endocrine Flashcards

1
Q

what does the pancreas secrete?

A

insulin
glucagon
amylin
somatostain

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2
Q

what do glucagon do

A

increases blood glucose via glycogenolysis (breakdown of glucagon)

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3
Q

what does amylin do

A

inhibits glucagon secretion after meals

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4
Q

what does insulin do

A

promotes glucose uptake by the cells

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5
Q

what are the actions of insulin?

A
  • decreases blood sugar
  • promotes uptake of blood glucose by cells
  • promotes storage of glucose in the form of glycogen
  • prevents the breakdown of fats and glycogen
  • inhibits gluconeogenesis (formation of new glucose)
  • increases protein synthesis (therefore has an impact on metabolic processes in the body)
  • Helps the movement of K+ into the cells
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6
Q

what is diabetes mellitus?

A

abnormal glucose regulation and nutrient storage

  • insulin deficiency or insulin resistance
  • 9 million canadians have this
  • 80% will die of stroke or heart disease
  • lifes shortened by 15 years
  • cost of this disease is lots. only insulin is covered by govt but everything else is not
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7
Q

what is the pathophysiology of diabetes mellitus type 1?

A
  • destruction of beta cells in pancreas
    -little or no insulin is produced
    -decreased amylin production
    -less amylin = impaired ability down glucagon going into blood stream (glucagon raised blood sugar)
    = hyperglycemia
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8
Q

causes of diabetes type 1?

A
  • most common in auto-immune response (immune destruction of the pancreas) **
  • genetically predisposed individuals
  • enviromental triggers
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9
Q

how many ppl have type 1 diabetes?

A

only 10%

  • earlier age of onset than type 2
  • diagnosis is around age 12
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10
Q

What occurs to a person when they have type 1 diabetes and there is too much sugar in the blood stream?

A

= hyperglycemia -> osmotic diuresis
this is because glucose takes water with it
-this causes lots of urination (polyuria)
-thirtiness (polydipsia) due to urinating more
-glucose will be present in urine- normal person wont have this

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11
Q

what conditions are a persons cell in when they have type 1 Diabetes?

A
  • the cells are starving (sugar cant get to cells)
  • results in weight loss
  • hunger (polyphagia)
  • breakdown fat for fuel (because glucose cant be used) (this is what causes ketonemia,ketonuria, and fruity breath)
  • fatigue- due to no fuel for cells
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12
Q

what are some manifestations of diabetes type 1?

A
  • hyperglycemia
  • polyuria
  • polydipia
  • polyphagia
  • weight loss
  • fruity breath
  • fatigue
  • recurrent infections
  • visual changes
  • paresthesia (burning/ prickling sensation in hands)
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13
Q

what is used to diagnose type 1 and type 2?

A
  • history and physical exam
  • lab tests
  • elevated plasma glucose
  • glucose tolerence test (2 samples, fasting, then receive sweet drink, then test (tells us in pancreas will respond)
  • randoma plasma glucose test
  • HbA1C (glycosylated hemoglobin) - glucose attaches to hemoglobin- this is useful because it tells u how long the sugar as been high- red blood cells only live for 120 days, so gives us a 3 month history
  • ketonuria (large amounts of ketone bodies in urine)
  • gluscosuria (large amounts of glucose in urine)
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14
Q

How can ppl with tyepe 1 manage thier diabeties?

A

-there is no cure, these ppl will need insulin and glood glucose testing forever

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15
Q

What is the pathophysiology of diabetes type 2?

A
  • gradual impairment (over many years) of beta cell function
  • progessive insulin resistance (linked to metabolic syndrome)
  • decreased ability of insulin to act on target tissue
  • higher levels on insulin is needed
  • less response to insulin - so pancreas will make more, so there will be higher levels of insulin, but beta cells of pancreas will become exhausted, but still functional= gradual impariment of these cells
  • hyperglycemia
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16
Q

what is the cause of diebetes type 2?

A
  • unknown but most likely genetic plus environment/ lifestyle
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17
Q

what are the characterists of type 2?

A
  • 90 % of ppl have this type
  • later age of onset, but this is starting to change and is seen in younger ppl now
  • more gradual onset
  • FN and metis are most likely to have this
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18
Q

What are some risk factors for diabetes type 2?

A
  • family history
  • age (older adult, but dropping)
  • obesity (very BIG risk factor- lol)
  • ethnicity
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19
Q

what does insulin resistance do to the body?

A
  • metabolic syndrome
  • central obesity
  • high blood pressure
  • high triglycerdies
  • low HDL cholesterol
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20
Q

how does a person with type 2 present?

A
  • fatigued
  • has recurrent infections
  • has visual changes
  • overweight or obese
  • dyslipidemic
  • hypertensive
  • abdominaly obesity - fat around the butt and thighs is more localized
  • abdominal fat is around the organs
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21
Q

how can a person with type 2 manage thier diabetes?

A
  • diet and excercise - drop in weight can decrease the need to use meds or even stop medication, and pancreas can recover= reduces insulin resistance. partially reversible disease
  • oral hypoglycemics - helps function of insulin- for ppl who still produce it, but has resistance
  • insulin- for thse who cant produce insulin
  • bariatric surgery- for profoundly obese pts
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22
Q

what are some acute complications of diabeties?

A
  • hypoglycemia
  • diabetic ketoacidosis (when the body starts breaking down fat at a rate that is much too fast. The liver processes the fat into a fuel called ketones, which causes the blood to become acidic)
  • hyperosmolar hyperglycemic nonketotic syndrome
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23
Q

what are some chronic complications of diabetes?

A
  • macrovasular disease
  • mircovascular disease
  • neuropathies
  • infection
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24
Q

what can cause a diabetic pt to have hypoglycemia?

A

from too much meds, too little food, or both

  • speed on onset can be rapid to within a few hours
  • when blood sugar is less than 4 mmol/L
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25
Q

what are some manifestations of hypoglycemia?

A
  • imparied LOC
  • less responsive -progresses to coma
  • brain needs continuous supply of glucose, so when it does, altered LOC occurs
  • tremors
  • cool, clammy, sweaty skin
  • increases heart rate
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26
Q

treatment of hypoglycemia?

A

glucose

  • any form of sugar
  • then recheck blood glucose
27
Q

what is diabetic ketoacidosis?

A
  • blood glucose than is greater than 14 mmol/L
  • pH decreases: acidosis
  • is a form of acidosis related to ketones
28
Q

what does diabetic ketoacidosis cause?

A
  • high blood pressure, cells starving, produce ketones and acid
  • causes lack of insulin = hyperglycemia
  • in type 1 predominantly
  • speed of onset is hours to days to a few days
29
Q

what are some manifestations of diabetis ketoacidosis?

A
  • hyperglycermia= glucose in urine = polyuria, polydipsia, hypotension, tachycardia
  • rapid weight loss, marked fatigue, seizures, coma
  • kussmals respiration (metabolic acidosis, resp compensation, fruity, acetone breath)
30
Q

treatment of diabetic ketoacidosis?

A
  • fluid replacement
  • correction of acidosis
  • insulin
31
Q

What is hyperosmolar hyperglucemia nonketocic syndrome?

A

blood glucose of more than 33 mmol/L

32
Q

what can cause HHNK?

A
  • in type 2 diabeties:
    -insufficient insulin
    -stress, illness, infection -makes it worse
    -speed of onset is slow, days or weeks
    hypersomolar means glucose is being urinated out and water is taken with it
33
Q

what are some manifestations of HHNK?

A
  • hyperglycemia - MORE glucose is lost in urine, polyuria (LOTS), polydispea, hypotension, tachycardia
  • profound fluid loss
  • no ketosis
  • no acidosis
34
Q

tx of HHNK?

A

insulin ro correct blood sugar

  • fluid replacement -profoundly dehydrated
  • outcome are worse- severe electroylte imbalance
35
Q

what does macrovascular mean?

A

big vessles

36
Q

what does microvascular mean?

A

tiny vessels

37
Q

what is the pathophysiology of chronic complications of diabeties?

A

-chronic hyperglycemia affects schwann cells (produce myelin that coat nerves)
that imparies peripheral nervous system, ion pumps, (chronic inflammation)
reduces antioxidants, attracts water to lens of eye

38
Q

how can diabeties cause atherosclerosis??

A

-glucose binds with proteins in blood vessel walls -traps LDL in blood vessels which causes atherosclerosis -triggers inflammation

39
Q

what is macrovasular disease?

A

Macrovascular disease is a disease of any large blood vessels in the body. It is a disease of the large blood vessels, including the coronary arteries, the aorta, and the sizable arteries in the brain and in the limbs. This sometimes occurs when a person has had diabetes for an extended period of time.
- complications can include atherosclerosis, MI, stroke, peripheral artery disease, foot ulcers

40
Q

what is microvascular disease?

A

Small vessel disease is a condition in which the walls of the small arteries are damaged.

  • includes ischemia of the eyes and kidneys
  • retionpathy (disease of retina) -scattered dead parts of the retina, bleeding in the retina, glacoma, cataracts

-nephropathy ( Nephropathy is the term used when the kidneys start to incur damage, which can ultimately lead to kidney failure)

41
Q

what is neuropathies?

A

ischemia to nerves, demyelination
-paresthesias (numbness, tingling, buring sensation typically in feet) - poor blood flow to feet = delayed healing
-gastric atony (poor tone of gut), paralytic blasser, impotence (erectile inability) in men
-impaired nervous function- dont feet when foot is injured, higher chance of foot infection
Infetion: impaired WBC function, high glucose enviroment

42
Q

what can help reduce chronic complications of diabeites?

A

-strict blood sugar control

43
Q

what does the posterior pituitary gland release?

A
  • releases two hormones
  • acts as a storage component
  • stores oxytocin and Antidiuretic hormone (ADH) , also known as vasopressin
44
Q

what does the hyperfunciton of ADH cause?

A
  • syndrome of too much ADH secretion
  • caused by something gone wrong in the pituitary (can be due to head trauma)
  • results in reabsorption of water
  • urine output decreases
  • serum sodium (decreases) -> dilutes the cells
  • person becomes hypotonic
45
Q

what does the hypofunction of ADH cause?

A
  • called diabeties insipidus
  • not enough ADH
  • caused by trauma to the pituitary -
  • results in excretion of water
  • profound urination (diuresis)
  • serum sodium increases (shrinks cell)
  • hypertonic
46
Q

what does the thyroid gland secrete?

A
  • thyroxin (t4) and Triiodothyronin (t3)
  • these increases metabolic rate
  • calcitonin, which decreases serum calcium levels
  • T4 and T3 are regulated by TSH (thyriod stimulating hormone)
47
Q

what are all the alterations in thyroid function?

A

Myxedema Coma hyperthyroidism (graves disease) -> thyroid storm

48
Q

what is hypothyroidism?

A
  • decreased levels of throid hormone
  • most common cause is hashimotos’ thyroiditis (autoimmine destruction of thyroid gland by T cells) -females are more likely to have this)
49
Q

manifestations of hypothyroidism?

A
  • fatigued
  • slows down
  • gain weight
  • cold
  • periorbital edema (swollen eyes)
50
Q

diagnosis for hypothyroid?

A
  • test thyroid stimulating hormone (TSH) then test T3 and T$
  • Tsh will be high
  • T3 and T4 will be low
51
Q

tx for hypothyroid?

A

synthetic forms of T3 and T4

52
Q

what does hypothyroidism in children cause?

A

Cretinism: cognitive impairment, and small figure

-thyroid hormones needed for physical growth and intellectual development

53
Q

what is hyperthyroidism?

A

increased levels of thyroid hormone

  • most common cause is graves disease (type 2 autoimmune)
  • autoantibodies bind to TSH hormone
  • minic the effect of TSH- stimultes production of T3 and T4
  • women are 10X more likely to have this
54
Q

Manifestations of Hyperthyroid?

A
  • increases heart rate
  • BP goes up
  • anxious
  • loss weight
  • diarrhea
  • buldging eyes (exophthamos)
55
Q

diagnosis for hyperthyroid?

A
  • two blood tests (TSH level will be lots)

- measure T3 and T4 (these levels will be low)

56
Q

Tx for hyperthryoid?

A

There is actually no way to stop an overactive thyroid, they actually have to destroy the gland and then make the person hypothyroid and then give them meds to bring levels back to normal.

57
Q

When testing a pt with hypert, what will T3 be like?

A

Low T3 levels

58
Q

when testing a pt with hypot, what will TSH levels be like?

A

high TSH levels

59
Q

what is the adrenal cortex responsible for secreting?

A
  • glucocorticoids
  • mineralocorticods
  • gonadotropins
60
Q

what is the adrenal medulla responsible for secreting?

A
  • epinephrine

- norepinephrine

61
Q

what ia hypercortisolism?

A

called cushing syndrome

Cushing’s syndrome is a collection of signs and symptoms due to prolonged exposure to cortisol. … Cushing’s syndrome is caused by either excessive cortisol-like medication such as prednisone or a tumor that either produces or results in the production of excessive cortisol by the adrenal glands.

62
Q

manifestations of cushings syndrome? (dysfunction of adrenal cortex)

A

-Affects metabolism of :
-Protein fat and carbohydrates
-Hyperglycemic
-Fat deposits (face-moon face, on upper back, and around belly)
-Arms and legs become thinner
-Thin skin- bruise easily
“moon face”
-buffalo hump

63
Q

what is hypocortisolism? (difference between primary and secondary adrenal insufficiency)

A
  • primary adrenal insufficiency = addison disease (rare)

- secondary adrenal insufficiency = sudden withdrawl of glucocorticoid therapy, gland atrophy during treatment