Electrolyte imbalances are common findings in many diseases. The kidney is a principally responsible organ for retention and excretion of electrolytes and fluids. But other mechanisms like hormonal interactions of antidiuretic hormone, aldosterone, and parathyroid hormone, and factors such as physiological stress play important roles in regulating fluid and electrolyte balance.
Electrolyte imbalances have a very broad range of signs and symptoms, from being completely asymptomatic to having fatal arrhythmias. The coexistence of one or more electrolyte imbalances in individuals with mixed medical conditions can create a complex clinical presentation. However, typically, each electrolyte imbalance presents with signs and symptoms that are more indicative of the specific imbalance.
Satyendra Dhar MD, @DharSaty
#Hyponatremia #hypokalemia
#hypocalcemia #hypophosphatemia
#hypernatremia #hyperkalemia
#hypercalcemia #hyperphosphatemia #electrolytes #electrolyte #algorithm
Pseudogout: pathogenesis and clinical findings
- Idiopathic (vast majority of cases) -> Mechanism unknown
- Familial chondrocalcinosis -> Overactivity of the NTPPPH enzyme and mutations in the ANKH gene, Incr pyrophosphate production
- Hyperparathyroidism -> Incr levels of parathyroid hormone produced, incr gut Ca2+ absorption
- Hemochromatosis -> Clearance of calcium pyrophosphate dihydrate (CPPD) crystals from joints is inhibited by iron
- Hypomagnesia -> The relative absence of magnesium impairs pyrophosphatase activity, reduces pyrophosphate breakdown
- Hypophosphatasia -> Defective mineralization of calcium and phosphorous in bones
- Chondrocalcinosis, seen on high-resolution ultrasound and/or x-ray
- CPPD Crystals - Positively birefringent (crystals appear blue parallel to axis of polarizer)
- PAINFUL, warm, swollen joint (sudden onset)
- Incr C-reactive protein (CRP); erythrocyte sedimentation rate (ESR)
- Subchondral sclerosis & cysts, joint space narrowing, and osteophytes seen on x-ray
#Chondrocalcinosis #Pseudogout #CPPD #Disease #Signs #Symptoms #Pathophysiology #Diagnosis
Digoxin Pharmacology and Pathophysiology
1) Na/K ATPase Pump - Digoxin works by directly binding to and inhibiting the action of the Na+/K+ ATPase pump. By blocking this pump, those sodium ions are NO longer pumped outside the cell and sodium increase.
2) The Na/Ca Exchanger - When digoxin blocks the Na+/K+ ATPase pump and intracellular sodium concentrations increase, the Na+2/Ca+2 exchanger compensates by becoming inhibited so it won't increase the intracellular sodium concentrations further. As a result, calcium ions are no longer exchanged for sodium and intracellular calcium concentration increases.
This increase of intracellular calcium causes:
- Increased contractility (force of contraction) of the heart
- Decreased heart rate (lengthens phase 4 and phase O of the cardiac action potential)
Watch the Potassium!
- Hyperkalemia (high potassium levels) is a side effect of digoxin toxicity. Since digoxin blocks the action of the Na+/K+ ATPase pump and prevents potassium from entering the cell, serum potassium levels can be elevated with toxic digoxin levels.
- Because digoxin binds to the same site as potassium on the ATPase pump, in states of hypokalemia (or low potassium levels), digoxin can more easily bind to the Na+/K+ ATPase pump (since there's less competition!) - because of this, it's important to make sure potassium levels stay within normal limits so digoxin toxicity isn't worsened.
by Cait E. Kulig, PharmD @CaitEKulig
#Digoxin #Pharmacology #Pathophysiology #cardiology
The crusade against “Ab”Normal Saline continues. This is a non-physiologic fluid that can harm our patients in several ways; however, this post will focus on the harms associated with its Chloride (Cl-) content.
Our Extracellular Fluid (ECF) is dominated by Na+ whose positive charges are balanced by Cl- and HCO3-. Our Intracellular Fluid (ICF) is dominated by K+ and Mg2+ whose positive charges are balanced by anions on proteins and organic phosphates. The ECF and ICF both work together to maintain this electroneutrality. When we infuse Normal Saline, we introduce a high amount of Cl- into the ECF making it more negative. The ICF responds by taking up an anion that, in reality, we actually need to remain in our ECF, HCO3-. Progressive loss of HCO3- inevitably leads to Metabolic Acidosis.
Metabolic Acidosis (H+) is a problem. It disrupts the activities of essentially all our vital organs leading to derangements in function. As acidemia worsens and (H+) accumulates in the ECF, the ICF tries to help out by taking up H+ to buffer against the drop in pH. However, for the ECF and ICF to remain electrically neutral, the ICF must now lose a positive charge of its own so in exchange for H+, K+ leaves the ICF and enters the ECF to maintain electroneutrality in both compartments. This is concerning as a too much K+ in the ECF causes Hyperkalemia, a complication which can easily be fatal if not immediately addressed.
Normal saline has been associated with an increased risk of renal failure possibly requiring dialysis or CRRT. The high CL- content induces renal vasoconstriction of the afferent arteriole which reduces renal blood flow and perfusion. Studies have correlated this even in healthy volunteers showing reduced renal blood flow with saline infusions. Many of the patients we are all treating are far from healthy, I’ll leave it to your imagination then to think of the possible outcomes.
Balanced crystalloids like LR are safer, more physiologic, and thus easier to use. The only thing “Normal” about saline is when we take it off a patients MAR.
#foamed #criticalcare #management #diagnosis #treatment #pharmacology #physiology #crystalloids
Common MRI Sequences - Basic MRI Brain Interpretation
• T1 Sequence - T1 is for anatomy. Since it’s anatomic, brain structures will reflect the same color as real life. So gray matter is gray on T1 & white matter is white on T1. So if you see an image where gray is gray & white is white—you know it’s a T1.
• T1 with Contrast - T1 is also for contrast. Contrast material helps us to see masses. Contrast can’t get into normal brain & spine bc of the blood brain barrier- but masses don’t have a blood brain barrier, so when you give contrast, masses will take it up & light up, making them easier to see.
• T2 Sequence - T2 sequences are water sensitive sequences. What is pathologic water in the brain? Edema! But this edema can be from many things.
• Diffusion Sequence (DWI) - Diffusion is primarily to detect stroke. Acute strokes are bright on diffusion. Not all that is bright on DWI is an acute stroke. This is because all diffusion does is detect how difficult it is for water to move. Anything that makes the space around water crowded and difficult to move will be bright on diffusion imaging. Classically from a stroke - When cells run out of ATP, the Na/K pump stops working & immediately water rushes in from osmotic pressure & the cells swell. These swollen cells fill the interstitium & restrict the movement of water. This is why strokes are bright on DWI! But other things can make it crowded and difficult for water to move. Tumors, hematomas and pus are also bright on diffusion.
• Gradient Sequence - Gradient imaging is sensitive to metals. And what’s the most important metal in body? Iron—bc iron is in blood. So gradient is our blood sensitive sequence. Blood is black on gradient. I remember this bc gradient is for metal—and when I think of metal, I think of blacksmiths forging metal products. So BLACKsmith=metal is BLACK on gradient. But other metals will be black too. Notably, calcium, which is in our bones and in many other lesions.
By Lea Alhilali, MD @teachplaygrub
#MRI #Sequences #Radiology #Neuroradiology #diagnosis #Brain #Interpretation
Rheumatology Workup - Laboratories Studies in Rheumatic Diseases
• Septic arthritis - Gram stain and culture of synovial fluid
• Gout or pseudogout - Compensated polarized light microscopy to examine a drop of synovial fluid for intracellular urate crystals (gout) or calcium pyrophosphate dihydrate crystals (pseudogout)
• Ankylosing spondylitis - Sacroiliac joint radiography to demonstrate bilateral sacroiliitis
• Osteoarthritis - Radiography of the affected joint
• Systemic lupus erythematosus (SLE) - Antinuclear antibody (ANA) test; if positive, test for Smith (Sm) and double-stranded DNA antibodies, which are more specific for SLE but present in only 30% and 60% of SLE patients, respectively
Screening Tests for All Types of Inflammatory Arthritis:
• Erythrocyte sedimentation rate (ESR)
• C-reactive protein (CRP)
• Rheumatoid factor (RF) and cyclic citrullinated peptide (CCP) antibody
• ANAs
RF test should be obtained when rheumatoid arthritis (RA) is considered at least moderately possible.
- Positive in as many as 20% of healthy elderly persons
- CCP antibody testing has higher specificity than the RF test but lower sensitivity
- >95% of patients with SLE have ANAs; thus, a negative ANA result is a strong indicator that SLE is not present.
CRP Level:
• A nonspecific measure of inflammation and is obtained as an alternative to obtaining the ESR.
• In contrast to the ESR, the CRP level:
(1) Can be measured on frozen serum
(2) Is not influenced by the presence of anemia or hyperglobulinemia
(3) Rises more rapidly in response to an inflammatory stimulus, and (4) may require more time for the laboratory result to be available (i.e., more than 24 hours, as opposed to 1 hour for the ESR).
Screening Tests for Acute Polyarthritis:
• Blood cultures
• Antistreptolysin O titer
• Parvovirus B-19 immunoglobulin G (IgG) and immunoglobulin M (IgM) levels
• Hepatitis B serology
• ANAs
• Additional tests: HIV test, a rubella titer, ACE level, CXR, ANCA test
Screening Tests for Chronic Polyarthritis:
• Complete blood count (CBC)
• ESR and CRP level
• ANAs
• RF and CCP antibody
• Chemistry profile, including liver function tests (LFTs) and a serum creatinine level
• Serum uric acid level
• Urinalysis
• Others – to consider: TSH level, serum ferritin level, and iron saturation of serum transferrin
Screening Tests for Diffuse Arthralgias and Myalgias:
• ESR and CRP level to exclude inflammatory disease (e.g., polymyalgia rheumatica)
• Creatine kinase and aldolase level to exclude myositis
• Thyroid testing
• Chemistry profile (e.g., calcium, phosphorus, electrolyte, glucose, and total protein) to exclude metabolic or endocrine disorders
Additional Tests for Diffuse Arthralgias and Myalgias:
• 25-hydroxy vitamin D level (in elderly housebound individuals, to exclude osteomalacia)
• Sacroiliac joint radiography (to exclude ankylosing spondylitis, especially in women younger than 45 years with neck, chest wall, and low back pain)
• HLA-B27 (to support a diagnosis of reactive arthritis)
• Hepatitis B and C serology testing
• Serum and urine protein electrophoresis (to exclude multiple myeloma)
• ANA and RF (if clinical features suggest RA, SLE, or another connective-tissue disease)
#Rheumatic #Disease #Rheumatoid #Arthritis #laboratory #workup #diagnosis #testing #Rheumatology
Diabetes Morning Hyperglycemia - Dawn Phenomenon vs Somogyi Effect
When patients FBG's are elevated each morning despite attempts at adjusting medication therapy, it's a good idea to assess the situation to determine if patient is experiencing the normal dawn phenomenon, or if they are actually experiencing Somogyi effect. Both are characterized by morning hyperglycemia, but they are for opposite reasons. All patients (even those without diabetes) experience dawn phenomenon, where the natural changes in growth hormones and insulin levels causes a natural hyperglycemia in the mornings. In patients without diabetes, the pancreas can adjust and release insulin to control the blood sugar. Although rare and not strongly evidenced, it's still good to know about the idea of Somogyi effect. This is when patients experience hypoglycemia in the late nights, and wake up with hyperglycemia as the body's overcompensating response to the hypoglycemia. If a patient actually does experience this, it's important to adjust or decrease the medication to prevent the night hypoglycemia, which would then resolve the morning hyperglycemia. ----
Although there is evidence disproving the Somogyi effect, I have had a patient in which I found them to be experiencing what I think was Somogyi effect. I ended up decreasing their evening insulin dose which actually ended up decreasing their morning FBG. This could have been from other reasons unknown to me since they did not have a CGM at the time for me to fully assess, but maybe? Have you experienced this in your practice?
Jarred Prudencio, PharmD - https://www.instagram.com/ambcarerx
#Dawn #Phenomenon #Somogyi #Effect #Fasting #Diabetes #Hyperglycemia #Diagnosis #Management #Endocrinology
