endo final

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:

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Treatment with isotonic saline bolus followed by infusion.

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Treatment for DKA to correct acidosis, indicated if pH

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IV administration, important but fluids are more pressing, weight-based dosing.

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Patient-specific based on deficiencies.

Sliding scale insulin:

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Inpatient glycemic control goal:

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Basal insulin initiation for Type 2 DM:

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10 units/day or 0.1-0.2 units/kg/day.

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Electrolyte disorders and mineral bone disease in CKD:

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Uremia in CKD:

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Anemia in CKD:

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Nephrotic syndrome in uncontrolled diabetic nephropathy:

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Regulation of glomerular filtration in the glomerulus:

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Causes of acute renal failure (ARF)/acute kidney injury:

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Decrease in blood flow to the kidneys.

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Damage directly to kidney tubules or parenchyma.

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Obstruction of the renal artery.

Drug-induced nephrotoxicity:

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Acid-base disorders:

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Acute and chronic causes.

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Acute and chronic causes.

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Causes mnemonic "MUD PILES."

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Causes mnemonic "USED CAR."

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Causes include vomiting and diuretic use.

Hyponatremia:

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Hypovolemic, euvolemic, and hypervolemic causes.

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Typically caused by hyperglycemia.

ADA guidelines for glucose goals:

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Diagnosis of Diabetes:

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