Categories
Respiratory Pathology

Rhinosinusitis

[et_pb_section fb_built=”1″ _builder_version=”3.26.3″][et_pb_row _builder_version=”3.26.3″][et_pb_column type=”4_4″ _builder_version=”3.26.3″][et_pb_post_title featured_image=”off” text_color=”light” _builder_version=”3.26.3″ title_letter_spacing=”6px” meta_font=”||on||||||” meta_text_color=”#000000″ use_background_color_gradient=”on” background_color_gradient_direction=”119deg” custom_margin=”0px|||0px|false|false” custom_padding=”36px||13px|27px|false|false” date=”off”][/et_pb_post_title][/et_pb_column][/et_pb_row][et_pb_row _builder_version=”3.25″][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_text _builder_version=”3.26.3″]

Should We Say Rhinosinusitis or Sinusitis?

Rhinosinusitis is preferred over sinusitis because inflammation of the sinuses usually occurs with the inflammation of the nasal mucosa.

    Rhinosinusitis Types

    Here are the types of rhinosinusitis, based on the duration of the symptoms:

    • Acute rhinosinusitis – < 4 weeks
    • Subacute rhinosinusitis – 4 to 12 weeks
    • Chronic rhinosinusitis – > 12 weeks
    • Recurrent acute rhinosinusitis – Four or more ARS episodes in a year per year, with interim symptom resolution.

    [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

    Categories
    CVS - Clinical/Cardiology Surgery

    How Does the Impella Ventricular Assist Device Work?

    [et_pb_section fb_built=”1″ _builder_version=”3.26.3″][et_pb_row _builder_version=”3.26.3″][et_pb_column type=”4_4″ _builder_version=”3.26.3″][et_pb_post_title featured_image=”off” text_color=”light” _builder_version=”3.26.3″ title_letter_spacing=”6px” meta_font=”||on||||||” meta_text_color=”#000000″ use_background_color_gradient=”on” background_color_gradient_direction=”119deg” custom_margin=”0px|||0px|false|false” custom_padding=”36px||13px|27px|false|false”][/et_pb_post_title][/et_pb_column][/et_pb_row][et_pb_row _builder_version=”3.25″][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_text _builder_version=”3.26.3″]

    Impella is a ventricular assist device, that is FDA approved for short-term support of the left ventricle. There is also a version that can be used for the right ventricle as well. The device can support 2.5 to 5 L/min of blood flow, the latter of which is considered a normal cardiac output.

    The device is minimally invasive and catheter-based, so it is usually placed by Interventional Cardiologists in the catheterization laboratory. It is an impeller driven, axial-flow pump (which derives its inspiration from the Archimedes pump from antiquity).

    The device is positioned so that the intake of the pump sits in the LV cavity and the outflow in the aorta, just above the aortic valve. In this way, the pump replaces the work done by the left ventricle and sucks up the oxygenated blood as it returns from the left atrium and forcibly delivers it into the aortic root (beginning part of the aorta).

    The oxygenated blood then feeds the coronary arteries and the rest of the body. By removing the blood from the LV cavity, the device reduces pre-load, and by ejecting it at a high velocity into the aorta, it reduces afterload. This has the net effect of “unloading” the left ventricle and thereby reducing the energy required by the LV to function. This, then, rests the LV and allows it to recover as the LVAD does the heart’s work. An impella placed in the RV works by the same principles, to help right ventricular function.

     

    Impella Videos :

    https://www.youtube.com/watch?v=ZgqKwG2HaxQ

    https://www.youtube.com/watch?v=A0q64bXxDQY

    https://www.youtube.com/watch?v=GhWB7T5QxMI

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]
      Categories
      Infectious Diseases

      Chagas Disease (American Trypanosomiasis)

      [et_pb_section fb_built=”1″ _builder_version=”3.22″][et_pb_row _builder_version=”3.25″][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_text _builder_version=”3.26.3″]

      Overview:

      Today’s lecture revolves around the discussion of Chagas disease, signs and symptoms, its manifestations and treatment.

      Chagas disease is an infectious disease caused by Trypanosoma cruzi, a parasite transmitted through the bite of Reduviid bug. The parasite is present in the feces of the bug.

      Chagas disease is predominantly found in South America, Central America, and Mexico. The Reduviid bugs hide in the crevices of the walls and roof during the day and come out at night to feed on the sleeping host.

      Most of the people who are infected with Trypanosoma cruzi don’t even know that they are infected. This disease is not transmitted from person to person like a number of contagious diseases.

      There are two phases of Chagas disease; acute and chronic. The acute phase may last for a few weeks or even months while the chronic phase can continue for decades or for the entirety of someone’s lifetime.

      An infected person may be asymptomatic or may present with a number of symptoms ranging from fever, fatigue, rash, body aches, cardiac complications or gastrointestinal complications.

      Treatment of Chagas disease involves getting rid of the parasite in acute infection or managing signs and symptoms in chronic phases. Steps should be taken to prevent the infection too. When left untreated, Chagas disease can lead to chronic lifelong and sometimes life-threatening manifestations.

       

      Trypanosoma Cruzi (the culprit of Chagas disease) :

      Before moving on to the detailed discussion about Chagas disease, let us first go through the life cycle of Trypanosoma cruzi.

      Trypanosoma cruzi is a protozoan that can live in humans, mammals and Reduviid bug (whose nickname is “kissing bug”.)

       

      Trypanosoma cruzi circulates in the blood of infected mammals in the form of   “trypomastigotes”.  When Reduviid bug bites and feeds on the infected mammal’s blood, it ingests the parasite. This parasite then subsequently matures in the bug’s intestine before being eliminated in its feces. When the bug bites the next mammal, the bug generally defecates near the site of the bite, allowing trypomastigotes in the feces to enter the host through a wound, intact skin or mucous membrane. Once the parasite gains entry into the host, it develops into an intracellular form called “amastigote”. The amastigote then multiplies producing trypomastigotes which are released in circulation, thus infecting other cells and tissues.

      This was briefly the life cycle of Trypanosoma cruzi parasite, now we continue with our discussion of Chagas disease.

       

      Risk factors

      There are several risk factors that increase the risk of transmission of the parasite. Some of the risk factors which increase the incidence of Chagas disease are described below:

      • Living in an area that contains the bug
      • Living in poor housing conditions e.g mud walls, thatched roofs, adobe huts in parts of the country residing the bug
      • Infection can also occur through infected transplanted organ
      • Transfusion of contaminated blood products
      • Vertical transmission from mother to child may also occur
      • And very rarely as a result of laboratory accident or contaminated food or drink

      Signs and symptoms

      Chagas disease has an acute phase and a chronic phase as mentioned earlier. Symptoms range from mild to severe or the person might even not be aware of the symptoms at all.

      Acute phase

      The acute phase lasts for the first few weeks or months of infection. The clinical features of acute phase include:

      • Fever
      • Fatigue
      • Body aches
      • Muscle pain
      • Headache
      • Rash
      • Loss of appetite
      • Diarrhea
      • Nausea
      • Vomiting
      • Mild enlargement of liver or spleen
      • Swollen glands
      • Swelling at the site of the bite

      Clinical features presented in this phase may go away but if left untreated, the infection persists and may progress to the chronic phase.

      Chronic phase

      The chronic phase of Chagas disease may continue for 10-20 years or even for the lifetime of a person. In severe cases, the chronic phase may present with:

      • Irregular heartbeat
      • Congestive heart failure due to dilated heart
      • Sudden cardiac arrest
      • Difficulty swallowing due to the dilated esophagus
      • Abdominal pain or constipation due to dilated colon

      Chronic “indeterminate” phase

      Along with the above-mentioned phases of Chagas disease, some of the infected people, following the acute phase of infection enter into an asymptomatic phase, known as chronic “indeterminate” phase. In this phase, few or no parasites are found in the blood.

      Most of the people are thus unaware of their infection as they are asymptomatic. Among them, many people remain asymptomatic throughout their lives but some may progress to develop the complications of chronic Chagas disease.

      Having mentioned the clinical features of Chagas disease let us understand the pathophysiology of this disease.

       

      Pathophysiology of Chagas disease :

      The main event destroying the peace in Chagas disease is the inflammatory process occurring as a response to the parasite.

      Dilated cardiomyopathy, the principal cardiomyopathy of Chagas disease starts with inflammation. Following inflammation, cellular damage occurs. The body attempts to recover from the cellular damage by causing fibrosis of cardiac tissue.

      Conduction abnormalities also accompany Trypanosoma cruzi infection. The inflammatory and non-inflammatory response of the heart leads to parasympathetic denervation of cardiac tissues.

      Cardiac manifestations may cause death in a person by producing arrhythmias, stasis of blood with embolism in a dilated heart, thrombi affecting several organs, or sudden cardiac death due to severe cardiac failure.

      Parasympathetic denervation due to inflammation also occurs in esophagus and colon. The esophagus is dilated because of loss of parasympathetic innervation (known as “megaesophagus”) and thus leading to swallowing difficulty. Dilation of the colon (known as “megacolon”) leads to abdominal pain and constipation producing complications of Chagas disease. 

       

      Diagnosis :

      After the host comes in contact with the feces of Reduviid bug, the incubation period of infection is about 5-14 days. Tests are used to diagnose a patient to begin treatment and prevent complications from occurring and include the following:

      • Microscopic examination:

      During the acute phase of infection, parasites may be seen circulating in the blood. Thick and thin blood smears stained with Giemsa stain are used for direct visualization of parasites.

      • Immunoassays:

      Test including complement fixation, indirect haemagglutination, indirect fluorescence assays, radioimmunoassays, ELISA and polymerase chain reaction (PCR) can be used to differentiate between the different strains of Trypanosoma. These immunoassays are usually used for the diagnosis of chronic Chagas disease.

       

      Treatment :

      Treatment is recommended for patients diagnosed early in the course of their disease (acute phase), babies with congenital infection (through vertical transmission), patients with reduced immunity (due to increased risk of aggressive disease) and many patients with chronic infection.

      Two approaches are used to treat Chagas disease; antiparasitic treatment (to kill the parasite) and symptomatic management (to manage the signs and symptoms of infection).

      • Medications:

      Antiparasitic medications are usually effective early in the course of the disease. Drugs of choice include azole or nitro derivatives such as benznidazole or nifurtimox. The parasitological cure of these drugs is high in children and low in adults. The reason might be the resistance of drugs or longer periods of infection in adults.

      • Symptomatic management:

      Symptomatic management involves managing the clinical features of the disease. For example for irregular heartbeats, pacemaker or medications may be used. Surgical procedures like subtotal colectomy are used to manage megacolon. Similarly, surgical procedures can also be used for the treatment of megaesophagus.

       

      Prevention and Control :

      No vaccines are available against Trypanosoma cruzi. Certain preventive measures that can be used in high-risk areas include:

      • Vector control by using insecticides to remove bugs from the residence
      • Insect repellent sprays or lotions can be used on exposed skin
      • Wearing protective clothing
      • Avoid sleeping in mud, thatch or adobe house
      • Screening of blood donations to prevent the spread of disease through blood transfusion

      Control strategies are directed towards transmission prevention through organ donation, blood donation, and mother to child transmission.

       

      References :

      1. First Aid for USMLE Step-1
      2. Robbins and Cotran Pathological basis of disease
      3. http://www.infochagas.org/en_GB/ciclo-de-vida-del-parasito
      4. https://en.wikipedia.org/wiki/Trypanosoma_cruzi
      5. https://www.cdc.gov/parasites/chagas/diagnosis.html
      6. https://www.mayoclinic.org/diseases-conditions/chagas-disease/symptoms-causes/syc-20356212
      7. https://en.wikipedia.org/wiki/Chagas_disease

       

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Microbiology

      Chaga’s Disease

      [et_pb_section fb_built=”1″ _builder_version=”3.19.5″][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Triatomine bugs bite the victim near the face at night. They suck their blood.
      After the bite, these bugs defecate on the victim.
      The bug’s feces contains Trypanosoma cruzi (T. cruzi)
      T. cruzi enters the victim’s blood via the mucous membrane, skin break, or when the victim scratches the bite area and unknowingly pushes the feces in the wound.

       

      Acute Phase

      During the acute phase (days to months) the victim has no symptoms or mild flu-like symptoms (fever, aches, rash, loss of appetite, diarrhea, vomiting, etc.)
      Liver, spleen, and lymph nodes might be mildly enlarged. A chagoma (swelling) at the site of the bite may develop.

      Less than 5% of the young patients may die due to severe inflammation, infections of the heart muscle (myocarditis) or brain (meningoencephalitis.)

       

      Chronic Phase

      This phase can last for decades. About 20%-30% of patients develop cardiac or gastrointestinal complications. Enlarged heart, arrhythmias, heart failure, can occur. Megaesophagus and megacolon may develop making it difficult to eat or poop.

       

      Diagnosis

      • Parasite in patient’s blood smear.
      • IgM in the acute phase.
      • PCR

      Reference: https://www.cdc.gov/parasites/chagas/diagnosis.html?fbclid=IwAR3y6jLjiwtC-pNqfFwl02xfbWKIoMA0aK_7nZX4n90aarT2old0YrXXIGo

      Treatment

      Benznidazole is FDA approved for children 2-12 years of age.
      Nifurtimox, not FDA approved, but available under the investigational protocol.
      Symptomatic treatment may be needed as well.

       

      Reference: https://www.cdc.gov/parasites/chagas/gen_info/detailed.html

       

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Endocrine System

      Insulin Dose Calculator

      [et_pb_section fb_built=”1″ _builder_version=”3.19.5″][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_code _builder_version=”3.19.5″]

      INITIAL INSULIN DOSE ASSESSMENTMedical disclaimer: this calculator is not for any specific patient

      1PERSON’S INFORMATION
      2INITIAL INSULIN DOSE




      By clicking calculate you agree to DrBeen’s medical disclaimer.
      [/et_pb_code][et_pb_text _builder_version=”3.19.5″]

      Reference article for the reasoning behind the dose calculation.

      Medical Disclaimer:

      This calculator is to help your provider calculate the initial insulin dose. This is not a prescription for any specific person. Insulin should only be administered with a provider’s prescription. This calculator does not establish a patient-doctor relationship between you and DrBeen or its affiliates/partners/associates/team members.

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]
      Categories
      Endocrine System

      Calculating Daily Insulin Dose

      [et_pb_section fb_built=”1″ _builder_version=”3.19.5″][et_pb_row custom_padding=”|||1px” _builder_version=”3.19.5″ background_color=”#f4f4f4″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″ custom_margin=”|||7px”]

      Medical Disclaimer: your physician/provider will give you the instructions and dosage needed for the insulin administration. The following information is for educational purposes and is not a prescription for any specific patient. Incorrect insulin dosage can cause severe hypoglycemia with dangerous outcomes.

      [/et_pb_text][/et_pb_column][/et_pb_row][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Understanding The Terms Related to The Insulin Administration

      Basal Insulin

      About 40-50% of the daily insulin dose is used during the intervals between meals and at night (fasting states.) This amount of insulin is usually constant.

      Bolus Insulin

      This dose of insulin is used for two purposes:

      • Reducing blood glucose levels that are higher than the goal/target level.
      • Disposing of the new blood glucose that will become available after eating carbohydrates/food.

      High Blood Sugar Correction Amount

      This is the amount of bolus insulin needed to correct high blood sugar. Generally, 1 unit of rapid-acting bolus insulin is needed to reduce the blood glucose level by 50 mg/dl. This drop can range from 15-100 mg/dl depending upon the individual, their state, time of the day, etc.

      Insulin to Carbohydrate Ratio

      This is the amount of carbohydrates that will be reduced by 1 unit of insulin. Generally, 1 unit of rapid-acting insulin will dispose of 12-15 grams of carbohydrates.

      Keep in mind that the amount of carbohydrate disposed of by 1 unit of insulin can vary. Some reasons for this variation are the following:

      • Different individuals respond differently to insulin.
      • Person’s health. For example fever, infections, etc.
      • Time of day, for example early in the morning our bodies produce hormones that increase blood glucose levels. This is called the dawn phenomenon. Usually, our natural insulin counters this effect, however, in diabetics this correction may not occur leading to high fasting glucose levels.
      • Blood glucose rebound as a result of insulin administration that causes hypoglycemia. This can occur in the morning after the administered insulin has caused hypoglycemia leading to the release of stress hormones that in turn work to release more glucose in the blood. This is called the Somogyi phenomenon.

      Worked-out Examples

      Initial Insulin Dose Calculator

      Calculate the amount of bolus insulin needed for the carbohydrates in the meal

      This is the insulin needed to dispose of the carbohydrates that you will eat in your meal.

      Assumption: your insulin sensitivity index is: 15gm per unit. Warning, this index is different for different people. You will have to determine your sensitivity index by repeatedly checking your blood glucose levels before meals, administering insulin, taking meals, and then checking the blood glucose levels. 

      Let’s say you will eat 1 cup of white rice. It has 45 grams of carbohydrates. (Reference: If you eat a cup of cooked long grain rice, you will be eating 45 grams of carbohydrates.)

      You will need 3 units (45/15) of bolus insulin (rapid-acting insulin) to dispose of this one cup of white rice.

      Calculate the amount of bolus insulin needed to correct the excess blood sugar

      Assumptions:

      • Your pre-meal goal/target blood glucose level is 120 mg/dl
      • The carbohydrate correction factor is 50 mg/dl

      Formulae:

      • (Pre-meal blood glucose) – (target pre-meal blood glucose level) = excessive blood glucose levels
      • Additional bolus insulin units = (excess blood glucose levels)/(carbohydrate correction factor)

      Before your meal, check your blood glucose level. Let’s say it is 270 mg/dl.

      Thus, 270 mg/dl – 120 mg/dl = 150 mg/dl

      This means your pre-meal blood glucose level is 150 mg/dl above the target level. We have to add bolus insulin (rapid-acting insulin) to correct this excessive blood glucose as well. The correction factor of 50 mg/dl means that we will have to administer 1 extra unit of bolus insulin for each 50 mg/dl of excess blood glucose.

      (Excess glucose)/(insulin correction factor) = additional bolus insulin units needed

      150/50 = 3 units of additional bolus insulin to correct for this excessive 150 mg/dl blood glucose

      The total bolus insulin (rapid-acting insulin) needed is 3 units.

       

      Summary

      For this patient who is going to eat two chapatis (30 grams carbohydrates) and has pre-meal blood glucose level of 270 mg/dl the bolus insulin levels will be 2 units (for chapatis) + 3 units (for the excessive pre-meal blood glucose level) = 5 total units.

       

      Calculating The Basal Insulin Dose

      Initial Insulin Dose Calculator

      First, we need to calculate the total daily insulin dose needed by the body. Then we will take 40-50% of this amount as the basal insulin (long-acting) amount needed. The rest of the insulin will be given via the bolus (rapid-acting) dosages (as calculated above.)

      Formulae:

      • Total daily insulin requirement = (total body weight in pounds) / 4
      • Total daily insulin requirement = (total body weight in kilograms) x 0.55

      Let’s work out an example

      Let’s say the patient’s weight is 216 pounds or 98 kilograms. Let’s calculate the total insulin required for this patient:

      • Calculating with pounds: Total daily insulin required = 217 lbs / 4 = 54.25 units
      • Calculating with kilograms: Total daily insulin required = 98 kg x 0.55 = 53.9 units

      The total daily insulin required by this patient is 54 units. (Warning do not administer this amount. Only 40% of this amount is needed in basal insulin.)

      Calculating the daily required basal (long-acting) insulin dose

      Daily basal (long-acting) insulin dose required = 40-50% of the total daily insulin required.

      • 40% = 54 units x 0.4 = 21.6 units of the basal (long-acting) insulin is required.
      • 50% = 54 units x 0.5 = 27 units of the basal (long-acting) insulin is required.

       

      Final Calculations for the whole day and one meal (mentioned above)

      For the patient in the examples above, the required insulin dosages are as follows:

      • Basal (long-acting) insulin: 21 to 27 units
      • Bolus (rapid-acting) insulin: 5 units needed when he/she was planning to take 2 chapatis and had a pre-meal blood glucose level of 270 mg/dl with a goal/target level of 120 mg/dl

       Initial Insulin Dose Calculator

       

      Reference: This UCSF article on the insulin dose calculation is excellent, though a little confusing to read.

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Endocrine System

      Daily Insulin to Oral Hypoglycemic

      [et_pb_section fb_built=”1″ _builder_version=”3.22″][et_pb_row _builder_version=”3.25″][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_text _builder_version=”3.26.3″]

      Disclaimer:

      This is not a prescription. Using medicines without the guidance of a licensed provider can be lethal.

       

      Adding once-daily insulin to  oral hypoglycemic  therapy in  T2DM patient

      • NPH or detemir at bedtime
      • Glargine or degludec in the  morning or at bedtime

       

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Endocrine System

      Beginning Therapy Type Two Diabetes Mellitus (T2DM) Patient

      [et_pb_section fb_built=”1″ _builder_version=”3.22″][et_pb_row _builder_version=”3.25″][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_text _builder_version=”3.26.3″]

      Disclaimer:

      This is not a prescription. Using medicines without the guidance of a licensed provider can be lethal.

       

      Asymptomatic patient with HbA1c < 7.6%  or close to HbA1c 0.5 to 1.5% above treatment goal

      •Lifestyle changes

      •Metformin-p starting with 500 mg at bedtime. Then 500 mg with breakfast. Dose increased slowly if needed.

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Renal Nephrology Renal System

      BUN:CR Ratio

      [et_pb_section fb_built=”1″ _builder_version=”3.19.5″][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Disclaimer:

      This is not a prescription. Using medicines without the guidance of a licensed provider  can be lethal.

       

      1. >20:1 prerenal.
        Example: dehydration
      2. 10-20:1 normal or postrenal.
        Example:kidney stones.
      3. <10:1 intrarenal.

      Example: A TN, glomerulonephritis.

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]
      Categories
      Pharmacology

      Common Cold Symptomatic & Treatment

      [et_pb_section fb_built=”1″ _builder_version=”3.19.5″][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Disclaimer:

      This is not a prescription. Using medicines without the guidance of a licensed provider  can be lethal.

       

       AnaIgesics

      2. Combination products of

      • Antihistamine
      • Decongestant

      3.  Cough maybe due to

      • Nasal obstruction or
      • Post nasal drip

      For cough dextromethorphan

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]
      Categories
      Endocrine System

      Insulin Initial Dose

      [et_pb_section fb_built=”1″ _builder_version=”3.22″][et_pb_row _builder_version=”3.25″][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_text _builder_version=”3.26.3″]

      Disclaimer:

      This is not a prescription. Using medicines without the guidance of a licensed provider can be lethal.

       

      Initial total insulin dose:

      0.2 to 0.6 units/kg/day in  divided doses.

      Conservative initial doses of 0.2 to 0.4 units/kg/day are often recommended to avoid the potential for hypoglycemia.

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Ear Nose Throat

      Rhinosinusitis Or Sinusitis?

      [et_pb_section fb_built=”1″ _builder_version=”3.19.5″][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Disclaimer:

      This is not a prescription. Using medicines without the guidance of a licensed provider  can be lethal.

       

      Rhinosinusitis is preferred  over sinusitis because  inflammation of the sinuses  usually occurs with

      the  inflammation of the nasal  mucosa.

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]
      Categories
      Authors and Contributors

      Dr. Ayesha Farooq

      [et_pb_section fb_built=”1″ fullwidth=”on” _builder_version=”3.19.5″ background_color=”#0c71c3″ background_image=”https://articles.drbeen.com/wp-content/uploads/2019/01/UNADJUSTEDNONRAW_thumb_2332.jpg&#8221; background_position=”top_left” background_blend=”multiply” global_module=”3792″ saved_tabs=”all”][et_pb_fullwidth_post_title text_color=”light” _builder_version=”3.19.5″ title_font=”Montserrat|700|||||||” text_orientation=”center” custom_padding=”||20px” custom_padding_last_edited=”off|desktop”][/et_pb_fullwidth_post_title][/et_pb_section][et_pb_section fb_built=”1″ _builder_version=”3.22″][et_pb_row module_class=” et_pb_row_fullwidth” _builder_version=”3.25″ width=”89%” width_tablet=”80%” width_last_edited=”on|desktop” max_width=”89%” max_width_tablet=”80%” max_width_last_edited=”on|desktop” make_fullwidth=”on”][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_text _builder_version=”3.19.5″]

      Ayesha Farooq is a final year medical student at Liaquat University of Medical and Health Sciences. Ayesha loves to conduct social awareness campaigns and workshops. She  actively participates in noble causes to help improve the society around her.

      She lives her life according to T.S., Eliot’s words:

      The purpose of living is to make life less difficult for each other.

      She feels strongly against exploitation and injustice of human rights. Ayesha is intrigued by the intricacies of medical sciences. She also has special interest in the workings of the human mind; she aspires to become a clinical psychiatrist.

      At Drbeen Ayesha is writing various sections in the immunology made easy book.

       

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Authors and Contributors

      Dr. Hassan Ahmad

      [et_pb_section fb_built=”1″ fullwidth=”on” _builder_version=”3.19.5″ background_color=”#0c71c3″ background_image=”https://articles.drbeen.com/wp-content/uploads/2019/01/UNADJUSTEDNONRAW_thumb_2332.jpg&#8221; background_position=”top_left” background_blend=”multiply” global_module=”3792″][et_pb_fullwidth_post_title text_color=”light” _builder_version=”3.19.5″ title_font=”Montserrat|700|||||||” text_orientation=”center” custom_padding=”||20px” custom_padding_last_edited=”off|desktop”][/et_pb_fullwidth_post_title][/et_pb_section][et_pb_section fb_built=”1″ _builder_version=”3.22″][et_pb_row module_class=” et_pb_row_fullwidth” _builder_version=”3.25″ width=”89%” width_tablet=”80%” width_last_edited=”on|desktop” max_width=”89%” max_width_tablet=”80%” max_width_last_edited=”on|desktop” make_fullwidth=”on”][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_image src=”https://articles.drbeen.com/wp-content/uploads/2019/01/Dr.-Hassan-Ahmad.jpeg&#8221; align_tablet=”center” align_last_edited=”on|desktop” _builder_version=”3.23″][/et_pb_image][et_pb_text _builder_version=”3.19.5″]

      Dr. Hassan Ahmad, M.B.B.S., studied at Rawalpindi Medical University.
      He has worked as the President of RIFAO (Rashida Iqbal Financial Aid Organization). He is currently serving as a member of the board of  directors at Capital Brand Technologies Private Limited. He also has experience in research work.

      At Drbeen he is working as the project director for Immunology Made Easy book.

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Authors and Contributors

      Dr. Mujtaba H Bukhari

      [et_pb_section fb_built=”1″ fullwidth=”on” _builder_version=”3.19.5″ background_color=”#0c71c3″ background_image=”https://articles.drbeen.com/wp-content/uploads/2019/01/UNADJUSTEDNONRAW_thumb_2332.jpg&#8221; background_position=”top_left” background_blend=”multiply” global_module=”3792″][et_pb_fullwidth_post_title text_color=”light” _builder_version=”3.19.5″ title_font=”Montserrat|700|||||||” text_orientation=”center” custom_padding=”||20px” custom_padding_last_edited=”off|desktop”][/et_pb_fullwidth_post_title][/et_pb_section][et_pb_section fb_built=”1″ _builder_version=”3.22″][et_pb_row module_class=” et_pb_row_fullwidth” _builder_version=”3.25″ width=”89%” width_tablet=”80%” width_last_edited=”on|desktop” max_width=”89%” max_width_tablet=”80%” max_width_last_edited=”on|desktop” make_fullwidth=”on”][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_image src=”https://articles.drbeen.com/wp-content/uploads/2019/01/Dr.-Mujtaba-H-Bukhari.jpg&#8221; align_tablet=”center” align_last_edited=”on|desktop” _builder_version=”3.23″][/et_pb_image][et_pb_text _builder_version=”3.19.5″]

      Dr. Mujtaba H Bukhari, M.B.B.S, B.Sc.

      Dr. Bukhari completed his M.B.,B.S., from Rawalpindi Medical University. He completed his bachelors in science from the University of the Punjab.

      He has worked as a demonstrator at Fawad Public School and Academy. He also has experience in research work. 

      At Drbeen Dr. Bukhari has contributed to the following sections in the immunology book:

      • Eosinophils
      • Basophils
      • Mast cells
      • Hypersensitivity reactions

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Authors and Contributors

      Umara Ayub M.D., M.B.A

      [et_pb_section fb_built=”1″ fullwidth=”on” _builder_version=”3.19.5″ background_color=”#0c71c3″ background_image=”https://articles.drbeen.com/wp-content/uploads/2019/01/UNADJUSTEDNONRAW_thumb_2332.jpg&#8221; background_position=”top_left” background_blend=”multiply” global_module=”3792″][et_pb_fullwidth_post_title text_color=”light” _builder_version=”3.19.5″ title_font=”Montserrat|700|||||||” text_orientation=”center” custom_padding=”||20px” custom_padding_last_edited=”off|desktop”][/et_pb_fullwidth_post_title][/et_pb_section][et_pb_section fb_built=”1″ _builder_version=”3.22″ custom_padding=”0|0px|54px|0px|false|false”][et_pb_row module_class=” et_pb_row_fullwidth” _builder_version=”3.25″ width=”89%” width_tablet=”80%” width_last_edited=”on|desktop” max_width=”89%” max_width_tablet=”80%” max_width_last_edited=”on|desktop” make_fullwidth=”on”][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” custom_padding__hover=”|||”][et_pb_image src=”https://articles.drbeen.com/wp-content/uploads/2019/01/Dr.-Umara-Ayub.jpg&#8221; align_tablet=”center” align_last_edited=”on|desktop” _builder_version=”3.23″ module_alignment=”center”][/et_pb_image][et_pb_text _builder_version=”3.19.5″]

      Umara Ayub M.D, M.B.A is a recent graduate of St. George’s University School of Medicine. She is planning to specialize in primary care with a focus on preventative medicine. Throughout her education, she has learned best, by creating drawings to help simplify concepts and better commit them to memory. She enjoys painting, sketching, calligraphy, and henna art in her spare time. Umara enjoys spending time with her family and traveling. She will utilize her MBA to help manage business, as well as give her a perspective into the business aspect of healthcare.

      At Drbeen Umara is working to create diagrams and illustrations for immunology book.

       

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Nervous System Nervous System Pathology

      INTRODUCTION TO PERIPHERAL NERVE DISORDERS

      Peripheral nerves consist of two principal cellular structures – motor or sensory cell with its axon and the myelin sheath covering it. Myelin sheath is produced by Schwann cells between each node of Ranvier. Blood supply is via vasa nervorum.

      Six principal mechanisms, some coexisting, cause nerve malfunction.

      1. Demyelination: When the Schwann cell is damaged, the myelin sheath is disrupted. This causes a marked slowing of conduction, seen for example in Guillain-Barre syndrome, post diphtheritic neuropathy, and many hereditary sensorimotor neuropathies.
      2. Axonal degeneration: The primary damage is in the axon, which dies back from the periphery. Conduction velocity tends to remain normal (cf. demyelination) because axonal continuity is maintained in surviving fibers. Axonal degeneration occurs typically in toxic neuropathies.
      3. Wallerian degeneration: This describes the changes following nerve section. Both the distal axon and the distal myelin sheath degenerate over several weeks.
      4. Compression: Focal demyelination at the point of compression. The myelin sheath is disrupted. This occurs typically in entrapment neuropathies e.g. carpal tunnel syndrome.
      5. Infarction: Micro infarction of vasa nervorum occurs in arteritis, e.g. polyarteritis nodosa, Churg Strauss syndrome and in diabetes mellitus. Wallerian degeneration occurs distal to the ischemic zone.
      6. Infiltration: Peripheral nerves are infiltrated by inflammatory cells in leprosy, by malignant cells in cancers, or granulomas in sarcoidosis.

      Important definitions required to understand neuropathies of any type:

      • Neuropathy simply means a pathological process affecting a peripheral nerve or nerves.
      • Mononeuropathy means a process affecting a single nerve. [From the web: damage to a single peripheral nerve.]
      • Mononeuritis multiplex (multiple mononeuropathy and or multifocal neuropathy) affects several or multiple nerves. [From the web: is the simultaneous malfunction of two or more peripheral nerves in separate areas of the body. It causes abnormal sensations and weakness.]
      • Polyneuropathy describes diffuse, symmetrical disease, usually commencing peripherally. The course may be acute, chronic, static, progressive, relapsing or towards recovery. Polyneuropathies are motor, sensory, sensorimotor and autonomic. They are classified broadly into demyelinating and axonal types, depending upon which principal pathological process predominates. It is often impossible to separate these clinically. Many systemic diseases cause neuropathies. Widespread loss of tendon reflexes is typical, with distal weakness and distal sensory loss. [From the web: is the simultaneous malfunction of many peripheral nerves throughout the body.]
      • Radiculopathy means disease affecting nerve roots
      • Plexopathy pathology of the brachial or lumbosacral plexus.
      • Myelopathy means disease of the cord.

      List of the causative categories of peripheral neuropathy and some examples of each:

      • Metabolic/endocrine: diabetes mellitus (autonomic and sensory neuropathy), uremia, and hypothyroidism.
        • Diabetes causes the damage by microvascular injury (vasa nervorum are damaged.) Capillary basement membrane thickening and endothelial hyperplasia cause narrowing of the lumen. This, in turn, leads to ischemic damage to the nerve.
        • Uremic neuropathy occurs in advanced renal failure. Usually, peripheral axons are damaged resulting in the segmental demyelination. An exact cause is not known, it is theorized that reduced thiamin, zinc, and biotin or reduced activity of transketolase can cause axonal damage.
        • Hypothyroidism can cause water retention. This, in turn, causes swollen tissue compressing and damaging the nerves.
      • Nutritional: deficiencies of vitamin B12, vitamin B6 (look for a history of isoniazid use), thiamine (“dry” beriberi), and vitamin E
      • Toxins/medications: lead poisoning (the classic symptom is wrist or foot drop; look for coexisting CNS or abdominal symptoms) or other heavy metals, isoniazid, vincristine, ethambutol (optic neuritis), and aminoglycosides (especially CN VIII)
      • Lead poisoning and heavy metal poisoning is due to increased reactive oxygen species production. Lead can also mimic other metals and act as a false cofactor with the enzymes. This results in the enzyme malfunction. Issues with heme synthesis are an example.
      • Immunization and autoimmune disorders: Guillain-Barré syndrome, SLE, polyarteritis nodosa, scleroderma, sarcoidosis, and amyloidosis
        • Guillain-Barre syndrome, usually after the GIT or upper respiratory tract infections. Immune system incorrectly attacks the myelin sheath cells.
      • Trauma: Carpal tunnel syndrome (entrapment of the median nerve at the wrist; usually due to repetitive physical activity but may be a presentation of acromegaly or hypothyroidism; look for positive Tinel and Phalen signs), pressure paralysis (radial nerve palsy in alcoholics), and fractures (causing nerve compression)
        • Tinel sign is tested by tapping on the median nerve.
        • Phalen sign is tested with the arms at 90 degrees and wrist joints opposed at 90 degrees. If in 30 seconds or so the tingling and numbness appear then the sign is positive.
      • Infectious: Lyme disease, diphtheria, HIV, and leprosy
        • In diphtheria, for example, the exotoxin binds to a cell with the B subunit and then the A subunit is phagocytosed. These subunits are released in the cytoplasm. A subunit binds with the elongation factor 2 and ADP-ribosylates it. This results in a reduction in protein synthesis and the cell die.

       

      Question: What test can be used to prove the presence of a peripheral neuropathy, regardless of cause?

      Answer: Nerve conduction velocity is slowed with a peripheral neuropathy.

      Categories
      Uncategorized

      Drbeen has more than half million friend and followers now!

      [et_pb_section fb_built=”1″ _builder_version=”3.19.5″][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Two years ago. I sat at my desk checking other successful brands in the field of medical education. I was awestruck by how many friends, fans, and followers they had. I felt that this was your way of saying thank you to those who were helping you. At this moment, I thought, I will never be able to do this. This recognition is reserved only for the best.

      Then I got to work – as you know, I always do. I wrote down my philosophy. When I die I hope people say, “he worked tirelessly to improve patient care.” I didn’t care if drbeen was small, or we practically had no fans or followers, or that we were a brand not even worth noticing.

      Two years later, we’ve just crossed half a million fans and followers this month. I am sitting at my desk, with eyes welling up. Overwhelmed with your love and support.

      I have no words to say you thank you, jump into my melting heart, feel it and know that it is my thanks to you. 💕🌹

      Thank you for your love and support. We will continue to offer our services and make them even better because you are worth it. Because YOU ARE IMPORTANT to us. Because we are nothing without you. Thank you again. 💕💕💕

      Love you

      Dr. Mobeen

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]

      Categories
      Surgery

      Question: surgery case – ID SUR1001

      [et_pb_section fb_built=”1″ _builder_version=”3.19.5″][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      64 y F with Hx of emphysema, HTN, laparoscopic hemicolectomy for Stage 2 colorectal cancer, and femoral hernia who presents with cramping abdominal pain, nausea, and vomiting. Her last bowel movement was yesterday morning. On exam, she has a distended abdomen with mild diffuse tenderness without rebound or guarding. She has a lump in her left groin which is reducible and non-tender.

      Vitals: T 37.2C, HR 98, BP 138/74, SpO2 93%.

      Her WBC is 10.1, Hb 11.4, BUN 39, Cr 1.1, LFTs normal. CT Abdomen / Pelvis shows dilated loops of small bowel with a transition point.

       

      What is the appropriate management?

      A) OR for exploratory laparotomy

      B) Admit, make NPO and place an NGT to low continuous suction

      C) OR for reduction and repair of a femoral hernia

      D) Admit, make NPO and do not place an NGT

      E) Admit and start a bowel regimen and give the patient an enema

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]
      Categories
      CVS Physiology

      CVS PHYSIOLOGY LECTURE # 20 STUDY NOTES: VENTRICULAR ACTION POTENTIAL

      [et_pb_section fb_built=”1″ _builder_version=”3.19.5″][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

       

      TYPES OF CHANNELS AND CONCENTRATIONS OF VARIOUS IONS

      1. Sodium Channels: The concentration of sodium ions outside the cell membrane is greater than that inside the cell. Therefore, there is a passive movement of sodium ions into the cell as the channels open. The sodium channels are voltage gated as they undergo conformational change in response to differences in potential across the membrane. The sodium channels have two types of gates that control the passage of sodium ions; the ‘H’ gate and the ‘M’ gate. At resting stage, the M gate is closed and the H gate is open. Upon stimulation by an action potential, the M gate opens and the channels become active, allowing sodium ions to travel into the cell. This opening of the channels is limited by time. After a fraction of a second, the H gates close spontaneously rendering the channels inactive. The sodium channels enter a refractory period during which they cannot be activated no matter how strong is the stimulus. At the same time, the M gate closes as well. As soon as the refractory period ends, the H channels open and the sodium channels are restored to their initial inactive state. The M gates remain closed till the arrival of the next action potential and the cycle is repeated.

         

      Click Here To Watch Video Lecture For This Topic

       

      Different states of the fast sodium channels and relative conformational states of the H and M gates are summarized in the table below:

      [/et_pb_text][/et_pb_column][/et_pb_row][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      SODIUM CHANNEL STATE

      [/et_pb_text][/et_pb_column][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      M-GATE (ACTIVATION GATE)

      [/et_pb_text][/et_pb_column][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      H-GATE (INACTIVATION GATE)

      [/et_pb_text][/et_pb_column][/et_pb_row][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Closed (Resting state)

      [/et_pb_text][/et_pb_column][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Closed

      [/et_pb_text][/et_pb_column][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Open

      [/et_pb_text][/et_pb_column][/et_pb_row][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Open (Active state)

      [/et_pb_text][/et_pb_column][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Open

      [/et_pb_text][/et_pb_column][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Open

      [/et_pb_text][/et_pb_column][/et_pb_row][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Inactivated

      [/et_pb_text][/et_pb_column][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Open

      [/et_pb_text][/et_pb_column][et_pb_column type=”1_3″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      Closed

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section][et_pb_section fb_built=”1″ _builder_version=”3.19.5″][et_pb_row _builder_version=”3.19.5″][et_pb_column type=”4_4″ _builder_version=”3.19.5″ parallax=”off” parallax_method=”on”][et_pb_text _builder_version=”3.19.5″]

      2. Potassium Channels: Physiologically, the cells are loaded with potassium ions. The concentration of potassium ions is relatively greater inside the cell. As a result, they tend to move out of the cell from a region of higher concentration to a region of lower concentration until -94 mV is the potential difference across the membrane.

      There are four types of potassium channels:

      • Potassium Leaky Channels: these are independent of any external factors and allow a constant leakage of potassium ions out of the cell.
      • Inward Rectifying Potassium Channels (IK1): These channels are voltage gated and they open or close in response to changes in membrane potential.
      • Inward Delayed Rectifying Potassium Channels: Also voltage gated.
      • Inward Rectifying Transient Potassium Channels: Open transiently for a very small amount of time.

      3. Calcium Channels: The calcium ions tend to move inside the cell as they are present in greater amounts outside the cell. They are classified as fast and slow calcium channels.

      4. Na/K ATPase: These are ATP dependent transmembrane proteins that actively pump sodium and potassium ions against their concentration gradient. 3 sodium ions are pumped out of the cell in exchange for 2 potassium ions into the cell. This creates a negative balance across the cell membrane which also corresponds to the negative RMP inside most cells.

      ROLE OF IONIC CHANNELS DURING AN ACTION POTENTIAL

      1. Rest State/Phase 4 of Action Potential: The Na/K ATPase works at the expense of energy to keep the resting membrane potential -90mV. Potassium leaky channels allow passive movement of potassium ions out of the cell in order to prevent excess negativity inside the cell and maintain the RMP.

         

      2. Rapid Depolarization/Phase 0 of Action Potential: Upon stimulation, the voltage dependent M gates of sodium channels open and rapidly allow sodium entry into the cells. An immediate spike in the positive direction is observed. The membrane potential rises from -90mV to +20mV. At this point, the H gates close and the sodium channels become refractory. The leaky potassium channels remain open.

         

      3. Transient Repolarization/Phase 1 of Action Potential: The inward rectifying transient potassium channels open. This happens for a very brief period of time during which potassium ions move out of the cell. A consequent drop in membrane potential is observed.

         

      4. Plateau/Phase 2 of Action Potential: The membrane potential remains constant during this part of the cycle as the resultant movement of ions in opposite directions balances the charge across the membrane. The calcium channels were triggered to open along with sodium ions at the start of the action potential. Due to their slow nature, the calcium channels take time to open. Opening of these channels and the movement of calcium ions inside the cell will oppose the negative charge produced by movement of potassium ions out of the cell. The movement of potassium ions is conducted by delayed rectifying potassium channels. Hence, the membrane potential is maintained at a constant value the entire time the calcium channels remain open.

         

      5. Repolarization/Phase 3 of Action Potential: At the end of Phase 2, the calcium channels start to close. The inward rectifying potassium channels open and along with the already open delayed rectifying potassium channels, they conduct potassium outflow. This would create a burst of positive charge leaving the cell. The membrane potential falls back to the RMP. The Na/K ATPase are reactivated to maintain RMP.

      [/et_pb_text][/et_pb_column][/et_pb_row][/et_pb_section]