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ABSN > endo - patho - E3 > Flashcards

endo - patho - E3 Flashcards

1
Q

synthesis and secretion of pituitary hormones are controlled by what

A

the hypothalamus

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2
Q

what hormones does the anterior lobe of the pituitary gland secrete

A

thyroid stimulating hormone (TSH)
adrenocorticotropic hormone (ACTH)

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3
Q

what hormones does the posterior lobe of the pituitary gland secrete

A

antidiuretic hormone (vasopressin)
oxytocin

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4
Q

ADH

A

released in response to high serum osmolality and/or hypotension & causes water retention via action in the kidneys

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5
Q

the adrenal medulla secretes

A

epinephrine and norepinephrine
(catecholamines)

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6
Q

in response to ACTH, the adrenal cortex secretes

A

Glucocorticoids (Cortisol)
Mineralcorticoids (Aldosterone)
Sex steroids (Androgens)

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7
Q

what do epi and norepi do

A

fight or flight
enhance/enlong the effect of the sympathetic nervous system

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8
Q

steroid hormones

A

-secreted by the adrenal cortex
-regulates the body’s response to normal & abnormal levels of stress
-made on demand
-activities: sugar, salt, & sex

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9
Q

what is the principal hormone of glucocorticoids

A

cortisol

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10
Q

functions of cortisol

A

-raise blood sugar
-protect against physiologic effects of stress
-suppress inflammatory and immune processes
-release muscle stores of proteins (maintains vascular system)
-increase blood cholesterol (raises our BP)

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11
Q

what is the principal hormone of mineralocorticoids

A

aldosterone

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12
Q

what regulates mineralocorticoids

A

renin-angiotensin system in the kidneys

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13
Q

functions of aldosterone

A

-maintain salt and water balance
-promotes excretion of potassium
-when triggered by angiotensin II, aldosterone promotes sodium retention & thus water retention

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14
Q

the thyroid secretes

A

triiodothyronine (T3, active form) and thyroxine (T4, either attached to proteins when not needed or freely in the tissues when needed)
T4 is converted to T3 when it reaches organs and tissues to aid in metabolism

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15
Q

what is a necessary component in synthesis of thyroid hormone

A

iodine

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16
Q

euthyroid

A

normally functioning thyroid gland

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17
Q

how many glands are in the parathyroid

A

4

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18
Q

parathyroid function

A

-produce and secrete parathyroid hormone (PTH) in response to hypocalcemia and break down bone to re-establish normal calcium in the blood
-Promotes vitamin D production

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19
Q

what is the primary use of looking at ACTH

A

dx of adrenal cortical dysfunction

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20
Q

sympathetic nervous system responses vs parasympathetic

A

Sym: pupils dilates, inhibits saliva, inc HR, dilates bronchi, inhibs peristalsis & secretion, converts glycogen to glucose, secretes adrenaline, inhibits bladder
Para: constricts pupils, stims saliva, slows HR, constricts bronchi, stims peristalsis & secretion, stims bowels

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21
Q

what is the patho behind why cushing syndrome happens

A

hypothalamus stimulates the release of ACTH which stimulates the adrenal cortex to produce glucort (cortisol) but there is too much of this process activated and we get increased cortisol levels

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22
Q

cushing syndrome definition

A

a collection of signs and symptoms associated with hypercortisolism

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23
Q

causes of Cushing’s

A

1) primary hyperfunction = Cushing’s syndrome
2) secondary hyperfunction = Cushing’s disease
3) exogenous steroids used in the mgt of various disease = Cushing’s syndrome

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24
Q

what is the most common cause of Cushing’s syndrome

A

exogenous steroids like predisone & dexamethazone

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25
Q

what does a patient lose when they have Cushing’s syndrome in regards to stress

A

the protective nature of stress -> in a healthy body, increased stress is used a protective mechanism for disease states
if a patient is having surgery, may need to give ACTH or Cortisol prior bc their body can’t respond to natural triggers

26
Q

what is a byproduct of Cushing syndrome

A

the pituitary decreases production of ACTH because the adrenal gland isn’t being stimulated so it will often atrophy

27
Q

clinical manifestations of Cushings

A

-glucose intol, hypergly
-htn, capollary friability
-muscle wasting/weakness, skin thinning, oesteoporosis & bone pain
-redistribution of fat to abdomen, shoulders and face
-impaired wound healing & immune response, inc risk of infection
-mood swings & insomnia

28
Q

what will a person physically look like with Cushings

A

-red cheeks
-fat pads on neck base
-abdominal stretch marks
-bruise easily
-pendulous abdomen
-thin arms and legs

29
Q

Addison’s disease

A

disease of the adrenal cortex that causes Hyposecretion of all 3 adrenocortical hormones
the most severe effect coming from the lack of cortisol

30
Q

Addison’s disease pathogenesis

A

the adrenal gland is destroyed causing the gland to stops secreting cortisol which causes a lack of negative feedback so the anterior pituitary increases the secretion of ACTH & a hormone called melanocyte to try and stimulate cortisol (which doesn’t happen)

31
Q

Addison’s Disease CM: early

A

anorexia, weight loss, weakness, malaise, apathy, electrolyte, skin hyperpigmentation

32
Q

Addison’s Disease CM: hypoaldosteronism

A

low aldosterone means we are not retaining sodium or water
hypotension, decreased vascular tone & CO, decreased BV, hypoNa (salt cravings), hyperK, dehydration

33
Q

Addison’s Disease CM: Hypocortisolism

A

low levels of cortisol = low levels of energy
hypoglycemia, weakness & fatigue, high levels of ACTH, & hyperpigmentation

34
Q

acute side effect of glucocorticoid replacement

A

remember w/ addison’s since deficient, show present as homeostatic person
-increased intraocular pressure
-fluid retention
-high BP
-mood swings
-hunger

35
Q

chronic side effect of cocorticoid replacement

A

clouded eye lens, weight gain (moon face & buffalo hump), high BS, increased risk for infection, thinning bones & fractures, suppressed adrenal gland hormone production (fatigue, loss of appetite, N/v, muscle weakness), thin skin, bruising, slow wound healing, hirsutism, striae

36
Q

Severe Cushing’s Syndrome

A

presents as an acute emergency and is defined by a massively elevated random serum cortisol at anytime or a 24 hr urine free cortisol more than 4 fold the upper limit + present w/ severe hypokalemia

37
Q

Severe Cushing’s Syndrome is typically associated with the onset of

A

sepsis, opportunistic infection, uncontrolled hypertension, heart failure, + more

38
Q

Severe Cushing’s Syndrome treatment

A

manage metabolic and electrolyte disturbances in rapid resolution and try to figure out cause

39
Q

Addisonian Crisis

A

a sudden insufficiency of serum corticosteroids (like you just got stabbed in your adrenal gland) or a sudden increase of stress or a sudden cessation of the corticosteroid drug
a medical emergency & if the body needs even more stress hormone, they just don’t have it

40
Q

Pheochromocytoma

A

Rare tumor of the adrenal medulla that produces excessive catecholamines
-90% of time it is benign
-risk factor: young - middle age

41
Q

Pheochromocytoma patho

A

excessive release of epi and norepi in response to SNS stimulation

42
Q

epi stimulates

A

alpha and beta receptors which are located in the heart, lungs and vessels

43
Q

norepi stimulates

A

alpha receptors

44
Q

what is the hallmark clinical manifestation of Pheochromocytoma

A

hypertension which presents w/ headaches, diaphoresis & tachycardia
-sporadic episodes can occur w/ anything that stimulates the SNS (stress, excitement, exercise or smoking)
BP can get to extremely high levels like 250/200)

45
Q

what environment should a person with Pheochromocytoma be in as they wait for treatment

A

a low stimulus environment

46
Q

what is our main concern with someone who has Pheochromocytoma

A

stroke risk d/t the high BP
treat as quickly as possible -> #1 treatment is surgery

47
Q

what can we give to patients w/ Pheochromocytoma as they wait to get surgery

A

alpha blockers bc the cause of the HTN is activation of alpha 1 receptors
-give 14 days prior & a little after

48
Q

Syndrome of Inappropriate AntiDiuretic Hormone (SIADH)

A

“An abnormal production or sustained secretion of ADH”
characterized by: fluid retention, serum hypoosmolality & hypoNa and concentrated urine
our body is inappropriately holding onto all the water it can

49
Q

SIADH etiology

A

-most common cause is a malignant tumor (Ex: Small cell carcinoma of the lung [Adenocarcinoma])
-CNS disorders like head trauma, stroke, brain tumor
-drug therapy: morphine, SSRIs, chemo drugs
-misc: hypothyroidism, infection

50
Q

SIADH patho

A

increasd ADH -> increased water reabsorption in the renal tubules -> increased intravascular fluid volume -> dilutional hypoNa & decreased serum osmolality

51
Q

SIADH osmolality labs

A

serum osmolality: low
urine osmolality: high
urine specific gravity: high
serum Na: low
urine output: low
weight: gain

52
Q

SIADH clinical manifestations

A

same as hypoNa
-dyspnea, fatigue
-neuro: lethargy, confusion, dulled sensorium, musical twitching, convulsions
-GI: impaired taste, anorexia, vomiting, cramps
if Na = 100-115, irreversible neurologic damage

53
Q

water intoxication in SIADH

A

When serum levels of NA become lower than what is INSIDE the cells (so vascular space Na levels are lower than the cell) -> cells will try and take in that water and they will swell causing further neurologic symptoms (confusion, lethargy, coma & death) b/c it is happening in the brain

54
Q

diabetes insipidus

A

“a deficiency of ADH or a decreased renal response to ADH”
characterized by excessive loss of water in the urine -> two forms
1) neurogenic (central)
2) nephrogenic

55
Q

neurogenic DI etiology

A

-cause: hypothalamus or pituitary gland damage
-associated w/ stroke, traumatic brain injury, brain surgery, cerebral infections
-has a sudden onset and is usually permanent

56
Q

nephrogenic DI etiology

A

-cause: loss of kidney function, often drug related (lithium -> bipolar med)
-associated w/ chronic kidney disease
-onset is slow and the disease is progressive

57
Q

DI patho

A

decreased ADH -> decreased water reabsorption in renal tubules -> decreased intravascular fluid volume -> increased serum osmolality (hyperNa) & excessive urine output

58
Q

DI osmolality labs

A

serum osmolality: high
urine osmolarity: low
urine specific gravity: low
serum Na: high
urine output: high
weight: loss

59
Q

DI clinical manifestations

A

-polyuria (up to 15L per day)
-polydipsia
-dehydration
-electrolyte imbalances
-if severe, hypovolemic shock (can lead to death)

60
Q

DI treatment for neurogenic

A

synthetic ADH replacement (desmopressin)

61
Q

DI treatment for nephrogenic DI

A

give thiazide (htcz) diuretic because it has a paradoxical effect so it decreases polyuria and increases urine osmolality

ABSN (161 decks)

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