Explain the pathophysiology of the three P’s (polyuria, polydipsia, polyphagia) with the given diagnosis of type 1 DM

Type 1 diabetes is characterized by chronic hyperglycemia. Polyuria refers to excessive urination. Hyperglycemia results in an increased filtered load of glucose in urine. Glucose osmotically pulls water leading to polyuria (McCance & Huether, 2019). On the other hand, polydipsia refers to excessive thirst. As with polyuria, polydipsia is a consequence of hyperglycemia. In an effort to extrude excessive blood glucose, the kidneys lose water as glucose is an osmotically active agent. The resulting loss of body fluid stimulates increased water uptake. Finally, polyphagia refers to excessive hunger. In diabetes, the glucose available can’t enter the cells for energy production due t insulin deficiency. Similarly, excessive loss of glucose in urine stimulates the body to crave for more glucose hence polyphagia (McCance & Huether, 2019).

Explain the genetic relationship and how this and the environment can contribute to type 1 DM

Type 1 DM is a consequence of cell-mediated and autoimmune destruction of the pancreatic beta cells. It is associated with a significant genetic predisposition particularly correlated with the major histocompatibility complex. For instance, polymorphisms of class II HLA genes encoding DR4-DR8, DR3-DR2, and DQ have been isolated in over 90% of patients with type 1 DM (McCance & Huether, 2019). On the other hand, environmental factors such as viral infection trigger an autoimmune response with the production of autoantibodies against glutamic acid decarboxylase, zinc transporter 8, islet cells, and tyrosine phosphatase, which causes progressive destruction of pancreatic beta cells leading to absolute lack of insulin.

How would you describe the pathophysiology of type 2 DM?

Type 2 DM is a consequence of peripheral insulin resistance and beta cell dysfunction. Peripheral insulin resistance stems from a complex interaction of environmental and genetic factors (Galicia-Garcia et al., 2020). For instance, central obesity results in an increase in plasma fatty acids, which interferes with insulin-dependent glucose uptake. Similarly, an increase in serine kinase activity in fat and muscle cells causes phosphorylation of insulin receptor substrate-1 leading to decreased glucose uptake. Finally, the accumulation of islet amyloid polypeptide in the pancreas causes diminished endogenous insulin production (Galicia-Garcia et al., 2020). Ultimately, there is a relative insulin deficiency leading to hyperglycemia.

What causes hypothyroidism

Hypothyroidism stems from low, inadequate production of thyroid hormones. Hypothyroidism results from an array of etiologies. It is termed primary when the abnormality is with the gland itself, while it is central or secondary when the thyroid gland is normal, but there is a pathology with the pituitary gland or hypothalamus. Primary causes of hypothyroidism include iodine deficiency, autoimmune thyroid disease, thyroid surgery, radiotherapy to the neck, and medications such as amiodarone and tyrosine kinase inhibitors (Orlander, 2022). On the other hand, secondary central hypothyroidism can result from a pituitary adenoma, brain/pituitary radiation, Sheehan syndrome, TRH resistance, TRH deficiency, tumors impinging the hypothalamus, and drugs such as opioids, steroids, and dopamine (Orlander, 2022).

References

Galicia-Garcia, U., Benito-Vicente, A., Jebari, S., Larrea-Sebal, A., Siddiqi, H., Uribe, K. B., Ostolaza, H., & Martín, C. (2020). Pathophysiology of type 2 Diabetes Mellitus. International Journal of Molecular Sciences, 21(17), 6275. https://doi.org/10.3390/ijms21176275