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Endocrine Flashcards

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1
Q

Hyperosmolar

A

(Low ADH) = Low water to particle ratio

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2
Q

Hypoosmolar

A

(High ADH) = High water to particle ratio

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3
Q

SIADH - Syndrome of inappropriate ADH

A

HIGH Level of ADH

Causes:
Tumors - ectopic production of ADH
Meds - narcotics, chemo, hypoglycemics, NSAIDs
Pulmonary disorders - pneumonia
Surgery - unclear reason
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4
Q

SIADH Patho

A

Enhanced renal water retention (CARDINAL FEATURE)

ADH acts in Renal collecting ducts. More ADH means more water reabsorbed.

Dilutional Hyponatremia - More water vs. same amount of salt

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5
Q

SIADH Manifestations

A

result from the Hyponatremic state

Thirst, Impaired taste, Anorexia, Dyspnea on exertion, Dulled sensorium, Serum Na levels rapidly decline, GI symptoms, No peripheral edema, extreme drops cause confusion/muscle twitching/convulsions/neurologic damage

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6
Q

DI - Diabetes Insipidus

A

LOW level of ADH

Causes:
Neurogenic Central DI - Low secretion
Neuro = brain

Nephrogenic DI - inadequate response to ADH by the kidneys
Nephro = kidneys

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7
Q

DI Pathophysiology

A

Partial/Total inability to concentrate urine (reabsorb water)

Water loss leads to:
Hypernatremia - high salt to water ratio
Hyperosmolality - high particle to water ration

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8
Q

DI Manifestations

A

Polyuria - excessive production of urine

Nocturia - waking up to piss

Thirst

Long-term DI: larger bladder capacity and hydronephrosis (dilation/distention of kidney)

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9
Q

Hypopituitarism

A

deficiency of one or more pituitary hormones (TSH, Corticotropin, Substance B, Prolactin)

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10
Q

Hypopituitarism (causes)

A

Inadequate supply of hormones from the pituitary to hypothalamus

Damage to pituitary gland

Inability of pituitary gland to produce hormones

May result from vascular infarction, aneurysm, or tumor

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11
Q

Hypopituitarism (patho)

A

Pituitary gland is very vascular and it sella turcica compartment

affected by inflammation and ischemia

Adenomas can compromise hormone output

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12
Q

Hyperpituitarism

A

hypersecretion of pituitary hormones

Primarily caused by pituitary adenomas

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13
Q

Hyperpituitarism (patho)

A

Local expansion of adenoma

i.e. Impinge on optic chiasm
Impinge on other nerves

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14
Q

Panhypopituitarism

A

deficiency of ALL pituitary hormones

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15
Q

ACTH deficiency

A

(loss of cortisol)

Nausea, vomiting, anorexia, fatigue, decreased urine output, and weakness. Potential death 2 weeks of complete absence of ACTH.

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16
Q

TSH deficiency

A

Cold intolerance, skin dryness, mild myxedema (swelling of skin/underlying tissue), decreased metabolic rate

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17
Q

FSH and LH deficiency

A

Females: Amenorrhea (no period), atrophic vagina, uterus, and breast.

Males: testicular atrophy and beard growth is stunted

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18
Q

GH (growth hormone) deficiency

A

Adults: fatigue, social withdrawal, loss of motivation, osteoporosis, altered body composition

Children: hypopituitary dwarfism

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19
Q

Pituitary adenoma manifestations

A

Manifestations are related to tumor growth and hormone hyper/hypo secretions.

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20
Q

Acromegaly

A

result of continuous hypersecretion of GH

*Almost always caused by GH-secreting adenoma

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21
Q

Acromegaly (patho)

A

GH secretion occurs over time and levels are never lost
If it occurs in children it develops into Gigantism
Connective Tissue proliferation and excess bone growth
High incidence of heart disease, hypertension, atherosclerosis
If untreated, associated with decreased lifespan

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22
Q

Acromegaly (manifestations)

A

Connective tissue proliferation - Large tongue, interstitial edema, enlarged overactive sweat glands, coarse skin and body hair

Bony proliferation - vertebral growth, enlargement of face, hands, and feet. Protruding forehead and lower jaw.

Symptoms of diabetes - polyuria and polydipsia

Hypertension is usually asymptomatic until heart failure symptoms develop

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23
Q

Hyperthyroidism

A

form of thyrotoxicosis in which excess amounts of TH (thyroid hormones) are secreted from the thyroid gland

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24
Q

Hyperthyroidism (causes)

A

Grave’s disease
Toxic Multinodular Goiter
Solitary toxic adenoma

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25
Hyperthyroidism (patho)
Genetic or environmental factors | Residual effects of puberty, pregnancy, or iodine-deficient states
26
Hyperthyroidism (mani)
Ophthalmopathy | Higher metabolism
27
Hypothyroidism
deficient production of TH by the thyroid gland
28
Hypothyroidism (causes)
Autoimmune thyroiditis: gradual inflammatory destruction of thyroid tissue by lymphocytes Congenital hypothyroidism: Infants born w/o thyroid tissue or with hereditary defects in TH synthesis Surgical removal of thyroid Radiation exposure to head and neck
29
Hypothyroidism (patho)
Autoimmune disorder Genetic disorder Medical trauma
30
Hypothyroidism (mani)
Lower metabolism: weight gain constipation cold intolerance
31
Myxedema Coma
related to hypothyroidism diminished consciousness due to severe hypothyroidism medical emergency: hypothermia w/o shivering hypoventilation hypotension Older patients at high risk
32
Graves disease
Autoimmune disease causing of 50-80% of hyperthyroidism Thyroid is stimulated by antibodies called Thyroid-stimulating immunoglobulins
33
Thyrotoxic crisis (Thyroid Storm)
rare emergency where patient suffers severe acute manifestations of hyperthyroidism pts are undiagnosed or partially treated **Hyperthermia, atrial tachycardia dysrhythmia, heart failure, dehydration, nausea and vomiting
34
hypothyroidism
Autoimmune thyroiditis: deficient production of TH due to tissue destruction by lymphocytes Puffy face brachycardia Cold intolerance Edema of extremities
35
Congenital Hypothyroidism
Normal growth is obtained with hormone replacement therapy symptoms after 4 months: difficulty eating protruding tongue hypotonic muscles of abdomen Constipation
36
Hypoglycemia
insulin shock or insulin reaction | *type 1 diabetes = at higher risk
37
Hypoglycemia (symptoms)
pallor, tremor, anxiety, tachycardia, palpitations, diaphoresis, headache, dizziness, irritability, fatigue, poor judgement, confusion, visual disturbance, hunger, seizures and coma
38
Diabetic ketoacidosis (DKA)
serious complication → deficiency of insulin and increase in levels of insulin counterregulatory hormones
39
DKA serum levels
serum glucose level >250 mg/dl serum pH
40
DKA symptoms
Kussmaul respirations, postural dizziness, CNS depression, ketonuria, anorexia, nausea, abdominal pain, thirst, polyuria
41
Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
severe dehydration: loss of electrolytes (potassium) → neurologic changes (stupor)
42
HHNKS serum levels
serum glucose >600 mg/dl serum pH >7.30
43
Somogyi effect
unique combo of hypoglycemia followed by rebound hyperglycemia rise in blood glucose occurs b/c of counterregulatory hormones which are stimulated by hypoglycemia → produce gluconeogenesis
44
Dawn phenomenon
early morning rise in blood glucose concentration w/ no hypoglycemia during night
45
Microvascular: Retinopathy (Nonproliferative)
microaneurysms, capillary dilation, soft and hard exudates, dot and flame hemorrhages, arteriovenous shunts
46
Microvascular: Retinopathy (Proliferative)
formation of new blood vessels, vitreal hemorrhage, scarring, retinal detachment loss of visual activity
47
Microvascular: Retinopathy (Maculopathy)
macular edema loss of central vision
48
Microvascular: Retinopathy (Hyperglycemic lens edema)
shunting of glucose to polyol pathway: hyperosmolar fluid in lens blurred vision
49
Microvascular: Retinopathy (Cataract formation)
chronic hyperglycemia | decreasing visual acuity
50
Nephropathy
glomerular basement mbn thickening, mesangial expansion, glomerulosclerosis, focal tubular atrophy; hyperperfusion and hyperfiltration nerve dysfunction and degeneration
51
Neuropathy
oxidative stress, poor perfusion and ischemia, loss of nerve growth factor nerve dysfunction and degeneration
52
peripheral neuropathy
oxidative stress, poor perfusion and ischemia, loss of nerve growth factor distal symmetric sensorimotor polyneuropathy w/ glove and stocking loss of sensation; loss of motor nerve function w/ clawed toes and small muscle wasting in hands and flexor muscles; Charcot joints; acute painful neuropathy w/ burning pain in legs and feet
53
autonomic neuropathy
oxidative stress, poor perfusion and ischemia, loss of nerve growth factor heart rate variability and postural hypotension; gastroparesis and diarrhea; loss of bladder tone, urinary retention, risk for bladder infection, ED and impotence in men
54
Neuropathy (skin and foot lesions)
loss of sensation, poor perfusion, suppressed immunity, increased risk of infection high risk for pressure ulcers and delayed wound healing; abscess formation; development of necrosis and gangrene, particularly of toes and foot; infection and osteomyelitis
55
Macrovascular (Cardiovascular)
endothelial dysfunction, hyperlipidemia, accelerated atherosclerosis, coagulopathies hypertension, CAD, cardiomyopathy, heart failure
56
Macrovascular (cerebrovascular)
endothelial dysfunction, hyperlipidemia, accelerated atherosclerosis, coagulopathies increased risk for ischemic and thrombotic stroke
57
Macrovascular (Peripheral vascular )
endothelial dysfunction, hyperlipidemia, accelerated atherosclerosis, coagulopathies claudication, nonhealing ulcers, gangrene
58
Infection
impaired immunity, decreased perfusion, recurrent trauma, delayed wound healing, urinary retention wound infections, UTI’s, increased risk for sepsis
59
Cushing syndrome
refers to clinical manifestations resulting from chronic exposure to excess cortisol
60
cushing disease
refers to excess endogenous secretion of ACTH
61
ACTH-dependent
overproduction of pituitary ACTH by pituitary adenoma or by ectopic secreting non pituitary tumor (small cell carcinoma of lung)
62
ACTH-independent
caused by cortisol secretion from rare benign or malignant tumor of one or both adrenal glands
63
Adrenal Cortex Dysfunction (mani)
weight gain (most common) → results from accumulation of adipose tissue in trunk, facial and cervical areas → “truncal obesity”, “moon face”, “buffalo hump”
64
Adrenal Cortex Dysfunction (patho)
1) normal diurnal or circadian secretion patterns of ACTH and cortisol are lost; 2) there is no increase in ACTH and cortisol secretion in response to a stressor
65
hyperaldosteronism
characterized by excessive aldosterone secretion by adrenal glands
66
primary hyperaldosteronism
promotes: increased renal sodium and water reabsorption w/ corresponding hypervolemia and hypertension; renal excretion of potassium extracellular fluid volume overload, hypertension and suppression of renin secretion are characteristic of primary disorders **hypertension and hypokalemia (hallmark manifestations)
67
secondary hyperaldosteronism
results from extra-adrenal stimulus of aldosterone secretion → most often angiotensin II through renin-dependent mechanism Patho: effect of increased extracellular volume on renin secretion varies **hypokalemic alkalosis, changes in myocardial conduction and skeletal muscle alterations may be seen (particularly w/ severe potassium depletion)
68
Addison disease
low levels of cortisol secretion either because of inadequate stimulation of the adrenal glands by ACTH or a primary inability of the adrenals to produce and secrete the adrenocortical hormones
69
Addison disease (patho)
primary adrenal insufficiency ``` Rare, most common in adults (30-60), more common in women autoimmune mechanisms that destroy adrenal cortical cells Chronic infections (TB) primary cause in underdeveloped countries ``` inadequate corticosteroid and mineralocorticoid synthesis elevated serum levels of ACTH (loss of negative feedback)
70
Addison disease (mani)
mild to moderate hypocorticolism: weakness and easy fatigability skin changes: hyperpigmentation and vitiligo anorexia, nausea, vomiting, and diarrhea development of hypotension that can lead to complete vascular collapse and shock
71
pheochromocytomas
tumor of the adrenal medulla: adrenomedullary hyperfunction chromaffin cell tumors rare, about 10% malignant
72
pheochromocytomas (patho)
excessive production of catecholamines because of autonomous secretion of the tumor
73
pheochromocytomas (mani)
persistent hypertension, headache, pallor, diaphoresis, tachycardia, and palpitations HTN results from increased peripheral vascular resistance acute episodes of HTN related to hypersecretion of catecholamine levels in the blood (affects cerebral blood flow) hypermetabolism and sweating related to chronic activation of sympathetic receptors in adipocytes hepatocytes, and other tissues glucose tolerance (catecholamine-induced inhibition of insulin release can be very vascular, rupture, and cause massive and potentially fatal hemorrhage
74
Hyperparathyroidism
hypersecretion of Parathyroid hormone (PTH) and hypercalcemia (hypophosphatemia) Muscular problems Headache, nausea, vomiting Fatigue, anorexia, depression Kidney stones (due to hypercalcemia in urine)
75
Primary Hyperparathyroidism
hypersecretion of Parathyroid gland itself usually due to adenoma
76
Secondary Hyperparathyroidism
hypersecretion in response to hypocalcemia
77
Hypoparathyroidism
hyposecretion of PTH and hypocalcemia (hyperphosphatemia) Dry skin, hair loss Bone deformities Low nerve excitement threshold muscle spasms, seizures, hyperreflexia

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