Acute Cholangitis

Legend says that Cholangitis was first defined in 1877 by Jean-Martin Charcot, at which time the

 pathognomonic triad of fever, right upper quadrant pain, and jaundice was described. Today, cholangitis is

 defined as the presence of increased hepatic intraductal pressure with a concurrent infection of the

 obstructed bile.

Chole: Derived from the Greek word “cholē” meaning bile.

Angio: Comes from the Greek “angeion” meaning vessel.

Cholangitis: Bacterial infection of the biliary tree.

The pathogens identified as causative agents of acute ascending cholangitis are gram-negative and

 anaerobic organisms, the most common including Escherichia coli, Klebsiella, Enterobacter,

 Pseudomonas, and Citrobacter.  

Iatrogenic introduction of bacteria commonly occurs post- ERCP in individuals with biliary obstruction.

Charcot triad has a high specificity (95.9%), while sensitivity is low (26.4%).

Tokyo guidelines (2018) have a sensitivity of 100% and specificity of 87.4%.

 

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Pseudo- Conditions in Medicine

 

The term ‘pseudo’ means ‘false’, ‘pretended’, ‘unreal’, or ‘sham’. Likely to be of Greek

origin, pseudes means false. There are a number of ‘pseudo’ terms and syndromes that we see

in the common practice. Even though the meaning of pseudo is unreal or sham, however

several medical conditions/ syndromes are true entities as described above.

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Acute Pulmonary Embolism

"D" sign:

In a physiologically normal heart, LV pressure > RV pressure. When viewing heart in a parasternal short

 axis during systole the LV maintains a circular appearance, bowing the intraventricular septum into the

 right ventricle. A D-shaped left ventricle or flattening of the interventricular septum with a D-shaped

 configuration is a feature described with significant RV overload / right heart strain such as that occurring

 with complications of a sizable pulmonary embolic event.

McConnell's sign:

An echocardiographic finding of segmental right ventricular wall‐motion abnormality with apical sparing,

 is highly specific in acute pulmonary embolism and may guide rapid intervention when other testing is

 not feasible.

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Thyroid storm

 

Thyroid storm is a rare and life-threatening condition characterized by an acute exacerbation of

 thyrotoxicosis (elevated free triiodothyronine or free thyroxine and suppressed thyrotropin) with severe

 clinical symptoms. It often results in multiorgan failure involving one or more organ systems such as the

 central nervous, cardiac, hepatic, pulmonary, respiratory, digestive, and gastrointestinal excretory

 systems.

Specific Strategic Steps for Treatment

• Therapy to control increased adrenergic tone: Beta-blocker
• Therapy to reduce thyroid hormone synthesis: Thionamide
• Therapy to reduce the release of thyroid hormone: Iodine solution
• Therapy to block peripheral conversion of T4 to T3: Iodinated radiocontrast agent, glucocorticoid, PTU, propranolol
• Therapy to reduce enterohepatic recycling of thyroid hormone: Bile acid sequestrant

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Urinalysis & Urine Sodium

     

Theophilus Protospatharius, a seventh-century physician who wrote the first manuscript focused

 exclusively on urine called "De Urinis", determined heating urine would precipitate proteins,

 documenting proteinuria as a disease state. French scholar named Gilles de Corbeil (12th century)

 classified 20 different types of urine, recording differences in urine sediment and color and introduced the

 "matula," a glass vessel in which a physician could assess color, consistency, and clarity.

Following includes the complete analysis of urine:

Visual exam

• Color. 

• Clarity

Dipstick test

• Acidity (urine pH). 

• Bilirubin. 

• Blood (hemoglobin). 

• Glucose. 

• Ketones

• Leukocyte esterase.

• Nitrites. 

• Protein

• Urine specific gravity test. 

Microscopic exam

• Crystals. 

• Epithelial cells. 

• Bacteria, yeast and parasites (infections). 

• Red blood cells (RBC). 

• Urinary casts: 

• White blood cells 

Fractional excretion of Sodium (FE Na).

• [(U Na x P Cr) / (P Na x U Cr)] x 100
• U = Urine, P = Plasma, Cr = Creatinine, Na = Sodium.
• Re-absorption and filtration accounted (Both).
• Should not be used with normal renal function.

Acute Kidney Injury (AKI)

• FE Na < 1%
• Urine sodium < 20 mEq/L.

Acute Tubular Necrosis (ATN)

• FE Na > 2%
• Urine sodium > 40 mEq/L.

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Capnography

CAPNOGRAPHY V/S PULSE OXIMETRYCAPNOGRAPHY 

• Provides a measure of ventilation – or concentration of CO2 exhaled air
• (aka end tidal CO2 or etCO2).
• Not effected by supplemental oxygen.
• Reflects breath-to-breath ventilation.
• Appear not normal if the patient has stopped breathing.
• Apnea or hypoventilation is detected immediately by capnography

PULSE OXIMETRY 

• Measures oxygenation or arterial blood oxygen saturation & pulse rate.
• Detects oxygen deficiency (hypoxia).
• May appear normal even if the patient has stopped breathing.
• Takes time to detect Apnea or hypoventilation.

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Hypoglycemia

Hypoglycemia In Diabetics

Type 1 DM/Type 2 DM,
Kidney disease: insulin not cleared out of circulation well.
Medications for Diabetic.

More frequently:
Meglitinides, 
Sulfonylureas,
Insulin 
Very infrequently:
Metformin,
GLP-receptor agonists,
SGLT-2, and 
DPP-4 inhibitor

Hypoglycemia In Non-Diabetics:

Hormonal dysfunction             

Addison's disease

Hypopituitarism

Non-B cell tumors.

Post-gastric bypass

Insulinomas.

Drugs: 

NSAID’s, phenylbutazone, propoxyphene,  

Quinine 

Lithium, TCA, chlorpromazine,   

Fluoxetine, sertraline,

ACE-inhibitors, arbs, beta-blockers.

Levofloxacin, trimethoprim-sulfamethoxazole, 

Mifepristone, 

Heparin

Mercaptopurine.

Haloperidol, pentamidine, 

Disopyramide, 

isoniazid, methotrexate, 

fenfluramine, thiazide diuretics,        

Opioid analgesic tramadol.

                                                          

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Liver Abscess

 

• Pyogenic abscess, accounts for 80% of abscess.
• Amebic abscess due to Entamoeba histolytica, accounts for 10%.
• Fungal abscess, accounts for < 10%.
• 50% of solitary liver abscesses occur in the right Liver lobe.
• Right hepatic lobe (~75%), less commonly left (20%) or caudate (5%) lobes.
• Pyogenic abscesses are usually polymicrobial.
• 50% of the bacterial cases develop by cholangitis. 
• Pyogenic Abscess- initial manifestation of an occult intra‐abdominal malignancy (up to 15%).
• Positive blood cultures in up to 50%.
• Most common organisms: E. coli, Klebsiella, Streptococcus, Staphylococcus, & anaerobes.
• K pneumoniae thought to be associated with colorectal cancer.
• Fever in 90% & abdominal pain in about 50-75%.
• In-hospital mortality estimated at 2.5% -19%

       Drainage of the abscess & antibiotic treatment are the cornerstones of treatment.

• Antibiotic Therapy: 

        If the size of the abscess < 3-5 cm
        Oral antibiotics are given after intravenous antibiotics are first administered. 

• Percutaneous Drainage: 

         Abscess > 5 cm
         Continuous fever despite 48-72 hours of ABX therapy
         Indications that the abscess may rupture
         U/S or CT-guided aspiration & drainage- first-line treatment. 

• Surgery:

          Where percutaneous drainage is impractical.
          When there are complications like rupture or numerous abscesses. 
          Open surgery or laparoscopic surgery.

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Electrolyte Replacement

Significant electrolyte depletion can result in serious complications. These guidelines are meant to assist with empiric dosing of electrolytes for inpatients. Doses may need to be adjusted based on patient-specific factors, including creatine & cardiac status; & responses to initial doses.

• Goal serum potassium concentration 4.0 – 5.0 mEq/L
• Goal serum ionized calcium concentration 1.12 – 1.3 mmol/L
• Goal serum magnesium concentration 2.0 – 2.4 mg/dL
• Goal serum phosphorus concentration 2.7 – 4.6 mg/dL

IV electrolyte replacement can produce life-threatening complications, serious arrhythmias & phlebitis; therefore, supplementation must be carefully monitored.  There are multiple underlying factors for electrolyte disorders in adult inpatients, including alterations in absorption, distribution, hormonal, and/or homeostatic mechanisms that can all cause disturbances. Treating the underlying cause and prescribing adequate therapy is essential for repletion. In addition, the intracellular vs. extracellular electrolyte concentrations must be considered. Due to distribution variances, labs may not directly correlate with true electrolyte levels. Therefore, continuous monitoring is essential to properly replete patients.

 

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Fluid Analysis

A systematic approach to the analysis of the fluid in conjunction with the clinical presentation helps to understand the etiology, narrow the differential diagnoses, & design a management plan. Includes biochemistry, microscopic examinations & infectious disease tests.

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Myasthenia gravis

 

 Chronic, constantly progressive disease. Initially, it affects the muscle tissues of the face, then spreads to the trunk. The following types of MG are distinguished:

• Ocular – the nerve endings in the cranial region are affected, and the eyelids fall asymmetrically. The patient complains of double vision and deterioration in visual acuity. Gradually focusing on one subject becomes difficult.
• Bulbar – the lesion extends to the masticatory muscles and tissues of the larynx. The patient’s voice changes, speech becomes quieter and nasal. Some consonants are very difficult to pronounce, and stuttering develops. Due to the penetration of fluid into the respiratory tract, the risk of pneumonia increases.
• Lambert-Eaton – the muscles of the arms, legs, and neck do not receive nerve impulses. It is difficult for the patient to coordinate these areas of the body. This form is diagnosed in the elderly and is characterized by rapid progression.
• Generalized – the muscles of the eyes are immediately affected, then the process spreads to the larynx, arms, legs, and hips. The main danger of this form is that the respiratory muscles are affected over time.

The disease is characterized by constant progression. 

Plasma exchange (PLEX) is first-line for severe exacerbation & usually causes improvement in a few days. It directly removes anti-acetylcholine receptor antibody from the body. May be more effective in MuSK+ patients.

IVIG may be useful for less severe exacerbations; takes longer to work (e.g., 2-3 weeks), but the efficacy may be more sustained. The dose of IVIG is 2 grams/kg, usually divided over 2 or 5 days.

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Drug-induced thrombocytopenia

1. Immune-mediated: Some drugs can trigger an immune response in the body, leading to the production of antibodies that attack and destroy platelets. This immune-mediated destruction of platelets is one of the common mechanisms in drug-induced thrombocytopenia. Examples of drugs associated with immune-mediated DITP include certain antibiotics (such as penicillin and sulfonamides), anti-inflammatory drugs (such as nonsteroidal anti-inflammatory drugs, or NSAIDs), and anticonvulsants.

2. Non-immune-mediated: Other drugs can cause thrombocytopenia through non-immune mechanisms, such as direct toxicity to the bone marrow where platelets are produced. Chemotherapy drugs, for example, can suppress bone marrow function and lead to a decrease in platelet production.

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