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ECOS Spring > Endocrine 1 and 2 > Flashcards

Endocrine 1 and 2 Flashcards

1
Q

Risk factors for Metabolic syndrome

A

Central adiposity- obesity Sedentary lifestyle genetics aging T2 DM Cardiovascular disease Lipid abnormalities

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2
Q

clinical presentation of elevated glucose

A

polyuria polydypsia polyphagia rapid weight loss increased hunger/weight gain recurrent UTIs tingling pain numb extremities

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3
Q

Criteria for diagnosis of T2 diabetes?

A

HbA1c >6.5% Fasting glucose >126 2 hr glucose >200 random glucose test >200

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4
Q

Diabetic foot exam?

A

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

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5
Q

complications in other organs with poorly controlled diabetes T2?

A

eye kidney NS Cardiovascular Skin Teeth Genitourinary

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6
Q

Clinical presentation of T1DM.

A

Polydipsia Polyuria Blurry vision Fatigue/Weakness Weight loss with hyperglycemia and ketonemia DKA-initial presentation 20/25%

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7
Q

differentiate T1 and T2 diabetes.

A

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
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8
Q

What is severe hyperglycemia and what disorders can come with this?

A
  • 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
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9
Q

How do you manage DKA and HHS?

A

Admit to hospital, generally need IV fluids, insulin and potassium replacememt. DO NOT treat as outpatient.

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10
Q

Acute disorders with diabetes- what is Hypoglycemia?

A
  • 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
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11
Q

What are the cholinergic and adrenergic responses to hypoglycemia? If nothing is done about these what are the consequences?

A

Cholinergic:

  • sweat, hunger, parasthesia

Adrenergic:

  • palpitations, tremor, anxiety

Hypoglycemic unawareness, serious cardiovascular morbitdity/mortality. The person no longer feels these affects

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12
Q

WHat is the most common cause of hypothyroidism in the US?

A
  • Hashimoto’s thyroiditis- autoimmune mediated
  • more prevalent in women
  • Insidious onset
  • may or may not have goiter
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13
Q

Hypothyorid symptoms?

A
  • Fatigue
  • Weakness
  • Dry skin
  • Feeling cold
  • Constipation
  • Weight gain
  • Changes in menses
  • Puffy hands feet fafce (myxedema)
  • Diffuse alopecia
  • Hyporeflexia
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14
Q

What will the lab results be for a person with Hypothyroidism?

A
  • TSH will be elevated and T4 will be low
    • low T4=primary hypothyroidism
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15
Q

Management for hypothyroidism?

A
  • Replace hormone with thyroxine (T4)
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16
Q

Causes of Hyperthyroidism?

A
  • Graves disease
    • most common cause in the US, autoimmune
  • Toxic multinodular goider
  • Toxic adenomas
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17
Q

Graves disesase signs?

A
  • 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

18
Q

Lab results for hyperthyroidism? Management?

A
  • TSH decreased
  • High T4 or T3 (Primary Hyperthyroidism)
  • Block thyroid hormone synthesis with anti thyroid drugs
  • Remove thyroid tissue with radioiodine ablation or thyroidectomy
19
Q

Types of thyorid masses?

A
  • 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
20
Q

Parathyroid function & regulation?

A
  • Maintain calcium levels in blood and tissues
  • Incerased calcium decreases PTH
  • Decreased Ca increasess PTH
21
Q

What are two examples of Hormone excess with the parathyroid galnds?

A
  • Primary hyperparathyroidism
  • Hereditary syndromes
22
Q

What is primary hyperparathyriodism?

A
  • Autonomously functioning adenomas are 80% of the causes
  • hyperplasia
  • rarely cancer
23
Q

Primary HPT symptoms?

A
  • Mostly asymptomatic
  • Renal stones
  • Abnormal bones
  • Abdominal moans-pain, N/V, constipation
  • Psychic groans- anxiety depression confusion
  • Neuromuscular symptoms weakness, easy fatigue, atrophy
24
Q

What is the second most common cause of Primary HPT?

A
  • Hypercalcemia of Malignancy
  • usually symptomatic
  • Calcium markedly elevated
25
Q

Labs for Primary HPT and management?

A
  • 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
26
Q

Hypoparathyroidism?

A
  • Most common occurs after damage or removal of PTH during a neck surgery
  • autoimmune pth destruction
  • rarely tissue resistance (psuedohypoparathyroidisim)
27
Q

Hypoparathyroidism signs?

A
  • 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
28
Q

Hypoparathyrodism labs and management?

A
  • 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
29
Q

Mineralocorticoids?

A

Regulate sodium and K handling in the kidney affecting BP and fluid volume

30
Q

Role of Glucocorticoids?

A

Aiding in glucose metabolism inflammatory and immune response to illness or injury and maintenance of BP and cardiac output

31
Q

Regulation of cortisol? disorders?

A

Hypothalamus-CRH

Pituitary- ACTH

Adrenal glands-Cortisol

  • Adrenal insufficiency can be primary or secondary
  • Excess- cushings disease
32
Q

Adrenal insufficiency?

A

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
33
Q

Adrenal insufficiency symptoms in glucocorticod and mineralocorticoid?

A

Glucocorticoid deficiency:

  • fatigue
  • weight loss
  • hypogloloycemia
  • postural hypotension
  • low BP

Minieralocorticoid deficiency:

  • salt craving
  • low BP and postural
  • Hyponatremia
  • Hyerkalemia
  • Hyperpigmentation (primary ONLY)
34
Q

Labs and management of adrenal insufficiency?

A
  • ACTH stimulation then measure cortisol, if abnormally low measure plasma ACTH renin and aldosterone.
  • Primary: replace glucorticoids and mineralocorticoids
  • Secondoary: replace glucocorticoid
35
Q

What is Cushing’s syndrome/disease?

A
  • 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!)
36
Q

Cushing syndrome signs?

A
  • 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
37
Q

Cushings syndrome labs and management?

A
  • 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
38
Q

Mineralocorticoid excess?

A

Aldosteronism: Conn’s syndrome:

  • Most common-adrenal adenomas
39
Q

hallmark of aldosteroniosm?

A

HTN with low potassium and normal sodium

40
Q

Management of aldosteronism?

A
  • Measure plasma renin and aldosterone if abnormal measure adrenal glands
  • Remove unilateral lesions surgically
  • Block excess aldosterone with mineralocorticoid antagonist
41
Q

Pheochromocytoma?

A
  • 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
42
Q

Pituitary tumors?

A
  • 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

ECOS Spring (12 decks)

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