Endocrine Disorders Flashcards

1
Q

Primary Thyroid Disorders

A

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

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2
Q

Secondary Thyroid Disease

A

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

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3
Q

Subclinical Thyroid Disorders

A

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

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4
Q

Hashimoto disease*

A

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

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5
Q

Postpartum thyroiditis*

A

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

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6
Q

Congenital hypothyroidism*

A

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&raquo_space; impaired neurologic development

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7
Q

Thyroid carcinoma*

A

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

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8
Q

Thyrotoxicosis*

A

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

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9
Q

Grave’s Disease*

A
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

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10
Q

Nodular thyroid disease*

A

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

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11
Q

Myxedema Coma*

A

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.

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12
Q

Thyrotoxic Crisis aka Thyroid Storm*

A

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

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13
Q

Name 3 adrenal gland disorders

A

Hyperaldosteronism
Cushing Disease
Addison Disease

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14
Q

Hyperaldosteronism*

A

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&raquo_space; HTN and hypokalemia
  • Increased aldosterone» water and sodium retention&raquo_space; increased blood volume» HTN
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15
Q

Cushing Disease*

A

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

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16
Q

Addison Disease*

A

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.

17
Q

Diabetes type I

A

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.

18
Q

Diabetes type 2

A

EPIDEMIOLGY: bout 1 in 11 adults have diabetes mellitus (90% have type 2 diabetes mellitus

ETIOLOGY:
Body cannot use insulin properly=INSULIN RESISTANT

19
Q

How can we assess diabetes?

A

Hemoglobin A1c >6.5%
Fasting Plasma Glucose >126 mg/dl
Random plasma Glucose >200mg/dl

20
Q

Hypoglycemia

A

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

21
Q

Diabetic Ketoacidosis (DKA)*

A

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.

22
Q

Hyperosmolar Hyperglycemic Non-ketotic Syndrome (HHS)*

A

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.

23
Q

Treatment of addison disease

A

life time steroid replacement

24
Q

Treatment of cushings disease

A

medication, radiation, surgery

25
Q

Treatment hypothyroid

A

thyroid hormone replacement

26
Q

Treatment hyperthyroid

A

antithyroid drugs, radioactive iodine therapy, surgery

27
Q

Examples primary hypothyroid disease

A
  • iodine deficiency
  • autoimmune
  • postpartum thyroiditis
  • congenital thyroiditis
  • idiopathic