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KCSU17 Patho/Pharm Submodule 1 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

autocrine

A

influences own tissue

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2
Q

juxtacrine

A

influences adjacent tissue

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3
Q

paracrine

A

influences neighboring tissue

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4
Q

endocrine

A

influences distant tissues

secreted, go thru blood to distant target

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5
Q

where are hormones broken down? (general)

A

in target tissue, liver, or kidney

short ghalf life

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6
Q

Hormone products of hypothalamus

6

A
  1. Corticotrophin (CRH)
  2. Gonadotrophin Releasing Hormone (GnRH)
  3. Growth Hormone Releasing Hormone (GHRH)
  4. Somatostatin
  5. Thyrotropin releasing hormone (TRH)
  6. Prolactin Inhibitory Factor (PIF)
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7
Q

highest level of control in endocrine system

A

hypothalamus

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8
Q

hypothalamus is controlled by ____

A

cortical centers in brain

response to emotions and sensory input (can be influenced by stress)

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9
Q

Pituitary

A

located in sella turcica

behind optic chasm

ant. and post.

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10
Q

Hypothalamus to anterior pituitary pathway

A

Hormones are made in hypothalamus

transported via pituitary portal circulation

arrive at anterior pituitary

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11
Q

hypothalamus to posterior pituitary pathway

A

hormones are made in hypothalamus

transported directly by neural network

posterior lobe

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12
Q

What are the targets of hypothalamus’ hormones

A

stimulation or inhibition of target cells in anterior lobe of pituitary

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13
Q

products of anterior pituitary

6

A
  1. adrenocorticotrophic hormone (ACTH) (Corticotrophin)
  2. Follicle stimulating hormone (FSH)
  3. Luteinizing hormone (LH)
  4. Growth hormone (GH)
  5. thyroid stimulating hormone (TSH)
  6. Prolactin
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14
Q

products of posterior pituitary

A
  1. ADH/vasopressin

2. oxytocin

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15
Q

Hormonal axes general steps

A
  1. hypothalamus secretes releasing hormones
  2. pituitary secretes trophic hormones (growth of gland)
  3. endocrine glands secrete circulating hormones with metabolic effects

circle back to give feedback to hypothalamus and pituitary

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16
Q

Hypothalamic pituitary adrenal axis

A
  1. Hyp. releases corticotrophin releasing hormone (CRH)
  2. adrenocorticotrophic hormone (ACTH) released by anterior pituitary
  3. ACTH stimulates adrenal cortex to release glucocorticoid and weakly simulates aldosterone release, trophic to adrenal gland

Gluc.: metabolism regulation, stress response
Aldos: blood pressure and water retention
trophic: growth of gland

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17
Q

hormones involved in hypothalamic pituitary adrenal axis

A

CRH
ACTH
glucocorticoid + aldosterone

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18
Q

results of the hypothalamic pituitary adrenal axis

A 
metabolism regulation 
stress respones (Via gluc.)

blood pressure regulation, water regulation (aldos.)

trophic = growth of the adrenal gland

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19
Q

Gonatrotrophin Pituitary Sex axis (not sure proper name ;) )

A
  1. Gonadotropin releasing hormone (GnRH) released by hypothalamus
  2. GnRH stimulates Follicle Stimulating hormone (FSH) and Luteinizing Hormone (LH) release by ant. pituitary
  3. stimulate estrogen/progesterone/testosterone in sex organs

secondary sex characteristics:
regulate growth of ovaries and testes, output of sex hormones, regulation of menstrual cycle

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20
Q

hormones in the Gonatrotrophin Pituitary Sex axis

A

GnRH
FSH/LH
progesterone/estrogen, testosterone

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21
Q

results of Gonatrotrophin Pituitary Sex axis

A

regulation of ovaries/testes growth
control output of sex hormones
regulation of menstrual cycle

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22
Q

Hypothalamic thyroid axis

A
  1. Thyrotropin releasing hormone (TRH) released by hypothalamus
  2. TRH stimulates release of thyroid stimulating hormone/thryotropin in anterior pituitary
  3. TSH stimulates release of T3 and T4 from thyroid, trophic to thyroid

results:
control of metabolism, growth of thyroid gland

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23
Q

hormones of Hypothalamic thyroid axis

A

TRH
TSH/thyrotropin
T3 and T4 (thyroxin)

somatostatin

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24
Q

results of Hypothalamic thyroid axis

A

metabolic control via T3 and T4

growth of thyroid gland

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25
Q

growth axis

A
  1. hypothalamus secretes growth hormone releasing hormone (GHRH)
  2. GHRH stimulates release of growth hormone/somatotropin (GH) in anterior pituitary
  3. GH stimulates liver to produce somatomedin (insulin like growth factors)

promotes cell growth
inhibits apoptosis

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26
Q

hormones of the growth axis

A

GHRH
GH/somatotrophin
somatomedin/IGFs

somatostatin

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27
Q

somatostatin

A

inhibits the growth axis

secreted by hypothalamus

inhibits release of TSH and GH by anterior pituitary

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28
Q

prolactin axis

A
  1. prolactin is released by ant. pituitary

2. prolactin stimulates milk production

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29
Q

prolactin is inhibited by

A

Prolactin Inhibitory Factor (PIF) and Dopamine from hypothalamus

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30
Q

prolactin inhibits

A

FSH and LH secretion

good bc it prevents you from getting pregnant directly after giving birth

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31
Q

prolactin release is stimulated by

A

estrogen, thyroid releasing hormone, nipple stimulation

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32
Q

prolactin levels are decreased artificially by

A
  1. drugs that mimic dopamine (levodopa, bromocriptine, Requip, Mirapex)
  2. drugs that block doapime receptors (which leads to increase of dopamine concentrations) [phenothiazines(chlorpromazine) butyrophenones(haloperidol)]
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33
Q

primary endocrine disorders

A

malfunction of the target organ

thyroid, adrenal gland, gonads

most common

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34
Q

secondary endocrine disorders

A

malfunction of pituitary

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35
Q

tertiary endocrine disorders

A

malfunction of hypothalamus

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36
Q

how are secondary and tertiary endocrine disorders diagnosed

A

checking levels of all the trophic hormones and functions of adrenal cortex (ACTH), thyroid gland (TSH), and gonads (FSH, LH)

bc if it is higher order disease, whole thing will be knocked out

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37
Q

panhypopituitarism

A

disorder where entire pituitary gland is destroy

caused by

  1. ischemia/infaction (sheenhan’s syndrome_
  2. tumor

very rare, presents subtly

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38
Q

functioning pituitary tumor

A

produces hormones
typically GH and prolactin

micro and macroadenomas

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39
Q

pituitary tumors and optic chiasm

A

optic nerves cross at the optic chiasm

when there is a pituitary tumor, as it grows, it compresses the optic bias and causes visual field cuts

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40
Q

bitemporal hemianopsia

A

visual field cuts where central vision is knocked out

caused by pituitary tumor growth and compression of the optic nerves at the optic chiasm

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41
Q

types of pituitary tumors

A
  1. pituitary adenoma (macro adenoma or micro adenoma)
  2. craniopharyngioma
  3. meningioma
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42
Q

pituitary adenoma

A

most often microdenomas

benign, functional

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43
Q

craniopharyngioma

A

benign or malignant
non function

face and oral cavity tumor

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44
Q

meningioma

A

benign and non function

tumor of the meninges

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45
Q

micro adenomas

A

less than 1 cm/ 10 mm

usually produce prolactin

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46
Q

prolactinomas symptoms:

A

galactorrhea (growth of breast tissue, breast milk production)

amenorrhea (bc prolactin surpasses FSH and LH)

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47
Q

treatment mechanisms

micro adenoma

A

a. dopamine agonists
stimulate the dopamine receptors to suppress prolactin secretion, shrinks growth

b. surgical removal (not easily done bc in hard to reach place)

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48
Q

macroadenomas

A

commonly secrete growth hormone
greater than 10 mm

different effect on adults and children

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49
Q

macroadenomas in adults

A

acromegaly

grow after bone epiphyses have closed

coarse facial features, thickening viscera, spade like hands, diabetes

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50
Q

diabetes and acromegaly

A

growth hormone stimulates the release of insulin like growth factors (looks like insulin) so has high blood sugar levels

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51
Q

micro and macro adenomas and size

A

microadenomas are found early when they are small, b/c they show symptoms at a small size

macroadenomas don’t show symptoms until larger than 10cm

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52
Q

colloid

A

found in thyroid, stores the inactive the thyroid hormone

when broken down, releases thyroxin in the blood

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53
Q

which is more active T4 or T3

A

T3 is more active

T4 is converted to T3

most is bound to albumin in blood (inactive)

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54
Q

thyroid hormone

A

rate controller for metabolic processes
determines energy levels

excess = hyperthyroid
deficiency=hypothyroid

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55
Q

hyperthyroidism s/s

cardiovascular:
neuromuscular: 
GI:
GU: 
metabolic:
dermatologic:
A

everything is very active, elevated FT4 and low TSH

cardiovascular: tachycardia, increased EF, more prone to heart failure
neuromuscular: tremor, hyperreflexia, irritable, restless, apathetic

GI: diarrhea (move thru GI quickly)

GU: menorrhagia (heavy periods)

metabolic: patients feel hot, weight loss
dermatologic: lush hair, moist, flushed skin

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56
Q

hypothyroidism s/s

cardiovascular:
neuromuscular: 
GI:
GU: 
metabolic:
dermatologic:
A

everything is slowed down

cardiovascular: bradycardia, decreased cardiac output
neuromuscular: sluggish, hyporeflexia, lethargic, placid, depressed

GI: constipation

GU: amenorrhea (spaced out periods)

metabolic: feel cold, weight gain
dermatologic: dry, flaky skin

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57
Q

Goiter

A

thyroid enlargement

via TH stimulant

may be euthrothyroid, hypothyroid, hyperthyroid

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58
Q

goiter structural classification

A

diffuse
nodular
substernal

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59
Q

function classification goiters

A

toxic (producing excess hormones) – hyperthyroid

non-toxic (not producing excess hormones)

once detected status must be determined

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60
Q

how to determine status of goiter

A

TSH check

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61
Q

disorders causing hyperthyroidism

A
  1. toxic nodular goiter
  2. graves disease
  3. hashimoto thyroiditis
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62
Q

toxic nodular goiter

A

nodule begins secreting TSH autonomously (without TRH)

elevated FT4 level, surpassed TSH

must rule out cancer

Hot nodule bc it is functional

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63
Q

grave’s disease

A

body produces antibodies that mimic TSH

stimulates thyroid– over production of thyroid hormones

elevated FT4 and suppressed TSH

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64
Q

Hashimoto thyroiditis

A

autoimmune

lymphocytic invasion of thyroid –> destruction of follicular cells (inc. TSH receptors)
causes destruction of colloids and uncontrolled release of T4 in blood

brief periods of hyperthyroidism then hypothyroidism

65
Q

Treatment for hyperthyroidism

A

propranolol
methimazole
I131 treatment

surgical

66
Q

Propranolol

brand name + MOA

A

hyperthyroidism

Inderal

non specifici beta blocker

blocks adrenergic effects of thyroid toxicity – decreases high cardiac output, tachycardia, restlessness and internal temp.

symptom relief

67
Q

methimazole

brand name + MOA

A

hyperthyroidism

blocks synthesis of thyroid hormone
gradual reduction of thyroid hormone (4-8weeks)

nasty side effects, but use in combo with propranolol

68
Q

I 131 treatment

A

radioactive iodine given
destroys the thyroid

ideal method but can’t give to pregnant women

69
Q

hypothyroidism hormone levels and treatment goal

A

decreased Ft4 and elevated TSH

goal is to replace deficient FT4 hormones and decrease TSH via negative feedback via Levothyroxine

70
Q

Levothryoxine

brand name + MOA

A

hypothyroidism

Synthroid

synthetic T4

full dose to younger, quarter dose to older (due to not wanting to cause stressors to the cardiac system)

71
Q

neonatal hypothyroidism

A

TH required for nervous system development

levels are maintained via transfer from mother

if not present, develop cretinism (stunted growth and retardation)

essential nonexistent in US

72
Q

Thyroid emergencies

A
  1. myxedema coma

2. thyroid storm

73
Q

myxedema coma

A

thyroid emergency

caused by profound hypothyroidism

can’t handle any kind of stress (narcotics, medical illness, surgery)

common in older women

74
Q

thyroid storm

A

thyroid emergency

severe hyperthyroidism

may occur without history of disease if rapid destruction

causes high fever, delirium, tachycardia, weight loss

75
Q

adrenal cortex secretions

A

glucocorticoids
mineralocorticoids
sex hormones (adrenal androgens)

76
Q

two layers of adrenal gland

A

adrenal cortex
adrenal medulla

completely separate organs almost

77
Q

adrenal medulla secretions

A

epinephrine and norepinephrine

78
Q

Glucocorticoid function (5)

A

Stress hormones

decreases glucose levels in nonessential tissues
increases breakdown of fat, protein
increases gluconeogenesis
inhibits protein synthesis (healthy go tissue)
suppresses inflammatory response

79
Q

mineralocorticoid funciton

A

keep fluid balance optimal

major part of blood pressure

major one is aldosterone

80
Q

adrenal androgens

A

important in females sexual health, negligible in men

81
Q

Disorders of adrenal gland

A
  1. primary adrenal insufficiency
  2. adrenal crisis
  3. cushing’s syndrome
82
Q

primary adrenal insufficiency

A

hypo function of adrenal cortex

LOW glucocorticoid and mineralocorticoid

no ability to increase glucocorticoid or mineralocorticoid in response to stress that causes adrenal crisis

83
Q

etiologies of primary adrenal insufficiency

A 
autoimmune 
infection (ex. TB) 
metastatic carcinoma
84
Q

addisons disease

A

autoimmune, causes primary adrenal insufficiency

cytotoxic lymphocytes and autoantibodies attach adrenal cortex

kill ability to make glucocorticoid – no response to stress

85
Q

metastatic carcinoma

A

primary cancer tumors in lung or breast metastasize in adrenal glands to grow and destroy adrenal tissue

86
Q

s/s of adrenal insufficiency

A
  1. low glucocorticoid (low blood sugar, low blood pressure, poor stress response – hypotension resistant to fluid resuscitation)
  2. low mineralocorticoid (chronic low sodium, high potassium, hypovolemia
87
Q

treatment of adrenal insufficiency

A

hydrocortisone
fludrocortisone

replace what is missing , lifelong

88
Q

hydrocortisone

brand name + MOA

A

cortex

glucocorticoid, considered most bioequivalent to cortisone

2/3 in AM, 1/3 in PM bc of cortisone surge before waking

89
Q

fludrocortisone

brand name + MOA

A

florin

mineralcorticoid
dosing once daily, prevents passing out or swelling

90
Q

adrenal crisis

A

preexisting insufficiency or borderline insufficiency is confronted with stressful event (HA, medical illness, infection, surgery)

causes RAPID loss of blood pressure

91
Q

cushing syndrome s/s

A

glucocorticoid excess

characterized by elevated blood glucose

muscle wasting, thin extremities, muscle weakness

osteoporosis, pathological fracture, thin skin easy tearing, stretch marks

redistribution of fat (truncal obesity, moon face)

92
Q

etiologies of cushing

A
  1. iatrogenic cortivosteroids
  2. ACTH producing pituitary adenomas (cushing disease)
  3. primary hyperfunctioning of adrenal cortex (tumor or hyperplasia)
  4. cancers that produce ACTH like proteins
93
Q

iatrogenic corticosteroids

A

we have given them steroids for respiratory disease, autoimmune disease, organ transplant or canter treatment but has caused dysfunction

not much we can do

decreased ACTH, decreased natural glucocorticoid

94
Q

ACTH producing pituitary adenomas

A

causes hyper function of adrenal cortex

cushing’s disease

increased glucocorticoid, increased ACTH

95
Q

primary hyper functioning of adrenal cortex caused by

A
  1. tumor on adrenal cortex
  2. adrenal hyperplasia

ignores ACTH, decreased ACTH levels

96
Q

hyperfunctionadrenal cortex tumor

A

usually benign

autonomously produces cortisol

primary adrenal cancer is rare

amenable to surgical rustication

** if removed, will have to wait for pituitary to get used to producing again ,will have to supplement and replace or may cause adrenal shock

97
Q

paraneoplastic syndrome

A

cancer found somewhere else (lung) that produces a similar protein to ACTH that fools adrenal glands into producing cortisol

98
Q

Name the cause:
low glucocorticoid (natural)
Low ACTH

A

Glucocorticoid excess caused by iatrogenic corticosteroids use

99
Q

Name the cause:

increased glucocorticoid
elevated ACTH

A

Glucocorticoid excess caused by pituitary adenoma

100
Q

name the cause:

increased glucocorticoid, decreased ACTH

A

Glucocorticoid excess caused by adrenal tumor

OR

papaneoplastic syndrome

101
Q

primary mineral corticoid

A

aldosterone

102
Q

primary aldosterone stimulus

A

kidney

minimally regulated by ACTH

103
Q

what stimulates renin production?

A

drop in renal profusion

104
Q

Renin changes ____ to ____

A

angiotensinogen to angiotensin-1

105
Q

ACE enzyme

A

converts angiotensin-1 to angiotensin-2 in the lungs

106
Q

angiotensin-2 fxn

A

causes vasoconstriction

aldosterone secretion from adrenal gland

107
Q

aldosterone fxn

A

causes nephron to retain sodium and water

increases blood pressure and renal profusion

108
Q

steps of RAAS loop

A
  1. renin produced in kidney in response to drop in renal perfusion
  2. Renin activates RAAS, changing plasma angiotensinogen to angiotensin-1
  3. Angiotensin-1 is converted to Angiotensin 2 but ACE in lungs
  4. angiotensin-2 causes vasoconstriction and aldosterone secretion
  5. aldosterone causes nephron to retain sodium (therefore water) ** increases BP and renal perfusion)
  6. Reapsorbtion of Na means that kidney must give up another positive ion (K or H) `
109
Q

hyperaldosteronism

A

mineralocorticoid excess

causes:
edema
elevated blood pressure
hypokalemia and metabolic alkalosis (wasting in urine bc must secrete to hold onto Na)

110
Q

etiologies of hyperaldosteronism

and treatment

A

adrenal adenoma (surgical removal of adenoma processing excess aldosterone)

adrenal hyperplasia (spironolactone[aldactone]– aldosterone antagonist, blocks effect at renal tubule)

111
Q

Hypoaldosteronism

A

minderalcorticoid deficiency

causes: low blood pressure, hyperkalemia, tendency toward acidosis

112
Q

most common cause of hypoaldosteroneism

A

diabetes

hyporeninemic hypoaldosteronism bc kidney damaged so can’t produce renin

113
Q

parathyroid hormone function (3)

A

increases Ca absorption from GI tract

mobilizes calcium from bone

decreases calcium loss from urine

*Required for calcium release response to hypocalcemia *

114
Q

vitamin D function (2)

A

facilitates calcium absorption in GI tract
deposits Ca in bone

activated by kidney

115
Q

what other ions have a role in calcium balance

A

magnesium and phosphorus

116
Q

active v. inactive calcium

A

active calcium- ionized

inactive - bound to albumin

117
Q

why are calcium levels important?

A

cardiac and skeletal muscle contraction

nerve conduction

coagulation cascade

118
Q

causes of parathyroid deficiency

A

iatrogenic (accidental) removal of glands during surgery of thyroid or other structure

autoimmune destruction of calcium receptors in parathyroid – no receptor, to stimulation to secrete

119
Q

3 types of parathyroid excess

A
  1. primary hyperparathyroidism
  2. secondary hyperparathyroidism
  3. tertiary hyperparathyroidism
120
Q

primary hyperparathyroidism 3 causes

A

only a problem on the gland itself:

  1. autonomous parathyroid adenoma
  2. parathyroid hyperplasia
  3. parathyroid cancer
121
Q

autonomous parathyroid adenoma

A

primary hyperparathyroidism

group of cells within a gland pump out PTH without stimulation/regard of Ca++ levels

most common cause, 85%

122
Q

parathyroid hyperplasia

A

primary hyperparathyroidism

enlargement of all 4 hyperparathyroid glands therefore increasing production of parathyroid hormone

123
Q

primary hyperparathyroidism s/s

A

most common in 50+, women (3x)

mild elevations of serum calcium
relatively asymptomatic

124
Q

diagnosing primary hyperparathyroidism

A

elevated serum calcium

elevated intact PTH

125
Q

primary hyperparathyroidism treatment

A

asymptomatic hypercalcemia may be treated by vigorous hydration (increasing amounts of calcium released from blood)

otherwise, treated surgically (removal of gland)

126
Q

secondary hyperparathyroidism causes

A

patients with chronic kidney disease

failing kidney is unable to excrete PO4 normally, instead excreting Ca

(secondary bc caused by CKD)

127
Q

secondary hyperparathyroidism pathophysiology

A

kidneys secrete Ca++ instead of PO4

low serum calcium causes high PTH secretion but can’t maintain Ca balance

failing kidney no longer produces vitamin D so Ca absorption decreases

results in renal osteodystrophy

128
Q

treatment of secondary hyperparathyroidism

A

diet management (more Ca++, decrease PO4)

Phos-lo (binds to phosphorus, increased excretion via GI)

Calcitriol/Rocaltrol (synthetic vitamin D, more calcium is absorbed in diet)

129
Q

tertiary hyperparathyroidism

A

occurs in pts with CKD following transplant

despite having normalized kidney, parathyroid continues to pump out excessive PTH (used to it)

treatment via surgery

130
Q

hormones of pancreas:

A

insulin

glucagon

131
Q

which hormone is trophic for pancreas?

A

somatostatin

132
Q

insulin

A

produced by beta cells

moves glucose from blood to cell

glycogen formation, suppresses glucose production from liver

133
Q

glucagon

A

released in response to cellular hypoglycemia

causes gluconeogenesis, glyconeolysis

glucose from cells to blood

134
Q

type 1 DM causes

A

immune mediated (90%)

idiopathic

circulating levels of insulin are negligible, insulinogenic stimuli elicit no response from pancreas

typically appears in children, teens

135
Q

immune mediated T1DM

A

autoantibodies attack islet cells (that produce insulin)

136
Q

idiopathic T1Dm

A

unknown stimulus cause death/dysfunction of beta cells

137
Q

symptoms of T1DM

A

polyphasia (with weight loss, despite normal intake)

polyuria (increased urinatoin due to osmotic diuresis)

polydipsia (increased thirst due to osmotic diuresis)

138
Q

Type 2 DM basic

A

gradual development of insulin resistance

pancreas tries to make more, but not enough. B cells die and glucose toxicity increases causing more rapid destruction

139
Q

symptoms of T2DM

A

asymptomatic

hyperglycemia or glucosuria found on routine lab

may report increased thirst or urination

140
Q

pathophysiology of T2DM

A

hyperinsulemia, hyperglycemia, increased free fatty acids results in

  1. endothelial cell dysfunction (impaired relaxation and proliferation of smooth muscle cells)
  2. inflammation (low grade inflammation, worsens resistance and arteriosclerosis, promotes clotting
141
Q

treatment options for T2DM (list classes) (5)

A
  1. metformin
  2. sylfonylureas
  3. incretin mimetics
  4. thiazolidineodiones
  5. SGLT2 inhibitors
142
Q

metformin

class, MOA, brand

A

brand: glucophage
no class

decreases glucose output by liver, sensitizes peripheral cells to insulin

1st line

doesn’t cause hypoglycemia, promotes weight loss

side effect: diarrhea (must discontinue if presents)

143
Q

glipizide

class, MOA, brand

A

Glucotrol
class: sylfonylureas

stimulates pancreatic beta cells to make more insulin

cheap, powerful BUT causes hypoglycemia and weight gain

144
Q

incretin mimetics

A

2 types:

  1. GLP-1 Agonists
  2. DPP4 inhibitors

don’t cause hypoglycemia and may cause weight loss

145
Q

eventide

class, MOA, brand

A

Byetta
class: incretin mimetics

synthetic GLP-1 (replaces what diabetic no longer makes)

inhibits glycogen release, slows gastric emptying, increases glucose dependent insulin secretion

patient fells full, eats less

MUST be injected :(

146
Q

Sitagliptin

class, MOA, brand

A

Januvia
class: incretin mimetics

inhibits dipeptidyl peptidase (which degrades GLP-1) therefore inhibiting GLP-1 breakdown

147
Q

pioglitazone

A

Actos
class: TZD

lower glucose by increasing glucose uptake in muscle and fatty tissue
decreases hepatic glucose production

multiple CI, cause weight gain

148
Q

canagliflozin

A

Invokana
Class: SGLT-2 inhibitor

inhibits glucose reabsorption after filtration by kidney

may cause weight loss, increases risk of UTI/DKA

149
Q

4 insulin options for diabetics

A

genetically engineered

  1. rapid acting insulin (insulin lisper)
  2. regular insulin
  3. NPH insulin
  4. Long acting insulin (insulin glargine/Lantus)
150
Q

rapid acting insulin

A

acts faster than endogenous insulin

two roles: mealtime coverage, insulin pump

pts must eat within 20 minutes and front load cards to avoid hypoglycemia

151
Q

regular insulin

A

slower onset, wears off in 5-7 hrs

not common used: primarily used as drip to treat severe hyperglycemia and DKA

152
Q

NPH insulin

A

slow onset (2x daily)
basal coverage
can be mixed with rapid acting insulin for mealtime and basal coverage

153
Q

Long acting insulin

A

inulin glargine (Lanthus)

basal Insulin, once daily injection

154
Q

why do we have multiple types of insulin to treat diabetes?

A

so that we can best mimic the physiologic activity of the pancreas

155
Q

T1DM is caused by

A

complete lack of insulin

only treatment option is to replace insulin

156
Q

T2DM caused by

A

insulin resistance, so many different options

157
Q

diabetic emergencies

A
  1. diabetic ketoacidosis

2. nonketotic hyperosmolar coma

158
Q

diabete ketoacidosis

A

common T1DM (young patients0

  • lack of insulin causes body to break down ketoacids in blood (decreasing blood pH – from 7.35 to 7.2) therefore impact enzyme function
  • patient develops dehydration from osmotic diuresis and hypokalemia

triggered by: n/v, surgery, stressor

develops rapidly, treated by giving insulin

159
Q

non-ketotic hyperosmolar coma

A

T2DM (older patients with poor access to fluids)

patient has enough insulin to prevent ketosis, but can’t satisfy cellular needs
severe osmotic diuresis occurs (need to get urine out so sucks up all water)

develops slowly, treated by hydration

KCSU17 Patho/Pharm Submodule 1 (12 decks)

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