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Human Anatomy & Physiology 2 > Endocrine and Immune 16, 20, 21 > Flashcards

Endocrine and Immune 16, 20, 21 Flashcards

1
Q

posterior lobe of pituitary synthesizes what hormones

A

ANSWER IS NONE OF THE ABOVE

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2
Q

gigantism vs acromegaly

A
  • gigantism occurs when growth hormone hypersecretion occurs before the fusion of the long bone epiphysis and is characterized by tall stature (tall)
  • acromegaly occurs when GH hypersecretion occurs after the fusion of the epiphysis leading to large extremities and characteristic facies (fat)
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3
Q

posterior pituitary

A
  • neurological tissue
  • remnant from the brain
  • comes down from the hypothalamus
  • comes down from the brain and its neural tissue
  • extension of the brain
  • does not synthesize any hormones
  • only stores hormones that the brain or the hypothalamus part of the brain synthesizes
  • hypothalamus synthesize the hormones
  • posterior stores oxytocin and antidiuretic hormone
  • oxytocin for milk let down and antidiuretic hormone for water retention
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4
Q

anterior pituitary

A
  • glandular tissue
  • comes up from soft palate
  • synthesizing and storing prolactin
  • genuine gland
  • synthesize growth hormone
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5
Q

oxytocin

A
  • for milk let down, not milk production
  • causes the female to release the milk and nourish the baby
  • oxytocin is synthesized by the paraventricular nuclei
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6
Q

prolactin

A
  • synthesized by the anterior pituitary
  • inhibited by dopamine
  • promote the breasts of the female to produce milk for the baby
  • released for milk production
  • inhibited by dopamine under normal circumstances
  • once the dopamin is not made, then prolactin can be released
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7
Q

antidiuretic hormone

A
  • antidiuresis, or anti urine production and water loss in urine
  • prevent urination
  • prevent the production of urine and therefore the loss of water
  • it will be produced when the body needs to conserve water or retain water, like when a patient is dehydrated overnight
  • act on the collecting tubules in the kidney and insert aquaporins, which has the kidneys synthesize and insert channels for absorbing water back
  • ADH is synthesized by the suprachiasmatic nuclei
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8
Q

two aspects to antidiuretic hormone

A
  • central nervous system
  • the posterior pituitary must release it, assuming the hypothalamus is synthesizing in the first place
  • nephrogenic
  • kidney has to physically respond to it by responding by synthesizing the aquaporins and inserting them into the collecting tubules, or kidney responding
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9
Q

diabetes insipidus

A
  • pathology with antidiuretic hormone
  • ADH is not being properly synthesized and released or its not being responded to properly by the kidney
  • former is central and the latter is nephrogenic
  • so either hypothalamus is not synthesizing it, the posterior pituitary is not releasing it, the kidneys are not responding
  • so it can be central haing to do with the brain or pituitary, or it can be nephrogenic relating to the kidney
  • inability to concentrate the urine
  • urine is not going to be concentrated and water is lost, which means the patient is going to be constantly dehydrated and thirsty (polydipsia)
  • they are going to be consisting drinking and that is all lost in the urine
  • patient will urinate dilute, clear, watery urine thats not concentrated because none of the water is retained
  • urine is clear
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10
Q

test if central or nephrogenic diabetes insipidus

A
  • give them vasopressin, another name for antidiuretic hormone
  • if the problem is central, that they are not synthesizing or releasing antidiuretic hormone, the urine will be corrected (urine is concentrated, not thirsty)
  • in reality, do urinalysis or a UA to check the osmolarity of the urine to confirm
  • if the vasopressin does not correct urine, it is nephrogenic, issue is the kidney cannot respond to it
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11
Q

growth hormone anterior pituitary

A
  • hypothalamus will synthesize growth hormone
  • it will promote the synthesis of growth hormone in the anterior pituitary
  • anterior pituitary responds to it by making growth hormone
  • then growth hormone will go to the liver and make IGF1, insulin-like growth factor 1
  • it will promote growth of bones, organs, and muscles
  • this is where children reach their growth spurt
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12
Q

gigantism vs acromegaly

A
  • gigantism = excessive growth hormone, while the child is still growing, so before the epiphyseal plates have closed
  • acromegaly = patient is done developing, they are adult now and release excess growth hormone later in life, epiphyseal plates have closed; get really coarse, rugged, thicker
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13
Q

thyroid hormone

A
  • hypothalamus is synthesizing TRH and that promotes the anterior pituitary to make thyroid stimulating hormone
  • thyroid stimulating hormone will go to the thyroid until the thyroid make thyroid hormone
  • TRH (thyroid releasing hormone) stimulate the pituitary to make thyroid stimulating hormone, which stimulates the thyroid to make thyroid hormone
  • T3 is more potent than T4 even though is has one less iodine
  • responsible for metabolism growth, sets metabolic rate
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14
Q

hyperthyroidism

A

too much thyroid hormone
- typical symptoms: tachycardia, racing heart, palpitations, sweating, feeling hot like feverish
- edema involved, diarrhea and weight loss

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15
Q

hypothyroidism

A

too little thyroid hormone
- typical symptoms: constipation, weight gain, hair loss, more fatigue,
- common cause is Hashimoto

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16
Q

Graves disease

A

Graves’ disease is an autoimmune disorder results hyperthyroidism
- bulging eyes
- caused by TSI or thyroid stimulating immunoglobulins, meaning they are antibodies
- they look like TSH from the pituitary, mimic TSH
- stimulate the thyroid excessively
- make an antibody that looks like TSH, the thyroid responds to it as if it is TSH, its over stimulated, it releases a lot of thyroid hormone causing hyperthyroidism

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17
Q

Hashimoto

A

Hashimoto’s disease, immune-system cells lead to the death of the thyroid’s hormone-producing cells; The disease usually results in a decline in hormone production (hypothyroidism)
- autoimmune, destroying thyroid
- anti-thyroid peroxidase antibodies attacking enzymes in the thyroid

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18
Q

subacute thyroiditis

A
  • a virus attacks the thyroid, ruptures all the follicles and releases a bunch of thyroid hormone
  • thyroid is kind of damaged and it doesn’t make anymore
  • it has to recover
  • so you get like a hyperthyroid situation and suddenly a hypothyroid situation
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19
Q

LH and FSH

A
  • sex hormone axis of the anterior pituitary involves GnRH, or gonadotropin releasing hormone to stimulate the gonads
  • gonadotropin releasing hormone from the hypothalamus will stimulate the anterior pituitary to release LH and FSH
  • luteinizing hormone is going to stimulate the testicles to release testosterone
  • follicle stimulating hormone is going to stimulate the ovaries to release progesterone and estrogen
  • FSH and the testicles will actually stimulate sertoli cells to release androgen binding peptide or ABP
  • FSH will promote the sertoli cells to release androgen binding peptide, which kind of concentrates testosterone and potential its effect or enhances it
  • LH stimulate the luteal cells and the testicles to release testosterone
  • FSH primary function in the female is to promote the synthesis and secretion of estrogen and progesterone
20
Q

ACTH Adrenocorticotropic hormone

A
  • ACTH stimulate the adrenal glands
  • adrenal glands sit above the kidneys and are endocrine glands
  • the hypothalamus will release corticotropin releasing hormone, CRH, which will stimulate the anterior pituitary to release Adrenocorticotropic hormone, which will stimulate the adrenal cortex
  • two primary regions of adrenal regions: adrenal cortex and adrenal medulla
  • adrenal medulla creates adrenaline aka epinephrine and norepinephrine
21
Q

pheochromocytoma

A
  • epinephrine and norepinephrine create tumor
  • patient is constantly releasing epinephrine or norepinephrine and having rushes of endocrine anxiety
22
Q

adrenal cortex

A
  • zona glomerulosa, zona fasciculata, and zona reticularis
  • zona glomerulosa synthesizes aldosterone to deal with salt management
  • aldosterone is what allows the kidney and the body to reabsorb sodium, so it can maintain sodium levels in the blood
  • sodium important to maintain blood pressure and blood volume
  • aldosterone is a mineralocorticoid
  • aldosterone allo kidney to reabsorb sodium and kick out or secrete potassium
23
Q

hypernatremia

A
  • excess aldosterone or excess sodium
24
Q

hypochelineia

A

low potassium levels

25
Q

Conn’s syndrome

A
  • excess aldosterone can be caused because of a tumor secreting too much aldosterone in the zona glomerulosa
  • cause hypernatremia and hypochloremia
  • also lead to hypertension or high blood pressure because where sodium goes water follows
26
Q

Addison’s disease

A

do not have enough aldosterone, adrenal insufficiency

27
Q
A
  • adrenal axis is CRH from the hypothalamus, ACTH from the anterior pituitary, stimulating the zona glomerulosa to synthesize aldosterone
  • ACTH stimulates the zona fasciculata to release cortisol
  • cortisol is a glucocorticoid and that deals with the management of sugar or glucose
  • cortisol is like the stress hormone
  • cortisol will maintain the tone of blood vessels and maintain body
  • excess glucocorticoids has an opposing effect on insulin which can lead to diabetes
  • it can end up causing the breakdown of muscle to raise glucose level, to use the amino acids and convert them to glucose
  • lead to muscle breakdown to raise glucose levels and then opposing insulin, raising them even further
28
Q

Cushing’s syndrome

A
  • cortisol excess can cause hypertension, hyperglycemia, the breakdown of muscle, the building of fat
  • get moon faces, because face is so bloated and filled with excess fat production
  • can get buffalo hump, fat production of the back of their neck
  • can get abdominal girth, abdomen swells with fat
  • get abdominal striae, purple stretch marks on abdomen
  • excess ACTH from the anterior pituitary
29
Q

zona reticularis

A
  • synthesize estrogen and testosterone
  • females have little testosterone and males have little estrogen
30
Q
A
  • zona glomerulosa, fasciculata, reticularis, then medulla
  • aldosterone, glucocorticoids like cortisol, estrogen/testosterone, and epinephrine/epinephrine
  • salt management, sugar management, sex management, excitement management
  • ACTH is not the only way to regulate aldosterone there is also RAS
31
Q

RAS renin angiotensin aldosterone system

A
  • kidneys detect that there is a low blood volume, they will release a hormone called renin
  • renin will go out and promote the activation of angiotensin, which begins as angiotensinogen, and then becomes angiotensin I
  • renin will activate ACE, which is angiotensin converting enzyme
  • angiotensin converting enzyme will stimulate the activation of angiotensin I to angiotensin II, which is the active form
  • angiotensin I through action of ACE, angiotensin converting enzyme, going to angiotensin II
  • its activity is promoted by renin from the kidneys after they have detected low blood volume
  • kidneys are like blood volume is low, must be low sodium, we need more aldosterone, release renin
  • so renin can promote the activity of ACE, so that ACE can activate angiotensin I to angiotensin II
  • angiotensin II is going to tense the blood vessels
  • it will promote thirst in the hypothalamus, drink more because blood volume is low, promote secretion of antidiuretic hormone
  • blood volume low, need to retain more water, antidiuretic concentrate more urine, tensed blood vessels to maintain blood volume, promoted thirst, promoted ADH to release to prevent urination of water, to retain more water, to maintain blood volume, angiotensin II once its activated by ACE, will go out and promote the secretion of aldosterone, aldosterone will promote the retention of sodium, that will retain water as well
32
Q

diabetes mellitus type one

A
  • autoimmune attack on the beta cells of the pancreas that produce insulin
  • so pancreas is destroyed, its autoimmune
  • occurs in younger folks
33
Q

diabetes mellitus type two

A
  • due to being overweight -
  • insulin resistance variety where they have, they are capable of producing insulin but they are so overweight the insulin is being opposed by cortisol levels and stress abd high cortisol, which is antagonistic to insulin
  • pancreas gets exhausted and shuts down
  • insulin is important because it allows the absorption of glucose into the cells and potassium
34
Q

diabetic ketoacidosis DKA

A
  • don’t have enough insulin, you not absorbing glucose
  • patient have glucose in their diet but are not able to absorb it
  • so it is high in their blood, they are glycemic
  • going to have polydipsia (excess thirst), polyphagia (excess eating), and polyuria (excess urination)
  • have a high blood sugar level like 500 (5 times norm)
  • its metabolising fat, releasing ketone bodies from the metabolism of fat, which cause ketosis, which is why it is called ketoacidosis because the ketones are acidic
  • breath smells like nail polish remover because they are breathing out acetone, ketone
  • diabetic emergency
  • first treat with fluids, then give potassium, then insulin
35
Q

fasting blood glucose

A
  • do twice to confirm results
  • level should be 75-100
  • above 100, insulin resistance, prediabetic
  • above 126, diabetes
36
Q

HBA1C

A
  • percentage of hemoglobin that is glycosylated
  • gives 3 month snapshot of glucose
  • should be a percentage 5.5-6, definitely below 6
  • sometimes in diabetics, they have insulin derangement, keep them below 6.5
37
Q

calcium management

A
  • parathyroid hormone, which is made by the parathyroid gland
  • parathyroid hormone is released when calcium levels are low
  • that will promote that will calcium from the bone and add it to the blood
  • stimulates the production of vitamin D and vitamin D helps absorption of calcium
  • high calcium levels, calcitonin which is made by the C cells in the thyroid, those will promote and take calcium from the blood to the bone
  • bone to blood in hypocalcemic state is parathyroid hormone
  • blood to bone in hypercalcemic state is calcitonin
  • lot of calcium = calcitonin
  • low calcium = parathyroid hormone
38
Q

immune system

A
  • innate = natural defenses: hydrochloric acid in stomach, skin keeps bacteria out, mucus
  • membrane attack complex = C3B and C5 through C9
  • these proteins are involved in MAC, membrane attack complex
  • these attack bacteria and destroy their cell walls in order and their cell membranes to kill bacteria
  • some white blood cells, neutrophils phagocytose bacteria and macrophages
39
Q
A
  • adaptive = 2 T lymphocytes and 1 B lymphocyte
  • CD4 lymphocyte is the one that is attacked by HIV; it activates the adaptive, sounds alarm
  • CD8 T lymphocyte aka cytotoxic cell attack viruses, tuberculosis, and fungi
  • CD4 activates the CD8 cytotoxic cell, the CD8 goes out and kills the cell thats infected with the virus
  • B cell can be activated by CD4
  • B cell activates into plasma cell to make antibodies
40
Q

MHC major histocompatibility complex

A
  • type 1 = all cells
  • types 2 = only antigen presenting cells
  • therefore immune cells will have type 1 and type 2
41
Q

five types of immunoglobulins

A
  • immunoglobulins = antibodies
  • proteins made by the B cells to attack foreign invaders
  • IgA = secretory, dimer, breast milk
  • IgM = acute, pentamer
  • IgG = chronic, specific, cross placenta
  • IgD = B cell receptor
  • IgE = allergies, bind mast or basophils
42
Q

hypersensitivity reactions

A
  • type 1 = allergic, IdE
  • type 2 = cytotoxic, antibody dependent
  • type 3 = immune complex mediated
  • type 4 = delayed, cell mediated
43
Q

HIV

A
  • RNA retrovirus that infects the CD4 T lymphocyte abd causes its apoptosis or programmed cell death
  • it causes it to burst and release more of the virus particles
  • CD4 should be above 1000
  • patient normal above 500
  • but if levels drop below 200, the patient has AIDs
  • AIDS = having below 200 CD4 count and having an AIDS defining illness like PCP pneumonia
  • HIV is the virus itself
  • AIDS is the final stage of an HIV infection
  • AIDS defining illnesses begin to appear when CD4 count drops below 500
44
Q

HIV makes 4 proteins

A
  • reverse transcriptase = what allows the RNA HIV, its a protein and an enzyme that will convert the RNA of the virus into DNA
  • integrase = what allows that viral DNA after it has been converted to integrate into your DNA, into the DNA of the T cell to infect it
  • protease = enzyme that cuts and activates the enzymes of HIV
  • entry and exit proteins - - all require protease to activate
45
Q

medications

A
  • antiretrovirals = block agents because HIV is a retrovirus
  • antiretrovirals can recover the CD4 count by 300
  • best to intervene before 800
  • use barrier contraceptives, frequent testing, PrEP, DiscoVe
  • window period 3 months
46
Q
A
  • parafollicular = secrete calcitonin
  • follicular = secrete thyroid hormone
  • HBA1C = lower the better, means more insulin
  • beta = insulin
  • alpha = glucagon
  • leftover healthy cells = memory cells
  • opsonization = attach to antigen to neutralize
  • positive selection = determine if class 1 or 2 MHC
  • negative selection = must not recognize self-antigens
  • HIV can hide for 4 months

Human Anatomy & Physiology 2 (4 decks)

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