Endocrine Disorders Flashcards
Primary Thyroid Disorders
ETIOLOGY: low levels of blood thyroid hormone due to destruction of the thyroid gland. AUTOIMMUNITY/hashimoto; cause has something to do with the thyroid gland itself
CLINICAL MANIFESTATIONS: fatigue lethargy sensitivity to cold depression muscle weakness pain in your joints or muscles constipation brittle hair or nails voice hoarseness puffiness in your face
PATHO:
thyroid does not produce enough T3 or T4
Secondary Thyroid Disease
ETIOLOGY: hypothalamus does not produce enough TRH and then pituitary does not produce TSH
CLINICAL MANIFESTATIONS: Goiter (enlarged thyroid) Fatigue. Weight gain. Cold intolerance. Constipation. Muscle soreness. Joint pain. Brittle nails.
PATHO:
the hypothalamus produces insufficient thyrotropin-releasing hormone (TRH) or the pituitary produces insufficient TSH. Caused by tumors, TBI, or SAH
Subclinical Thyroid Disorders
ETIOLOGY: It’s called subclinical because only the serum level of thyroid-stimulating hormone from the front of the pituitary gland is a little bit above normal
CLINICAL MANIFESTATIONS: depression. constipation. fatigue. goiter (this appears as swelling in the front of the neck due to an enlarged thyroid gland) weight gain. hair loss. intolerance to cold.
PATHO:an early, mild form of hypothyroidism, a condition in which the body doesn’t produce enough thyroid hormones. High TSH and normal T4 and T3
Hashimoto disease*
ETIOLOGY: under active thyroid gland (hypothyroidism); autoimmune; associated with increased risk of thyroid cancer
CLINICAL MANIFESTATIONS: Fatigue and sluggishness cold intolerance Constipation Brittle nails Hair loss ENLARGEMENT OF THYROID Unexplained weight gain Muscle aches, tenderness and stiffness Joint pain and stiffness Muscle weakness Excessive or PROLONGED MENSTRUAL BLEEDING MEMORY LAPSES bouts of hyperthyroidism
PATHO: condition in which your immune system attacks your thyroid; related to HLA-DR5 and HLD DR3
Postpartum thyroiditis*
ETIOLOGY:
autoimmune destruction of thyroid gland within 1 year of giving birth; usually have a hx hypothyroid
MANIFESTATIONS Anxiety Irritability Rapid heartbeat or palpitations Unexplained weight loss Increased sensitivity to heat DIFFUSE, PAINLESS GOITER Fatigue Tremor Insomnia
PATHO: autoimmune: Hyperthyroid phase few months after delivery for up to 8 weeks then body goes Hypothyroidism that can last up to 6 months
Congenital hypothyroidism*
ETIOLOGY: thyroid tissue is absent
CLINICAL MANIFESTATIONS:
JAUNDICE (yellow skin or eyes)
sleeping longer or more often than usual.
constipation
a large soft spot (fontanel) on the head.
large, swollen tongue.
weak ("floppy") muscle tone.
swelling around the eyes.
poor or slow growth.
PATHO:
Results in absent thyroxine»_space; impaired neurologic development
Thyroid carcinoma*
ETIOLOGY:
tumor
CLINICAL MANIFESTATIONS:
A lump (nodule) that can be felt through the skin on your neck
Changes to your voice, including increasing hoarseness
Difficulty swallowing
Pain in your neck and throat
Swollen lymph nodes in your neck
PATHO:
thyroid undergo genetic changes (mutations) which leads cells multiplying and loose ability to die and accumulate»tumor
Thyrotoxicosis*
ETIOLOGY: an excess of thyroid hormone in the body
CLINICAL MANIFESTATIONS:
nervousness, diminished sleep, tremulousness, tachycardia, increased appetite, weight loss, and increased perspiration and signs are goiter, occasionally with exophthalmos, and rarely with pretibial myxedema.
PATHO: you have a low level of thyroid stimulating hormone, TSH, in your bloodstream, which causes your body to make more thyroid hormone which leads to excess
Grave’s Disease*
ETIOLOGY: • A condition that results in elevated thyroid hormone • Increased T3 and T4, decreased TSH Hyperthyroidism women 20-40
CLINICAL MANIFESTATIONS: BULGING EYES (only in Graves' disease) EXOPTHALMUS DERMOPATHY-Thickening and reddening of the skin, especially on the shins and upper feet (only in Graves' disease) Irritability or nervousness. Tiredness or muscle weakness. Heat sensitivity. Trouble sleeping. Rapid and irregular heartbeat. GOITER WEIGHT LOSS DESPITE INCREASED APPETITE
PATHO:
Autoimmune (Type II hypersensitivity)
-thyroid stimulating autoantibodies which causes an excess production of thyroid hormone
Nodular thyroid disease*
ETIOLOGY:
Thyroid nodules are solid or fluid-filled lumps that form within your thyroid
CLINICAL MANIFESTATIONS:
Trouble with swallowing or breathing. Hoarseness or voice change. Pain in the neck.
PATHO:
Overgrowth of normal thyroid tissue, Thyroid cyst., Chronic inflammation of the thyroid, Multinodular goiter., Thyroid cancer., Iodine deficiency
Myxedema Coma*
ETIOLOGY:
Decreased LOC associated with severe hypothyroidism
CLINICAL MANIFESTATIONS:
CONFUSION, DIFFICULTY BREATHING
cold, low temp, weakness
PATHO:
a result of long-standing, undiagnosed, or under treated hypothyroidism and is usually precipitated by a systemic illness.
Thyrotoxic Crisis aka Thyroid Storm*
ETIOLOGY:
life-threatening health condition that is associated with untreated or under treated hyperthyroidism; HYPERMETABOLIC STATE
CLINICAL MANIFESTATIONS: a rapid heartbeat. a high temperature. DIARRHEA and being sick. yellowing of the skin and eyes (jaundice) severe agitation and confusion. loss of consciousness. LIVER FAILURE INSULIN RESISTANCE LID LAG
PATHO:
decrease in thyroid binding proteins, rapid increase in free hormone, and decrease in ability to physiologically compensate
Name 3 adrenal gland disorders
Hyperaldosteronism
Cushing Disease
Addison Disease
Hyperaldosteronism*
ETIOLOGY:
• Excess aldosterone secretion by adrenal cortex which leads to hypertension; ; overproduction from both adrenal glands; rare genetic disorder
CLINICAL MANIFESTATIONS:
headache, facial flushing, arrhythmias (d/t hypokalemia), muscle weakness, constipation
PATHO:
- Excess aldosterone»_space; HTN and hypokalemia
- Increased aldosterone» water and sodium retention»_space; increased blood volume» HTN
Cushing Disease*
ETIOLOGY:
Increased cortisol d/t too much ACTH being produced
-effects women more than men
-ACTH high
CLINICAL MANIFESTATIONS: MID SECTION WEIGHT GAIN MOON FACE; PURPLE STRIAE osteoperosis
PATHO:
pituitary adenoma
• Loss of circadian rhythm of ACTH and cortisol
• Inability to increase ACTH in response to stress
Addison Disease*
ETIOLOGY:
Adrenal insufficiency; destruction of the outer layer of the adrenal glands
chronic adrenal insufficiency d/t atrophy or destruction of adrenal gland and cause deficiency in cortisol and aldosterone
CLINICAL MANIFESTATIONS:
loss of appetite, weight loss, dehydration, fatigue, low blood glucose, low BP
SKIN HYPERPIGMENTATION
SALT CRAVINGS
PATHO:
the immune system attacks the outer portion of the adrenal glands (the cortex), where cortisol and aldosterone are made.
Diabetes type I
EPIDEMIOLGY:
15 per 100,000 people
-sudden onset, polyuria, polydipsia, polyphagia and unexplained weight loss; usually effects 30 year old and less
-INSULIN DEPENDENT
ETIOLOGY: A chronic condition in which the pancreas produces little or no insulin. one of the most common chronic diseases in childhood, is caused by insulin deficiency following destruction of the insulin-producing pancreatic beta cells.
Diabetes type 2
EPIDEMIOLGY: bout 1 in 11 adults have diabetes mellitus (90% have type 2 diabetes mellitus
ETIOLOGY:
Body cannot use insulin properly=INSULIN RESISTANT
How can we assess diabetes?
Hemoglobin A1c >6.5%
Fasting Plasma Glucose >126 mg/dl
Random plasma Glucose >200mg/dl
Hypoglycemia
TIMING OF ONSET:
The timing of onset of symptoms relative to the time of meal ingestion
CLINICAL MANIFESTATIONS:
AMS, tachycardia, palpitations, diaphoresis, tremors
•*Brain needs glucose – this is an emergency
LAB RESULTS:
Glucose <47mg/dl in first 48 hours of life or < 70mg/dl in children and adults
PATHO:
Causes:
•Exogenous: medication, alcohol, exercise
•Endogenous: tumors of pancreas, inherited disorders
•Functions: Hyperalimentation, liver disease
Diabetic Ketoacidosis (DKA)*
TIMING OF ONSET: develop quickly, sometimes within 24 hours
CLINICAL MANIFESTATIONS: polyuria, thirst, polydipsia, kussmaul respirations, ketones in urine
-hyperglycemia, hyperketonemia, metabolic acidosis
LAB RESULTS:
blood pH < 7.3, serum bicarbonate < 18 mEq/L, anion gap > 10 mEq/L and increased serum osmolarity.
serum glucose level greater than 250 mg per dL
PATHO: Relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism. common causes are underlying infection, disruption of insulin treatment, and new onset of diabetes.
Hyperosmolar Hyperglycemic Non-ketotic Syndrome (HHS)*
TIMING OF ONSET: take days or weeks to develop.
CLINICAL MANIFESTATIONS:
fever, BLURRED VISION, extreme thirst, frequent urination, and CONFUSION/HALLUCINATION,
LAB RESULTS:
blood glucose level of 600 mg/dL and low ketone levels are the main factors for diagnosis of HHNS
-EXCESS SUGAR PASSED IN URINE
PATHO:
Elevated levels of counter regulatory hormones (glucagon, catecholamines, cortisol, and growth hormone) initiate HHS by stimulating hepatic glucose production through glycogenolysis and gluconeogenesis, leading to hyperglycemia, intracellular water depletion, and subsequent osmotic diuresis.
Treatment of addison disease
life time steroid replacement
Treatment of cushings disease
medication, radiation, surgery
Treatment hypothyroid
thyroid hormone replacement
Treatment hyperthyroid
antithyroid drugs, radioactive iodine therapy, surgery
Examples primary hypothyroid disease
- iodine deficiency
- autoimmune
- postpartum thyroiditis
- congenital thyroiditis
- idiopathic
