Scenario 1: Syndrome of Antidiuretic Hormone (SIADH)
A 77-year-old female was brought to the clinic by her daughter who stated that her mother had become slightly confused over the past several days. She had been stumbling at home and had fallen twice but was able to walk with some difficulty. She had no other obvious problems and had been eating and drinking. The daughter became concerned when she forgot her daughter’s name, so she thought she better bring her to the clinic.
HPI: Type II diabetes mellitus (DM) with peripheral neuropathy x 30 years. Emphysema. Situational depression after death of spouse 6-months ago
SHFH: – non contributary except for 40 pack/year history tobacco use.
Meds: Metformin 1000 mg po BID, ASA 81 mg po qam, escitalopram (Lexapro) 5 mg po q am started 2 months ago
Labs-CBC WNL; Chem 7- Glucose-102 mg/dl, BUN 16 mg/dl, Creatinine 1.1 mg/dl, Na+116 mmol/L,
K+4.2 mmol/L, CO237 m mol/L, Cl–97 mmol/L.
The APRN refers the patient to the ED and called endocrinology for a consult for diagnosis and management of syndrome of inappropriate antidiuretic hormone (SIADH).
Question:
1. Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH
An overabundance of the hormone antidiuretic causes a condition known as the syndrome of inappropriate Request Unlock antidiuretic hormone (SIADH). (ADH). The hypothalamus in the brain secretes ADH, which is then stored and released by the pituitary gland. ADH regulates the body’s water balance by releasing excess and storing essential fluids. Due to water retention, electrolyte levels drop when ADH is increased. Hyponatremia, or low salt levels, is a severe consequence of SIADH that may lead to cramps, nausea, vomiting, disorientation, seizures, and death. Hydrocephalus, Guillain-Barre syndrome, multiple sclerosis, AIDS, Rocky Mountain spotted fever, lung cancer, gastrointestinal cancer, genitourinary cancer, lymphoma, sarcoma, asthma, lung infections, cystic fibrosis, medications, anesthesia, hereditary factors, and sarcoidosis are all potential causes of SIADH. Hypoglycemic medicines, antidepressants, antipsychotics, opioids, general anesthetics, chemotherapeutic agents, nonsteroidal anti-inflammatory drugs (NSAIDs), and synthetic ADH are only some of the pharmaceuticals that might trigger SIADH. Our patient’s COPD puts her at risk of developing SIADH. Lexapro, metformin, and ASA are all potential triggers for SIADH, all of which our patient is now taking.
Scenario 2: Type 1 Diabetes
A 14-year-old girl is brought to the pediatrician’s office by his parents who are concerned about their daughter’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with her school activities. She had been seemingly healthy until about 4 months ago when her parents started noticing these symptoms. She admits to sleeping more and gets tired very easily.
PMH: noncontributory.
Allergies-NKDA
FH:- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process
SH: denies alcohol, tobacco or illicit drug use. Not sexually active.
Labs: random glucose 244 mg/dl.
DIAGNOSIS: Diabetes Mellitus type 1 and refers to an endocrinologist for further work up and management plan.
Question
1. Explain the pathophysiology of the three P’s for (polyuria, polydipsia, polyphagia)” with the given diagnosis of Type I DM.
Polyuria is the excessive production of urine. A high blood sugar level has a diuretic effect due to its Request Unlock osmotic nature. Glycosuria occurs when the kidneys’ glomeruli filter more glucose than the renal tubules can reabsorb, leading to excessive water loss.
Polydipsia is a condition characterized by excessive thirst. Intracellular dehydration and hypothalamus stimulation of thirst come from the body’s cells being osmotically drawn to the higher concentration of glucose present in the blood.
Polyphagia is intense or uncontrollable hunger. Cellular deprivation, caused by the breakdown of stored carbs, lipids, and protein, leads to an increase in appetite.
Scenario 2: Type 1 Diabetes
A 14-year-old girl is brought to the pediatrician’s office by his parents who are concerned about their daughter’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with her school activities. She had been seemingly healthy until about 4 months ago when her parents started noticing these symptoms. She admits to sleeping more and gets tired very easily.
PMH: noncontributory.
Allergies-NKDA
FH:- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process
SH: denies alcohol, tobacco or illicit drug use. Not sexually active.
Labs: random glucose 244 mg/dl.
DIAGNOSIS: Diabetes Mellitus type 1 and refers to an endocrinologist for further work up and management plan.
Question
1. Explain the genetics relationship and how this and the environment can contribute to Type I DM.
Autoimmune polyendocrine insufficiency patients’ sera included Request Unlock islet cell autoantibodies (ICAs). Beta cells, which secrete insulin, generate autoantigens that then travel through the body’s circulatory and lymphatic systems. Autoantigen is then presented by antigen-presenting cells after being processed. Type 1 DM is thought to result from a complex interplay between genetic predisposition and environmental factors, although the precise nature of this connection is unclear. Viruses, air pollution, stress, immunizations, microbial ecology, family density, and cow’s milk proteins are all examples of environmental variables. Hyperglycemia, increased thirst and urination, weariness, and a family history of the disease are also present.
Scenario 3: Type II DM
A 55-year-old male presents with complaints of polyuria, polydipsia, polyphagia, and weight loss. He also noted that his feet on the bottom are feeling “strange” “like ants crawling on them” and noted his vision is blurry sometimes. He has increased an increased appetite, but still losing weight. He also complains of “swelling” and enlargement of his abdomen.
PMH: HTN – well controlled with medications. He has mixed hyperlipidemia, and central abdominal obesity. Physical exam unremarkable except for decreased filament test both feet. Random glucose in office 333 mg/dl.
Diagnosis: Type II DM and prescribes oral medication to control the glucose level and also referred the patient to a dietician for dietary teaching.
Question:
1. How would you describe the pathophysiology of Type II DM?
Insulin resistance, poor control of hepatic glucose generation, and the decline in B-cell activity that ultimately leads to Request Unlock B-cell failure are the hallmarks of type II diabetes. The failure of insulin-sensitive tissues to properly react to insulin and faulty insulin release by pancreatic B-cells constitute type 2 diabetes.
In order to maintain a steady blood sugar level, the molecular processes involved in insulin production, storage, and secretion, as well as its detection, are strictly controlled. A metabolic imbalance, and hence the illness, may originate from a malfunction in any of the systems involved. Hyperglycemia, a consequence of insulin resistance, insufficient insulin secretion, and excessive or incorrect glucagon production, characterizes type 2 diabetes mellitus, a constellation of dysfunctions. It’s often linked to being overweight.
Scenario 4: Hypothyroidism
A patient walked into your clinic today with the following complaints: Weight gain (15 pounds), however has a decreased appetite with extreme fatigue, cold intolerance, dry skin, hair loss, and falls asleep watching television. The patient also tearfulness with depression, and with an unknown cause and has noted she is more forgetful. She does have blurry vision.
PMH: Non-contributory.
Vitals: Temp 96.4˚F, pulse 58 and regular, BP 106/92, 12 respirations. Dull facial expression with coarse facial features. Periorbital puffiness noted.
Diagnosis: hypothyroidism.
Question:
What causes hypothyroidism?
The inability of the thyroid gland to produce enough Request Unlock thyroid hormone (TH) is the root cause of hypothyroidism. Due to a lack of thyroid function, TH synthesis drops and TSH and TRH are secreted at higher levels in those with primary hypothyroidism. Thyroiditis, surgical or radioactive therapy for hyperthyroidism that results in thyroid tissue loss, drug side effects, and endemic iodine shortage are the most prevalent causes. Congenital abnormalities in the pituitary or thyroid glands may cause the condition in newborns and young children.