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Showing posts with label Infographics. Show all posts
Showing posts with label Infographics. Show all posts

Lower extremity edema is a multifaceted clinical presentation characterized by the abnormal accumulation

 of interstitial fluid within the subcutaneous tissues of the lower limbs. This phenomenon often manifests

 as visible swelling, which may be pitting or non-pitting in nature, contingent upon its underlying etiology.

 The pathophysiology involves an intricate interplay of increased capillary hydrostatic pressure, reduced

 oncotic pressure, lymphatic obstruction, or enhanced capillary permeability. Etiologies are diverse,

 spanning systemic conditions such as congestive heart failure, chronic kidney disease, and hepatic

 dysfunction, to localized factors like venous insufficiency, lymphedema, or trauma. A meticulous history

 and physical examination, supplemented by diagnostic adjuncts including duplex ultrasonography or

 laboratory investigations, are imperative to delineate the causative mechanism and guide targeted

 intervention.
 


Common features and patterns:
  • Color:
  1. Red or erythematous: Common in inflammatory or allergic reactions.
  2. Purple or purpuric: May suggest vascular or hematologic issues, such as small blood vessel inflammation (vasculitis).
  3. White or hypopigmented: Seen in fungal infections or depigmentation disorders.
  4. Brown or hyperpigmented: May occur in chronic skin conditions or post-inflammatory hyperpigmentation.
  • Texture:
  1. Flat (macular): Rash appears as flat, discolored spots.
  2. Raised (papular or nodular): Bumps that may be small or large.
  3. Scaly or flaky: Seen in psoriasis or fungal infections.
  4. Smooth or shiny: Can occur in viral rashes or early dermatitis.
  • Moisture:
  1. Dry and cracked: Common in eczema or chronic irritation.
  2. Moist or oozing: May suggest infection, blistering, or acute contact dermatitis.
  • Distribution:
  1. Symmetrical: Seen in systemic causes like eczema, psoriasis, or drug reactions.
  2. Localized: Often indicates contact dermatitis or insect bites.
  3. Peripheral patterns: Rashes that concentrate around the edges of the palms can be seen in certain fungal infections.
  • Associated Symptoms:
  1. Itching: Common in eczema, scabies, or allergic reactions.
  2. Pain or burning: Suggests irritation, infection, or vascular issues.
  3. Blisters: Seen in contact dermatitis, hand-foot-and-mouth disease, or bullous skin conditions.
  4. Peeling or desquamation: Seen after infections (e.g., scarlet fever) or in conditions like Kawasaki disease.
  • Causes & Features:
  1. Contact Dermatitis: Red, itchy patches, sometimes with vesicles or blisters.
  2. Atopic Dermatitis: Chronic, itchy, scaly rash; may worsen with exposure to irritants.
  3. Psoriasis: Thick, scaly, silvery patches, often with well-defined edges.
  4. Hand-Foot-and-Mouth Disease: Small, red spots or blisters on palms, soles, and sometimes around the mouth.
  5. Fungal Infections (Tinea Manuum): Asymmetric scaling and redness, often with peeling.
  6. Scabies: Small, red papules with linear burrows, typically between fingers.
  7. Drug Reactions: Diffuse rash that can affect the palms, often accompanied by systemic symptoms.

 

TREMOR

Involuntary, rhythmic, shaking movement of part of the body

Occur when muscles repeatedly contract and relax.

Classification:

  • Physiologic (Normal)
  • Abnormal (Pathologic)
  • Essential (Hereditary disorder)
  • Cerebellar (Damage to cerebellum)
  • Secondary (medication, or substance use, etc.)
  • Psychogenic (Psychologic factors)


 

Individualize BP-lowering therapy and treatment targets in people with frailty, high risk of falls, very

 limited life expectancy, or symptomatic postural hypotension.

Treatments that delay progression of CKD with a strong evidence base include RASi and SGLT2i. In

 people with CKD and heart failure, SGLT2i confer benefits irrespective of albuminuria.

Initial dips in eGFR are expected following initiation of hemodynamically active therapies, including both

 RASI and SGLT2i. GFR reductions of ≥30% from baseline exceed the expected variability and warrant

 evaluation.

CKD is not a contraindication to an invasive strategy for people with acute or unstable heart disease.

 Imaging studies are not necessarily contraindicated in people with CKD and the risks and benefits should

 be determined on an individual basis.

  • A substance is more radiopaque if it contains atoms of high atomic number (AN) such as calcium, iodine, barium, or lead.
  • Bone, which contains calcium (AN 20), is more radiopaque than soft tissue, which is made up mostly of carbon (AN 6), hydrogen (AN 1), and oxygen (AN 8). 
  • Iodine (AN 53) is the key constituent of radiocontrast material and lead (AN 82) is an effective barrier to x-rays.


The eye is very complex and contains various tissues and structures that work together to provide vision.

 Eye problems can range from benign, self-resolving processes to malignant, and possibly metastatic

 tumors. Eye disorders can be caused by various factors, resulting in various signs and symptoms. They

 can be as trivial as minor irritation or pain all the way to blurred vision or blindness. Strabismus is a

 visual disorder in which the eyes are misaligned and point in different directions. When the eyes are

 misaligned, typically one eye will fixate on objects of interest while the other eye turns in (esotropia), out

 (exotropia), down (hypotropia), or up (hypertropia).



  • Monitor for changes in BP, serum creatinine, & serum K+ within 2–4 weeks of initiation or increase in the dose of an ACEi or ARB. 
  • Continue ACEi or ARB therapy unless serum creatinine rises by > 30% within 4 weeks following initiation of treatment or an increase in dose.
  • FDA recommends, metformin should NOT be used with serum creatinine ≥ 1.5 mg/dl in men & ≥ 1.4 mg/dl in women or with decreased creatinine clearance in people > 80.
  • Recommended is treating patients with T2D, CKD, & an eGFR ≥ 30 ml/min per 1.73 m2 with metformin.


ADA/KDIGO Consensus Statements:


All patients with Type 1 diabetes or Type 2 diabetes and CKD should be treated with a

comprehensive plan, outlined and agreed by health care professionals and the patient 

together, to optimize nutrition, exercise, smoking cessation, and weight, upon which are

layered evidence-based pharmacologic therapies  aimed at preserving organ function and 

other therapies selected to attain intermediate targets for glycemia, blood pressure, and lipids.


Myocardial Infarction:

Classified into 5 types based on etiology and circumstances:

  • Type 1: Spontaneous MI caused by ischemia due to a primary coronary event (eg, plaque rupture, erosion, or fissuring; coronary dissection).
  • Type 2: Ischemia due to increased oxygen demand (eg, hypertension), or decreased supply (eg, coronary artery spasm or embolism, arrhythmia, hypotension).
  • Type 3: Related to sudden unexpected cardiac death. 
  • Type 4a: Associated with percutaneous coronary intervention (signs and symptoms of myocardial infarction with cTn values > 5 × 99th percentile URL). 
  • Type 4b: Associated with documented stent thrombosis. 
  • Type 5: Associated with coronary artery bypass grafting (signs and symptoms of myocardial infarction with cTn values > 10 × 99th percentile URL).

Infarct location

  • Right ventricular infarction usually results from obstruction of the right coronary or a dominant left circumflex artery; it is characterized by high RV filling pressure, often with severe tricuspid regurgitation and reduced cardiac output.
  • An inferoposterior infarction causes some degree of RV dysfunction in about half of patients and causes hemodynamic abnormality in 10 to 15%. RV dysfunction should be considered in any patient who has inferoposterior infarction and elevated jugular venous pressure with hypotension or shock. RV infarction complicating LV infarction significantly increases mortality risk.
  • Anterior infarcts tend to be larger and result in a worse prognosis than inferoposterior infarcts. They are usually due to left coronary artery obstruction, especially in the anterior descending artery; inferoposterior infarcts reflect right coronary or dominant left circumflex artery obstruction.

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 “cholÄ“” 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%.

 

 


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.


"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.

 

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

     

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.


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.

                                                          

 

  • 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.



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.

 


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.


 

 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.


  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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