessary for the synthesis of normal Hgb A. Thalassemia is the result of a mutation in any of the four alpha-globin genes or two beta-globin genes.

    Thalassemia is found in people from Africa, Southeast Asia, China, India Pakistan, the Middle East, Greece, Italy and the places from which these people have emigrate. T/F

    2 million Americans carry the thalassemia trait but only 1,000 are affected by the most severe form. T/F

    The thalassemias are a heterogeneous group of single gene disorders in which the production of normal hemoglobin is suppressed partially or completely because of defective synthesis of β- or α-globin chains. The clinical severity depends on the number of defective globin chains, the amount of globin expression from an individual gene and other genetic characteristics. The disease varies from uniformly fatal (α thalassemia major) to very mild. Beyond hydrops fetalis, thalassemia major is the most severe form of thalassemia. It manifests with growth failure, progressive pallor, hepatosplenomegaly, and bony changes during infancy. It is often fatal in the first few years of life if transfusion therapy is not initiated. Patients with the heterozygous form β- or α-thalassemia trait are at the other end of the severity spectrum. These mildly anemic, asymptomatic patients are at risk for having affected offspring and require genetic counseling. Between these two extremes are thalassemia intermedia patients, who do not initially require chronic transfusion therapy but suffer varying clinical manifestations of thalassemia. Their clinical course is deceptively severe and often deteriorates with age. These patients should be followed closely for complications of ineffective erythropoiesis and organ failure.

    2 million Americans carry the thalassemia trait but only 1,000 are affected by the most severe form. T/F

    What is the most severe form of Thalassemia?
    Beta-Thalassemia Major

    What is the Beta-Thalessemia intermedia?
    Milder form of the disease than those diagnosed with Beta-Thalessemia major and may only require support with occasional blood transfusions.

    Which chromosome are four alpha-globin genes found?
  30. Guest

    Guest Guest

    Endometrial carcinoma is the most common malignancy of the female genital tract in the Western world and the fourth most common cancer in women after breast, lung, and colorectum. Developing countries and Japan have incidence rates four to five times lower than Western industrialized nations, with the lowest rates being in India and south Asia (1).

    In the United States, it is anticipated there will be 42,160 new cases and 7,780 deaths from the disease in 2009 (2). Black women have a 40% lower risk of developing the disease but a 54% greater risk of dying from it, mainly because of late diagnosis (3).

    Two different clinicopathological subtypes of endometrial cancer are recognized: the estrogen-related (type I, endometrioid), and the non-estrogen-related (type II, nonendometrioid). Each subtype has specific genetic alterations, with endometrioid tumors showing microsatellite instability and mutations in PTEN, PIK3CA, K-ras, and CTNNBI (β-catenin), although nonendometrioid (predominantly serous and clear cell) tumors exhibit p53 mutations and chromosomal instability (

    Endometrial carcinoma
    Approximately 80% of newly diagnosed endometrial carcinomas in the Western world are endometrioid in type (4). Any factor that increases exposure to unopposed estrogen (e.g., estrogen-replacement therapy, obesity, anovulatory cycles, estrogen-secreting tumors) increases the risk of these tumors, whereas factors that decrease exposure to estrogens or increase progesterone levels (e.g., oral contraceptives or smoking) tend to be protective (1).

    The average age of patients with endometrioid cancer is approximately 63 years, and 70% or so are confined to the corpus at the time of diagnosis. Their 5-year survival is approximately 83% (5). By contrast, the average age of patients with nonendometrioid cancer is 67 years, and at least half have already spread beyond the corpus at the time of diagnosis. Their 5-year survival is approximately 62% for clear cell carcinomas and 53% for papillary serous cancers (5).

    Endometrial cancer may occasionally develop after radiation treatment for cervical cancer. In such cases, the majority are diagnosed at an advanced stage of disease and are high-risk histological subtypes. Their prognosis is poor but does not appear to be significantly worse when compared to patients with high-stage, high-grade sporadic cancers (6).

    The autonomic nervous system is pivotal in modulating the hemodynamic response to shock. The response to hypotension is vasoconstriction. Baroreceptors located in the aortic arch and carotid arteries are stimulated by changes in perfusion pressure, identified as a decline in the stretch of vessel walls during systole. Both increases and decreases in systolic pressure prompt the transmission of afferent reflex signals to vascular control centers located in the brainstem. These centers control release of the catecholamines norepinephrine from terminal sites of sympathetic nerves adjacent to vascular smooth muscle and epinephrine from the adrenal medulla. Sympathetic postganglionic neurons release norepinephrine into synaptic junctions, and binding to α-adrenergic receptors increases perivascular smooth muscle constriction. In response to increased sympathetic tone, receptors in the heart cause an increase in the heart rate and contractility. Furthermore, epinephrine released from the adrenal medulla circulates in blood and can bind α- and β-adrenergic receptors throughout the body. Baroreceptors stimulated in response to hypotension release ADH from the supraoptic and paraventricular nuclei of the hypothalamus, which circulates and contributes to constrict arterioles. Vasopressin has an additional longer acting compensatory response to hypotension because as a hormone it increases renal water absorption and expands ECF volume. Baroreceptors respond to hypertension by stimulating a reflex reduction in catecholamine release.
  31. Guest

    Guest Guest

    Cawthorne head exercise
    Balance exercises were first developed by Terrence Cawthorne, an English ear doctor. Called
    Cawthorne Exercises, these seemingly simple maneuvers can often help you regain control of your
    balance and help you lead a more healthy life. You should do them the first thing in the morning and just
    before you go to bed.
    You might get dizzy when you first start the exercises. With time though, your feeling of
    unsteadiness should gradually lessen or disappear altogether. It might take 4 weeks before you can do all
    of the exercises without getting dizzy. Above all else, please be patient!
    You should do the exercises in each level at least 10 times before you go on to the next level.
    Remember to do the exercises twice daily; once on getting up in the morning, and just before you
    go to bed at night.
    Level 1 Exercise
    While sitting on the side of your bed or on a sturdy chair, without moving your neck at all, do the
    following maneuvers:
    • Look up as far as you can with your eyes, then look down as far as you can.
    • Look from side to side as far as you can with your eyes.
    • Focus your eyes on your index finger when your arm is stretched out in front of you. Then try to
    maintain focus on that finger as you bring it toward your nose.
  32. divakar.

    divakar. Guest

    Regarding the blood supply to the chest wall:
    (a) The posterior intercostal arteries supply the 11 intercostal spaces.
    (b) The internal thoracic artery arises from the subclavian artery and supplies the upper six intercostal spaces.
    (c) The neurovascular bundle passes around the chest wall in the subcostal groove deep to the internal intercostal muscle
    (d) The intercostal spaces are drained by two anterior veins and a single posterior intercostal vein.
    (e) The posterior intercostal vein drains into the internal thoracic vein

    (a) False – there are usually nine pairs of posterior arteries from the postero-lateral margin of the thoracic aorta, distributed to the lower nine intercostal spaces.
    The first and second spaces are supplied by the superior intercostal artery, branches of the costocervical trunk from the subclavian artery.
    (b) True
    (c) True
    (d) True
    (e) False – posterior intercostal veins drain into the brachiocephalic vein and azygos system. The anterior veins drain into the musculo-phrenic and internal thoracic veins.

    Regarding the azygos venous system:
    (a) The azygos vein at the level of the fourth thoracic vertebra arches over the root of the right lung to end in the superior vena cava (SVC).
    (b) About 10% of the population have an azygos lobe.
    (c) The thoracic duct and aorta are to the right of the azygos vein.
    (d) The second, third and fourth intercostal spaces on the right, drain via the right superior intercostal vein into the azygos vein.
    (e) In congenital absence of IVC the azygos vein enlarges.

    (a) True
    (b) False – in 1% of the population, the azygos vein traverses the lung before entering the SVC resulting in the azygos fissure. The azygos ‘ lobe’ is not a true segment.
    (c) False – they are to its left.
    (d) True – hemiazygos, accessory hemiazygos, oesophageal, mediastinal, pericardial and right bronchial veins drain into the azygos system.
    (e) True – in the azygous continuation of the IVC, the azygos is a large structure, but otherwise the anatomy is unaltered. This may be confused with a mediastinal mass.
  33. kim.

    kim. Guest

    The skull varies considerably in shape and consists of a superior portion, the vault, and an inferior portion, the base. Along the base lie the orbits, sella turcica, and the temporal bones. The skull bones are composed of outer and inner tables of compact bone separated by the diploic space containing bone marrow. The inner table contains grooves for vascular structures such as the middle meningeal artery branches, and care should be taken not to confuse these for linear fractures. Pacchionian depressions house arachnoid granulations that are related to venous lacunae communicating with the superior sagittal sinus. From the midline they commonly extend 2.5 to 3.0cm, and any inner table depression beyond that distance should be considered suspicious, possibly an inner table erosion secondary to a neoplasm.[1] Beyond age 3, the cranial sutures appear similar to those of adults, and portions undergo actual closure at variable ages. Normal intracranial calcifications involve the dura, pineal gland, habenular commissure, choroid plexus, arachnoid granulations, and basal ganglia. The latter can be seen in hypothyroidism and pseudohypothyroidism but are most often physiological.
  34. kim.

    kim. Guest

    For the spine, the lateral view is the single most useful projection because it can demonstrate most post-traumatic lesions of the cervical spine.[2] The lateral projection clearly demonstrates the vertebral bodies, apophyseal joints, anterior arch of the atlas, atlanto-odontoid distance, odontoid process, spinous processes, and disc spaces. A mandatory requirement is the demonstration of the C7 vertebral body. The four smooth contour lines of the normal cervical spine are apparent on the lateral view and should be evaluated to exclude interruption or angulation. The lines include the anterior and posterior vertebral lines, the spinolaminar line (defines the posterior margin of the spinal canal), and the posterior spinous line. Evaluation of the prevertebral soft tissues can also be performed because the retropharyngeal and retrotracheal spaces are adequately demonstrated and may be pathologically widened in traumatic or nontraumatic conditions
  35. kim.

    kim. Guest

    Intrauterine Environment
    The womb generally is dark, but under certain conditions light can transmit to the fetus. A behavioral response by a fetus to light has been described (136). Transmission through all the tissue is limited to small amounts of red, or long-wavelength, light. Probably only 2% of incident light reaches the uterus (D. Sliney, personal communication, June 1992). In later pregnancy, the head of the human fetus is in the vertex position, the neck is flexed, and the face is posterior, thereby diminishing exposure. It is unlikely that light exposure is a necessary condition for the fetus, or that periodic exposure to low levels of long-wavelength light is harmful. Aspects of the light-dark cycle that reach the fetus probably are mediated more by maternal sources such as rest-activity cycles and hormones than by light directly. After birth, ambient light increases markedly, although typically the room is kept dim and cycled with dark to some extent. A prolonged wake period linked to catecholamine release occurs during this transition to extrauterine life. In dim light, the newborn is more likely to open his or her eyes.
  36. kim.

    kim. Guest

    Mounting data indicate that light has potent biological effects that are not considered routinely in standard NICU care. An association between light and ROP was first suggested by Terry in 1946. Potential mechanisms to account for phototoxicity as one of the contributing factors in ROP have been proposed and are consistent with the oxygen toxicity hypotheses: damage to endothelial cells, alteration of normal retinal metabolism, disruption of the normal regenerative process of the retina, and generation of free radicals. There is no evidence that light is a necessary condition for ROP or that maintaining a preterm infant in the dark will completely prevent it. Seiberth and colleagues found no difference in incidence of ROP for preterm infants (birth weight less than 1,250 g) who had opaque eye patches day and night from birth to 35 weeks of gestation compared to an unpatched control group. The daytime ambient light levels were already low (30 to 40 lux, or approximately 3 to 5 ft-c), and the control group had cycled lighting at night. Three converging lines of evidence lend empirical support to an association between light and ROP. In a prospective but nonrandomized study, preterm infants for whom the light levels were reduced for the duration of their hospital stay had a lower incidence of ROP compared to a similar group of preterm infants exposed to standard bright levels of nursery light. The same effect was found in both NICUs studied. Similar findings were reported by Hommura and colleagues. Reynolds and colleagues reported no difference in incidence of ROP for preterm infants who wore light-reducing goggles compared to infants who did not; however, the goggles were discontinued at 31 weeks of gestation. In a separate study, increased ROP was identified in the region of the retina that is more exposed to light—specifically, more in the regions around 3 o'clock and 9 o'clock compared to the superior and inferior regions. In addition, preterm infants with a higher degree of retinal pigment are less likely to develop ROP than infants with less retinal pigment. Retinal pigment is protective against phototoxicity.
  37. divakar.

    divakar. Guest

    Pregnancy lasts ____ days (___ weeks)

    - Calculated from the first day of ____

    -Trimesters divided in to __weeks-__ weeks-___ weeks
    280 days, 40 weeks

    - first day of last menstrual period (LMP) based on 28 day cycle

    - 13;14;13

    Gravida definition


    - number of pregnancies a woman has regardless of outcome

    - pregnant once

    - pregnant 2 or more times

    Parity: definition



    - number of deliveries after 20 weeks gestation

    - never delivered an infant after 20 weeks

    - delivered an infant beyond 20 weeks

    - two or more deliveries

    "Florida Power And Light"
    Full Term, Premature, Abortions, Live children

    Stage 1 of labor
    - Latent = ____ contractions become progressively better coordinated and cervix effaces and dilates to ___ cm

    - Active: the cervix becomes fully dilated and the presenting part descends well into the ____
    - irregular; 4cm

    - midpelvis

    Stage 2 of labor

    - Time from full ____ to delivery of fetus
    - cervical dilation

    Stage 3 of labor

    - begins after ____ and ends with ____
    - highest risk of ____
    - after delivery; delivery of placenta
    - hemorrhage

    This is defined as a purposeful stimulation of uterine contractions for the goal of delivery prior to the onset of spontaneous labor
    - Induction

    The umbilical vein, carrying oxygenated (80% saturated) blood from the placenta to the fetal body, enters the portal system. A portion of this umbilical-portal blood passes through the hepatic microcirculation, where oxygen is extracted, and thence through the hepatic veins into the inferior vena cava. The majority of the blood bypasses the liver through the ductus venosus, which directly enters the inferior vena cava, which also receives the unsaturated (25% saturated) venous return from the lower body. Blood reaching the heart via the inferior vena cava has an oxygen saturation of about 70%, which represents the most highly oxygenated blood in the heart. Approximately one-third of blood returning to the heart from the inferior vena cava preferentially streams across the foramen ovale into the left atrium, where it mixes with the relatively meager pulmonary venous return. Blood flows from the left atrium into the left ventricle, and then to the ascending aorta.
    The proximal aorta, carrying the most highly saturated blood leaving the heart (65%) gives off branches to supply the brain and upper body. Most of the blood returning via the inferior vena cava enters the right atrium, where it mixes with the unsaturated blood returning via the superior vena cava (25% saturated). Right ventricular outfow (O2 saturation of 55%) enters the aorta via the ductus arteriosus, and the descending aorta supplies the lower body with blood having less O2 saturation (about 60%) than that flowing to the brain and the upper body.
    The role of the ductus arteriosus must be emphasized. Right ventricular output enters the pulmonary trunk, from which its major portion bypasses the lungs by flowing through the ductus arteriosus to the descending aorta. Although the descending aorta supplies branches to the lower fetal body, the major portion of descending aortic flow goes to the umbilical arteries, which carry deoxygenated blood to the placenta.

    Contraindications to induction of labor
    "PAF PAPI"

    - placenta or vasa previa
    - abnormal fetal lie (breach)
    - Funic presentation (cord prolapse)
    - Prior classical uterine incision
    - Active genital herpes
    - Pelvic structural deformities
    - Invasive cervical carcinoma

    Chorioamnionitis, cesarean delivery, iatrogenic prematurity, respiratory morbidities in newborn are risk of ____

    Should not induce prior to ____ weeks and should be at least 36 weeks since last ______; 30 weeks since ____ detected on doppler
    - 39 weeks
    - positive pregnancy test
    - heart rate
  38. Guest

    Guest Guest

    Where are the Kupfer cells found?
    Kupffer cells are the resident macrophages that line the sinusoids of the liver.

    What is the function of the Kupfer cells?
    Kupfer cells are phagocytic and are responsible for clearing hepatic sinus blood of bacteria and other foreign materials.

    What is the portal triad in the liver?
    The portal triad is a portal vein, an hepatic artery and a bile duct in the liver. (they are located at the six corners of each hexagon hepatic lobule)

    Can the liver act as a reservoir for blood?
    yes- it can store up to 500 ml of blood at a time. Autotransfusion is controlled by the autonomic innervation and can release blood in response to intense sympathetic stimulation.

    What is the arterial buffer system in the liver?
    the increase n hepatic arterial flow in response to a decrease in portal vein blood flow.

    What are the seven functions of the Liver?
    1. Storage and filtration of blood
    2. Blood Coagulation
    3. carbohydrate, fat and protein metabolism
    4. Secretion of bile
    5. Storage of vitamins
    6. Storage of iron
    7. Detoxification and excretion of drugs
    (also hormone production (IGF-1 for childhood growth

    The liver metabolizes carbohydrates: describe
    1. Gluconeogenesis
    2. Glycogenolysis
    1. Gluconeogenesis: the production of glucose from amino acids
    2. Glycogenolysis: the breakdown of glycogen into glucose
    3. Glycogenesis:the formation of glycogen from glucose

    What are 4 roles of the liver in protein metabolism?
    1. produces most proteins (except IGG)
    2. syntheisizes lipoproteins
    3. converts amino acids by oxidative deamination into carbohydrates and FA for prod of ATP
    4. produces urea which removes ammonia

    What are the three likely abnormalities with chronic alcoholism?
    1. thrombocytopenia,
    2. leukopenia
    3. Anemia
  39. Guest

    Guest Guest

    Habit of mirror-gazing and silly smiles

    A 16 year old lady is in love with an aged famous doctor. She writes secret letters and sends him gifts, with no reciprocation. Recently her mother observed her habit of mirror-gazing and silly smiles. She has history of leaving home for days,without informing anybody. What is the probable diagnosis:-
    a) de-Claurembault's syndrome
    b) Dissociative fugue
    c) Nymphomania
    d) Simple schizophrenia.
  40. Guest

    Guest Guest

    Ans is: b) Dissociative fugue
  41. Guest

    Guest Guest

    The patient with complaints of urinary incontinence or urinary retention cannot be diagnosed reliably on the basis of history and physical alone. Urodynamics is an attempt to measure bladder and urethral function objectively. Videourodynamics adds anatomic detail to these measurements with the addition of a fluoroscopy unit, which allows real time imaging of the bladder and urethra during filling and voiding. The information obtained is useful for both the diagnosis and prognosis of urologic disease.
    Urologic disease may result from a number of different etiologies. Neurologic diseases are associated with bladder and urethral dysfunction, and generalizations can be made about the type of dysfunction based upon the type of disease and the level of the lesion. These inferences are not reliable. For example, among patients with spinal cord injury, we assume the following: Cervical injury is associated with detrusor external sphincter dyssynergia (DESD); thoracic injury is associated with detrusor hyperreflexia (DH) and DESD; and lumbar and sacral injuries are associated with detrusor areflexia (DA). Kaplan et al. (1) showed that although these generalizations are largely true. There are statistically significant numbers of patients with
    cervical injury who have DA and patients with sacral injury with DESD. Patients with thoracic and lumbar lesions had even greater variation in their urodynamic findings in the same study.
    This study shows clearly why individual patients require urodynamic testing rather than making treatment plans based on assumptions about dysfunction from the level of the lesion. Chancellor et al. (2) showed that even patients with incomplete injuries to the thoracolumbar spine often have occult neurogenic bladder dysfunction, including 41% of patients with ASIA E impairment (otherwise completely neurologically intact).
  42. Guest

    Guest Guest

    Managing Opioids
    Morphine’s metabolite, morphine-3 glucuronide, accumulates with renal insufficiency and may produce toxicity in the form of sedation, confusion, or myoclonus. Many preparations are inexpensive.
    Methadone acts as an opioid agonist and an N-methyl d-aspartate (NMDA) antagonist. The latter mechanism may provide advantages in neuropathic pain. Methadone is particularly inexpensive. The pace of titration is more gradual than other strong opioids due to its prolonged terminal half-life but intermediate duration of analgesia. Fatal ventricular arrhythmias have occurred with methadone at high doses (such as greater than 300 mg/day), particularly when prescribed to patients with heart disease and metabolic disarray. Thus methadone prescribing should be reserved for clinicians with experience. Fentanyl transdermal patches are changed every 72 h or sometimes every 48 h. Febrile patients may have a more rapid and less predictable accumulation of drug in the subcutaneous tissue. For patients requiring very high doses of opioids, it may be impractical to use transdermal fentanyl beyond a few hundred mcg per hour (i.e., three or four 100 mcg/h patches) which is equivalent to the potency of 300–400 mg/day of oxycodone.
    Sustained-release tablet formulations of oxycodone, morphine, or oxymorphone tablets must not be cut, crushed, or chewed because that violates the sustained-release structure of the tablets which leads to release of the entire dosage. Sustained-release morphine also comes in capsules containing time-release beads. The beads can be sprinkled on applesauce for ingestion, maintaining the extended release effects
  43. sada.

    sada. Guest

    Prolonged exposure and binding of ligand to receptor that leads to desensitization of the activated receptor where it does not respond to drug anymore
    Homologous Desensitization

    G Protein coupled receptor: G alpha stimulates
    Adenylyl cyclase

    G Protein coupled receptor: G beta gamma stimulates
    Phospholipase C

    THIS ACTION on the C-terminus of the Gprotein coupled receptor results in a decrease in ability for proteins to bind to the receptor --> Desensitization
    Phosphorylation causes Beta arrestin to attach to the receptor

    What phosphorylates the G protein coupled receptor?
    Beta adrenergic receptor kinase phosphorylates the receptor on the C-terminal

    Activation of a receptor causes a second messenger system that desensitize an unrelated class of receptors
    cross talk - heterologous desensitization

    How will heterologous desensitization be seen in a patient?
    Patient being treated with a series of medications can result in a diminished clinical response to a new drug upon first exposure - can incorrectly attribute it to genetic variability / enzyme metabolism
  44. Guest

    Guest Guest

    characteristics of pain
    duration, quality, location, radiation, frequency, alleviating or precipitating factors, associated symptoms

    chest pain in acute coronary syndrome
    substernal opressive quality described as tightness, heaviness or pressure; in MI pain lasts >20-30min; constant in frequency, precipitated by exercise, radiates to left shoulder

    inferoposterior MI can present with upper abdominal pain, nausea, hypotension and dizziness or fainting (due vagal reflexes)

    transient ischemia is releived with nitroglycerin
    associated symptoms are diaphoresis, tachypnea and anxiety

    musculoskeletal or pulmonary chest pain
    described as sharp or knife-like and reproduced by changes in position or palpation

    nonspecific but seen in MI or pulmonary embolism

    blood pressure in evaluation of chest pain
    difference of >20mmHg between two arms suggests aortic dissection (70%); hypotension is seen in massive pulmonary embolism or cardiac shock and it could also be seen in inferoposterior MI

    fever in evaluation of chest pain
    suggests pneumonia or mediastinitis
  45. Guest

    Guest Guest

    WHO criteria formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

    1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
    2. Changes in serial ECG tracings
    3. Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin

    The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.[58] According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.
  46. Guest

    Guest Guest

    Diagnosing lymphoma requires the biopsy of an involved or enlarged lymph node and subsequent microscopic examination of the specimen by a pathologist. Additional tests include a Complete Blood Count and blood chemistries to determine how well the other organs are functioning. CT scans, MRIs and PET scans may also be ordered to determine the extent of additional organ involvement. Cytogenetic studies will determine chromosomal abnormalities which may help in choosing which drug should be utilized for treatment. Since there are so many types of lymphoma, many factors will influence treatment
  47. Guest

    Guest Guest

    signs of atherosclerosis
    corneal lipid rings
    narrowed retinal arteries
    pigment and hair changes in legs
    may be seen in acute coronary syndrome

    chest wall exam in chest pain evaluation
    check for tender areas, respiratory motion, respiratory retractions or accessory muscle use; if palpation reproduces the pain consider musculoskeletal etiology

    heart sounds in chest pain evaluation
    wide physiologic splitting of S2 (inspiration) --> right bundle branch block or right ventricular infarction
    paradoxical splitting (expiration) --> LBBB or anterior/lateral infarction
    S3 --> heart failure
    S4 --> angina or infarction;
    aortic regurgitation --> aortic dissection
    mitral regurgitation --> angina or infarction due to papillary muscle dysfunction

    lung auscultation in chest pain evaluation
    assymetry of breath sounds in spontaneous pneumothorax; absent lung sounds in spontaneous pneumothorax or pleural effussion
  48. Guest

    Guest Guest

    Protein metabolism:
    A. Proteins contain about 40 per cent nitrogen.
    B. Chains containing >100 amino acid residues are called proteins.
    C. Proteins yield 4 calories per gram absorbed.
    D. During pregnancy, there is a rise in the plasma concentration of triglycerides.
    E. During pregnancy, there is a rise in the plasma concentration of albumin.

    A. False. Protein on average is composed of 16 per cent nitrogen and 84 per cent of carbon, hydrogen and sulphur combined.
    B. True. Peptide chains contain 2–10 amino acid residues, while polypeptide chains contain >10 to over 100 amino acid residues.
    C. False. The yield is 4 kcal per gram absorbed.
    D. True.
    E. False. In the case of pre-eclampsia, where the liver is affected, there is a further fall in albumin concentration.

    Uric acid:
    A. Is the end-product of pyrimidine metabolism in humans.
    B. Is excreted mainly in the bile.
    C. Is highly soluble in body fluids.
    D. The normal blood level is 4 mg/dL.
    E. Its plasma levels do not change significantly during pregnancy.

    A. False. It is the end-product of purine metabolism in humans.
    B. False. It is excreted mainly in the urine, but some is excreted in the bile.
    C. False. It is not very soluble in body fluids.
    D. True.
    E. True. The clearance of uric acid is increased, but this is balanced by increased tubular reabsorption.

    Carbohydrate metabolism:
    A. The principal carbohydrate used in body metabolism is galactose.
    B. Glycolysis is the process of glycogen formation.
    C. The pentose shunt is active in all cells of the body except red blood cells (RBCs).
    D. The tricarboxylic acid (TCA) cycle is the common pathway for the oxidation of dietary carbohydrates, fats and proteins to CO2 and H2O.
    E. Acetoacetic acid and beta-hydroxybutyric acid are known as ketone bodies.
    A. False. The principal carbohydrate used in body metabolism is glucose.
    B. False. Glycolysis is the process whereby glycogen is broken down to either pyruvate (aerobic metabolism) or lactate (anaerobic metabolism).
    C. False. The pentose shunt is active in all cells of the body, including fat and RBC.
    D. True.
    E. True. When carbohydrate supply is limited, the body uses fats for energy. Excess acetyl CoA may be produced, which condenses to acetoacetyl-CoA, the origin of the ketone bodies.
  49. Guest

    Guest Guest

    Gastroenteritis is an illness characterized by inflammation of tissue lining any part of the gastroenteric tract including the stomach and small and/or large intestines. Gastroenteritis is a common disease which can affect all individuals and which can have an important impact on health and physical development. Worldwide, nearly one in every five childhood deaths – approximately 1.5 million a year – is due to diarrhea, which
    kills more children than AIDS, malaria, and measles combined.The principles of preservation of gastrointestinal pathogens in fecal specimens include:
    — Enteric pathogens do not replicate in feces during transport at room temperature, since this is not their optimal living environment. Some protozoa, however, undergo maturation in feces before they become infectious (e.g. Cyclospora cayatenensis).
    — Although often present in high levels during acute infection, enteric pathogens can be shed intermittently and in low numbers especially during asymptomatic or subclinical infections or in the convalescent phase.
    — Bacteria, viruses, and some protozoa are generally susceptible to subsequent freeze–thawing treatment.
    — Conventional diagnostic procedures including production of environments, which permit only the growth of specific bacterial pathogens, might hamper the recognition of co-infections.
    — The action of proteases and nucleases in feces may degrade targets essential for diagnostic procedures
  50. veena.

    veena. Guest

    Age-related “degenerative change†of aortic valves is
    the most common cause of adult aortic valve stenosis
    encountered in North America. Traditionally valve
    “degenerative†calcification was thought to be passive
    in nature representing dystrophic calcification of
    degenerated material from wear and tear of the valve
    tissue. Increasingly, this theory has been shown to be
    incomplete. Early there is endothelial dysfunction
    from wear and tear, and hemodynamic shear stresses,
    followed by lipid accumulation, inflammation, alteration
    of cytokines, growth factors and valve matrix
    metalloproteinases [3]. The process of valve calcification
    has much in common with atherosclerosis and
    bone formation [4–6]. Progression of aortic valvular
    disease in patients from the general population has
    been associated with many of the traditional risk factors
    for atherosclerotic disease including systemic
    arterial hypertension, hyperlipidemia, and diabetes
    mellitus [7–10]. Stenotic aortic valves have a larger
    amount of lipid compared to non-stenotic valves The lipid may oxidize and attract inflammatory cells.
    Early cusp yellow discoloration and fibrosis eventually
    evolves into an arch of calcium extending from the
    base of each cusp like an inverted “uâ€

    Mitral annular calcification (MAC) is a common finding
    in the hearts of elderly patients, especially females.
    Although MAC has been considered to be an agerelated
    finding, it probably is a pathological process
    due to degenerative changes in the mitral annulus. Its
    incidence is low in those under the age of 50 years;
    however, the incidence of MAC increases to become
    common in the elderly. It is a progressive process,
    albeit at a slow pace in most patients. In association
    with mitral valve disease, especially mitral valve prolapse
    (myxomatous/floppy mitral valve), the condition
    may occur in younger patients. MAC occurs at an earlier
    age, is more exaggerated and has a more rapid progression
    in those with calcium metabolic abnormalities
    such as hyperparathyroidism and chronic renal failure,
    especially in those who are dialysis dependent

    Mitral annular calcification (MAC)
    Mitral annular calcification is usually localized to
    the mitral ring, invariably the most common site being
    the base of the posterior mitral leaflet .
    Rarely the calcium extends onto the mitral leaflet
    . This process generally starts at the base of
    the leaflets and the tips of leaflets remain mobile
    . MAC may be distinguished from post-rheumatic
    changes by the lack of leaflet commissural
    fusion and the fact that the leaflet is not diffusely diseased.
    MAC may also fix or tether the posterior leaflet
    to the underlying calcified mass, restricting the leaflet
    motion and contributing to valve insufficiency. Loss
    of the normal left ventricle squeezing motion during
    systole due to rigidity, also contributes to mitral insufficiency.
    When liquefactive degeneration of the calcific
    mass occurs, extension to the posterior left atrial
    wall has been described

    Protein misfolding, which literally means ‘‘incorrect folding,’’ is associated with
    a number of pathological states in humans, collectively termed protein
    misfolding diseases. In some cases the disease arises because a specific protein
    is no longer functional when adopting a misfolded state or undergoes a severe
    trafficking impairment (loss-of-function diseases). In most diseases, however,
    the pathological state originates because misfolding occurs concomitantly with
    aggregation, and the underlying aggregates are detrimental (gain-of-function
    diseases). The question of why proteins misfold and self-assemble into wellorganized
    fibrillar aggregates characterized by an extensive b-sheet structure,
    generally referred to as amyloid or amyloidlike fibrils, is very complex and
    cannot be answered exhaustively even in several pages. Despite these difficulties,
    it is fascinating to try to address this issue, particularly by describing a few
    concepts that are well established, have general validity, and benefit from a
    general consensus in the scientific community. In this challenge we start by
    describing our current knowledge of why and how proteins misfold in vitro.

    A newly synthesized polypeptide chain usually folds into a functional, globular
    conformational state characterized by a well-defined, persistent secondary and
    tertiary structure . In this conformation, generally termed the folded or
    native state, a protein is generally stable and soluble and has a minimal
    propensity to undergo aberrant aggregation, particularly because most of its
    hydrophobic moieties and a large portion of the backbone are sequestered
    inside the protein . Even the regions located on the protein surface that
    may potentially retain a residual ability to trigger an undesired intermolecular
    association between folded protein molecules, such as the peripheral strands of
    b-sheets, are protected by structural adaptations developed during evolution
    [1]. Therefore, the first and necessary event that generally triggers the aggregation
    process of a normally globular protein into structured amyloidlike fibrils is
    the adoption of a nonnative partially or globally unfolded state [2,3

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