FINAL: endocrine & dermatology Flashcards

1
Q

what is gigantism?

A

when epiphysial plates of long bones are still open (before puberty), and there is excessive GH

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2
Q

when does acromegaly occur?

A

result of GH production after the closure of epiphysial plates (post-puberty age). After sexual maturation and long bone can’t grow anymore, it increases the size of internal organs, distorts bone (fascial, nasal, jaw, toes) that have no epiphysial plates

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3
Q

There are a number of disorders that may increase the pituitary’s GH output in gigantism and acromegaly, what is the most common?

A

most commonly it involves a GH producing tumor called PITUTITARY ADENOMA (tumor), derived from distinct type of cell (somatotrophs)

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4
Q

acromegaly most commonly affects who?

A

middle age adults

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5
Q

what are complicatios of acromegaly?

A

compression of optic chiasm leading to loss of vision in outer visual fileds (bi-temporal hemianopia); increased palmar seating and sebum production; severe HA; arthiritis and carpal tunnel syndrome; enlarged heart; hypertension; diabetes mellitus; HT and KD failure

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6
Q

what are some tx options for acromegaly?

A

Endonasal Transphenoidal surgery; Trans-sphenodial surgery; medication or radiostatic neurosurgery; prolactinoma

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7
Q

what is Congential Hyothyroidism (CHT)?

A

thyroid hormone deficinecy present at birth

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8
Q

what is Cretinism?

A

outdated medical term for Congenital Hypothyroidsim: if this condition is untreated for several months after birth, it can lead to growth failure and permanent mental retardation - Creatinism. TX consists of daily dose of oral application of thyroid hormone (thyroxine)

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9
Q

what is presentation of hypothyroidism?

A

pituitary pressing on active

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10
Q

what is the primary, secondary, and tiertiary order of endocrine system?

A

III: Releasing Hormone from Hypothamalmus ; II: Stimulating Hormone from Anterior Pituitary (also called Adenohypophysis); I: periphery gland

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11
Q

what is Negative Feedback Regulation of Hormone Release in the Hypothalamic-Pituitary axis?

A

once peripheral glands fulfilled “their obligations” to secrete normal amount of primiary/peripheral hormones, they will feedback to secondary level (anterior pituitary) and to tertiary level (hypothalamus) to stop further “push” for production of corresponding primiary hormones. Opposite is also true: if peripheral glands do not secrete minimally normal amount of primary hormones, empty receptors of corresponding trophs (cells of anterior pituitary) and hypothhalamic nuclei will activate production of releasing and tropic/stimulating factors to encourage primary glands to “secrete better”

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12
Q

if there are problems with the primary level (the peripheral glands) of the endocrine system, it looks like?

A

if perhperial glands are “lazy” (deficient state, for instance Thyroid organ not producing enough T3 or T4), the anterior pituitary and hypothalamus will increase secretions of Stimulating Hormones and Releasing Factors correspondingly. When peripheral hormones are in excess, the further production of stimulating and releasing factors / hormones will be inhibited. [so hormones moving in OPPOSITE direction]

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13
Q

If there are problems with Secondary Level (overproduction or underprodution of Stimulating Hormones) due to pituitary tumors (could be secreting excessively or just inactively pressing on “troph” cells), the behavior of primary glands will be?

A

the primiary glands will mimick their “commanders in chiefs” [so hormones move in SAME direction]. Meaning the primary glands will secrete the same order as their “boss”, which means the negative feedback stopped working as the secondary level exhibits pathological condition

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14
Q

If lab tests HIGH Cortisol Level and LOW ACTH level, possible dx is?

A

tumor in adrenal gland (in primary level, bc hormones are opposite)

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15
Q

If lab tests HIGH cortisol level with HIGH ACTH level, dx is?

A

Tumor in the anterior pituitary (secondary level, bc hormones move in same direction)

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16
Q

in Secondary Level: Anterior Pituitary, what are corresponding hormones?

A

Thyrotrophs - thyroid stimulating hormones; Corticotrophs - ACTH (adenocortiocotrophic hormones) & MSH; Gonadotrophs - LH & FSH; Somatotrophs - GH

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17
Q

In Negative Feedback Inhibition, if the hormone cortisol of peripheral gland binds ot its receptor in cells in the hypothalamus and anteior pituitary, and has the effect of ,

A

inhibiting secretion of Tropic hormones (corticoropin releasing hormones CRH in this case) and Adrenocorticotropic Hormone (ACTH). LESS CRH secretion leads to LESS ACTH secretion, which leads to less stimulation of cortisol secretion by cells of zona fasciculata of adrenal cortex

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18
Q

what is usefullness of negative feedback inhibition?

A

that it results in Hormonal Homeostasis - the maintenance of hromone levesl within particular appropriate physiological range. *For example: if adrenal gland is damaged, this will decrease secretion of cortisol. There wil be decrease in degree of negative feedback inhibition on Hypothalamus and Anterior Pituitary. Resulting in MORE CRH and ACTH secretion. More ACTH will stimulate the remaining adrenal tissue to grow and sevrete more cortisol, brining cortisol back up to normal daily level of secretion.

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19
Q

if there is problems with the anterior pituitary on the second level of the endocrine system, then it is ALWAYS?

A

Adenoma - tumor of the brain (it can even be benign)

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20
Q

what is the most common cause of hyperthyroidism?

A

Grave’s Disease

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21
Q

what is pathogenesis of Graves’ disease?

A

it is an autoimmune reaction on unknown interrupting immune tolerance factor (smoking?, pregnancy?, etc). It results in production of self anti-bodies (IgG), over-stimulating TSH receptors of thyroid gland. As a result, thyroid gland secretes excessive amounts of T3 and T4. Natural TSH will be eventually supressed by auto-antibodies. TSH is LOW, and T3/T4 are oth HIGH (mimics primary profile of endocrine condition)

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22
Q

what are hallmark features of Graves’?

A

exophthalmos, heat tolerance, nervousness, insomina, fine and silky hair alopecia, alternating diarrhea, tremors, irregular and heavy menstruations, psychosis at times: signs of excessive BMR

23
Q

what is most common cause of hypothyroidism?

A

aging, followed by Hashimoto’s auto-immune thyroiditis

24
Q

what is the pathogenesis of Hashimoto’s?

A

the immune system creates self-immunoglobulins agains TG core molecule of thyroid follicles. Eventually core substrate (thyro-globulin) is damaged and the thyroid hormones can not be synthesized in sufficent amounts.

25
Q

what are clinical presentations of established hypothyroidism?

A

cold intolerance, facial myxedema, fatigue, gaining weight, and other features of decreased BMR, including brittle and dry hair alopecia. In initial statges, might be misdx with hyperthyroidism. Endocrine profile mimics primary endocrine disorders as well: TSH is HIGH, and T3/T4 is LOW

26
Q

what is Cushing syndrome/Disease?

A

an Endocrine condition, characterized by excessive production of cortisol and aldosterone

27
Q

what is most common cause of Cushing’s SYNDROME?

A

Sterioid medications when administered for a long period of time to suppress persistent inflammatory state.

28
Q

what is Cushing DISEASE?

A

it is type of Cushing Syndrome, when anterior pituitary adenoma secretes excessive ACTH, pushing adrenal gland to produce excessive amounts of steroid hormones: cotrisol (predominantly), aldosterone, and precursors for sex hormones. Hence, Cushing’s DISEASE is secondary profile of Cushing’s Syndrome: ACTH is up –> Cortisol is up as well: negative feedback is not working

29
Q

what constitute a set of clinical hallmarks of Cushing’s Syndrome?

A

Bufallo hump, moon face, central obesity, thin lower limbs, hirsutism, arterial hypertension, change in mental status (depression, anxiety, psychosis, diabetes mellitus, osteoporosis, induced by excessice steroid hormones)

30
Q

what is Addison’s Disease?

A

it is adrenal insufficiency

31
Q

what are the causes of Addison’s?

A

Could be due to infections, neoplasia, auto-immune. But it is largely, unknown

32
Q

what is typical presentation of primary Addison’s due to adrenal corticol insufficiency as a major cause?

A

there is fatigue, muscle weakness, hypotension, craving for salt and brown/bronze discolorations (“bronze diabetes”) dye to excessive ACTH and MSH production as a result of primary cortisol deficiency (cortisol is LOW –> ACTH/MSH is HIGH, per primary profile). **the discolorations are caused by MSH in primary profile of Addison’s as it is by-product of ACTH secretion.

33
Q

what is typical presentation of seondary Addison’s caused by pituitary adenoma, which is not producing anything but rather pressing and disabling corticotrophs of anterior pituitary?

A

it is same presentation as primary Addison’s MINUS the discolorations. ACTH/MSH is LOW –> Cortisol and Aldosterone are LOW (secondary profile with disabled feedback regulation). **the discolorations are caused by MSH in primary profile of Addison’s as it is by-product of ACTH secretion.

34
Q

what is Thyroid Storm?

A

extreme symptoms of hyperthyroidism, including severe arrhythmias, anxiety, MI, and or cerebral hemorrhages.

35
Q

why do Hyperthyroid patients and their physicians need to be careful about aspirin supplementation and treatment?

A

Asprine intake may increase circulating levels of T3/T4 and cause thyroid storm.

36
Q

Different names for Graves’ Disease is?

A

Basedow’s syndrome, or Basedow’s disease, or exophthalmic goiter

37
Q

what is Addison’s (Addisonian) Crisis?

A

also called “adrenal crisis” is a constellation of symptoms that indicate severe adrenal insufficiency. May be from previously undiagnosed Addison’s or an intercurrent problem (ex. infection, trauma), or it may develop in those on long-term oral glucocorticoids who have suddenly stopped taking their medication.

38
Q

Tiertiary, Releasing Horomes of the Hypothalamus are?

A

Thyroid Releasing Horomes (TRH); Corticotrophin-releasing horomes (CRH); Gonadotrophin-releasing horomes (GnRH); Growth Hormone-releasing horomes (GHRH)

39
Q

secondary, stimulating or trophic hormones are?

A

Thyroid Stimulating Horomes (TSH); Adrenocorticotrophic hormones (ACTH) and Melanin Stimulating Hormones (MSH); Lutinizing horome (LH) and Follicle-stimulating hormone (FSH); Growth Horome (GH)

40
Q

primary glands are?

A

Thyroid; Adrenal gland & melanocytes; Testes & ovaries; Tissues

41
Q

what is Psoriasis?

A

common inflammatory dermatological condition of, most probaby, auto-immune or inherited nature.

42
Q

what are triggering factors of psoriasis?

A

stress, antimicrobial medications, tanning salons, bacterial or viral infections, dryness of the skin, injury to the skin, some drugs, stress and UV radiation.

43
Q

what is pathogenesis of psoriasis?

A

abnormally rapid maturation and recyling of jeratinocytes. Normally, keratinocytes develop from epidermal stem cells and mature within 28 days. In psoriasis, due to auto-immune inflammation, the cycle of keratinocytes maturation is much shorter. It takes about 2 weeks (1/2 of the normal cycle time). Eventually, all layers of the skin may be affected and the skin appears scaling as per inability to discard all mature cells, ready for the exfoliation.

44
Q

what does psoriasis look like?

A

skin appears with different types of scaling rashes, including guttae (drop-like papules), plagues, and pustules. Under the scrapped scales, one may find minature petechial bleeding spots (Auspitz points of hemorrhaging skin).

45
Q

psoriasis affects what parts of the body?

A

can affec any part of the body skin inclyding either mostly extensor of flexor surfaces of extremities; scalp, as well as entire trunk. Joints may simultanesouly affected by debilitating psoriatic arthritis. Nails might be affected as nail thickening, yellowing and pitting.

46
Q

what is ABCDE system of screening for skin malignancies?

A

Asymmetry; Borders; Color; Diameter; Extension – this means that any skin lesion, which is noticed to have asymmetry, irregular borders, irregular or abnormal color, is more in diameter than 5-6mm, and appears to be extended or growing either in perimeter or in depth, represents RED FLAG for immediate medical referal

47
Q

first degree burn affect?

A

superficial, affect epidermis only, present as red, painful and swollen

48
Q

second degree burns affect?

A

partial thickness, affect epidermis and dermis. Present as painful, red, swollen and with BLISTERS

49
Q

third degree burns affect?

A

full thickness, affect deeper layers; may be non-painful, white or charred, and perceived as numb areas

50
Q

severity of burn is determined by what 2 parameters?

A

body surface area affected and by depth; also relevant to age, inhalation, and how much skin is burned

51
Q

which parts of body when burned are considered SEVERE and require immediate medical attention?

A

lips, hand, genitals

52
Q

what are the clinical presentations of Cushing’s DISEASE

A

loss of peripheral vision, headaches, blotchy discolorations

53
Q

what population most often develops Cushing’s

A

females, as it leads to infertility due to Cushing’s causing an androgenic state & imbalance of their ovaries.