Looks like no one added any tags here yet for you.
T3 and T4
Both T3 and T4 are 99.5% bound to plasma proteins, mainly thyroid-binding globulin and albumin.
T3 activity
T3 activity is 5-10x greater than T4 activity.
T4
T4 is the main negative feedback hormone.
Central diabetes insipidus
An ADH deficiency leads to the condition known as central diabetes insipidus, characterized by polyuria, polydipsia, headaches, and other symptoms.
Polyuria
Increased urine production.
Polydipsia
Increased thirst.
Headache
A symptom of central diabetes insipidus.
Increased plasma osmolarity
A consequence of central diabetes insipidus.
Seizures
Can occur due to central diabetes insipidus.
Hormones working together
Hormones typically work in concert to produce a desired effect or physiologic outcome.
Exponential response
Hormones working together can produce effects 5x greater than what they would alone.
IGF-1
Most of the effects of GH are mediated by the production of IGF-1, which is produced after GH binds the GH receptor on the cell membranes of liver cells.
GH
Growth hormone.
IGF-1
Insulin-like growth factor 1, mediated by STH.
Estrogen
Estrogen is the dominant hormone in the follicular phase of the menstrual cycle, inhibiting FSH release, promoting endometrial thickening, and promoting the LH surge.
FSH
FSH levels increase during the follicular phase for growth/development.
LH surge
Estrogen promotes the LH surge during ovulation, necessary for follicular maturation and ovulation.
Corpus luteum
Estrogen is secreted by the corpus luteum in the luteal phase, but progesterone is the main hormone secreted by the corpus luteum in the luteal phase.
Insulin in liver
Insulin in the liver increases glucose uptake, lipogenesis, glycogenesis, and decreases glucose output, gluconeogenesis, and glycogenolysis.
Insulin resistance
Insulin resistance is the failure of normal amounts of insulin to elicit the expected response.
Sulfonylureas
Sulfonylureas act on SUR to inhibit ATP-sensitive K+ channels and stimulate insulin secretion from pancreatic β-cells.
GLP-1 receptor agonists
Long-acting GLP-1 receptor agonists act on incretin receptors on pancreatic β-cells to increase cAMP levels and stimulate insulin secretion.
DPP-4 inhibitors
DPP-4 inhibitors inhibit the enzyme DPP-4, increasing GLP-1 levels in type 2 diabetes.
Prandial state
In the prandial state, pancreatic β-cells secrete insulin, promoting glucose uptake, glycogenesis, and lipogenesis.
Metformin
The main clinical benefit of metformin is reduced glucose production by the liver, inhibiting gluconeogenesis and improving insulin sensitivity.
Vitamin D metabolism
In CKD, the kidneys are unable to convert inactive vitamin D to active vitamin D, leading to deficiency.
Myxedema coma
Pharmacological management of myxedema coma includes IV glucocorticoid, levothyroxine ± liothyronine IV, and supportive care.
Vascular access techniques
Native arteriovenous (AV) fistula, synthetic AV graft, and venous catheters are used for hemodialysis, each with different longevity and complications.
Overflow incontinence
Medications that exacerbate overflow incontinence include alpha-adrenergic agonists and anticholinergics.
Intradialytic hypotension
Intradialytic hypotension is treated and prevented through patient positioning, fluid and electrolyte administration, changing dialysis settings, and the use of midodrine.
Prerenal, intrinsic, and postrenal AKI
Differentiate between prerenal, intrinsic, and postrenal acute kidney injury based on the underlying causes.
Medications to discontinue in AKI with low blood pressure
ACEI/ARBs, NSAIDs/COX-2 inhibitors, and diuretics should be discontinued in patients with AKI and low blood pressure.
Medications needing dose reduction in renal impairment
Various medications, including antimicrobials, acyclovir, chemotherapy drugs, NSAIDs, and immunosuppressants, require dose reduction in renal impairment.
Supportive measures in AKI
Supportive measures in AKI include assessing volume status, using crystalloids for volume depletion and loop diure
Hyperglycemic crisis treatment categories:
undefined
Treatment with isotonic saline bolus followed by infusion.
undefined
Treatment for DKA to correct acidosis, indicated if pH
undefined
IV administration, important but fluids are more pressing, weight-based dosing.
undefined
Patient-specific based on deficiencies.
Sliding scale insulin:
undefined
undefined
undefined
undefined
Inpatient glycemic control goal:
undefined
undefined
Basal insulin initiation for Type 2 DM:
undefined
undefined
10 units/day or 0.1-0.2 units/kg/day.
undefined
undefined
Electrolyte disorders and mineral bone disease in CKD:
undefined
undefined
undefined
undefined
undefined
Uremia in CKD:
undefined
undefined
undefined
undefined
Anemia in CKD:
undefined
undefined
undefined
undefined
Nephrotic syndrome in uncontrolled diabetic nephropathy:
undefined
undefined
undefined
Regulation of glomerular filtration in the glomerulus:
undefined
undefined
Causes of acute renal failure (ARF)/acute kidney injury:
undefined
Decrease in blood flow to the kidneys.
undefined
Damage directly to kidney tubules or parenchyma.
undefined
Obstruction of the renal artery.
Drug-induced nephrotoxicity:
undefined
undefined
undefined
Acid-base disorders:
undefined
Acute and chronic causes.
undefined
Acute and chronic causes.
undefined
Causes mnemonic "MUD PILES."
undefined
Causes mnemonic "USED CAR."
undefined
Causes include vomiting and diuretic use.
Hyponatremia:
undefined
Hypovolemic, euvolemic, and hypervolemic causes.
undefined
Typically caused by hyperglycemia.
ADA guidelines for glucose goals:
undefined
Diagnosis of Diabetes:
undefined
undefined
undefined
undefined
undefined