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Study decks > Patho - Disorders of Endocrine Disease and Diabetes Mellitus > Flashcards

Patho - Disorders of Endocrine Disease and Diabetes Mellitus Flashcards

1
Q

what is GH?

A

GH is regulated by hypothalamic release of growth hormone-releasing hormone (GHRH) to anterior pituitary gland, liver is the target
-GH increases lean body mass, reduces fat mass, induces liver to
release glucose under conditions of hypoglycemia

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2
Q

what can GH excess lead to?

A

hyperpituitarism
-gigantism (children)
-acromegaly (adults)

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3
Q

what can GH deficiency lead to?

A

hypopituitarism
-dwarfism (decreased linear growth)
-adults = decreased muscle mass but also very vague symptoms

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4
Q

gigantism etiology

A

-primary pituitary adenoma (tumor on gland)
-idiopathic
-radiation
-trauma

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5
Q

gigantism pathogenesis

A

-begins in childhood before epiphyseal (plates) closed
-excessive GH production causes increased linear growth
-associated with hypogonadism (delay puberty) leading to delayed epiphyseal closure

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6
Q

gigantism CM

A

-accelerated growth velocity (>95% pediatric growth chart)
-increased stature, height, linear growth
-untreated, may grow to 8ft tall with increased risk of cardiomegaly and heart failure

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7
Q

acromegaly etiology

A

pituitary tumor (leading to excess GH)

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8
Q

acromegaly pathogenesis

A

-prolonged excess production of GH
-primarily bone and connective tissue
-slow and progressive (insidious)

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9
Q

acromegaly CM

A

-large hands and feet*
-protrusion of lower jaw
-coarse facial features
-signs of osteoporosis
-change in hand, shoe, glove size
-HTN
-arthritis (overgrowth of tissue)
-CAD/CHF
-DM
-enlarged adrenal gland
-amenorrhea (absence of meneses)
-HA
-sweating
-weakness
-deep voice*

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10
Q

what is GH deficiency associated with?

A

-prolonged labor or breech delivery
-chromosomal anomalies
-congenital malformations: midacial abnormalities (cleft lip/palate)
-midline brain tumors
-head trauma
-nystagmus (rapid, uncoordinated eye movement), retinal abnormalities

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11
Q

GH deficiency CM

A

-hypoglycemia
-growth below 3rd percentile
-dental eruption delayed
-irregular setting of permanent teeth
-thin hair, poor nail growth
-greater fat mass, decreased muscle mass, delayed bone formation
-delayed puberty

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12
Q

GH deficiency pathogenesis

A

-decreased/defective GH secretion
-defective generation of or impaired response to somatomedin (impaired mediation)

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13
Q

what happens in antidiuretic hormone disorders?

A

ADH (vasopressin) secreted by posterior pituitary gland in response to changes in blood osmolarity
-ADH acts directly on renal collecting ducts and distal tubules, increasing membrane permeability and reabsorption of water
-ADH regulates that body’s water balance by controlling amount of water reabsorbed by the kidneys
-> disorders = excessive water retention or excessive polyuria

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14
Q

types of diabetes insipidus (hypothalamic, nephrogenic, transient)

A

hypothalamic: unable to secrete/produce ADH, usually r/t trauma
nephrogenic: renal tubules unresponsive to ADH
transient: r/t pregnancy, produced by the accelerated metabolism of ADH

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15
Q

what is diabetes insipidus?

A

lack of vasopressin (ADH) action that leads to inability to concentrate urine and H20, leading to large volume of dilute urine

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16
Q

diabetes insipidus etiology

A

related to insufficiency of ADH – damage to posterior pituitary, head trauma, intracranial tumors, neurosurgery, drugs, pregnancy, idiopathic

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17
Q

diabetes insipidus pathogenesis

A

lack of ADH, decreased water reabsorption in kidneys – may be permanent or transient

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18
Q

diabetes insipidus CM

A

-large volume of dilute urine
-thirst
-increased serum of sodium (b/c concentration isnt eliminated)
-neurological symptoms
-dehydration
-nocturia in adults
-bed wetting in children

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19
Q

what is SIADH?

A

levels of vasopressin (ADH) elevated at times during which physiologic secretion of ADH from posterior pituitary would normally be suppressed
-because the clinical abnormality is a decrease in osmotic pressure of body fluids, the hallmark of SIADH is hypo-osmolality, resulting in hyponatremia. frequently indicator of underlying disease

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20
Q

SIADH etiology

A

abnormal production of ADH, lung tumors, drugs, head surgery/trauma, anesthetics

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21
Q

SIADH pathogenesis

A

excessive secretion of ADH leads to excessive H2O retention leading to hyponatremia and H2O intoxication

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22
Q

SIADH CM

A

-fluid retention
-hyponatremia
-lethargy
-confusion
-cerebral edema
-seizures
-coma
-muscle cramps
-weakness
-decreased urine output
-weight gain

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23
Q

what is hyperthyroidism

A

increased levels of thyroid hormones = increased metabolism
low TSH, high T3 & T4

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24
Q

what is hypothyroidism

A

decreased levels of thyroid hormones = decreased metabolism
high TSH, low T3 & T4

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25
Q

hyperthyroidism etiology (primary, secondary)

A

primary
-autoimmune (Graves disease)
-thyroid tumor/goiter

secondary
-pituitary adenoma
-exogenous thyroid (medications)

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26
Q

hyperthyroidism pathogenesis

A

-thyroid follicular cell hyper function, excess of T3 and T4 (Graves)
-excess secretion of TSH (secondary)

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27
Q

hyperthyroidism CM

A

history
-weight loss
-increased appetite
-nervousness
-heat intolerance
-palpitations
-diarrhea
-irritability
-insomnia

physical
-warm, moist skin
-thin, fine hair
-increased BP, HR
-hyperreflexia
-fine tremor
-eyelid, retraction, lag (eye rolls down)
-enlarged thyroid

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28
Q

graves disease etiology

A

autoimmune or idiopathic

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29
Q

graves disease pathogenesis

A

IgG autoantibodies bind to and stimulate TSH receptors on thyroid. the result is excess production of T3 and T4 which leads to hypermetabolic state. thyroid hyperplasia (enlargement) and hypersecretion (increased production) result

30
Q

thyroid storm and CM

A

-form of life-threatening thyrotoxicosis
-excessive amounts of thyroid hormones acutely released into circulation
-extreme state of hyperthyroidism “hyperthyroidism on steroids”
-presence of excessive thyroid hormone causes rapid increase in metabolic rate

CM
-hyperthermia
-tachycardia
-agitation
-seizures
-exophthalmos (bulging eyes)
-palpitations
-restlessness
-NVD

31
Q

what is goiter

A

-enlargement of thyroid gland in attempt to compensate for inadequate thyroid hormone
-may be present in hyperthyroidism or hypothyroidism
-may be so large that cause respiratory complications
-may be benign or malignant

32
Q

hypothyroidism etiology (primary, secondary)

A

primary (disfunction/distruction)
-autoimmune (Hashimoto Thyroiditis)
-iatrogenic (surgery, RAIU ablation)
-congenital d/t dysgenesis
-iodine deficiency

secondary (what arises from primary)
-pituitary failure
-anti-thyroid medications

33
Q

hyperthyroidism pathogenesis

A

-thyroid follicular cell hyperfuntion (from constant stimulation) and increased T3 and T4 (Hashimoto)
-excess secretion of TSH (secondary pituitary)

34
Q

hypothyroidism CM (infants)

A

-dull appearance, thick, tongue and lips
-prolonged neonatal jaundice
-poor muscle tone
-bradycardia, mottled extremities
-umbilical hernia
-hoarse cry

35
Q

what is Hashimoto’s thyroiditis? pathogenesis?

A

most common form of hyperthyroidism, more common in females over 50

autoimmune inflammation and destruction if thyroid cells

36
Q

Hashimoto’s thyroiditis CM

A

-decreased BMR
-weakness, lethargy, cold intolerance, decreased appetite
-bradycardia, mild/moderate weight gain
-elevated serum cholesterol and triglycerides
-enlarged thyroid, dry skin, constipation
-depression, difficulties with concentration/memory
-menstrual irregularity

37
Q

what is myxedema?

A

-severe hypothyroidism.
-accumulation of proteins in interstitial spaces results in increase of interstitial fluids causing edema.
-altered mental state, altered thermoregulation, hx of precipitating event (trauma, infection/sepsis).
-non-pitting edema commonly in pretibial & facial areas.
-may progress to Myxedema coma (hypothyroid crisis)
-result of severe or prolonged hypothyroidism & may be life-threatening.

38
Q

what is parathyroid gland

A

-serum CA+ levels provide feedback for Parathyroid hormone (PTH) secretion
-PTH maintains normal CA+ levels by increasing bone resorption of CA+, and reabsorption from kidneys and intestines.
So….
-decrease in CA+ = PTH release = bone reabsorption
-elevation in CA+ = suppression of PTH secretion

39
Q

hyperparathyroidism etiology

A

-chief cell adenomas (most common)
-hyperplasia
-renal failure
-idiopathic

40
Q

hyperparathyroidism pathogenesis

A

PTH increases resorption of CA+ and release of phosphorus & CA+ by bones, increases bicarb excretion & decreases acid excretion leading to hypokalemia & metabolic acidosis

41
Q

hyperparathyroidism CM

A

-depression
-paresthesias
-impaired vision
-HTN
-nausea
-renal calculi
-bone pain
-abdominal pain
-bone demineralization
-dehydration
-may be asymptomatic

42
Q

hypoparathyroidism etiology

A

-removal of parathyroid gland during thyroidectomy
-idiopathic
-autoimmune

43
Q

hypoparathyroidism pathogenesis

A

Inability to maintain normal serum CA+ concentrations due to decreased PTH

44
Q

hypoparathyroidism CM

A

-dysrhythmias
-abdominal cramps
-irritability/anxiety
-paresthesias
-muscle spasms
-dry scaly skin
-tetany (twitchiness)
-laryngeal stridor

45
Q

addison disease etiology

A

destruction/dysfunction of adrenal cortex

46
Q

addison disease pathogenesis

A

-destruction of adrenal cortical tissue causes adrenal gland hypofunction -hyposecretion of aldosterone, cortisol & androgens
-decreased aldosterone=loss of Na+ and H20=hypovolemia and hypotension
-K+ retained resulting hyperkalemia

47
Q

addison disease CM

A

-depression, fatigue, decreased libido
-hypotension
-EKG changes
-muscle weakness
-skin hyperpigmentation (bronze look)
-ND
-anorexia
-hyperkalemia
-hyponatremia
-hypoglycemia

48
Q

cushing’s syndrome etiology

A

-pituitary Adenoma
-adrenal adenoma (benign)
-adrenal carcinoma (malignant)
-abnormal ACTH (CA)
-exogenous steroids (common)

49
Q

cushing’s syndrome pathogenesis

A

adrenal cortex hyperfunction results in excess production of cortisol & aldosterone. syndrome caused by chronic exposure to excessive circulating levels of glucocorticoids

50
Q

cushing’s syndrome CM (hx, physical)

A

history:
-weight gain
-fatigue
-oligomenorrhea
-weakness
-easy bruising
-peptic ulcers
-poor wound healing
-decreased libido
-hypokalemia

physical
-central obesity
-muscle wasting
-striae
-hyperglycemia
-hypertension
-hirsutism (excessive hair growth)
-buffalo hump
-acne
-glycosuria (high sugar levels in urine)
-moon face

51
Q

hyperaldosteronism etiology

A

adrenal tumor or excessive circulating renin

52
Q

hyperaldosteronism pathogenesis

A

excessive production & excretion of aldosterone by the adrenal cortex causing Na+ and H20 retention by the kidney

53
Q

hyperaldosteronism CM

A

-HTN
-hypokalemia
-renal damage
-cerebral infarcts (brain infarctions, disruption of blood flow)
-fluid retention
-tetany (muscle spasms)
-electrolyte imbalances
-muscle weakness

54
Q

what is pheochromocytoma? etiology?

A

tumor of adrenal medulla causes excessive production of secretion of catecholamines

neoplasia syndromes

55
Q

pheochromocytoma pathogenesis

A

tumor causes excessive secretion of epinephrine/norepinephrine

56
Q

pheochromocytoma CM

A

-HTN
-agitation
-headache
-palpitations
-tachycardia
-NVD
-polyuria
-tremors

57
Q

diabetes diagnosis criteria

A

-Random glucose > 200 mg with classic signs and symptoms
-OR: fasting glucose > 126 mg, twice
-OR: HbA1C >6.5
-OR: BG>200 mg/dl 2 hrs after a 75-g oral glucose load

58
Q

type 1 DM
type 2 DM

A

Type I DM: Destruction of pancreatic beta cells leads to insulin dependence
-complete insufficiency
-Must have exogenous insulin.

Type II DM: Decrease in beta cell wt or #, or insulin resistance.
-Insulin receptors in target tissues become insensitive or resistant to insulin.
-May be controlled with diet & exercise or oral agents.

59
Q

DM type 1 etiology

A

-Damaged pancreatic B cells by genetic, environment, or immunologic factors
-May be autoimmune
-Absolute insulin deficiency d/t B-cell failure

60
Q

DM type 1 risk factors

A

-Generally in younger, thinner, “acute” onset
-Genetic predisposition
-May effect any age group, 20% develop DM after age 30
-Heredity

61
Q

DM type 1 pathogenesis

A

-Autoimmune destruction of pancreatic B cells causes Insulin deficiency.
-This leads to uncontrolled glucose production by liver & hyperglycemia.
-Glucose spills into urine causing osmotic diuresis & excessive amounts of urine(polyuria).
-Loss of fluids leads to excessive thirst (polydipsia).
Without insulin, body cannot use carbs so uses proteins & fats for energy leading to weight loss.
-Breakdown of nutritional stores leads to excessive hunger (polyphagia).
-Lipolysis (breakdown of fat) produces ketone bodies that lead to acidosis.
-DKA—severe metabolic, fluid, and electrolyte disturbances.

62
Q

DM type 1 CM

A

-Onset may be associated with ketoacidosis.
-Polyuria: d/t osmotic diuresis
-Polydipsia: d/t fluid loss.
-Polyphagia: d/t gluconeogenesis (Breakdown of stored glycogen)
-Wt. loss: Impaired metabolism
-Glycosuria: glucose urine (kidney cannot reabsorb glucose)

63
Q

what is diabetic ketoacidosis?

A

-occurs primarily in type 1 diabetes
-fat metabolism produces ketones leading to acidosis
-results in severe metabolic, fluid, and electrolyte disturbances
-may be life threatening

64
Q

diabetic ketoacidosis precipitating factors

A

-non-compliance
-stress
-infection
-trauma
-pregnancy
-thyroid storm

65
Q

diabetic ketoacidosis CM

A

-abdominal pain
-nausea
-vomiting
-metabolic acidosis
-fruit breath odor
-Kussmaul’s respirations (deep, rapid, regular)
-altered LOC
-coma
-death if untreated

66
Q

DM type 2 etiology

A

-Etiology unknown but obesity is single most important risk factor.
-Decreased tissue sensitivity & responsiveness.
-Genetic predisposition

67
Q

DM type 2 risk factors

A

-Obesity (% body fat)
-H/o gestational DM, HTN, dyslipidemia, high triglycerides
-Sex (female), age, family hx & ethnicity all factors in determining risk
-Sedentary lifestyle

68
Q

DM type 2 pathogenesis

A

Three abnormalities:
1. Resistance of insulin in peripheral tissues, mostly muscle & fat but also liver
-Decreased tissue sensitivity & responsiveness to insulin.
-Decrease in # of insulin receptors
2. Defective insulin secretion in response to glucose stimulus
-Deficiency of insulin related to Beta cell dysfunction
3. Increased glucose production by liver

69
Q

DM type 2 CM

A

-Polyuria
-Polydipsia (excessive thrist)
-Blurred vision
-Weight gain

70
Q

what is nonketotic hyperglycemic hyperosmolar coma?

A

-Extreme hyperglycemia
-Polyuria (excessive urination) in attempt to decrease glucose concentration
-Polyuria leads to profound dehydration and hyperosmotic state
-Neurological manifestations related to hypernatremia

71
Q

hypoglycemia etiology

A

-Insufficient food intake
-Unplanned activity
-Inappropriate insulin or sulfonylurea dose

72
Q

hypoglycemia symptoms

A

-Pallor
-Tremor
-Diaphoresis
-Palpitations & anxiety
-Hunger
-Visual disturbance
-Weakness
-Paresthesias
-Confusion
-Agitation
-Coma
-Death

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