​Kembara Xtra - Medicine - Hypersplenism 
Hypersplenism, or excessive spleen activity, manifests as the following symptoms: Splenomegaly, which occurs frequently but not always.
- Cytopenias with corresponding bone marrow hyperplasia of precursors - Splenectomy to resolve cytopenias

Splenomegaly and hypersplenism are not the same thing.
As shown in immune thrombocytopenic purpura (ITP) and autoimmune hemolytic anemia, the spleen can become overactive without growing larger. Similar to this, hypersplenism is not always present in splenomegaly.

Epidemiology 
In patients with cirrhosis and portal hypertension (HTN), it may be as common as 30–70%. 

Pathophysiology and Etiology 

The sequestration of produced blood components by an enlarged spleen causes peripheral cytopenias and concurrent bone marrow precursor hyperplasia.
● The following list includes several of the typical etiologies. Hypersplenism can be brought on by almost any splenic or hematologic condition: - Contaginous
 Malaria, Brucellosis, and Tuberculosis
Leishmaniasis, Ehrlichiosis, Schistosomiasis, Histoplasmosis, Candidiasis, Viral, Syphilis, and Hematologic Infectious Endocarditis
Polycythemia vera and myeloproliferative diseases
Hematologic malignancies, primary hypersplenism, ITP, and neoplastic hemolytic anemias
Melanoma and several carcinomas
Gaucher disease, storage disorders, and metastatic malignancies
Niemann-Pick illness
Sarcoidosis, Amyloidosis, Congestive Felty syndrome, Systemic lupus erythematosus, and Inflammatory Glycogen Storage Disease
Cirrhosis and cardiac arrest
 Splenic or portal vein thrombosis Congenital portal vein abnormalities

Patients may complain of abdominal fullness or the spleen protruding through the abdominal wall. They may also express early satiety if the spleen is compressing the stomach.
Particularly with viral infections, patients may complain of pain in the left upper quadrant. Spleen enlargement in lymphoproliferative diseases can go unnoticed unless there is splenic infarction. Given that the spleen is situated near to the diaphragm, the phrenic nerve may convey a feeling of fullness to the C3-C5 dermatomes in the left shoulder.
There could be signs of the hypersplenic underlying condition.

Splenomegaly on a clinical examination
The typical spleen cannot be touched. In the proper clinical setting, a palpable spleen always denotes an underlying problem such as splenomegaly, which leads to hypersplenism, or it may denote a wandering spleen. Additionally, spleen can be palpated in cases of acute asthma exacerbation and chronic obstructive pulmonary disease without the presence of splenomegaly.
● Start off by percussion Traube semilunar space, bordered superiorly by the left 6th rib, inferiorly by the left costal margin, and laterally by the left anterior axillary line. Typically, this area is hollow. The percussion in this region may become dull due to splenic enlargement. The dullness may also be brought on by pleural or pericardial effusions. Additionally, if the patient just consumed a substantial meal, this region could be difficult to percussion.
Gently place your hand on the patient's belly while they are supine to avoid any rapid contractions of the abdominal muscles that can make palpation difficult. By flexing the knees in the direction of the abdomen, you can achieve greater abdominal relaxation. The spleen moves medially and caudally as it grows. Beginning with the right lower quadrant, palpate your way to the umbilicus in the left upper quadrant. Ask the patient to take a deep breath, which will move the diaphragm and, in turn, the spleen into the examiner's hands if there is any uncertainty about whether the spleen has extended over the costal margin.
Petechiae, purpura, or ecchymosis: if thrombocytopenia is present; Jaundice: if hemolytic anemia is present or in advanced cirrhosis; Lymphadenopathy: in hematologic or solid organ cancers. It can be observed in infectious etiologies as well.


Laboratory Results 

Any and all cell lines may be lowered on CBC, leading to the following outcomes: 
Blood loss
Thrombocytopenia and leukopenia

Initial tests (lab, imaging): CBC, reticulocyte count, and haptoglobin if anemia is present.
If there is hemolysis, there should also be signs of unconjugated hyperbilirubinemia, an increased reticulocyte count, an increased LDH, and decreased haptoglobin.
US, CT, Tc-99m sulfur colloid scintigraphy, PET, and MRI are all available.

Tests in the Future & Special Considerations

Testing for particular infectious etiologies may be necessary based on additional history and exam findings: 
EBV serologies, HIV ELISA with Western blot, PPD for tuberculosis, HIV blood parasite smear for malaria and other parasitic diseases, JAK2 mutation in polycythemia vera, Hgb electrophoresis in hereditary hemoglobinopathies, and Hgb electrophoresis

Bone marrow biopsy and liver biopsy for cirrhosis and other storage disorders are two diagnostic procedures. Interpretation of Tests
bone marrow precursor hyperplasia, particularly that which is associated with the patient's unique cytopenias


Treatment Patients with hypersplenism cannot be prescribed any specific medicine. Treating the underlying illness is the most crucial intervention.
If ITP is the cause, the following treatments may be helpful for the patient: If an infectious etiology is found, treatment with the proper antibiotic treatments may assist to ameliorate the cytopenias. - Prednisone or methylprednisolone - IVIG - Rituximab.

Surgery: Splenectomy is a common surgical procedure for people with severe, uncontrolled cytopenias; laparoscopic surgery is preferred over open surgery.


Caution 

Pneumococcal, meningococcal, Haemophilus influenzae, and influenza vaccinations should be given to splenectomized patients at least 14 days before the procedure.

Wait at least 14 days after the splenectomy before getting immunized if this can't be done (for example, in cases of emergency splenectomy).
Vaccine against pneumococci
 The pneumococcal polyvalent-23 vaccine (PPSV23) for use in fully immunized adults and children under the age of two
Pneumococcal polyvalent-13 vaccine (PCV13) for infants and early children 2 months of age as part of standard vaccination schedule PCV13 for children >2 years of age, adolescents, and adults in addition to PPSV23. For scheduling of administration, consult the CDC.
Current recommendations call for a single PPSV23 revaccination five years after the first dose and again at age 65, at least five years following the first dose.
- Influenza vaccination
All unvaccinated children under the age of five should receive one dose of the conjugate vaccination against H. influenzae type B (Hib).
Children under the age of 5 should also receive vaccinations.
For timing, consult the CDC.
Additionally, vaccinated people can receive additional vaccination doses.
- Meningitis vaccinationMeningococcal conjugate vaccination (MCV4) recommended for individuals aged 2 to 55 Meningococcal polysaccharide vaccine (MPSV4) for people over 55; recertification is advised every five years.
– Although patients are not at higher risk from influenza itself, infection with influenza may place patients at higher risk for subsequent bacterial infections, hence influenza vaccination should be given annually based on prevalent circulating strains.

More frequently used, radiofrequency ablation (RFA) can successfully stop hypersplenism from returning. Whether there are any differences between RFA and splenectomy in terms of postoperative infection hazards is unknown at this time. Total and partial splenic embolization and shunting are additional options to splenectomy, albeit these procedures are still in development and require further research to assess their efficacy and morbidity in comparison to splenectomy.

Admission 
Hypersplenism by itself typically does not justify admittance. All patients, however, should be constantly watched for cytopenia-related problems, such as bleeding and infection, as well as splenomegaly-related consequences, such as an elevated risk of splenic rupture. Some patients' huge spleens squeeze their stomachs, making it difficult for them to take in enough food orally.
Patients who have had splenectomies are more susceptible to infection and sepsis following the procedure, particularly when Streptococcus pneumoniae is involved. Clinical decompensation can happen within hours if there are fevers, chills, or discomfort indicative of an underlying infection. While the evaluation is being conducted, empiric broad-spectrum antibiotics should not be delayed. The following are examples of typical empiric regimens: Vancomycin 1 g IV q12h and Ceftriaxone 2 g IV q24h Vancomycin 1 g IV q12h and Levofloxacin 750 mg IV q24h in patients with -lactam allergies 

Continuous Care: Adult splenectomized patients should be instructed to keep a watchful eye out for fever or rigors at home, since these symptoms could be a precursor to bacteremia. They should be told to start taking antibiotics right away before going to a hospital for testing. Early use of antibiotics has been demonstrated to lower mortality from severe post-splenectomy sepsis. Despite the lack of controlled trials, some regimens include the following: - 875 mg of amoxicillin-clavulanate PO BID
500 mg of cefuroxime axetil PO BID.
Levofloxacin 750 mg PO or moxifloxacin 400 mg PO daily are two examples of extended-spectrum fluoroquinolones that can be administered to patients who are allergic to beta-lactam antibiotics.
● Up until age 5 or at least three years after splenectomy, daily antibiotic prophylaxis with penicillin VK or amoxicillin is advised in children who have undergone splenectomy to prevent severe post-splenectomy sepsis: Ages 2 months to 5 years: 125 mg PO BID, and older than 5 years: 250 mg PO BID

Patients who have had their spleens removed should receive in-depth counseling on the possibility of developing severe sepsis after having their spleens removed, as well as the importance of getting a quick medical checkup if they have any worrying symptoms like fever or chills.

​Kembara Xtra - Medicine - Hypersensitivity Pneumonitis 
Extrinsic allergic alveolitis (EAA) is another name for hypersensitivity pneumonitis (HP).
HP is a widespread inflammatory condition of the lung parenchyma brought on by an immune response to antigenic aerosolized particles present in various environments. Classification is based on the relevant time period:
- Acute: fever, chills, myalgias, diaphoresis, and nausea; cough and dyspnea are frequent but not always present. occurs between 4 and 12 hours following a strong dose of a provoking substance. Within 12 hours to several days following removal from exposure, symptoms go away. Complete resolution happens in a few of weeks.
- Subacute: primarily brought on by repeated low-level antigen exposure, with the potential for a low-grade fever in the first week; cough, dyspnea, exhaustion, anorexia, and weight loss that appear over the course of days to weeks.
- Chronic: caused by repeated exposure in either acute or subacute cases; long-lasting and progressive cough; exhaustion; weight loss; may result in fibrosis and respiratory failure.
The term "farmer's lung" refers to a type of HP that affects only farmers; the bacterium that causes it can be found in moldy hay or straw. Modern farming techniques have led to new and distinct etiologies for farmer's lung.


Epidemiology Not well defined; likely to happen in adults as a result of occupational exposure, however some home environmental exposures are also seen HP is becoming more and more recognized as a significant contributor to fibrotic interstitial lung disease.

Incidence 0.9/100,000
Prevalence
Farmer exposure ranged from 1 to 19 percent; bird watchers from 6 to 30 percent; and others from 1 to 8 percent.


Pathophysiology and Etiology 
Immunologic reaction types III and IV (hypersensitivity reaction involving immune complexes) are brought on by the binding of inhaled antigens to IgG.

T cell-mediated immunological inflammatory response is one example of a cellular response.
Workers in agriculture, horticulture, or dairy cattle (1), (2)
- Moldy grain, silage, and hay are caused by thermophilic actinomycetes like Faenia rectivirgula.
- Thymus vulgaris and Thermoactinomyces sacchari mold on pressed sugar cane
- Tobacco plants: Scopulariopsis brevicaulis and Aspergillus sp.
Saccharopolyspora rectivirgula, T. vulgaris, and Aspergillus spp. cause worker's lung in the mushroom industry. Thermophilic actinomycetes, T. vulgaris, F. rectivirgula, and Aspergillus sp. cause riddler's lung in the potato industry.
- Coffee worker's lung: coffee bean dust Penicillium caseifulvum, Aspergillus clavatus - Cheese washer's lung:
- Tea plants: Tea grower's lung

 Ventilation and water-related contamination: Amoebae, Nematodes, Yeasts, and Bacteria infected humidifiers and air conditioners
- Shower without ventilation: Epicoccum nigrum
- Cladosporium species, Mycobacterium avium complex, hot-tub lung
Aureobasidium sp. causes sauna taker's lung, and Trichosporon cutaneum causes summer-type pneumonitis.
- Aerosolized endotoxin and M. avium complex in the swimming pool lifeguard's lung - Cephalosporium and Penicillium spp. in contaminated basement pneumonitis - Handling of birds and poultry - Bird fancier's lung: droppings, feathers, serum proteins
- Serum proteins in the lung of poultry workers
- Sera for turkey-handling illness
- Serum proteins in the canary fancier's lung
- Feathers and serum proteins cause duck fever
Laboratory worker's lung: proteins, urine, serum, and serum from handling animals used in veterinary medicine
- Dried, powdered neurohypophysis is a symptom of pituitary snuff taker's disease.
- Furrier's lung: pet fur
- Bat serum protein: bat lung
- Workers' lung from fish food: fish meal
- Coptic lung: mummies wrapped in cloth
- Shell of a mollusk Sea snail with pearl oyster shells, HP lung disease: oyster shells
Cereal grain, grain dust, and flour: grain measurer's lung
- Sitophilus granarius, a cause of Miller's lung
Lumber milling, construction, wood stripping, paper, and wallboard manufacturing - Malt worker's disease: Aspergillus fumigatus, Aspergillus clavatus - Wood dust pneumonitis: Alternaria sp., Bacillus subtilis
- Trichoderma sp., Pullularia, Graphium, and Aureobasidium pullulans in sequoiosis
- Cryptostroma corticale, the cause of maple bark disease
- Suberosis: Trogon viridis, Penicillium glabrum; Wood trimmer's disease: Rhizopus sp., Mucor sp.; Wood pulp worker's disease: Penicillium sp.
Manufacturing of plastics, paints, electronics, and chemicals 
Diphenyl diisocyanate and toluene diisocyanate are chemical HPs. B. subtilis enzymes are found in the lungs of detergent workers.
Alveolitis caused by the Pauli reagent: sodium diazobenzene sulfate
Copper sulfate causes vineyard sprayer's lung. Pyrethrum causes pyrethrum.
Bible printer's lung: moldy typesetting water - Epoxy resin lung: phthalic anhydride
Pseudomonas fluorescens, an aerosolized metalworking fluid, causes machine operator's lung
Cotton mill dust byssinosis in textile workers and nylon, tannic acid, and potato starch lung disease in velvet workers
Fusarium species, which produces aflatoxin, infects upholstery fabric. Puffball spores, which cause lycoperdonosis.
Genetics
No evidence of a distinct genetic tendency, but potential genetic predisposition involving the MHC class II and tumor necrosis factor alpha (TNF-) genes.


Risk Elements 

The chance of acquiring HP increases with contact with organic antigens. Risk may be increased by viral infection at the time of exposure.
Compared to smokers, nonsmokers have a higher incidence of HP. Smoking is assumed to provide "protective" effects because nicotine is believed to suppress macrophage activation and lymphocyte proliferation and function. - Smokers' antibodies react less strongly to inhaled antigens. Smokers are more likely to develop chronic disease, and their mortality rate is higher.

Prevention 
Avoiding offending antigens and/or wearing protective gear

Constrictive bronchiolitis is a condition that is related.

Diagnoses The most popular yet unreliable diagnostic criteria are: (i) a history, physical examination, and pulmonary function tests (PFTs) showing diffusion or restriction illness. The most frequently affected lung parameter, DLco, may be normal in up to 22% of patients, (ii) radiologic imaging consent with interstitial lung disease, (iii) exposure to a known cause, (iv) evidence of sensitization in BAL fluids (serum precipitins and/or lymphocytosis), and (v) exposure to a recognized cause ● There are six important predictors: exposure to a known antigen, precipitation of positive antibodies (if known), recurring symptom episodes, inspiratory crackles, symptoms 4 to 8 hours after exposure, and weight loss.
Acute form: appears 4–12 hours after exposure.
Chest tightness, cough, dyspnea without wheezing, fever, chills, diaphoresis, headache, nausea, and malaise.
Symptoms can continue for hours or days.
Sequela (previous subacute, chronic): occurs over days, weeks, or months and includes a progressive or gradual productive cough, exhaustion, anorexia, and weight loss that may result in respiratory failure.

 Symptomatic relief when not at work or home

clinical assessment 
Sequela or chronic symptoms include inspiratory crackles, increasing hypoxia, weight loss, diffuse rales, clubbing, and occasionally wheezing. Acute symptoms include fever, tachypnea, and diffuse fine rales.

Differential Diagnosis Acute: acute infectious pneumonia caused by Pneumocystis jiroveci pneumonia, mycoplasma, influenza (or other viral pneumonia), aspiration, and asthma

Chronic conditions include P. jiroveci pneumonia, sarcoidosis, chronic bronchitis, chronic obstructive lung disease, tuberculosis, collagen vascular disease, and idiopathic pulmonary fibrosis.

The majority of cases are covered by the following antigens: pigeon and parakeet sera, dove feather, Aspergillus sp., Penicillium, S. rectivirgula, and Thalassomonas viridans PFTs: The typical profile is a restrictive pattern with low diffusing capacity; could also have an obstructive pattern BAL with serum precipitins and lymphocytosis (greater than 10)
Positive antigen-specific inhalation challenge testing involves re-exposure to the environment and an in-hospital challenge to the suspected antigen, but it is not standardized.

 Chest x-ray (CXR): used to obviate the presence of other diseases
- Acute: interstitial pattern in various lung field distributions, ground-glass infiltrates, nodular or striated patchy opacities. Up to 20% might be typical.
- Sequela/chronic: emphysematous alterations, upper lobe fibrosis, nodular or groundglass opacities, volume loss

 Chest CT scan; non-HP-specific patterns:
- Acute: air trapping, ground-glass opacities, and poorly defined centrilobular nodules on expiratory imaging.- Chronic: honeycombing, fibrosis, ground-glass attenuation, irregular opacities, bronchiectasis, decrease of lung volume
Usually begin with CXR; may move to HRCT depending on results. High-resolution CT (HRCT) mid-to-upper zone predominance of centrilobular ground glass or nodular opacities with evidence of air trapping

Diagnostic techniques and other lung biopsies:

Transbronchial: Shows extensive foam cells, peribronchial fibrosis, and tiny, poorly formed noncaseating granulomas close to respiratory or terminal bronchioles.
Open lung biopsy yields the most information when the disease is advanced; it displays different organizing pneumonia patterns, centrilobular and perilobular fibrosis, and multinucleated giant cells with clefts.

Caution 

Farmers' HP must be recognized from organic dust toxic syndrome (ODTS), which causes feverish, toxic reactions to inhaled dusts. Farmers get nonimmunologic responses 30–50% more frequently than HP. ODTS is connected to a day of extremely high exposure.

The patient should be kept fully away from repeated exposure to the causing antigen, with the exception of cases of acute pneumonitis and hospitalization for workup (BAL, lung biopsy). The best treatment for disease is provided by this action.

First Line of Medicine
Avoiding the offending antigen is the main treatment, which causes the condition to regress.

Corticosteroids assist manage exacerbation symptoms, but they have no lasting positive effects.
Prednisone: 20 to 50 mg daily; first treatment, 1 to 2 weeks with taper; for patients with severe symptoms 

Next Line
Patients with wheezing and chest tightness may have symptomatic relief from bronchodilators and inhaled corticosteroids.

In more severe situations, oxygen might be required.
When medical treatment is ineffective for serious instances, lung transplantation may be the only option.


Referral 

Advisory for a pulmonologist or immunologist


Admission 

Supportive care, when required, to sustain breathing and oxygenation
Changes in mental status, oxygen need, and unstable breathing
Requirement for invasive testing (lung biopsy)

Patient Follow-Up Monitoring

Depending on the severity and course, the initial follow-up should be weekly to monthly.

Serial CXR, PFTs, and circulating antibody levels should be performed after therapy.



Education of Patients 

Keep in mind that prolonged exposure can cause acute symptoms to disappear (the patient may stop being aware of the connection between exposure and symptoms).

Fibrosis is a factor that indicates a poor prognosis.

Acute: If the offending antigen is removed early in the course of the disease, there is a good chance that the pathologic findings will be reversed. Sequela/chronic: Corticosteroids have been shown to temporarily enhance lung function but have no discernible effect on the long-term prognosis.


Progressive interstitial fibrosis with eventual respiratory failure is a complication.
Cor pulmonale and failure of the right heart

​Kembara Xtra - Medicine - Hyperprolactinemia
When the lactotroph cells of the pituitary gland are affected either physiologically or pathologically, the result is hyperprolactinemia, which is an abnormal spike in serum prolactin levels.

Prevalence of Epidemiology
Predominant sex: female (70%) > male (30%) Predominant age: reproductive age
Men come with headache, visual abnormalities, and erectile dysfunction; women are more likely to experience changes in menstruation and galactorrhea, and men have adenomas that are often larger due to the delayed start of symptoms.


Pathophysiology and Etiology 

 The anterior pituitary's lactotrophs, which make prolactin, are controlled by: - Dopamine and other inhibitory substances are produced in the hypothalamus and transported to the pituitary stalk by the hypothalamic-pituitary arteries.
Thyrotropin-releasing hormone (TRH) is the main stimulatory agent.
● The following are some examples of hyperprolactinemia causes: - Physical
- Increased estrogen-related pregnancy
- Nursing or nipple stimulation - Stress, including the aftermath of surgery
- Pharmaceuticals Usually, concentrations fall between 20 and 100 ng/mL (2)[A].
Prochlorperazine and metoclopramide are two dopamine (D2) blockers. Antidepressants include tricyclic antidepressants (TCAs); paroxetine (an SSRI) induces transitory hyperprolactinemia, which typically recovers in 7 to 10 days. Dopamine depleters include methyldopa and reserpine. Verapamil (but not other calcium channel blockers; believed to reduce hypothalamic dopamine production) Older antipsychotics include haloperidol, fluphenazine, and risperidone (the level of elevation with risperidone is higher than with other antipsychotics). Newer antipsychotics include asenapine, iloperidone, and lurasidone, which may cause elevation but do so less frequently than the older antipsychotics.
- Hypothyroidism brought on by increased TRH
Herpes zoster, trauma, or post-thoracotomy disorders of the chest wall; prolactin-secreting adenoma in the anterior pituitary (microadenoma: 1 cm; macroadenoma: >1 cm). Pituitary stalk disruption or compression
Meningioma, astrocytoma, Craniopharyngioma, Rathke Cleft Cyst
Metastases and head injury
 Infiltrative and inflammatory conditions
- Reduced prolactin clearance (cirrhosis, cocaine, chronic renal failure) - Idiopathic hyperprolactinemia, which occurs often in people with serum prolactin levels between 20 and 100 ng/mL for no apparent reason.

Based on clinical history, physical examination, and laboratory results, a diagnosis is made. 

The following symptoms and indicators of pituitary enlargement may also be present: Galactorrhea, amenorrhea or oligomenorrhea, infertility, osteoporosis or osteoopenia, decreased libido, impotence, and weight gain. - Headache - Bitemporal hemianopia, a visual field impairment
- Hypopituitarism (a result of the tumor's strain on nearby structures).
Additionally, they could exhibit symptoms of comorbid conditions: - Cushing disease - Hypothyroidism
Acromegaly and MEN-1 syndrome, or multiple endocrine neoplasia,

Clinical evaluation, visual field tests, cranial nerve examination, and examination for lesions on the chest wall 


Multiple Diagnoses 
Macroprolactinemia: While not biologically active, macroprolactin, a polymer of multiple prolactin units, is detectable by immunologically based laboratory testing. Consider this diagnosis and inform the lab if the patient has increased prolactin (PRL) despite being asymptomatic. Treatment is not necessary.

Serum prolactin (most reliable results if examined fasting, in the morning; eating only has a modest effect on concentrations, therefore fasting is not essential, but if elevated levels recur on a fasting samples) is a laboratory finding that can be used to diagnose many diseases. In postmenopausal women, a value of >25 g/L is abnormal, >25 g/L is normal, and >30 g/L or more frequently denotes a prolactinoma.

Luteinizing hormone (LH)/follicle-stimulating hormone (FSH) if amenorrheic; pregnancy test; thyroid-stimulating hormone (TSH); Initial Chem Panel Tests (Lab, Imaging)

A single blood prolactin test can confirm the diagnosis if the result is higher than the upper limit of normal.
Pituitary MRI: the best imaging modality. 
Levels should be obtained before a breast exam and a CT scan should be done if an MRI is not appropriate.

Tests in the Future & Special Considerations

formal visual field testing if there is a suspicion of a pituitary adenoma

Management 
Stop using any problematic medications, if any.
Treat the root causes.
Observation alone may be an option for asymptomatic people with minor prolactin increases.

● Medications recommended for: - Hypogonadism symptoms, such as decreased libido
- Galactorrhea, if the patient finds it irritating
- Fertility is restored
- A pituitary tumor
- Combating osteoporosis

Dopamine agonist medications: Lower serum prolactin levels and shrink most lactotroph adenomas in size.
Due to its effectiveness and manageable adverse effect profile, cabergoline (Dostinex) is now the first-line option. It is dosed at 0.25 mg twice weekly or 0.50 mg once weekly.
The reduction of chronic hyperprolactinemia, galactorrhea, and amenorrhea/oligomenorrhea was more pronounced with cabergoline than with bromocriptine, despite the latter being more expensive. Has been demonstrated to lessen erectile dysfunction in hyperprolactinemic men; has recently been linked to significant improvements in body mass index, total HDL and LDL cholesterol levels, and insulin sensitivity; a decrease in proinflammatory markers; and a reduction in carotid intima-media thickness.– Adverse effects (better tolerated if administered at night with food and at low doses with slow titration):  Nausea/vomiting Headache, lightheadedness, and exhaustion
Contraindications for postural hypotension
Unmanageable hypertension
Cardiac valvular illnesses
 Fibrotic conditions of the pericardium, the lungs, or the retroperitoneum
Bromocriptine (Parlodel): This medication has the longest clinical history and is chosen by certain clinicians when treating infertility. It is dosed BID; start with 1.25 mg once at bedtime or after supper for a week, then increase to BID. Both are efficient in shrinking tumors and easing symptoms.

SE is diminished by cabergoline compared to bromocriptine (5)[A].
In the US, pergolide (Permax) is no longer in use.
Don't stop the medication suddenly if the patient is still taking it.
ADVANCED THERAPIES
Prolactin levels were reduced in virtually all patients with radiation, and in over 25% of patients with low complication rates, in those with medically and surgically refractory prolactinomas.

Surgical procedures Medical treatment for adenomas is effective in 80–90% of individuals. In some circumstances, surgery is advised: - Resistance or intolerance to medical care - Headache
- Loss of visual acuity - CSF leak from tumor apoplexy or shrinking
A high recurrence rate (up to 40%), CSF leakage, meningitis, pituitary insufficiency, and temporary diabetes insipidus are among the risks associated with cranial nerve deficiency.


Take Action 

After one month, recheck the lab results; if they are normal, continue the initial dose. Increase cabergoline to 1.25 mg two to three times per week or bromocriptine to 5 mg twice day if lab levels do not drop but the patient shows no negative effects.
patient observation

 If there is no tumor and prolactin levels are normal after at least 2 years of treatment, one might think about reducing and ceasing medication. However, this decision must be carefully monitored because the tumor could recur.
Take into account: - Annual formal visual field assessment - Serial MRIs if clinically necessary 
pregnant women's issues

Dopamine agonists are indicated for usage if neurologic symptoms are present but are not approved for use during pregnancy or if pregnancy is confirmed in a woman with hyperprolactinemia who wishes to get pregnant.

Bromocriptine should be used to treat microprolactinoma if symptoms are present. Pregnancy should be confirmed monthly before stopping bromocriptine.
With macroprolactinomas, a specific, personal plan is created. Options include stopping bromocriptine at conception and carefully monitoring prolactin levels and VS, with or without MRI scan evidence of tumor enlargement; prenatal transsphenoidal surgery with tumor debulking; and continued bromocriptine use throughout pregnancy, with a risk to the fetus.
Careful monitoring of visual fields during each trimester; prolactin levels are not need to be checked as they are often elevated owing to pregnancy.

Educating the Patient 

Talk about the dangers of untreated hyperprolactinemia.
Headache, reduced visual acuity, weakened bones, and infertility


Prognosis: If PRL levels have stayed normal for 1 to 2 years after therapy, you could want to discontinue taking your medications.
Approximately 5–10% of macroadenomas can develop into macroadenomas.
Follow-up imaging is not necessary unless there are indications of a growing malignancy. >10 years, 7% probability of prolactin-secreting microadenoma progression 


Complications: For patients on large doses of cabergoline, cardiac US is advised every two years. If a pituitary adenoma develops, there is a risk of permanent visual field loss.

​Kembara Xtra - Medicine - Hyperparathyroidism 
an abnormality in the body's regular regulatory feedback processes that causes an overproduction of parathyroid hormone (PTH)

Primary hyperparathyroidism (HPT) is characterized by excessive PTH release as a result of intrinsic parathyroid gland malfunction and a failure to respond to calcium-induced feedback inhibition.
The proper increase in PTH production in response to possible hypocalcemia and/or hyperphosphatemia is known as secondary HPT. Lack of vitamin D, kidney disease, low calcium intake, poor calcium absorption, and/or phosphate loading can all contribute to this. Tertiary HPT: autonomous hyperfunction of the parathyroid gland in the setting of long-term secondary HPT

Female > male (3:1) Predominantly postmenopausal females Epidemiology Incidence
Prevalence
In the US, primary HPT affects 1 in 500 to 1 in 1000 people.

Pathophysiology and Etiology 

PTH is primarily controlled by calcium concentrations.
The four parathyroid glands, which can be found behind the thyroid's four poles in different places, produce PTH.
Ectopic or supernumerary glands (more than four glands), which are most frequently found in aberrant sites.
PTH stimulates osteoclastic activity, which increases bone resorption, and releases calcium from bone.
PTH boosts the reabsorption of calcium in the kidneys' distal tubules.
PTH enhances the conversion of 25-hydroxycholecalciferol (25[OH]D) to 1,25-dihydroxycholecalciferol (1,25[OH]2D or active vitamin D) in the kidneys, increasing phosphorus excretion by reducing reabsorption. 1,25(OH)2D enhances osteoclastic activity and bone resorption in addition to increasing calcium and phosphate absorption from the GI tract and kidneys.
Primary HPT: Uncontrolled PTH generation and release as a result of the absence of the extracellular calcium's usual feedback regulation, which results in an increase in serum calcium.
- One-sided adenoma (80–85%)
- Multiple endocrine neoplasia (MEN) type I or MEN type IIA, which may occur sporadically or in conjunction with diffuse hyperplasia (10–15%) of the four parathyroid glands.
- Dietary changes - Secondary HPT: adaptive parathyroid gland hyperplasia and hyperfunction due to reduced calcium - Parathyroid carcinoma (1%), a very rare and severe form -
A lack of vitamin D reduces the body's ability to absorb calcium.
Chronic renal illness brought on by a calcium shortage causes the following symptoms:
Loss of the renal parenchyma results in hyperphosphatemia.
 Hypocalcemia resulting from impaired calcitriol synthesis
General resistance to PTH in the skeletal and renal systems Tertiary HPT: autonomous oversecretion of PTH after protracted parathyroid stimulation

Genetics MEN type I and MEN type IIA: MEN-I gene mutation screening should be performed on patients with multiple gland hyperplasia who do not also have renal illness.
Infants born missing both calcium-sensing receptor (CaSR) gene alleles have neonatal severe primary HPT.
Familial hypocalcciuric hypercalcemia (FHH): deletion of one CaSR gene allele. HPT—jaw tumor syndrome.
Isolated familial HPT


Risk Elements 
Age-related renal disease, inadequate nutrition, radiation exposure, and/or family history

Prevention 
Calcium and vitamin D consumption should be adequate to prevent subsequent HPT.

Associated Conditions include chronic renal failure, vitamin D insufficiency, and the MEN I and MEN IIA syndromes.


Asymptomatic patients make up about 80% of people with histories of current illness.
stones in the kidney (15–20%)
- Osteitis fibrosa cystica (5%), characterized by "salt and pepper" appearance of the head, tapering of the distal clavicles, bone cysts, and brown tumors of long bones.
- Hypercalcemia symptoms such as mental confusion, memory loss, polyuria, polydipsia, constipation, bone pain, poor focus, altered mental status, weariness, and muscle weakness
Past medical history - The following illnesses may be linked to HPT: MEN syndrome (MEN I linked to pituitary adenomas, pancreatic cancers, and parathyroid hyperplasia; MEN IIA linked to medullary thyroid cancer, pheochromocytoma, and parathyroid hyperplasia); nephrolithiasis (in 20-30% of cases); nephrocalcinosis; pancreatitis; gastro


clinical assessment 
Physical findings that are connected to the underlying cause of HPT may be discovered. Limited usefulness; 70–80% of patients have no visible symptoms or indicators of disease.

Differential Diagnosis: PTH Production Increased: Ectopic PTH production is uncommon. It confirms the diagnosis of primary HPT in the majority of instances, but first, rule out:
– FHH: A 24-hour urine calcium:creatinine ratio can rule out FHH.
Lithium and thiazide diuretics

Causes of nonparathyroidism
Multiple myeloma, lymphoma, leukemia, prostate cancer, Paget disease, and lung (squamous cell) carcinoma are examples of malignancies. Granulomatous illnesses include sarcoidosis, TB, berylliosis, histoplasmosis, and coccidioidomycosis.
- Drugs: milk-alkali syndrome and vitamin D poisoning
- Endocrine: acute adrenal insufficiency and hyperthyroidism

Laboratory Results 

Initial examinations (lab, imaging)
Frequently discovered by unintentional hypercalcemia on standard lab tests. Checking ionized calcium is the best method.

 To calculate adjusted calcium, multiply the patient's albumin level by 0.8 and the serum calcium value in mg/dL. Since the uncorrected calcium is normal, some people may have mild hypercalcemia for years without it being noticed.
If hypercalcemia is verified, check your PTH level next.
- PTH dependent: Primary HPT is suggested by high or (abnormally) normal PTH.
PTH-independent hypercalcemia is indicated by undetectable or low PTH levels.
● Low serum phosphate and significant 24-hour urine calcium excretion are possible additional results.
● A high phosphorus level in secondary HPT indicates chronic renal failure; a low phosphorus level indicates another cause, typically a 25(OH)D shortage. Both of these are frequent reasons for increased PTH levels in the presence of normal adjusted calcium levels.

Tests in the Future & Special Considerations
A ratio of >0.02 between the 24-hour urine calcium concentration and creatinine clearance and 0.01 between the two may indicate FHH, which is a significant result because FHH does not require surgery.

All individuals with primary HPT should have their 25(OH)D levels routinely checked. Delay making management decisions in cases of vitamin D deficiency (20 ng/mL or 50 nmol/L) until levels are kept >20 ng/mL (50 nmol/L).

Other/Diagnostic Procedures
Diagnostic imaging is not necessary. Planning for surgery is necessary, particularly for minimally invasive parathyroidectomies (MIP).
- Imaging is also recommended for repeat surgery to pinpoint hyperplasia or an ectopic parathyroid gland.
Imaging techniques for localization prior to surgery
- Technetium-99m sestamibi with or without single-photon emission computed tomography (SPECT): It is frequently wrong in multigland illness but has the highest reported success rate for localizing solitary parathyroid adenomas.
- Neck ultrasound (US): painless, noninvasive, and radiation-free; however, operator skill is required for accuracy.
- Four-dimensional CT (4D-CT) may be superior to sestamibi-SPECT and US for primary localisation.
- In terms of diagnostic usage, positron emission tomography (PET) with C-methionine (MET-PET) is comparable to US and technetium-99m sestamibi with SPECT.
- The most common methods for locating ectopic mediastinal glands are CT and MRI.

Medication Primary HPT: Operative management is curative; the following are the indications for surgical surgery.
For individuals who cannot or are awaiting surgery:
- Bisphosphonates (alendronate): Help to preserve bone density and decrease bone turnover; avoid in kidney disease (GFR 35).
CaSR in the parathyroid gland is activated by calcimimetics (cinacalcet) (1)[B], which inhibits PTH secretion. No long-term data on its impact on constitutional, cognitive symptoms, or fractures; FDA-approved for symptomatic individuals who are not surgical candidates.
- Raloxifene, a selective estrogen receptor modulator, inhibits PTH-mediated bone resorption
– The benefits of estrogen replacement therapy must be weighed against the dangers of recognized systemic side effects; it is not advised as a first-line treatment.
○ Can be utilized by postmenopausal women who reject or do not undergo surgery
Secondary HPT: The underlying cause is frequently the focus of treatment.
- Calcium replenishment - Analogs of vitamin D (calcitriol and paricalcitol)
- Sevelamer, a phosphorus-binding agent
Calcimimetic (cinacalcet) - Tertiary HPT - Medical treatment is generally not recommended and is not curative.

Surgical Procedures 95–98% of patients with primary HPT respond to operational management. It is the initial line of pediatric treatment. Additionally, it is frequently the initial course of treatment for young adults up to 50 years old.

Parathyroidectomy indications include primary HPT symptoms, nephrolithiasis, and fragility fractures.
Osteitis fibrosa cystica - primary HPT without symptoms
Age 50 years Serum Ca+ level >1 mg/dL above normal
24-hour urine calcium >400 mg/day (>10 mmol/day) and increased stone risk by biochemical stone risk analysis are associated with creatinine clearance 60 mL/min.
Nephrolithiasis or nephrocalcinosis found on an x-ray, an ultrasound, or a CT scan
 Bone density reduction in the lumbar spine, femoral neck, whole hip, or distal third of the radius with a T-score of less than 2.5
The only confirmed curative treatment for HPT is surgical excision of the affected gland or tissue.
The following surgical options are available:
- MIP using intraoperative PTH levels (high sensitivity 79-95% to predict location of single parathyroid adenoma) and preoperative sestamibi scan with SPECT/US/4D-CT, which results in less pain, smaller incisions, improved cosmetic results, lower morbidity, and a shorter hospital stay than open neck exploratory surgery.
Follow postoperative serum calcium, magnesium, and phosphorus levels; keep an eye out for the "hungry bone" syndrome associated with hypocalcemia.
Patients may require oral calcitriol and calcium supplements first, followed by an IV calcium infusion postoperatively.
Though it is currently less prevalent, hungry pain syndrome can be extremely severe.
Additionally, hemorrhage and airway compromise concern for patients
Keep a close eye on renal function.

Admission 
For severe symptoms caused by critical hypercalcemia, IV fluid rehydration, IV bisphosphonate treatment, and SC calcitonin (4 U/kg q12h) are all necessary.

Take Action 
Calcium and PTH levels need to be serially monitored in asymptomatic patients with primary HPT.
patient observation
A bone density scan every one to two years and annual measurements of blood calcium and creatinine are enough for patients with primary HPT who are asymptomatic.


Diet
Dietary calcium limitation is advised in cases of hypercalciuria or increased 1,25(OH)2D levels.
Otherwise, a maximum of 1,000 mg of calcium should be consumed per day.
Limit the phosphate in your diet for secondary HPT.


The significance of routine lab examinations Symptoms of severe hypercalcemia

Prognosis In primary HPT, the prognosis is excellent following surgery thanks to the elimination of several preoperative symptoms.

Complications Associated with Elevated Calcium and/or High PTH Levels

​Kembara Xtra - Medicine - Hypernatremia 
Serum sodium (Na) concentration >145 mEq/L, which often denotes a hypertonic state

The equilibrium between total body water (TBW) and total body Na is reflected in the Na concentration. Water relative to sodium deficiency is the cause of hypernatremia.
Hypernatremia typically comes from net water loss or, less frequently, from main Na gain. Dehydration is defined as hypernatremia from water loss. Hypovolemia is defined as concurrent water and salt loss.

Patients who can acquire water and have functioning thirst mechanisms won't experience hypernatremia.


Epidemiology Incidence: More prevalent in the very young and elderly; occurs in 1% of elderly hospital patients; seen in roughly 9% of ICU patients


Pathophysiology and Etiology 

Due to the potent impact of the thirst mechanism, hypernatremia usually only affects patients who do not have easy access to water, such as babies, patients who are intubated, people who have changed mental status, or people who have hypodipsia.

The most frequent cause of hypernatremia is water loss that is out of proportion to salt loss. Excessive water loss is caused by the factors listed below:
- Transdermal loss due to burns or profuse perspiration (examples include illness, newborns exposed to radiant heaters, heat exposure, and intense exercise).
- Loss of urine
Nephrogenic diabetes insipidus (DI) (congenital or caused by renal dysfunction, hypercalcemia, hypokalemia, or medication-related, such as lithium) and Central DI (caused by head injury, stroke, or meningitis) are two types of diabetes insipidus. Post-ATN diuresis - Gastrointestinal loss Osmotic diuresis: glucose, urea, and mannitol
 Enterocutaneous fistula Osmotic diarrhea: lactulose, malabsorption, and some forms of infectious diarrhea
NG suction and vomiting
Because of inadequate water intake, disorders of the thirst mechanism (such as cerebral lesions, intrinsic hypodipsia, and chronic volume enlargement in mineralocorticoid excess) can cause hypernatremia.
Hypernatremia is less frequently brought on by excess Na (an increase in total body Na). Excess total body Na may originate from the following condition:
- IV infusion of hypertonic NaCl or NaHCO3 for the treatment of metabolic acidosis, hyperkalemia, or brain damageIngestion of sea water, excessive use of NaHCO3 antacids, improper preparation of newborn formula and tube feeding, and an abundance of Na in dialysate solutions
Acute hypernatremia can cause the cerebral veins to burst, which can result in focal intracerebral and subarachnoid hemorrhages as well as potentially irreparable neurologic impairment.

Genetics Some types of DI may run in families.

Risk factors include: infants and children; elderly patients (who may also exhibit a diminished thirst response to osmotic stimulation via an unknown mechanism); patients who are intubated or have altered mental status; acute gastrointestinal illness; poorly controlled diabetes mellitus; prior brain injury; surgery; diuretic therapy, particularly loop diuretics; and lithium therapy.


Treatment and/or prevention of the underlying cause
Keep patients well-hydrated, properly mix newborn formula, and never salt any purchased infant formula.


Gastroenteritis, altered mental status, burns, and head damage are associated conditions.

presenting the history Head injury, fever, heat exposure, polyuria, nausea, vomiting, diarrhea, and polyuria all have a history of causing water loss or impairing thirst.

 Neurologic symptoms frequently occur:
- Mild: anorexia, thirst
Moderate symptoms include confusion, myalgia, twitching muscles, tiredness, and irritability.
- Severe: seizure (particularly if hypernatremia develops quickly), coma

Severe symptoms are likely to occur with sudden rises in plasma Na levels or at concentrations >160 mEq/L. The severity of symptoms correlates with the rate of the increase in Na as well as the degree of hypernatremia.

clinical assessment 

 Tachycardia, hypotension, orthostatic hypotension, dry mucous membranes, and poor skin turgor are indications of water or volume loss.
Lethargy, weakness, tremor, focal impairments (in situations of intracerebral bleeding/lesion), disorientation, coma, and seizures are examples of neurologic abnormalities.

Differential diagnosis, hyperosmotic coma, salt intake, hypertonic dehydration, hypothyroidism, and Cushing syndrome are all possible diagnoses.


Initial test results from the laboratory and imaging
Blood tests for sodium, potassium, BUN, creatinine, glucose, calcium, and osmolality (and, if necessary, serum lithium)
Hemoglobin/hematocrit levels (which could be higher than normal due to hemoconcentration)
Na and osmolality in urine
Low urine osmolality: DI is suggested by urine osmolality (typically 300 mOsm/kg) serum osmolality.
The causes of intermediate urine osmolality (300 to 800 mOsm/kg) include partial DI, osmotic diuresis, and hypovolemia.
- High urine osmolality (>800 mOsm/kg) may indicate salt consumption or extrarenal water loss.
Low urine sodium levels (10) typically indicate volume depletion, but they can also result from dilution when combined with excessive urine production from DI.
- Osmotic diuresis may be the cause of intermediate urine Na.
- Consuming salt is suggested by high urine Na.

Tests in the Future & Special Considerations
Antidiuretic hormone (ADH) stimulation distinguishes between central and nephrogenic DI; in nephrogenic DI, urine osmolality does not rise in response to ADH or desmopressin.
To rule out cerebral abnormalities in individuals with central DI or hypodipsia using head CT/MRI

Management 
The underlying cause of hypernatremia must be addressed in addition to the water deficiency.
As the speed of correction relies on the severity of the symptoms and the rate at which hypernatremia develops, ascertain the length of the hypernatremia.
Acute hyponatremia is a relatively rare condition that can result from salt consumption, extreme hyperglycemia, or acute DI.
- Infuse D5W at 3 to 6 mL/kg/hr to reduce serum Na by 1 to 2 mEq/L/hr. - Check serum Na every 1 to 2 hours to ensure correction is occurring at the required rate.
– D5W infusion should be decreased to 1 mL/kg/hr once serum Na falls to 145 mEq/L until serum Na returns to normal.
– In 24 to 48 hours, try to cure hypernatremia.
Chronic hypernatremia (lasting more than 48 hours): Delay fast correction to avoid cerebral edema.
Check serum Na every 4 to 6 hours to assess whether the correction is occurring at the required pace. D5W infusion at 1.35 mL/kg/hr.
Correct at a rate of no more than 0.5 mEq/L/hour or 10–12 mEq/L/day.
Infusion rates frequently need to be changed to allow for persistent water losses.
Hyponatremia combined with hypernatremia Before treating hypernatremia, treat severe volume loss with isotonic IV fluids:
- Once hemodynamic stability is achieved, 0.45% saline can be used to treat hypovolemia and hypernatremia simultaneously because every 2 mL of this solution contains 1 mL of saline and 1 mL of water.
When hypernatremia and hypervolemia coexist, hypervolemia can be treated with diuretics while hypernatremia is being corrected. However, concurrent diuretic use will increase urinary water losses and may call for higher water replenishment.
If you have mild hypernatremia, think about oral water replacement.
Dialysis is an option if acute kidney damage and conventional treatment have failed. High infusion rates of D5W may generate hyperglycemia. Hyperglycemia-induced osmotic diuresis may increase urinary water losses and require higher water replenishment.


First Line of Medicine
Instead of using medications, most treatments use hypotonic IV fluids or water.
Medication may be used to treat DI

Desmopressin acetate (DDAVP), a centrally injected analgesic, should be administered parenterally to patients with acute symptoms and intranasally or orally for chronic therapy.
- Free water replacement: To prevent glycosuria when administering large amounts of water in DI, use 2.5% dextrose in water.
- For chronic but not acute treatment, sulfonylureas/thiazide diuretics may be considered.

Nephrogenic DI should be treated with NSAIDs and diuretics.
- Amiloride hydrochloride 5 to 10 mg PO BID Second Line: Hydrochlorothiazide 25 mg PO BID or Indomethacin 50 mg PO TID
A number of case reports and case series have demonstrated the effectiveness and safety of employing continuous renal replacement therapy (CRRT) to treat hypernatremia in critically ill patients with CHF and severe burns. NSAIDs should be taken into consideration in nephrogenic DI.


Referral 

A nephrology referral would be advantageous if there was underlying renal involvement brought on by hypernatremia.

Admission 

The following criteria must be met before a patient can be discharged: stabilization of the blood Na level and relief of symptoms in a symptomatic patient with serum Na >155 mEq/L.

Patient Follow-Up Monitoring
Daily weight, electrolytes, and blood glucose for a time after correction Periodic monitoring of urine osmolality and urine output in DI Regular neurologic assessments throughout acute correction 

Ensure sufficient nourishment throughout the acute phase of the condition. After the acute phase has passed, the patient may consider a sodium-restricted diet.

Patients with nephrogenic DI need to limit their salt intake and consume a lot of water.

The majority of patients recover, however neurologic damage is possible.


Complications include: CNS thrombosis/hemorrhage; seizures; and chronic hypernatremia, which has a greater death rate if it persists for longer than two days.
Serum Na >180 mEq/L (>180 mmol/L): frequently causes lingering CNS injury

​Kembara Xtra - Medicine - Hyperkalemia 
An electrolyte disease known as hyperkalemia is characterized by a plasma potassium (K) concentration that is greater than 5.5 mEq/L (or 5 mmol/L).

Hyperkalemia slows down the heart's ability to beat and can cause deadly arrhythmias.
Normal K regulation occurs when ingested K reaches the portal circulation and the pancreas responds by releasing insulin. K entrance into cells is facilitated by insulin. Angiotensin I is activated by K in the renal circulation, which promotes renin release from juxtaglomerular cells. Angiotensin I is then converted to angiotensin II in the lungs. Aldosterone secretion is stimulated by angiotensin II's action in the adrenal zona glomerulosa. At the renal collecting ducts, aldosterone causes sodium to be retained while K is expelled.
● four main factors
- Increased load: exogenous from a high intake or endogenous from tissue release, frequently accompanied by a decrease in excretion – Reduced excretion: caused by a lower glomerular filtration rate or a problem with aldosterone secretion – Cellular redistribution: changes from intracellular to extracellular space (the majority of K is intracellular); pseudohyperkalemia: associated with red cell lysis during blood sample collection or transport; thrombocytosis; or leukocytosis Geriatric Considerations
comorbid diseases, decreased renin and aldosterone, and an increased risk of hyperkalemia

Prevention Incidence
Patients with older ages, male sex, worse renal function, comorbidities, and usage of renin-angiotensin-aldosterone system inhibitors have greater incidence rates.
Prevalence can reach 50% in individuals with chronic kidney disease, compared to 1%–10% of hospitalized patients and 2%–3% of the general population.

Pathophysiology and Etiology 
Hemolysis of red blood cells in a phlebotomy tube, a symptom of pseudohyperkalemia (most frequently bogus result) Leukocytosis (reverse pseudohyperkalemia) with thrombolysis
Thrombocytosis, Hereditary Spherocytosis, Infectious Mononucleosis, Traumatic Venipuncture, and Clenching of the Fists During Phlebotomy (Spurious Result) Pseudohyperkalemia in families
Increasing K intake - Giving chronic renal disease patients salt replacements - Eating more bananas, potatoes, melons, citrus juice, and avocados
- Consuming ignite match heads and clay
Transcellular redistribution (shift) insulin shortage, metabolic acidosis, and hyperglycemia (also known as diabetic ketoacidosis or hyperosmolar hyperglycemia condition) - Impaired K excretion - Tissue injury (rhabdomyolysis, burns, trauma), cocaine addiction, high sweating during exercise, and renal insufficiency or failure
- Addison's illness
- Primary hyporeninemia and primary hypoaldosteronism - Type IV renal tubular acidosis (hyporeninemic hypoaldosteronism) - Mineralocorticoid deficiency - Cirrhosis - Obstructive uropathy - Congestive heart failure
Medication-induced (many) Genetics Sickle cell disease Amyloidosis Gordon syndrome Systemic lupus erythematosus
Familial hyperkalemic periodic paralysis and congenital adrenal hyperplasia are linked to various inherited diseases and disorders. 

Acidemia, massive cell lysis (rhabdomyolysis, burns, trauma), use of K-sparing diuretics, excessive K supplementation, and comorbid illnesses such chronic kidney disease, diabetes, heart failure, and liver disease are risk factors. 

Prevention Low K diet compliance and use of oral supplements in persons at risk


Chronic kidney illness, end-stage renal disease, congestive heart failure, myocardial infarction, rhabdomyolysis, liver disease, and the use of drugs like ACE inhibitors or angiotensin II receptor blockers are all associated conditions.

Serum K levels above the normal range (3.5 to 5.0 mEq/L) is the diagnosis. 

Presenting History Abdominal pain Palpitations Numbness Neuromuscular cramps, myalgias, muscle weakness, or paralysis

Clinical examination findings include: Weakness or flaccid paralysis of the extremities; decreased deep tendon reflexes; and 

Laboratory Results 

Renal function: BUN and creatinine Serum electrolytes
K, creatinine, and osmoles in urine (to determine fractional excretion of K and transtubular K gradient, all of which evaluate renal processing of K)
Conditions that could affect lab results K moves from the intracellular to extracellular area during acidemia.
Cortisol, aldosterone, and renin levels to test for mineralocorticoid deficit after other explanations have been checked out include: - Insulin deficiency - Hemolysis of sample When K 7 mEq/L, diagnostic procedures and other ECG abnormalities typically occur.
Lengthening of PR interval, loss of P wave, widened QRS Sine wave at very high K Can eventually result in arrhythmias such as bradycardia, ventricular fibrillation, and asystole. Peaked T wave with shortened QT interval in precordial leads (most common, typically earliest ECG change; however, neither sensitive nor specific).

Management 
Stabilize myocardial membranes with calcium gluconate IV 1,000 mg (10 mL of 10% solution) over 2 to 3 minutes; with continuous cardiac monitoring; repeat if necessary after 5 minutes; effect starts to take effect within minutes but only lasts 30 to 60 minutes; should be used in conjunction with definitive therapies. - Calcium chloride can also be used, albeit it requires central or deep vein infusion to prevent tissue necrosis.
Get extracellular K into the cells.
- Nebulized albuterol and other -agonists had an additive effect with insulin and glucose (at 10 to 20 mg/4 mL saline for >10 minutes—4 to 8 times bronchodilation dose) (5)[B].
- Close monitoring is required, especially for the first hour or two after injection. - Dextrose 50% 1 amp (if plasma glucose 250 mg/dL) and insulin 10 U IV may drive K intracellularly but do not lower total body K. This combination may cause hypoglycemia.
- Although sodium bicarbonate isn't typically advised, it may be beneficial in cases of severe metabolic acidosis.
Remove any extra K from your body.
When dialysis is not easily available, cation exchange resins are a definite therapeutic option but need to be administered in multiple doses.Kayexalate (sodium polystyrene sulfonate), patiromer calcium (Veltassa), and zirconium cyclosilicate are cation exchangers in the gastrointestinal system that bind K.
In particular, patiromer is preferred because it increases tolerance and reduces side effects in both acute and chronic contexts.
- Patiromer calcium (Veltassa): 8.4 g PO per day (study doses range from 4.2 to 16.8 g BID). This takes between 7 and 24 hours to reduce K. If more time is needed, repeat this every 12 hours.
- Kayexalate (sodium polystyrene sulfonate): 15 g PO or 30 g rectally; this lowers K in 1 to 4 hours.
If need, repeat this every six hours.
Enema has a quicker impact than PO.
Furosemide 40 mg IV every 12 hours or as a continuous infusion
- When other treatments are ineffective, hemodialysis is the only option. When situations like digitalis toxicity, rhabdomyolysis, end-stage renal illness, severe chronic kidney disease, or acute kidney injury are present, this may be necessary. One should also keep an eye out for postdialysis rebound– Although there is little clinical evidence, diuretics (loop and thiazides) can be used to manage persistent hyperkalemia.
Treatment for chronic hyperkalemia involves reviewing medications and stopping any that may be causing the condition.
- Advice on eating foods high in K.
- Thiazide and loop diuretic medication for diuretic therapy.


Caution: Kayexalate, which contains sodium polystyrene sulfonate, may make patients who already have fluid overload due to renal or cardiac failure worse.
Due to the significant risk of intestinal necrosis, sodium polystyrene sulfonate should not be used in individuals who are postoperative, have a bowel blockage, or have ileus.
Rapid calcium injection may cause a deadly dysrhythmia in people who have digitalis poisoning. With considerable caution, calcium should be infused slowly over 20 to 30 minutes in 5% dextrose. Digoxin-specific antibody fragment treatment is favored.

Furthermore Treated 

Replaced mineralocorticoids 
Consider a trial of fludrocortisone 0.1 mg daily for 3 to 5 days (in patients with moderately advanced chronic kidney disease, consider maintaining or increasing diuretics in tandem with the assistance of a nephrology consulting service) if the patient does not have a contraindication (greater than stage 1 HTN, volume overload, history of heart failure).

Admission 

If hyperkalemia is severe, treat it first before doing any diagnostic tests.
Intravenous calcium to stabilize the myocardium (use caution if digoxin toxicity or digoxin-induced hyperkalemia exists; this medication can result in heart block). 
Insulin (10 U IV, typically given with 50 mL of 50% glucose [if serum glucose 250 mg/dL] to prevent hypoglycemia]); repeat if elevation persists.
Inhaled 2-agonist (albuterol nebulized)
Stop using any medications (such as exogenous K and K-sparing diuretics) that could raise K levels.
If there are ECG changes or if K is greater than 6 mEq/L (6 mmol/L), you should be admitted for cardiac monitoring.

Patient Follow-Up Monitoring
Serum Until the patient has stabilized and recurrent hyperkalemia is no longer a danger, K levels should be monitored again every 2 to 4 hours.
The recommended daily intake of potassium is 80 mEq (80 mmol). A lot of foods contain K. Bananas, orange juice, other citrus fruits and juices, figs, molasses, seaweed, dried fruits, almonds, avocados, lima beans, bran, tomatoes, tomato juice, cantaloupe, honeydew melon, peaches, potatoes, and salt alternatives are some foods that are exceptionally high in K (>6.4 mEq/serving). Alfalfa, dandelion, horsetail nettle, milkweed, hawthorn berries, toad skin, oleander, foxglove, and ginseng are just a few of the herbal remedies that can raise K levels.


Discuss a low-K diet with a dietician.

Prognosis Associated with poor prognosis in patients with chronic kidney disease and heart failure Associated with poor prognosis in emergency medicine, with trauma, tissue necrosis, K+ supplementation, metabolic acidosis, if calcium gluconate is used to treat hyperkalemia, if AKI, or if hyperkalemia lasts for an extended period of time

 Potential side effects of using ion-exchange resins to treat hyperkalemia include volume overload and intestinal necrosis. Complications Life-threatening heart arrhythmias

​Kembara Xtra - Medicine - Hyperemesis Gravidarum 
Around 70–80% of pregnancies experience nausea and vomiting at some point during the pregnancy.
Hyperemesis gravidarum, a more severe form of morning sickness that affects 0.5–2% of pregnancies, can have serious negative medical and psychological repercussions.
One of the most frequent reasons for hospitalization during pregnancy is hyperemesis gravidarum, which is still diagnosed based on clinical judgment.
Although morning sickness is common during pregnancy, hyperemesis gravidarum is a rare condition. hyperemesis gravidarum is associated with several adverse fetal outcomes including preterm delivery, low birth weight, small for gestational age, low 5-minute Apgar scores, and neurodevelopmental delay.
● Intractable vomiting that disrupts a pregnant woman's fluid and electrolyte balance as well as nutrition is known as hyperemesis gravidarum:
It is typically present in the first 8 to 20 weeks of pregnancy and is thought to have both biological and behavioral components.
- Linked to high levels of the hormone human chorionic gonadotropin (hCG) and estrogen Symptoms typically start around two weeks after the first missed period, peak around week twelve, and disappear by week twenty.
Endocrine/metabolic, gastrointestinal (GI), and reproductive system(s) affected

Epidemiology Other risk factors include prior history of hyperemesis, preexisting diabetes, hyperthyroid disease, psychiatric illness, asthma, and GI issues. It typically affects young women, primiparous women, nonsmokers, and non-Caucasians.
Incidence
In 0.5–2% of pregnancies, hyperemesis gravidarum occurs.
Prevalence
The most typical reason for hospitalization during the first half of pregnancy and the second most typical reason for hospitalization overall for pregnant women is hyperemesis gravidarum.

Pathophysiology and Etiology 

The cause is unknown. Pregnancy hormones, hyperthyroidism, hyperparathyroidism, liver dysfunction, autonomic nervous system dysfunction, CNS tumor, Addison disease, and maybe psychological problems are some of the suggested implications.

Genetics

higher chance if hyperemesis gravidarum runs in the mother's family

Risk factors include nulliparity, many pregnancies, migraine and motion sickness histories, black or Asian women, gestational trophoblastic illness, female fetuses, and a possible link to Helicobacter pylori infection.

Prevention 

Small, frequent meals; avoiding an excessively empty or full stomach; anticipatory advice for dietary practices to prevent dehydration and nutritional depletion

Diagnosis
Although there are many different ways to define hyperemesis gravidarum, it frequently includes persistent nausea and vomiting throughout pregnancy, symptoms of dehydration, and electrolyte abnormalities after ruling out more serious causes of extreme nausea and vomiting.


Providing a history; feeling queasy; vomiting with retching more than three times per day; decreased urine production; being tired; feeling dizzy while standing; and having a poor appetite

Clinical examination, thyroid evaluation, >5% weight loss from pre-pregnancy weight, significant ketonuria, high urine specific gravity, and other signs of dehydration

Multiple Diagnoses 

Other typical reasons of vomiting need to be taken into account:
Anxiety, gastroenteritis, gastrotritis, reflux esophagitis, peptic ulcer disease, cholelithiasis, cholecystitis, Pyelonephritis, appendicitis, pancreatitis, hyperparathyroidism, hypercalcemia, thyrotoxicosis, and H. pylori infection are just a few of the conditions that can affect the digestive system.


Laboratory Results 

The purpose of the initial laboratory tests for hyperemesis gravidarum is to assess the clinical condition of the mother and rule out any other potential causes of nausea and vomiting.

Initial examinations (lab, imaging)
Glucosuria, albuminuria, granular casts, and hematuria may be seen on a urine test; ketosis is more likely to occur. Thyroid-stimulating hormone (TSH), free T4.
- Dehydration and abnormal electrolyte levels brought on by nausea and vomiting - Acidosis - Liver enzymes and bilirubin levels - Hematocrit - Hepatitis panel - Calcium - Albumin
Tests in the Future & Special Considerations
Unless there is a worry about a hydatidiform mole or multiple gestations, in which case ultrasonography may be conducted, no imaging is recommended.


Other/Diagnostic Procedures

only recommended if additional diagnoses listed in the following section need to be ruled out:
 An upper abdomen ultrasonography if nausea and vomiting are thought to be the result of cholecystitis or pancreatitis.
The suspected reason of nausea and vomiting is appendicitis, according to an abdominal MRI.

Interpretation of Tests
A positive urine analysis for ketones and a high specific gravity point to starving ketosis and volume depletion, respectively.
TSH and free T4: If TSH is suppressed with high free T4, further testing is required to rule out overt hyperthyroidism. Transient hyperthyroidism (suppressed TSH with normal free T4) may be present in about 50% of hyperemesis gravidarum cases.

Dehydration can result in low potassium, low sodium, increased BUN, and elevated levels of creatinine and electrolytes.
Liver enzymes and bilirubin levels: Mild AST and ALT elevations occur in about 50% of cases and settle on their own.
When liver enzyme levels are dramatically increased, other etiologies must be taken into account.
Hematocrit: Volume contraction due to dehydration results in an increase.
Hepatitis panel: Take into account and rule out Hepatitis A, B, and C as a possible cause of hyperemesis.
Calcium: Hypercalcemia brought on by hyperparathyroidism is a rare occurrence.
Albumin: Low albumin levels may be a sign of malnutrition brought on by nausea and vomiting.
TREATMENT
The first-line therapies for hyperemesis gravidarum are pyridoxine and doxylamine (pregnancy Category A)(1)[C]. Metoclopramide or ondansetron (pregnancy Category B) come next, and then prochlorperazine, methylprednisolone, or promethazine (pregnancy Category C), depending on the drug.

General Actions 
Treat electrolyte imbalances and dehydration before dealing with nausea.
Ondansetron carries an FDA warning for concerns of QT prolongation. IV fluids, either normal saline or 5% dextrose normal saline (with consideration for potential thiamine deficiency). For severe cases, consider PO thiamine 25 to 50 mg TID or IV 100 mg in 100 mL of normal saline over 30 minutes once weekly. In a pregnancy-related situation, the danger is unknown. Although the bulk of recent research seem to indicate no increased risk of prenatal deformity, this is still a contentious topic.

Medication: Pyridoxine (vitamin B6) 25 mg PO or IV every 8 hours, with a daily maximum dose of 200 mg; antihistamines (such as diphenhydramine 25 to 50 mg every 4 to 6 hours; doxylamine 12 mg PO BID; meclizine 25 mg PO every 4 to 6 hours; and dimenhydrinate 25 to 50 mg PO every 4 to 6 hours); and the combination product Diclegis (sustained-release pyridoxine
Promethazine or prochlorperazine, for example, are phenothiazines.
- Safety measures: In infants, phenothiazines are linked to extrapyramidal effects, extended jaundice, and hyper- or hyporeflexia.
Methylprednisolone 16 mg PO/IV q8h for two to three days, then taper over two weeks if the initial three-day treatment is successful; only used in severe instances with unknown benefit
Ondansetron 4–8 mg PO every eight hours
pregnant women's issues
All prenatal drugs should weigh the risks and advantages for the mother and the fetus.
Initial Line
Pyridoxine (vitamin B6) 10 to 25 mg PO or IV every eight hours helps alleviate symptoms in women with mild to moderate motion sickness and has a favorable safety profile. The daily maximum is 200 mg.
If nausea and vomiting persist, combine pyridoxine 25 mg PO every eight hours with doxylamine succinate 12.5 mg. Both drugs work better together than they do separately.
With refractory vomiting, 350 mg PO TID of ginger pills may be given.

Antihistamines like dimenhydrinate, meclizine, and diphenhydramine are on the second line. It is best to stop using doxylamine-pyridoxine before beginning a new antihistamine.
Promethazine 12.5 mg PO or rectally, Metoclopramide 10 mg PO every eight hours, and Ondansetron 4 to 8 mg PO or IV every eight hours


Referral: Inpatient management is necessary for IV fluids and antiemetics when symptoms are resistant to outpatient treatment.
Referral to gastroenterology or surgery if an other diagnosis is more consistent with the cause of the nausea and vomiting.

 If a referral to psychiatry or psychology is necessary, they may also take that into consideration.

Further Therapies 
Although their effectiveness is debatable, glucocorticoids (methylprednisolone 16 mg IV every eight hours for 48 to 72 hours) can be explored in severe and resistant instances.
Cimetidine and ranitidine as an additional therapy to lessen heartburn and acid reflux

Surgical Techniques 

Rarely, tube feeding or parenteral nourishment is used if all pharmacologic and nonpharmacologic therapies fail and weight loss persists. Parenteral feeding is recommended over enteral nutrition, which can reduce nausea and vomiting. Enteral nutrition can be administered via the gastric or duodenal routes.

Healthcare Alternatives 

Acupressure and acupuncture have conflicting results, although ginger 350 mg PO every six hours may be helpful.
In cases of severe hyperemesis, acupressure bands at the Neiguan point are a successful adjuvant therapy.
Medical hypnosis might be a useful addition to the standard course of medical treatment, but further research is required.

Admission, usually outpatient therapy, enteral volume and nutrition repletion, but early enteral tube feeding does not enhance maternal or perinatal outcomes. In rare severe cases, parenteral therapy in the hospital or at home may be necessary.


Constant Care 
10% of hyperemesis gravidarum individuals experience symptoms throughout the entire pregnancy.

Take Action 

The degree of nausea and vomiting can have an impact on one's overall quality of life and future prospects for conception.

patient observation
If the condition is severe, daily weight checks should be performed. Ketosis, hypokalemia, and acid-base abnormalities brought on by hyperemesis should all be carefully watched for.

Diet: As tolerated, bland or watery diet

 A diet high in protein and carbs, such as fruit, cheese, eggs, steak, chicken, vegetables, toast, crackers, and rice, is recommended for outpatients. High-fat foods and spicy meals should be avoided by patients. Every hour or so, encourage tiny quantities at a time.

Modification of Lifestyle 
Psychosocial problems, such as potential ambivalence regarding the pregnancy, should be paid attention to.
To prevent volume depletion, patients should be advised to routinely consume tiny amounts of fluid.
Steer clear of specific meals that are known to irritate the sufferer.
Nutrients that are wet to dry (sherbet, broth, crackers with gelatin on them, toast)

Self-limited sickness with a favorable prognosis if the patient's weight is kept at >95% of pre-pregnancy levels.
The mortality rate for pregnant patients who develop hemorrhagic retinitis is 50%.


Fetal complications: Patients with >5% weight loss are associated with intrauterine growth retardation and fetal anomalies. Maternal complications include vitamin deficiency, dehydration, and malnutrition. In severe cases, Wernicke encephalopathy secondary to thiamine deficiency, coma, and even death.
Poor weight gain is linked to a somewhat higher risk of small for gestational age births (2,500 g or less) and early births (37 weeks or less).Hemorrhagic retinitis and damage to the liver

​Kembara Xtra - Medicine - Hypercholesterolemia 
Elevated cholesterol is a substantial risk factor for atherosclerotic cardiovascular disease (ASCVD), according to the basic description.

Subtypes of lipoprotein
- Low-density lipoproteins (LDL): the main therapeutic target
- Atheroprotective effects of high-density lipoproteins (HDL)
TG: Triglycerides

Cardiovascular (CV) system is/are impaired.

Epidemiology 
Hypercholesterolemia affects 7% of children and adolescents in the United States between the ages of 6 and 19 and 28% of Americans over the age of 20.
Prevalence
As people age, disease incidence and prevalence rise.

Pathophysiology and Etiology 
The pathophysiology
- When cholesterol builds up in vascular walls, fatty streaks develop into fibrous plaques.
– Plaque rupture is a result of plaque instability brought on by inflammation.
– The pathogenesis of atherosclerosis, inflammation, and vascular reactivity is multifaceted.
Hypercholesterolemia's etiology
Obesity, diet, excessive alcohol consumption, hypothyroidism, diabetes, inflammatory disease, liver disease, nephrotic syndrome, chronic renal failure, and medications (thiazide diuretics, carbamazepine, cyclosporine, progestins, anabolic steroids, corticosteroids, protease inhibitors, antipsychotics, isotretinoin) are secondary causes. The primary cause is genetic (familial dyslipid

Genetics Familial hypercholesterolemia (FH) - Elevated LDL levels since birth - Heterozygous FH prevalence is 1:300 globally.
- High risk of coronary heart disease at younger ages and a propensity for atherosclerotic disease in early adulthood. Homozygous FH patients often pass away before the age of 20. - Early lipid-lowering medication therapy has been demonstrated to minimize the risk of ASCVD.
It is advised that first-degree relatives get early lipid screening.

Risk Elements 

Obesity, physical inactivity, family history, smoking cigarettes, and binge drinking are all risk factors. Saturated dietary fat has a complicated link with hypercholesterolemia and coronary artery disease.

Preventive measures, regular exercise, weight management, and a diet low in saturated fats (grade 1B)


Accompanying Conditions 
Obesity, high blood pressure, and diabetes mellitus (DM)


DIAGNOSIS
U.S. Preventive Services Task Force (USPSTF) screening recommendations: total cholesterol and HDL cholesterol (HDL-C) every five years for men and women under 40; neither a recommendation for nor a recommendation against screening for adults aged 21 to 39; neither a recommendation for nor a recommendation against screening for children and adolescents.

American diabetic Association: diabetic patients should get yearly dyslipidemia screenings

Child Safety Considerations
The National Heart, Lung, and Blood Institute recommends that all children between the ages of 9 and 11 and between the ages of 17 and 21 get a comprehensive lipid screening. The American Academy of Pediatrics gave their approval to this.
Children who have a family history of familial hypercholesterolemia or early coronary artery disease should be screened.

Review potential secondary etiologies; evaluate other ASCVD risk factors; present history.

clinical assessment 

Non-specific findings; possible BMI calculation and xanthoma examination

Laboratory Results 

Initial examinations (lab, imaging)

Lipid panel (preferably not fasted). LDL is often computed and reliable if TG is less than 350 mg/dL.
If you have hypertriglyceridemia (TG > 440 mg/dL) or a condition that can elevate TG, including pancreatitis, perform fasting blood tests.

In cases of extremely high LDL (>190 mg/dL) or TG (>500 mg/dL), consider the genetic explanation.

Administration Caution 
Multiple rules are in place. LDL target targets are once again emphasized in the 2018 American College of Cardiology/American Heart Association (ACC/AHA) cholesterol guidelines. Patients with existing CV disease should be regarded as high risk (secondary prevention), hence risk stratification should only be used for primary prevention.
U.S.: ACC/AHA cholesterol recommendations (2)
– The ACC/AHA states that four groups gain from statin therapy:
Initial LDL-C rise >190 mg/dL: high-intensity statin
Patients 40 to 75 years old with diabetes and LDL-C >70 mg/dL should take a moderate-intensity statin.
Based on pooled cohort equations, ASCVD risk: Visit the calculator at http://tools.acc.org/ASCVD-Risk-Estimator (comment on calculator below).
10-year ASCVD risk is 5% with a Mediterranean diet and regular exercise.
10-year ASCVD risk 7.5-20%: moderate-intensity statin, discuss with patient; 10-year ASCVD risk 5-7.5%: moderate-intensity statin; 30- to 49%-lower LDL-C target; 10-year ASCVD risk 7.5-20%: moderate-intensity statin
High-intensity statin with a target to lower LDL-C by >50% for patients with 10-year ASCVD risk >20%
Secondary ASCVD prevention: high-intensity statins with an aim to lower LDL-C by more than 50%. In very high-risk ASCVD patients, add ezetimibe if LDL levels are greater than 70 mg/dL following maximal statin therapy.
Age >75 years: as tolerated, moderate- or high-intensity statin therapyVery high-risk ASCVD is defined as having numerous high-risk conditions as well as at least one significant ASCVD event:
Important ASCVD occurrences
Ischemic stroke history, symptomatic peripheral arterial disease, acute coronary syndrome, or previous myocardial infarction
Age over 65, heterozygous FH, a history of CABG or PCI, diabetes mellitus, high blood pressure, chronic renal disease, current smoking, a history of congestive heart failure, and LDL-C >100 mg/dL while receiving the best medical care are all high-risk factors.
 The threshold calculated risk at which to treat patients is a matter of debate: The 10-year ASCVD risk estimated by the pooled cohort equations is greatly inflated (by at least 50%). Therefore, go over the advantages and disadvantages of statin therapy with your patients. Consider the patient's age.
United States: USPSTF advice on statin use Adults between the ages of 40 and 75 who do not smoke, have dyslipidemia, hypertension, diabetes, or diabetes with a projected 10-year CVD event risk of 10% or higher: statins with a low to moderate dose (grade B recommended)
- People aged 40 to 75 who have no prior history of cardiovascular disease, at least one CVD risk factor, and an estimated 10-year CVD event risk of 7.5–10%: Low- to moderate-dose statins are advised (grade C).
- Adults 76 years and older without a history of CVD: insufficient data to recommend.
Guidelines for lowering cholesterol from the National Institute for Health and Care Excellence (NICE), United KingdomNICE advises individuals under primary prevention consideration to make lifestyle changes before beginning any statin therapy. The 10-year risk can be assessed using QRISK2 at https:// qrisk.org/three/.
- Start taking atorvastatin 20 mg if your 10-year risk of cardiovascular disease is greater than 10% and you have no history of the disease.
- If there is a known CVD and a 10-year risk of CVD is greater than 10%, begin taking 80 mg of atorvastatin.
Consider taking atorvastatin 20 mg if you're under 85 years old to lower your risk of suffering a nonfatal myocardial infarction, while there is some debate over its efficacy.
– Start atorvastatin 20 mg if estimated glomerular rate is less than 60 or if you have type I diabetes.
ALERT
To prevent acute pancreatitis in hypertriglyceridemia with TG>500 mg/dL, TG reduction becomes the main objective until 500 mg/dL. Unless TGs continue >500, statin medication is typically advised as a first line of treatment. Fibrates may be taken with statins with caution due to an increased risk of rhabdomyolysis.


Prior to starting drug therapy, cornerstone therapies including medication and therapeutic lifestyle changes should be tried.
The majority of persons over 75 years old do not benefit from starting statin medication for primary prevention, according to the available data (ALLHAT-LLT).
4–12 weeks after starting a drug, check the lipid panel to assess response and/or adherence.
- Unless there is a concern about the patient's adherence, subsequent monitoring is generally not recommended.

Statins, the first-line HMG-CoA reductase inhibitors

 Sorted according to intensity
- High intensity (reduces LDL-C by >50%): atorvastatin 40 to 80 mg/day, rosuvastatin 20 to 40 mg/day; - Moderate intensity (reduces LDL-C by 30-49%): atorvastatin 10 to 20 mg/day, rosuvastatin 5 to 10 mg/day; - Low intensity (reduces LDL-C by 30%): simvastatin 20 to 40 mg/

Pregnancy, lactation, or active liver disease are contraindications.

Adverse effects: Mild myalgia is frequently experienced.
- Elevated liver transaminases: alanine aminotransferase (ALT) is measured before to medication to establish baseline; if ALT is greater than three times the upper limit of normal, do not start a statin; routine monitoring is not advised.
- Association with an increase in diabetes cases: 0.1 extra cases per 100 people taking a moderate-intensity statin and 0.3 extra cases per 100 people taking a high-intensity statin.
- Myopathies (quite uncommon but poorly understood)
- Intolerance to statins
Think about switching statins.
Reduced dosage
The majority of patients who have previously stopped taking statins because of side effects are able to resume taking the same or a different statin and tolerate it.
ALERT
Warning from the U.S. Food and Drug Administration: Due to an elevated risk of myopathy, simvastatin at 80 mg/day should not be prescribed.
If there are no symptoms of myopathy, patients who have been taking this medication for more than a year can continue.
 The following dosage limitations are used to lower the risk of myopathy:
Simvastatin 10 mg/day with amiodarone, verapamil, and diltiazem is the upper limit; simvastatin 20 mg/day with amlodipine and ranolazine is the upper limit.

Some HMG-CoA reductase inhibitors may interact negatively with hepatitis C antiviral drugs.
Visit https:// www.hepdruginteractions.org/checker to verify interactions.
When using statins, stay away from grapefruit juice as it may raise the risk of statin myopathy.


pregnant women's issues
Statins are not recommended during pregnancy, and lactation may be risky.

Next Line
If LDL-C is >70 mg/dL on maximum statin therapy, second-line medications are now advised for primary prevention.
Ezetimibe - Can be used alone or in combination with a statin; monotherapy (10 mg/day) or ezetimibe/simvastatin - Effect: lowers LDL-C; one randomized controlled trial shows combination therapy with statin has modest benefits in lowering CV events and CV-related mortality following acute coronary syndromes.
Fibrates, of which the most effective are gemfibrozil and fenofibrate, have a moderate impact on lowering LDL and a strong positive impact on raising HDL. Most patients in more recent research do not have a mortality benefit.
Niacin improves HDL but there is no proof that it leads to better results; it shouldn't be used frequently.
PCSK9 inhibitors, such as monoclonal antibodies alirocumab and evolocumab. The latest research suggests secondary prevention reduces CVD incidence without impacting all-cause death incidence, however it is very expensive.


Healthcare Alternatives 
Omega-3 fatty acids with use of fish oil
Flaxseed, canola oil, soybean oil, almonds, and fatty fish are the sources of this compound. Its effect is to lower TG and LDL levels while raising HDL.
Mortality reduction and overall CV benefit are questionable.

Admission

Recommend rechecking a fasting lipid panel 4–12 weeks after discharge if lipid panel was tested while patient due to myocardial infarction as the initial lab may not have been as accurate.

Take Action 

150 minutes a week of moderate-intensity exercise raises HDL, reduces TC, and aids in weight management.
patient observation
If the first ALT is within the normal range, routine monitoring of liver function tests is no longer advised.
DIET The risk of CV disease is decreased by plant-based diets and the Mediterranean diet, which are high in legumes, fruits, vegetables, nuts, fish, and olive oil.

Complications 

Peripheral artery disease, a myocardial infarction, and a cerebrovascular event

​Kembara Xtra - Medicine - Hydronephrosis 
Dilatation of the renal calyces and pelvis is referred to as hydronephrosis, and hydroureter (dilatation of the ureter) may also be present.

 Obstructive uropathy, which describes the harm to the renal parenchyma brought on by urinary tract obstruction (UTO), should not be confused with hydronephrosis.

Epidemiology: Congenital abnormalities make hydronephrosis more common in children than in adults; it is more common in women for adults under 60 and in males for adults over 60.

Pathophysiology and Etiology 
Hydronephrosis is characterized by elevated pressure in the urine collecting system, which most frequently results from an obstruction of some kind.
Nonobstructive hydronephrosis may be acute or chronic, partial or total, and unilateral or bilateral, and it may be caused by diabetes insipidus or a physiological shift during pregnancy.
The GU system may be obstructed at one of the following levels:
Congenital occlusion of the ureteropelvic junction (UPJ), nephrolithiasis, transitional cell cancer, sloughed renal papillae, blood clot, and fungal ball Nephrolithiasis, transitional cell carcinomas, strictures, sloughed renal papillae, retroperitoneal fibrosis, and extrinsic compression are all conditions that affect the ureter. - Bladder: posterior urethral valves, extrinsic compression, neurogenic bladder
Prostatic hypertrophy, malignancy, and strictures in the urethra
As a result of ureteral reflux, strictures, ureteral compression (from peritransplant lymphoceles, hematomas), and bladder dysfunction, hydronephrosis in a transplanted kidney is more frequent than in native kidneys.
Child Safety Considerations
Antenatal hydronephrosis is typically detected by the US as early as the 12th or 14th week of pregnancy in 1-5% of pregnancies.
An increased risk of postnatal pathology exists in children with prenatal hydronephrosis.
The US exam is the first step in the postnatal evaluation process; further tests, such the voiding cystourethrogram (VCUG), depend on how severe the postnatal hydronephrosis is. It is the most frequent reason for abdominal mass in newborns.
VUR, congenital UPJ blockage, neurogenic bladder, and posterior urethral valves are common etiologies in children, and pediatric diagnostic algorithms differ from adult ones due to distinct differential diagnoses requiring age-appropriate testing.

pregnant women's issues
80% of pregnant women experience physiologic hydronephrosis, which is more noticeable on the right than the left.
Despite its high incidence, most cases of ureteral dilatation are asymptomatic; if they are, ureteric calculus should be taken into consideration and urinary infection must be ruled out. Dilatation is caused by hormonal effects, external compression from an expanding uterus, and intrinsic changes in the ureteral wall.

Symptoms vary depending on the source, severity, location, and degree of obstruction, as well as the patient's medical history.
Hydronephrosis can be accompanied by pain, ranging from nebulous, sporadic discomfort to severe renal colic, despite the fact that it is frequently asymptomatic.
May be related to hematuria

Vomiting and nausea may be brought on by pain or an infection.
The presence of a urinary infection is suggested by fever and chills.
Anuria denotes total obstruction of both kidneys, or unilateral obstruction of one kidney.

Due to poor urine concentration in partial blockage, polyuria may develop.
Chronic kidney disease (CKD) symptoms include anorexia, fatigue, weight gain, edema, shortness of breath, changes in mental status, and tremors due to a protracted blockage.
Weak pee stream, nocturia, straining to urinate, overflow incontinence, urgency, and frequency are signs of bladder outlet obstruction.
General medical and surgical history includes the following conditions: malignancy (extrinsic compression), radiotherapy (ureteric stricture/fibrosis), surgery (iatrogenic obstruction), trauma hematoma or fibrosis, gynecologic disease (extrinsic compression from endometriosis, ovarian masses, and uterine prolapse), smoking (urothelial cancer), and drugs (methysergide-induced retroperitoneal 

clinical assessment 

General indications of volume overload from renal failure include edema, rales, and hypertension (HTN).
- Tachycardia, tachypnea, and diaphoresis with pain
- High fever, if there is an infection
Pelvic exam: pelvic mass, uterine prolapse, palpable enlarged prostate (cancer or benign), urethral meatal stenosis, and phimosis (may be evident, especially in thin youngsters) Abdominal exam: CVA pain, palpable bladder, rarely palpable abdominal mass 

Laboratory Results 
Urinalysis with microscopy reveals pyuria, proteinuria, crystalluria, and hematuria.
Midstream urine sensitivity and culture: Rule out UTI.
Elevated urea and creatinine may be signs of obstructive uropathy, according to the basic metabolic panel. A type 4 distal RTA due to blockage may be indicated by hyperkalemic nonanion gap metabolic acidosis.
Before considering ureteral instrumentation, evaluate the platelet count if there is an infection. CBC: anemia of CKD, leukocytosis.
Prostate-specific antigen (PSA): adult males over 50, abnormal digital rectal exam, or symptoms of bladder outlet blockage 
For detecting malignant cells in urothelial cancers, urine cytology
The majority of the time, US and noncontrast CT scanning are successful at identifying the existence and origin of obstruction.
US: Sensitivity 90%, specificity 84.5% of preferred screening test for hydronephrosis. does not evaluate function and hardly ever determines the kind and degree of impediment. The severity or duration of the obstruction have no relation to the degree of hydronephrosis.
Benefits include the ability to detect renal parenchymal illness (reduced renal volume, increased cortical echogenicity, cortical thinning, and cysts); lack of radiation or contrast exposure; and safety during pregnancy, contrast allergy, and renal failure. - Erroneous good results False-negative findings in 15.5% of cases include parapelvic cysts, VUR, excessive diuresis, and a normal extrarenal pelvis. 10%: retroperitoneal fibrosis, acute obstruction, and calyceal dilatation mistaken for renal cortical cysts. Noncontrast helical CT (NHCT): test of choice for suspected nephrolithiasis. 94–96% sensitivity and 94–100% specificity were reported. Stone is most frequently discovered at the UPJ, pelvic brim, and vesicoureteric junction, which are levels of ureteric luminal constriction. Perinephric stranding, hydronephrosis with hydroureter close to the degree of obstruction, and renal enlargement are typical features in acute obstruction. Renal atrophy may be observed if persistent.
Benefits include not exposing patients to contrast material, saving time and money, and detecting extraurinary pathology.- Drawbacks: does not evaluate function or degree of obstruction; exposes the user to more radiation, albeit reduced radiation dose procedures have demonstrated equivalent accuracy.
Diuretic renal scintigraphy (DTPA or MAG-3 radionuclide renal scan) is only recommended for assessing hydronephrosis without obvious blockage.
Determines total and divided renal function (right vs. left), as well as the existence of real blockage.
- The T1/2 for the tracer's washout is assessed following the administration of furosemide for 20 minutes. T1/2; >20 minutes is blocked, 10 to 20 minutes is ambiguous, and 15 minutes is considered normal by some specialists.
Advantages: safe in contrast allergy and renal dysfunction; no contrast exposure
False-positive results False-negative findings: dehydration or insufficient diuretic challenge; delayed excretion due to renal failure; large dilatation producing a water-reservoir effect of delayed excretion without obstruction.
Multiphase CT with contrast - Stones and edema are found in the non-enhanced phase.
- The parenchymal phase shows decreased enhancement of the renal parenchyma in the presence of acute obstruction; it can identify extraurinary causes of obstruction and estimate the relative glomerular filtration rate (GFR) of each kidney with accuracy comparable to that of a radioactive renal scan. - The delayed phase makes it possible to see soft tissue filling deficiencies (such urothelial carcinoma) and the collecting system.
When NHCT and US are nondiagnostic, magnetic resonance urography (MRU) is recommended. provide information on anatomical structure, function, and prognosis; sensitivity is comparable to US or NHCT for nephrolithiasis (70%) but superior for soft tissue causes, such as strictures. Advantages: no radiation exposure; safe throughout pregnancy; Drawbacks: more expensive; takes longer (35 minutes as opposed to 5 minutes); it is less accessible than CT. Due to the potential of nephrogenic systemic fibrosis, gadolinium is contraindicated in renal failure, especially when GFR is 30 mL/min.
Tests in the Future & Special Considerations
Due to the possibility of developing bacteremia from a urine infection in an obstructed urinary system, fever should be treated as a medical emergency when it occurs in conjunction with hydronephrosis.

Other/Diagnostic Procedures

It is occasionally necessary to do a biopsy, retrograde pyelogram, or cystoscopy to identify the obstruction (for example, a tiny urothelial carcinoma that was missed on imaging) or to check that the distal ureter is healthy before pyeloplasty. Furthermore, such procedures are frequently required to get a firm pathologic diagnosis for mass lesions.

Treatment Prompt drainage is advised in cases of UTI, impaired renal function, or unbearable/persistent pain. Medical treatment: correction of fluid and electrolyte imbalances, pain management, and antibiotics as an adjuvant to drainage if infection is present. - Urethral or suprapubic catheter for obstruction of the bladder outflow
VUR is frequently treated conservatively with antibiotics; surgical care may be necessary in severe instances in children or women of reproductive age. - Ureteric obstruction: retrograde (cystoscopic) or antegrade (percutaneous) stenting.
Medical expulsive therapy (MET) is recommended for urethral stones smaller than 10 mm in patients with managed discomfort, no symptoms of sepsis, and normal renal function.

Procedures Pyeloplasty (open or laparoscopic) and minimally invasive stricture incision (endopyelotomy) are employed with equivalent results in cases of congenital UPJ obstruction and hydronephrosis caused by obstruction.
- Nephrolithiasis: The first line of treatment for impacted upper urethral stones under 2 cm is extracorporeal shock wave lithotripsy (ESWL).
While ureteral stenting prior to ESWL or postureteroscopy is not related with any additional benefit and is linked with greater discomfort and morbidity, ureteroscopy with or without intracorporeal lithotripsy has lower retreatment rates but higher complication rates and longer hospital stays.
- Nephroureterectomy for transitional cell carcinoma - Ureterolysis for idiopathic retroperitoneal fibrosis (releases ureters from inflammatory mass)
Nonobstructed hydronephrosis - VUR: ureteric reimplantation, endoscopic suburethral injection - Prostate disorders: numerous treatment techniques, including transurethral resection of the prostate (TURP) and radical prostatectomy

Admission

Pyonephrosis, an obstruction and infection coexisting, is a genuine urologic emergency needing prompt drainage.
Retrograde (cystoscopic) stenting is frequently challenging, necessitating implantation of percutaneous nephrostomy tube(s), yet both are equally effective.

Follow-up Until renal function stabilizes, serial monitoring of kidney function (electrolytes, BUN, and creatinine) and blood pressure is required.
The severity of renal impairment determines the frequency of monitoring.
A follow-up US to check on the progress of the hydronephrosis after the renal function has stabilized. Consider diuretic radionuclide testing to rule out ongoing blockage if hydronephrosis persists.

Recovery of renal function relies on the etiology, whether a UTI is present or not, and the severity and length of the blockage.
Even after days of total obstruction, some healing is still possible, however some lasting damage may manifest within the first 24 hours. Diagnostic testing has a low predictive value; delays in therapy can result in irreparable kidney damage. It's quite difficult to foresee how incomplete obstruction will proceed.


Complications 

Urine stasis increases the risk of infection and the production of kidney stones. Obstruction results in gradual renal atrophy and irreversible kidney function loss.
Urine extravasation in the perinephric region may result in the spontaneous rupture of a calyx.
Postobstructive diuresis: pronounced polyuria following blockage alleviation
– primarily brought on by fluid and nutrient excess, but may be made worse by decreased renal tubular concentrating power. Over 500 mL/hr of urine may be produced.
– Only enough hypotonic fluid (about 0.45% NaCl) should be added to replace urine losses in order to prevent volume depletion. The diuresis will continue if urine production is replaced with equal volumes of saline.

​Kembara Xtra - Medicine - Hydrocephalus 
Hakim first identified normal pressure hydrocephalus (NPH) as a clinical triad of gait instability, incontinence, and dementia (mnemonic: wet, wobbly, wacky) in 1957. The condition has two types: idiopathic and obstructive, the latter of which is typically brought on by physical trauma such as post-trauma, meningitis, or subarachnoid hemorrhage. It is also characterized

Precautions: Idiopathic NPH (iNPH) is most common in those over 60; it is extremely rare in people under 40. Patients over 60 who fall to the ground should be evaluated for NPH.
More than 10% of study participants exhibited NPH results.


Epidemiology 

The secondary type can develop at any age, although the iNPH form primarily affects elderly people who are at least 40 years old.
● estimated to play a role in 6% of dementia cases overall
Incidence
between 1.1% and 2.2%. Uncertain diagnosis hinders obtaining correct data (2).
The prevalence increases from 1.3% in the over-65 age group to 5.9% in those who are 80 years and older. It is believed that 2,000,000 people in Europe and 700,000 people in the United States are affected (as opposed to 400,000 people with multiple sclerosis).


Pathophysiology and Etiology 

Idiopathic hydrocephalus is a communicative condition of reduced CSF absorption (not overproduction), not overproduction. The predominant notion in iNPH contends that suboptimal venous compliance compromises baseline CSF evacuation by subarachnoid granulations.
Scarring is probably present in secondary NPH.
● There is a pressure gradient between the ventricular system and subarachnoid space as a result.
In response to a higher pressure set point, CSF synthesis declines (albeit it still exceeds the amount of CSF absorbed).
Elevated pressure causes the ventricles to dilate and the brain parenchyma to constrict, which disrupts the normal flow of blood to the brain and causes ischemia alterations that result in tissue loss and damage.
● Some people think that the idiopathic form results from immature subarachnoid granulations that have consistently failed to remove enough CSF throughout childhood.
● Several factors could cause secondary NPH, including:
- Head injury (most often)
- Subarachnoid bleeding
- Chronic meningitis (tuberculosis, syphilis) - Paget disease of the skull - Resolved acute meningitis
RISK ELEMENTS
Head injury, subarachnoid hemorrhage, meningitis, or encephalitis are causes of the secondary type.

Diagnosis 
The secret to an early diagnosis is a thorough history and examination.

Gait instability typically first shows up in the past, then mentation abnormalities, and finally urinary incontinence. The past is typically insidious and progressive.
Behavioral alterations observed frequently: Many times the physical results are preceded by depression, mania, or psychotic symptoms, which frequently do not respond well to conventional therapy.
Difficulty starting motion: Feet seem "glued to the floor." Wide-based and shuffling gait; turning looks to be done "en bloc."
With subcortical dementia of NPH, inattention, forgetfulness, and lack of spontaneity are frequently observed.
Urinary urgency was first, then lack of restraint, and then outright incontinence.
A minimum of three to six months of symptom persistence and progression.
A distant trauma or infection points to a secondary as opposed to an idiopathic form.
No behavioral, neurological, or other medical problems (including structural causes of CSF flow restriction) can account for the symptoms
It is crucial to have a qualified informant who is familiar with the patient's premorbid status because memory impairment may be present.
Frontal lobe function is adversely impacted more than memory function (early identification may be possible with objective testing).
Parkinson's disease symptoms like bradykinesia and stiffness are frequently seen.

Clinical examination findings include: decreased step height and length; decreased walking speed (cadence); widened standing base; swaying of the trunk during walking; decreased fine motor speed and accuracy; impaired recall for recent events; impaired ability to perform multistep tasks or interpret abstractions; and useful "get up and go" testing (standing from a chair, walking 10 steps, turning, and returning to start).

Alzheimer disease (which may be a concomitant illness in as many as 75%) is the differential diagnosis.
Parkinson disease, chronic alcoholism, intracranial infection, multi-infarct dementia, subdural hematoma, cancerous meningitis, collagen vascular diseases, depression, syphilis, vitamin B12 insufficiency, and urologic conditions are only a few of the conditions that are mentioned.
Case report pointing to Lyme disease as a potential source of comparable imaging and clinical traits (curable with antibiotic therapy)


Laboratory Results 
Initial examinations (lab, imaging)
Complete blood count, vitamin B12, folate, thyroid-stimulating hormone (TSH), syphilis serology, and metabolic profile

Blood alcohol content and drug abuse analysis
Urine testing
Imaging is crucial for CSF analysis, which includes an opening pressure of less than 245 mm H2O (a value higher than this excludes iNPH by definition).
– As opposed to ventricular enlargement seen in other forms of dementia where brain atrophy is present, computed tomography (CT) or magnetic resonance imaging (MRI) (preferred imaging study) show ventriculomegaly (particularly lateral and 3rd ventricles) with preservation of the cerebral parenchyma. Recent research has demonstrated that a tight convexity, or restricted subarachnoid space, correlates with possible or confirmed iNPH.
– When comparing NPH to other conditions, T1-weighted MRI images combined with the Evans index (the ratio of the width of the lateral ventricles to the maximum internal diameter of the skull) and the callosal angle provide acceptable accuracy (AUC = 0.96). Evans index greater than 0.3 suggests NPH (1).
Diagnostic procedures and other CSF removal help determine the precise diagnosis and forecast surgical treatment outcomes.
High-volume (30 to 70 mL) spinal tap to remove CSF ("tap test") Comparison of gait analysis before and after CSF removal should be performed within 24 hours (a 20% improvement indicates a positive test), especially when combined with concurrent executive function improvement.


No medicine is notably useful for management.
The use of carbonic anhydrase inhibitors (acetazolamide) in conjunction with repeated lumbar punctures has only been reported anecdotally.
Levodopa may be used to rule out Parkinson's disease (NPH will show little to no improvement to dopamine agonist).


Referral 
Consultation with a neurologist or a neurosurgeon is useful in suspected situations when other treatable medical disorders have been ruled out.
Recent cohort studies have shown that clinical improvement occurs after shunt surgeries. At one year after the surgery, gait stability, cognitive scores, and urine continence parameters all improved.

Further Treatments 

Gait training and the use of ambulation aids are advised, but their effectiveness is limited.

Surgical Techniques 
The only available treatment is to implant a ventricle-atrial or ventricle-peritoneal shunt from a lateral ventricle that drains into the right atrium or peritoneal cavity through a tunnel under the skin. Recent research has shown that using a lumbar-peritoneal shunt is noninferior since it is technically simpler and linked to less problems.
Patients with symptoms that have been present for less two years are more likely to have improvement after shunting. Age has not been found to have a deleterious impact on shunting response. Patients who had symptoms for many years but were previously undetected have shown improvement.
 Endoscopic third ventriculostomy is becoming more popular because it eliminates shunt-related postoperative problems like late shunt infection and blockage.

Admission for a scheduled surgical procedure

Follow-Up Evaluation and environment modification for fall hazards
A determination of your capacity to drive safely in a motor vehicle
patient observation

 Conduct additional cognitive tests to assess the dementia's condition after treatment.
Improvements in walking speed and incontinence can both be quantified.

Prognosis 
Deterioration occurs over time in natural history. Inability to walk, stand, sit, or turn over in bed causes the patient's axial skeletal stability to deteriorate.

Complications 
In addition to the standard surgical risks, complications in patients undergoing surgery include cerebral infarcts, bleeding, infection, and seizures. This is because NPH is a disorder that affects people over 65.
Misalignment of the shunt, particularly when symptoms return following successful shunt implantation and infections of the urinary tract, skin deterioration, pressure ulcers, and infections as movement impairment worsen also part of the complications.