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Summer Patho > Endocrine > Flashcards

Endocrine Flashcards

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
Q

Hyperthyroidism (patho)

A

Genetic or environmental factors

Residual effects of puberty, pregnancy, or iodine-deficient states

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26
Q

Hyperthyroidism (mani)

A

Ophthalmopathy

Higher metabolism

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27
Q

Hypothyroidism

A

deficient production of TH by the thyroid gland

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28
Q

Hypothyroidism (causes)

A

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

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29
Q

Hypothyroidism (patho)

A

Autoimmune disorder
Genetic disorder
Medical trauma

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30
Q

Hypothyroidism (mani)

A

Lower metabolism:
weight gain
constipation
cold intolerance

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31
Q

Myxedema Coma

A

related to hypothyroidism

diminished consciousness due to severe hypothyroidism

medical emergency: hypothermia w/o shivering
hypoventilation
hypotension
Older patients at high risk

32
Q

Graves disease

A

Autoimmune disease causing of 50-80% of hyperthyroidism

Thyroid is stimulated by antibodies called Thyroid-stimulating immunoglobulins

33
Q

Thyrotoxic crisis (Thyroid Storm)

A

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
Q

hypothyroidism

A

Autoimmune thyroiditis: deficient production of TH due to tissue destruction by lymphocytes Puffy face brachycardia Cold intolerance Edema of extremities

35
Q

Congenital Hypothyroidism

A

Normal growth is obtained with hormone replacement therapy

symptoms after 4 months: difficulty eating
protruding tongue
hypotonic muscles of abdomen
Constipation

36
Q

Hypoglycemia

A

insulin shock or insulin reaction

*type 1 diabetes = at higher risk

37
Q

Hypoglycemia (symptoms)

A

pallor, tremor, anxiety, tachycardia, palpitations, diaphoresis, headache, dizziness, irritability, fatigue, poor judgement, confusion, visual disturbance, hunger, seizures and coma

38
Q

Diabetic ketoacidosis (DKA)

A

serious complication → deficiency of insulin and increase in levels of insulin counterregulatory hormones

39
Q

DKA serum levels

A

serum glucose level >250 mg/dl

serum pH

40
Q

DKA symptoms

A

Kussmaul respirations, postural dizziness, CNS depression, ketonuria, anorexia, nausea, abdominal pain, thirst, polyuria

41
Q

Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)

A

severe dehydration: loss of electrolytes (potassium) → neurologic changes (stupor)

42
Q

HHNKS serum levels

A

serum glucose >600 mg/dl

serum pH >7.30

43
Q

Somogyi effect

A

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
Q

Dawn phenomenon

A

early morning rise in blood glucose concentration w/ no hypoglycemia during night

45
Q

Microvascular: Retinopathy (Nonproliferative)

A

microaneurysms, capillary dilation, soft and hard exudates, dot and flame hemorrhages, arteriovenous shunts

46
Q

Microvascular: Retinopathy (Proliferative)

A

formation of new blood vessels, vitreal hemorrhage, scarring, retinal detachment

loss of visual activity

47
Q

Microvascular: Retinopathy (Maculopathy)

A

macular edema

loss of central vision

48
Q

Microvascular: Retinopathy (Hyperglycemic lens edema)

A

shunting of glucose to polyol pathway: hyperosmolar fluid in lens

blurred vision

49
Q

Microvascular: Retinopathy (Cataract formation)

A

chronic hyperglycemia

decreasing visual acuity

50
Q

Nephropathy

A

glomerular basement mbn thickening, mesangial expansion, glomerulosclerosis, focal tubular atrophy; hyperperfusion and hyperfiltration

nerve dysfunction and degeneration

51
Q

Neuropathy

A

oxidative stress, poor perfusion and ischemia, loss of nerve growth factor

nerve dysfunction and degeneration

52
Q

peripheral neuropathy

A

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
Q

autonomic neuropathy

A

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
Q

Neuropathy (skin and foot lesions)

A

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
Q

Macrovascular (Cardiovascular)

A

endothelial dysfunction, hyperlipidemia, accelerated atherosclerosis, coagulopathies

hypertension, CAD, cardiomyopathy, heart failure

56
Q

Macrovascular (cerebrovascular)

A

endothelial dysfunction, hyperlipidemia, accelerated atherosclerosis, coagulopathies

increased risk for ischemic and thrombotic stroke

57
Q

Macrovascular (Peripheral vascular )

A

endothelial dysfunction, hyperlipidemia, accelerated atherosclerosis, coagulopathies

claudication, nonhealing ulcers, gangrene

58
Q

Infection

A

impaired immunity, decreased perfusion, recurrent trauma, delayed wound healing, urinary retention

wound infections, UTI’s, increased risk for sepsis

59
Q

Cushing syndrome

A

refers to clinical manifestations resulting from chronic exposure to excess cortisol

60
Q

cushing disease

A

refers to excess endogenous secretion of ACTH

61
Q

ACTH-dependent

A

overproduction of pituitary ACTH by pituitary adenoma or by ectopic secreting non pituitary tumor (small cell carcinoma of lung)

62
Q

ACTH-independent

A

caused by cortisol secretion from rare benign or malignant tumor of one or both adrenal glands

63
Q

Adrenal Cortex Dysfunction (mani)

A

weight gain (most common) → results from accumulation of adipose tissue in trunk, facial and cervical areas → “truncal obesity”, “moon face”, “buffalo hump”

64
Q

Adrenal Cortex Dysfunction (patho)

A

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
Q

hyperaldosteronism

A

characterized by excessive aldosterone secretion by adrenal glands

66
Q

primary hyperaldosteronism

A

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
Q

secondary hyperaldosteronism

A

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
Q

Addison disease

A

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
Q

Addison disease (patho)

A

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
Q

Addison disease (mani)

A

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
Q

pheochromocytomas

A

tumor of the adrenal medulla:
adrenomedullary hyperfunction
chromaffin cell tumors
rare, about 10% malignant

72
Q

pheochromocytomas (patho)

A

excessive production of catecholamines because of autonomous secretion of the tumor

73
Q

pheochromocytomas (mani)

A

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
Q

Hyperparathyroidism

A

hypersecretion of Parathyroid hormone (PTH) and hypercalcemia (hypophosphatemia)

Muscular problems
Headache, nausea, vomiting
Fatigue, anorexia, depression
Kidney stones (due to hypercalcemia in urine)

75
Q

Primary Hyperparathyroidism

A

hypersecretion of Parathyroid gland itself usually due to adenoma

76
Q

Secondary Hyperparathyroidism

A

hypersecretion in response to hypocalcemia

77
Q

Hypoparathyroidism

A

hyposecretion of PTH and hypocalcemia (hyperphosphatemia)

Dry skin, hair loss
Bone deformities
Low nerve excitement threshold
muscle spasms, seizures, hyperreflexia

Summer Patho (4 decks)

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