The pt most likely has Polycythemia vera, a myeloproliferative disorder characterized by uncontrolled Erythrocyte production. Pts frequently present with nonspecific symptoms (HA, weakness, diaphoresis), aquagenic pruritus, facial plethora (reddish complexion), and splenomegaly. Associated conditions include PUD (altered mucosal blood flow d/t increased viscosity) and gouty arthritis (higher red cell turnover). Lab studies show increased erythrocyte mass, thrombocytosis, leukocytosis, and low EPO levels.
Polycythemia vera is caused by abnormal transduction of EPO growth signals. EPO receptor has no intrinsic kinase activity and must interact with Janus Kinase 2 (JAK2), a cytoplasmic (non-receptor) tyrosine kinase, to initiate downstream signaling.
"Hot as a hare, red as a beet, dry as a bone, mad as a hatter, blind as a bat, full as a flask, fast as a fiddle."
Toxicity results from inhibition of cholinergic transmission at Muscarinic receptors
S/S: fever, mucosal and axillary dryness, cutaneous flushing, nonreactive mydriasis, delirium and urinary retention as well as decreased bowel sounds and tachycardia
Can be caused by TCAs (amitryptyline) or antihistamines
A 22 yo woman is brought to the ED d/t a day of fever, HA, nausea, vomiting and myalgias that began suddenly last night. This morning, the patient was lethargic, difficult to arouse, and confused. She is an exchange student who came to the US 3 months ago, and her med hx is unknown. Temp is 102.9 F, bp is 100/60 mmHg, pulse is 112 bpm, and resp 18/min. PE shows nuchal rigidity. Skin exam shows petechial rash. Leukocyte count is elevated and LP with CSF gram stain establishes the diagnosis. What is the primary component of the vaccine that could have prevented the patient's current condition? Glucocorticoids are potent stimulators of liver gluconeogenesis and upregulate the synthesis of key gluconeogenic enzymes (PEP carboxykinase, glucose-6-phosphatase). Glucocorticoids also increase hepatic glycogen reserves by increasing expression of glycogen synthase, thereby improving glucose availability during periods of acute stress.
Peripherally, glucocorticoids antagonize the actions of insulin in skeletal muscle, favoring catabolism and proteolysis to provide substrates for gluconeogenesis and glycogenesis in the liver. This can manifest as proximal weakness (glucocorticoid myopathy)
Glucocorticoids are predominantly catabolic, causing muscle weakness, skin thinning, impaired wound healing, osteoporosis, and immunosuppression. However, they increase hepatic synthesis of gluconeogenic and glycogenic proteins to increase glucose availability.
Alzheimer: early, insidious, short term memory loss
- Language deficits, spatial disorientation
- later= personality changes
Vascular: stepwise decline, early executive dysfunction
- deep white matter changes on neuroimaging
Frontotemporal: early personality issues
- apathy, disinhibition, compulsive behavior
- frontotemporal atrophy on imaging
Dementia with lewy bodies: VISUAL hallucinations, spontaneous parkinsonism, fluctuating cognition
NPH: ataxia, incontinence, dilated ventricles
A signal receptor protein in the plasma membrane that responds to the binding of a signaling molecule by activating a G protein.
The receptors that bind glycoprotein hormones (TSH, FSH, LH) contain 3 major domains:
-an extracellular domain responsible for ligand binding
-a transmembrane domain is made up of nonpolar, hydrophobic amino acids (ala, val, leu, ile, phe, tryptophan, met, pro, gly) anchoring the transmembrane region of the protein to the hydrophobic core of the phospholipid layer
-an intracellular domain coupled with heterotrimeric G proteins
Depolarizing neuromuscular-blocking agent that, like ACh, attaches to nicotinic AChR and depolarizes Neuromuscular end plate. Unlike ACh, succinylcholine is not degraded by AChE, resulting in continuous stimulation of the endplate. Thus, succinylcholine-induced depolarization remains isolated to the end plate, resulting in flaccid paralysis. With continuous administration of succinylcholine, the continuous depolarization of the endplate gives way to gradual repolarization as the nAChR becomes desensitized to the effects of succinylcholine. This termed phase II block.Can cause K+ release and life-threatening arrhythmias in pts at high risk for hyperkalemia, including those with burns, myopathies, crush injuries, and denervating injuries or disease. It is a cannabinoid that contains THC. It lasts 1-4 hrs and stimulates cannabinoid receptors (CB1 and CB2) to produce effects on mood, perception and cognition. Produces a mild euphoria with inappropriate laughter, sedation, slowed reflexes, impaired motor coordination, distorted sensory perceptions and cognitive impairment.
Characteristic physiologic signs: conjunctival injection, tachycardia, increased appetite, and dry mouth
Is metabolized in the liver, distributed and stored in lipophilic tissues and slowly released. It remains in the body for a long time, it can be detected in the urine up to 30 days after daily use has ceased.