Endocrine 1 and 2 Flashcards
Risk factors for Metabolic syndrome
Central adiposity- obesity Sedentary lifestyle genetics aging T2 DM Cardiovascular disease Lipid abnormalities
clinical presentation of elevated glucose
polyuria polydypsia polyphagia rapid weight loss increased hunger/weight gain recurrent UTIs tingling pain numb extremities
Criteria for diagnosis of T2 diabetes?
HbA1c >6.5% Fasting glucose >126 2 hr glucose >200 random glucose test >200
Diabetic foot exam?
1/yr or each visit inspect for skin breaks red callused areas pallor dryness, palpate for pedal pulses, cap refill, temp, special test for sensation
complications in other organs with poorly controlled diabetes T2?
eye kidney NS Cardiovascular Skin Teeth Genitourinary
Clinical presentation of T1DM.
Polydipsia Polyuria Blurry vision Fatigue/Weakness Weight loss with hyperglycemia and ketonemia DKA-initial presentation 20/25%
differentiate T1 and T2 diabetes.
T1:
- Presents in childhood
- Insulin secretion is deceased or absent
- Normal insulin sensitivity when controlled
- Insulin dependence permanent
- Pancreatic antibioidies
T2:
- Presents at puberty
- Insulin secretion varies
- Sensitivity decreased
- Dependence is variable
- No antibodies
What is severe hyperglycemia and what disorders can come with this?
- Glucose higher than 250 mg/dL
- DKA: (more common type 1) insulin deficiency + glucagon excess leads to gluconeogenesis, glycogenolysis and ketone body formation in liver
- Hyperglycemia hyperosmolar state: (more common type 2) relative insulin deficiency + inadequate fluid intake resulting in severe dehydration
- extra sugar in plasma goes to urine, water followos leading to dehydration, severe electrolye also
How do you manage DKA and HHS?
Admit to hospital, generally need IV fluids, insulin and potassium replacememt. DO NOT treat as outpatient.
Acute disorders with diabetes- what is Hypoglycemia?
- Most commonly caused by drugs to treat DM
- prevalence of 70% in diabetics
- If patient is confused, altered mental status or siezures Glucose should be checked
What are the cholinergic and adrenergic responses to hypoglycemia? If nothing is done about these what are the consequences?
Cholinergic:
- sweat, hunger, parasthesia
Adrenergic:
- palpitations, tremor, anxiety
Hypoglycemic unawareness, serious cardiovascular morbitdity/mortality. The person no longer feels these affects
WHat is the most common cause of hypothyroidism in the US?
- Hashimoto’s thyroiditis- autoimmune mediated
- more prevalent in women
- Insidious onset
- may or may not have goiter
Hypothyorid symptoms?
- Fatigue
- Weakness
- Dry skin
- Feeling cold
- Constipation
- Weight gain
- Changes in menses
- Puffy hands feet fafce (myxedema)
- Diffuse alopecia
- Hyporeflexia
What will the lab results be for a person with Hypothyroidism?
- TSH will be elevated and T4 will be low
- low T4=primary hypothyroidism
Management for hypothyroidism?
- Replace hormone with thyroxine (T4)
Causes of Hyperthyroidism?
- Graves disease
- most common cause in the US, autoimmune
- Toxic multinodular goider
- Toxic adenomas
Graves disesase signs?
- Hyperactivity/irritability
- Heat intolerance
- Palpitations
- Weight loss increased appetite
- Decreased menses
Keys:
- Tachycardia
- Tremor
- Goiter
- Warm moist skin
- Eyelid retraction -exopthalmos
- Hyperreflelxia
Thyroid is diffusely enlarged, firm, not nodular
Lab results for hyperthyroidism? Management?
- TSH decreased
- High T4 or T3 (Primary Hyperthyroidism)
- Block thyroid hormone synthesis with anti thyroid drugs
- Remove thyroid tissue with radioiodine ablation or thyroidectomy
Types of thyorid masses?
- Goiter: enlarged gland result of biosynthetic defects, iodine deficiency, autoimmune
- leads to increaSed TSH stimulating thyroid growth
- Nodular disease: disordered growth of thyroid cells
- benign or malignant growth
- thyroid cancer most common malignancy of endocrine system
- Nodules 3-7% by exam and 50% by ultrasound
- benign or malignant growth
Parathyroid function & regulation?
- Maintain calcium levels in blood and tissues
- Incerased calcium decreases PTH
- Decreased Ca increasess PTH
What are two examples of Hormone excess with the parathyroid galnds?
- Primary hyperparathyroidism
- Hereditary syndromes
What is primary hyperparathyriodism?
- Autonomously functioning adenomas are 80% of the causes
- hyperplasia
- rarely cancer
Primary HPT symptoms?
- Mostly asymptomatic
- Renal stones
- Abnormal bones
- Abdominal moans-pain, N/V, constipation
- Psychic groans- anxiety depression confusion
- Neuromuscular symptoms weakness, easy fatigue, atrophy
What is the second most common cause of Primary HPT?
- Hypercalcemia of Malignancy
- usually symptomatic
- Calcium markedly elevated
Labs for Primary HPT and management?
- Verify Ca, check PTH,
- If abnormally high measure calcium excretion in urine
- Check electrolytes twice to ensure elevation wasn’t a lab error
- Remove PTH glands
Hypoparathyroidism?
- Most common occurs after damage or removal of PTH during a neck surgery
- autoimmune pth destruction
- rarely tissue resistance (psuedohypoparathyroidisim)
Hypoparathyroidism signs?
- Uncontrollable painful spasms in face hands arms feet
- Pins and needls hands feet around mouth
- Chvostek’s sign: tap facial nerve and get facial musle contraction
- Trousseau’s sign: induction of carpal spasm by inflation of sphygmomanometer above systolic for 3 min, results in muscle spasm due to neuromuscular irritablity from hypocalcemia
Hypoparathyrodism labs and management?
- Labs: verify calcium check PTH, if abnormally low measure ca excretion in urine
- Use medicatinos and dietary modification to increase calcium, no PTH replacements available
Mineralocorticoids?
Regulate sodium and K handling in the kidney affecting BP and fluid volume
Role of Glucocorticoids?
Aiding in glucose metabolism inflammatory and immune response to illness or injury and maintenance of BP and cardiac output
Regulation of cortisol? disorders?
Hypothalamus-CRH
Pituitary- ACTH
Adrenal glands-Cortisol
- Adrenal insufficiency can be primary or secondary
- Excess- cushings disease
Adrenal insufficiency?
Primary:
- autoimmune destruction of adrenal gland (Addison’s)
- Destruction of gland by infection hemorrhage infiltration, metastases
- Genetic diseases cause distinct enzymatic blocks in steroidgenesis
Secondary:
- Suppression of HPA axis from too much glucocorticoids exogenously given (most common!)
- Hypothalmus or pituitary failure to release hormones
Adrenal insufficiency symptoms in glucocorticod and mineralocorticoid?
Glucocorticoid deficiency:
- fatigue
- weight loss
- hypogloloycemia
- postural hypotension
- low BP
Minieralocorticoid deficiency:
- salt craving
- low BP and postural
- Hyponatremia
- Hyerkalemia
- Hyperpigmentation (primary ONLY)
Labs and management of adrenal insufficiency?
- ACTH stimulation then measure cortisol, if abnormally low measure plasma ACTH renin and aldosterone.
- Primary: replace glucorticoids and mineralocorticoids
- Secondoary: replace glucocorticoid
What is Cushing’s syndrome/disease?
- Cushing Syndrome =Hypercortisolism, chronic exposure to excess glucocorticoid from any etiology
Causes:
- ACTH dependent: pituitary adenoma producing too much ACTH resulting in excess cortisol (Cushings Disease) could also be ectopic secretion
- ACTH independent: adrenocorticol adenoma or carcinoma
- Iatrogenic: medical use of glucocorticoids for immunosuppression or treatement of inflammatory disorders (most common!)
Cushing syndrome signs?
- Weight gain around abdomen
- moon face, red cheecks
- buffalo hump
- purple stria in abdomen and breasts
- thin arms and legs
- easy bruising, hirituism
- weakness
- abnormal menses
- decreased libido
- emotional lability
- depression
Cushings syndrome labs and management?
- Dexamethasone suppression test and measure cortisol levels
- Measure cortisol directly, either 24 hr urinie excretion or midnight plasma cortisol
- If high measure plasma ACTH
- Remove tumor in adrenal gland, pituitary, etc.
- Block cortisol synthesis with meds
Mineralocorticoid excess?
Aldosteronism: Conn’s syndrome:
- Most common-adrenal adenomas
hallmark of aldosteroniosm?
HTN with low potassium and normal sodium
Management of aldosteronism?
- Measure plasma renin and aldosterone if abnormal measure adrenal glands
- Remove unilateral lesions surgically
- Block excess aldosterone with mineralocorticoid antagonist
Pheochromocytoma?
- Catecholamine producing tumors from symp or parasymp NS. Extremely rare
- Triad of symptoms: palpitations, headache, profuse sweating
- Dominant sign is HTN, usually its episodic
- Management: remove turmor, localize turmor, measure catecholamines or metanephrines in urine or plasma
Pituitary tumors?
- Usually pituitary adenomas
- Common features are headaches and vision loss
- Other symptoms depend on what hormone the tumor is ssecreting
- Evaluate and manage:
- Screen for endocrine functions
- remove tumors
- block hormone excess
- monitor with imaging
