Exam 3 Flashcards
Calcitonin
- regulates calcium levels in blood in response to HIGH calcium levels in blood
- released from the parafollicular cells in the thyroid gland
Parathyroid hormone
- regulates calcium levels in the blood in response to LOW calcium levels
- hypofunction leads to hypocalcemia
Hypoparathyroidism symptoms
- hyperphosphatemia
- hypocalcemia -> positive Chvosteks (tetany)
- neuromusclar irritability/ hyperexcitability
- bronchospasm
- laryngospasm
- seizures
- cardiac arrythmia -> leads to prolonged QT interval
- impaired cardiac function -> decreased excitation-contraction coupling
Hyperparathyroidism symptoms
- hypercalcemia -> excess bone resorption
- hypercalcemia symptoms ->
- muscle weakness
- kidney stones from high calcium accumulation
- vomiting and constipation
- polyuria -> kidney loses urine concentrating abilities
- dehydration from vomiting and polyuria
- depressed nervous system and mental state
- mental depression due to decreased perfusion to brain due to low BV
- hypertension due to increased cardiac output from inc SV due to high calcium entry-> calcium release coupling occurring
Parathyroid biological functions
in bones:
PTH binds to osteoblasts -> release osteoclast activating factors OAFs -> lead to bone resoprtion, releasing phosphate ions and calcium ions into the blood
in kidneys:
- PTH stimulates calcium reabsorption to increased blood calcium
- PTH stimulates phosphate excretion to prevent formation of calcium phosphate crystals
- activates 1 alpha dehydroxylasse which converted vitamin D in 1,25 (OH), 2 Vit D which allows for calcium reab from the small intestine
Hypoparathyroidism causes
- thyroidectomy
- damaged parathyroid gland
- PTH gene mutation
- inhibition of PTH release due to chronic hypomagnesemia
Pseudohypoparathyroidism causes
- genetic disorder with dysfunctional PTH receptors -> PTH is present but goes undetected
Synergy
the total effect is greater than the sum of all of the individual effects of the hormones
3 Hormone chemical structures
Biogenic amine hormone
peptide/protein/glycoprotein hormone
steroid hormone
Biogenic amine hormone
derived from the amino acid Tyrosine (polar)
- L-dopa, dopamine, norepinephrine, epinephrine
Peptide/ protein/glycoprotein
derived from chain of amino acids (polar)
- oxytocin, insulin, follicle stimulating hormone
Steroid hormone
derived from cholestrol (nonpolar)
- testosterone
Locations for receptors
- membrane/ cell surface -> bind polar hormones that can not enter
- cytoplasm or nucleus -> bind nonpolar hormones that can enter the cell
Permissiveness
- hormone binds it’s own receptors but in doing so it’s biological action increases the release of another hormone or the expression of receptors for that hormone, thereby increasing the other hormones effect
Cooperativity
- hormones work together on the same target tissue to achieve the desired biological effect
Posterior Pituitary
- connected to neurosecretory centers in hypothalamus via the hypothalemic- hypophyseal tract
- receives oxytocin and ADH via axonal transport
- stores and releases these two hormones into the body
Anterior pituitary
- connected to neurosecretory centers in the hypothalamus via hypothalemic- hypophyseal portal system
- receives CRH, TRH, GHRH, GRIH, PHH, PIH, GnRH
- these hormones act on the endocrine cells (target tissues) to release stimulating hormones which then are sent out into the body
CRH
corticotropin releasing hormone -> activates corticotrophs to release ACTH adrenocorticotropic hormone to send to the kidney
TRH
thrytropin releasing hormone -> activates thyrotrophs to release TSH thyroid stimulating hormone in the thyroid gland
HPT axis
hypothalamus TRH -> pituitary TSH -> thyroid gland T3 and T4 -> tissues -> negative feedback to hypothalamus and pituitary if T3 or T4 are high levels
HPA axis
hypothalamus CRH -> pituitary ACTH ( can also do negative feedback loop) -> zona fesiculata
in the adrenal gland cortisol -> negative feed back loop
Iodine
thryoid can pick up 3 to 4 iodide atoms as it is synthesized making T3 or T4
Stimulatory factors for thyroid release
- TRH
- TSH
- exposure to the cold
Inhibitory factors for thyroid release
- excess iodide -> Wolff - Chaikoff effect
- high levels of T3 and T4 already in blood
Biological actions of thyroid hormone
- inc BMR -> inc body temperature
- inc EPO production
- inc inotropic and chronotropic action of heart
- permissive effect on the catecholamines -> can couple with SNS during fight or flight to lead to thyroid storm
- GI motility increased
- regulates normal pulmonary function via medullary respiratory centers
- regulates reproduction through HPG axis
Hyperthyroidism symptoms
- inc BMR -> high body temp
- low heat tolerance -> hyperhydrosis
- inc appetite (GI motility) but decreased weight
- protein breakdown for energy -> lose muscle mass- bone breakdown for energy -> osteoporosis
- diarrhea due to GI motility -> metabolic alkalosis -
>hyperventilation
- tachycardia, palpitations, arrrythmia, fibrillation
- hypertension from rapid heart rate and high SV from increase in beta 1 effect on the heart
- thinning of skin due to fat breakdown in the hypodermis
- irritability/ restlessness -> high energy
- Goiter and exophthalmus in Graves’ disease
-excess leads to thyroid swelling and swelling behind the eyes
Hypothyroidism/ Myxedema symptoms
- dec BMR -> dec body temp -> hypothermia
- weight gain -> reduced breakdown of fat for energy
- cardiovascular problems -> reduced AV and SV nodal stimulation -> bradycardia
- edema development leading to enlarged heart which undergoes CARDIOMEGALY, reducing SV and CO
- constipation due to dec in GI motility
- anemia -> low EPO levels leads to low erythrocyte synthesis which can cause low oxygen circulation
- also linked to pernicious anemia because of constipation/ GI issues
- Renal issues -> the GFR is decreased due to reduced beta adrenergic effectiveness and renin release -> reduced GFR leads to lower water excretion -> lower water excretion means that excessive fresh water consumption can cause hypo-osmotic hypervolemia and water intoxication
- paranoid psychosis
- Goiter in primary hypothyroid -> low T3 and T4 means that you lack the NFB effect and TSH is produced in excess
Water intoxication/ poisoning process
Hemorrhaging, sweating or vomitting combined with drinking large amounts of fresh water
- hyponatremia
- decreased osmolarity of blood plasma and the IF
- the cells now have higher osmolarity
- cells pull large amount of water from IF via filtration force of the OPif
- cells swell, rupture and cause severe issues like coma, seizure or death
Adrenal Gland
outer layer (zona glomerulosa) -> secretes renin middle layer (zona fasciculata) -> secretes cortisol inner layer (zona reticularis) -> secretes adrenal androgens - ACTH regulates both the fasciculata and the reticularis
Biological effects of cortisol
- increased appetite
- inhibited glucose uptake -> hyperglycemia
- stimulates gluconeogenesis in liver -> more glucose release
- stimulates catabolism of proteins -> not the liver need those enzymes
- increases CO and TPR via permissive effect on catecholamines
- renal effect -> high levels stimulate sodium and water reabsorption -> inc BV -> VR -> EDV- > SV -> CO -> BP
- regulates HCl levels in stomach -> high levels mean high levels of HCl which decreases formation of prostaglandins -> peptic ulcers in the stomach
Cortisol drug uses
antiinflammatory
- decreases capillary permeability
- cause vasoconstriction
- inhibits vasodilation, release of histamine, diapedesis (leukocyte movement into tissues)
- phospholipidase A is inhibited which prevents prostaglandin formation
immunosuppressant
- prevents leukocyte maturation with involution of the thymus
- inhibits leukocyte movement/ function by inhibiting diapedesis
- leads to leukocyte apoptosis
Cushing symptoms
hypercortisolism
- moon face
- trunkal obesity
- fungal infections
- muscle weakness from protein catabolsim
- osteoporosis from bone breakdown/ catabolism
- hypertension from inc TPR and CO
- diabete/ glucose intolerance
Aldosterone excess syndrome symptoms
1- hypernatremia
2- hypokalemia
3- hypervolemia
4- hypertension
5- alkolosis because the K+ excretion brings H+ with it in a symport system
6- vasoconstriction due to permissive effect with catecholamines
7- orthostatic/ posterial hypotension -> baroreceptors are blunted due to hypokalemia which hyperpolarizes them -> do not get immediate baroreceptors signals being sent to the medulla
8- sodium escape -> aldosterone causes excessive fluid retention which then activates the RV to excrete ANH which causes sodium and water to be excreted
9- chronic headaches due to high BV and thus increased perfusion
Adrenal Insufficiency (AI) Syndrome
- low cortisol and aldosterone
- hyponatremia -> lacking the aldosterone which helps to reabsorb sodium -> hypovolemia
- hypotension -> lack of TPR from lack of vasoconstriction permissiveness and lack of BV due to lack of aldosterone
- hypoglycemia -> due to lack of cortisol action helping with keeping glucose in the blood (syncope, confusion, drowsiness, shaking, sweat) neuroglucopenia
- hyperpigmentation -> in addison’s syndrome ACTH levels are high but they just do not get turned into cortisol -> ACTH co-secreted alongside melonocyte stimulating hormone MSH via POMC -> more melanin in the membranes in your mouth or anal cavity
Adrenal Medulla
Tyrosine -> L-dopa -> dopamine -> norepinephrine -> epinephrine (biogenic amines)
Stimuli for Catecholamine release
- SNS activation
- hypoglycemia
- hemorrhaging
- stress
Factors of catecholamine levels
- production rate
- concentration of MAO (monoamine oxidase) which breaks down the catecholamines
Fight or flight basics
- inc TPR from vasoconstriction in most tissues except for heart and skeletal muscle
- inc CO from SA and AV node and cardiomyocytes activation
- decreased GI activity
- sweating
- pupillary dilation via contraction
- nutrient release
- glycogenolysis, gluconeogenesis, lipolysis - bronchodilation -> hyperventilation -> more oxygen
drugs for catecholamine levels
tyramine -> in fermented food inc catecholamine release
monoamine oxidase inhibitors MAOI’s -> reduce the breakdown of catecholamines -> antidepressants as they increase the effect of epinephrine and norepinephrine and dopamine
cocaine and amphetamines -> prevent the breakdown or diffusion of the catecholamines out of the synapse
Alpha cells
glucagon
Beta cells
insulin
delta cells
somatostatin
epsilon cells
ghrelin
F cells
pancreatic peptide
Glucagon
- secreted by the pancreatic alpha cells when glucose levels are LOW in blood
- glucagon targets the liver for breakdown of glycogen into gluocse for the blood glycogenolysis/ gluconeogenesis
- diminishes glucagon stimulus
Insulin
- secreted by the pancreatic beta cells when glucose levels are HIGH in blood
- insulin secreted and targets the liver and body cell tissues to take up the glucose
Insulin release stimuli
hyperaminoacidemia
hyperglycemia
vagal stimulation via muscarinic receptors
incretins from digestive processes
THE BIOLOGICAL EFFECT FROM DIGESTIVE INSULIN WILL ALWAYS BE GREATER THAN THE SAME AMOUNT BEING INJECTED
insulin biological actions -> stimulatory
- maintains glucose levels by stimulating glucose uptake in cells
- stimulates cellular uptake of amino acids
- stimulates glycolysis -> production of glycogen from the glucose / storage
- glycogenesis
- lipogenesis -> pulls lipids out of blood and into fat cells which convert it into
- stimulates protein synthesis -> uptake glucose and used in ribosomal protein synthesis
- somatostatin synergy for inhibiting glucagon release
insulin anabolic or catabolic?
anabolic
insulin inhibitory biological actions
- inhibits glycogenolysis
- inhibits lipolysis
- inhibits the release of glucagon via synergy with somatostatin i.e. the paracrine effect
- inhibit gluconeogenesis in the liver because the production of glucose from non carbohydrates
Insulin effect on potassium?
causes hypokalemia
- biological action brings potassium into the cell, reducing outside levels
- leads to prolonged QT interval due to lengthened T interval because of the lower activation of IKr channels prolonging the repolarization phase but hyperexcitabilitiy
Diabetes mellitus effect on potassium
hyperkalemia
- shortened QT interval due to high activation of IKr channels shortening the T-interval ->. shorter QT
- longer QRS because less negative so fewer Na+ channels available so the depolarization phase for the ventricles is prolonged
- lower excitability
Diabetes Mellitus Type 1
- onset because of damage to the beta cells in the pancreas
- molecular mimicry leads to autoimmune response attacking the beta cells
- low weight
- insulin is not secreted -> low endogenous levels
- 30% concordance
- low insulin means hyperketoacidosis
Diabetes Mellitus Type 2
- obesity cause
- prolonged hyperglycemia -> prolonged hyperinsulinemia -> desensitzation of receptors to insulin
- normal or high endogenous insulin
- weight gain
- 90% concordance
- associated with high insulin levels that just can not be used
DM Symptoms (Catabolic disease)
Look at slide 58
- hyperglycemia
- polyuria due to somotic diuresis -> glucosuria
- polydipsia becuase of dehydration and hyperosmolar blood
- hypertension in TYPE 2 because of high level of fat in blood -> excessive lipolysis leaves a bunch of fatty plaque in the blood
- Type 1 -> excessive lipolysis as insulin dependent cells can’t pick up glucose -> ketogenesis of ketone acids-> ketones -> ketoacidisosis-> metabolic acidosis -> Kussmaul breathing -> hyperventilation to try to compensate -> acetone on breath as it is a gas
- retinopathy -> the lens gets glycosylated and the retina and optic nerve leading to blindness
- neuropathy in extremities -> gets decubitus wounds
- poor wound healing -> glucose makes a tasty snack for pathogens and microbes
- hyperkalemia because lack of movement in
Acetone breath for Type 1
excessive lipolysis as insulin dependent cells can not pick up glucose for energy -> keogenesis -> creation of ketone acids ( acetone, acetoacetic acid, beta hydroxybuttryic acid) -> ketoacidosis -> metabolic acidosis -> Kussmaul breathing -> extreme hyperventilation -> acetone breathed off -> fruity breath
Normocalcemia
9 to 11 mg / 100 cc
regulation hormones
1,25 (OH)2 Vit D
calcitonin
parathyroid hormone
Adrenal insuffiency -> low Aldosterone and low cortisol
- hyponatremia -> absence of aldosterone so it fails to bring it in
- hypotensions -> low blood volume due to lack of aldosterone and fluid retention
- low TPR because the vasoconstrictor permissiveness is not present - anorexia -> low appetite due to lack of cortisol
- weight loss
- hypoglycemia -> no cortisol to
