Hormones Flashcards
Steroid vs non- steroid hormones (5- each)
Steroid:
- lipid soluble
- bound to a protein carrier
- receptor on the INSIDE of target cell
- mobil receptor model
- rapid long lasting response
Non-steroid:
- water soluble
- unbound
- receptor in the OUTSIDE of target cell
- 2nd messenger model
- short acting response
what is the Mobile-receptor model
Steroid hormone passes through the cell wall and binds to a receptor; that receptor complex then moves in to the nucleus; induces transcription; leading to translation= new protein made; that protein causes an effect.
what is the second messenger model
non-steroidal hormone CANNOT pass though the cell membrane; it binds to an external receptor; leading to the activation of an internal pathway change; activating second messenger
Which gland does the hypothalamus secret to?
Without the hormones the target glands will…
With excess hormone the glands will… EG…
- anterior pituitary
- not enough= atrophy
- too much= undergo hyperplasia and hypertrophy
Hypertrophy and hyperplasia of the Thyroid gland: Hyperthyroidism
Anterior Pituitary
Posterior Pituitary
Adenohypophysis, “aneno”= gland, “A” think Anterior
Neurohypophysis, “neuro”, posterior
Adenohypophysis
Neurohypophysis
-the gland and the mode of communication
- Hypothalamus communicates with the ANT PIT by secreting regulatory hormones into the BLOOD STREAM (via infundibula)
- Hypothalamus communicates with the POST PIT by direct NEURONAL connections
After simulation they each release their hormones into systemic blood supply
Thyroid Hormone (TH) Function (4)
Affects growth and maturation of tissues, cell metabolism, heat production, and oxygen consumption
Calcitonin
who secretes it
function
Secreted by the thyroid
- Regulation of blood calcium and bone density
- Inhibition of osteoclasts/ stimulation of osteoblasts
- Too much Ca++ in the blood= secrete calcitonin to move Ca++ into bone (increasing its density)
- Calcitonin decreases blood Ca++ and increases bone density!
Parathyroid Hormone function
hypersecretion
hyposecretion
-Antagonist (works opposite) to Calcitonin
-Stimulation of osteoclasts (bone breakdown, increasing Ca++ in blood)
hypersecretion leads to osteoporosis
hyposecretion leads to decreased vit D release from kidney
Pancreatic Islet Cells (2)
function
- Alpha cells – secrete Glucagon
- Beta cells – secrete Insulin
Alpha cells
Beta cells
-secrete Glucagon
“you secrete glucose when your glucagon is gone” (hypoglycemic)
Works in the liver to secrete glucose and raise blood sugar.
-secrete Insulin when hyperglycemic to lower blood sugar.
Works in the liver to take up glucose and store as glycogen.
How do beta cells work to facilitate the rate of glucose uptake by cells?
Glucose requires facilitated diffusion to enter cell. Insulin binds in insulin receptors and stimulates the opening of the glucose channel.
Therefore insulin is the KEY that allows our cells to take up sugar
How do alpha cells work to increase blood glucose?
The liver is stimulated:
- Glycogenolysis- breakdown of glycogen
- Gluconeogenesis- formation of glucose from non-sugar products
- Lipolysis- break down of fat into sugar, keto body
Adrenal cortex (3 hormones) 80% of an adrenal gland’s total weight
Adrenal medulla (1)
- Aldosterone
- Cortisol
- Weak androgens and estrogens
Innervation by SNS
-Catecholamines (Epi/norepi) into blood
Adrenal Cortex
3 layers and what they regulate
1) Glomerulosa (salty)- Mineralcorticoids (aldosterone), regulates Na+
2) Fasciculata (sweet)- Glucocorticoids (cortisol), increase blood glucose
3) Reticularis (sex)- Weak Androgens (DHEA), sex development
(SALTY) Mineralocorticoids- Aldosterone
what it does
what this causes in the DCT
what it is regulated by
Aldosterone turns on Na+/K+ pump in the DCT and collecting duct of cells
↑ Na+ uptake
↑ Na retention with LOSS of K+ and H+
Regulation by the renin-angiotensin system
(SWEET) Glucocorticoids - Cortisol
Released with bodily stress ↑ blood sugar by gluconeogenesis Anti-inflammatory Growth suppression Influences awareness and sleep habits Inhibits bone matrix-protein matrix (decrease bone density)
(SEX) Adrenal estrogens and androgens
estrogen and Androgens
function
Estrogen secretion is minimal (vs. ovary)
Needed in men b/c no ovary
Androgens – weak
DHEA
Converted by peripheral tissues to stronger androgens such as testosterone
Needed in women b/c no testes
Panhypopituitarism
what it is
cause
“pan”=all, “hypo”; ant pit hormones are low
Due to infundibulum damage
Hypopituitarism
what it is
cause
s/s
deficiency in 1 or more pituitary hormones
Usually due to pituitary infarction (narcotic effect of decreased blood flow)
Hyperpituitarism
what it is
cause
s/s
hypersecretion of in 1 or more pituitary hormones
Commonly caused by a benign slow-growing pituitary adenoma
s/s:
Headache and fatigue
Visual changes (b/c a tumor is growing next to the optic tract, pushing on it)
Hyposecretion from those cells that are most sensitive to pressure from the growing tumor (FSH-and LH-secreting cells)
Acromegaly
Hypersecretion of GH during adulthood
Increase metabolic effects (sim. to hypothyroidism)
Continued bone growth of nose, chin, hands, feet (will NOT grow in height)
Connective tissue changes (cardio and respiratory concerns)
Hypersecretion of prolactin
what it is
cause
s/s: male vs female
(most common pit. adenoma)
Caused by prolactinoma
In a non-breast feeding females – amenorrhea, galactorrhea, hirsutism and osteopenia (loss of bone density)
In males – hypogonadism, erectile dysfunction, impaired libido, oligospermia and ↓ ejaculate volume
SIADH
what it is
cause
s/s
Syndrome of inappropriate anti-diuretic hormone secretion (Hypersecretion of ADH)
Small cell lung cancer
Brain injury or infection (post op.)
Sepis
Psychiatric/drugs
Water intoxication (hyponatremia, hypoosmolality)
Decreased blood concentration, too much water in blood stream resulting in high BP and risk of ICP.
Low volume, high concentration urine output
Polyuria
Polydipsia
Polyuria- excessive urine output
Polydipsia- excessive thirst
what does Diabetes mean?
“to siphon” (water!)
Polyuria- excessive urine output
Polydipsia- excessive thirst
B/c water is being excessively siphoned out of the blood into urine
Diabetes Insipidus vs Mellitus
Insipidus: Not sweet pee
ADH problem
No relationship to sugar
Mellitus: sweet pee Excessive glucose in the urine (should have none) Insulin problem Excessive hyperglycemia Type I and type II
Diabetes insipidus what it is s/s Neurogenic Nephrogenic Psychogenic
Insufficiency of ADH
Polyuria and polydipsia, hypernatremia, hypersomolality (thin concentration)
Inability to concentrate urine
Constantly dehydrated
-Neurogenic
Insufficient amounts of ADH
from post pit
-Nephrogenic
Inadequate response to ADH
from kidney
-Psychogenic (not really DI)
Excessive consumption leads to similar findings
(hypernatremia)
Hyperthyroidism what it is Main disorder s/s Thyrotoxic crisis
Increase T3 and T4- TRH and TSH are low due to negative feedback.
Graves- autoimmune: Antibodies binds to TSH receptor leading to inappropriate over activation of T4 and T3. The hypothalamus tries to turn down the over activation by turning down TSH.
Increased Metabolism: Warm/sweaty (fever), weight loss (hungry), thinning hair, tachy, insomnia, exopthalmos, goiter
Thyrotoxic crisis: prolonged thyrotoxicosis. Excessive stimulation the over works the heart, BP, leading to cardio events. Can be fatal.
Thyrotoxicosis:
the state in which the entire body is experiencing the hyperthyroid effects
can result from dysfunction of the pituitary, the thyroid gland, ectopic thyroid tissue, or the ingestion of excessive amounts of TH medication
Hypothyroidism what it is Main disorder s/s Myxedema coma
(most common thyroid disorder)
decreased T3 and T4; increased TRH and TSH to compensate
Hashimotos- autoimmune: antibody binds to T4 and T3 causing direct autoimmune attack to the thyroid.
Fatigue, weight gain (decreased hunger), hair loss, cold, brady, decrease HR, decrease BP (risk of coma)
Periorbital myxedema (bags around the eyes)
Goiter
Myxedema coma: low metabolic functioning leading to decreased neurologic function. Can be fatal
Hyperparathyroidism
what it is
s/s
Excess secretion of PTH (antagonist to calcitonin) from one or more parathyroid gland.
Usually secondary to a chronic disease Hypercalcemia Hypophosphatemia Hypercalciuria: kidney stones Pathologic fractures (from decreased bone density)
Hypopararthyroidism
Abnormally low PTH levels leads to low blood Ca++ (thus leaning to hypocalcemic effects)
Usually caused by parathyroid damage during thyroid surgery
Adrenal Cortex:
Cushing disease
Cushing syndrome
Cushing disease (big cushion of steroids) Excessive anterior pituitary secretion of ACTH (high cortisol levels)
Cushing syndrome
Excessive level of cortisol regardless of cause
Diabetes Mellitus
what it is
s/s
Diabetes Mellitus = disorder of glucose metabolism related to insulin
Hyperglycemia- leading to the 3 P’s: polydipsia, polyuria, polyphagia. Weight loss, fatigue
3 P’s of DM:
- polydipsia: increased thirst from polyuria
- polyuria: the PCT is maxed out and cannot absorb all glucose; it also attracts water!
- polyphagia: tissues are not getting the resources they need; turns on hunger in the brain
HbA1c (Glycated hemoglobin test)
Monitors long term (120 day) blood sugar levels to prevent severe cardiovascular and neurologic complications
Amount of sugar attached to hemoglobin during production in the bone marrow
Type I
what it is
cause
(Insulin Dependent) =no insulin
Pancreatic atrophy and specific loss of beta cells and loss of insulin production
Typically early in life, BUT can be later in life
Due to genetic autoimmune (most common), viral attack on beta cells
Pancreatic damage: pancreatitis, trauma, resection
Type II
what it is
cause
(Insulin Resistant) =has insulin but it doesn't function Prolonged hyperglycemia (years) leads to increased resistance by insulin receptors Chronic type II, may lead to a loss of insulin (NOT type I, "insulin dependent")
More common (90%) Risk factors: *Genetic susceptibility* Environmental factors- socioeconomic status (be kind). Obesity (diet and lifestyle)
Over time; decrease Beta cell response to plasma glucose
Chronic Conditions of Diabetes Mellitus:
prolonged hyperglycemia destroying tissues leading to decreased vascular flow
Microvascular disease (DM Types I and II)
(small vessel) Retinopathy Nephropathy Neuropathy Infection (most concerning) decreased specificity, blood flow, immune functioning; especially peripheral leading to amputations
Macrovascular disease (Type II)
(large vessel) Atherosclerosis!!! Coronary artery disease Stroke Peripheral artery disease
Acute Conditions Primarily of DM Type I
Hypoglycemia: Insulin shock or reaction Diabetic ketoacidosis (DKA)
Acute Conditions Primarily of DM Type I: Diabetic ketoacidosis (DKA)
Leads to serious complications
-decrease Insulin leading to increase counter regulatory hormones (Catecholamines, cortisol, glucagon, GH)
-Ketoacidosis from not having enough glucose and leads to the breakdown of fats & proteins
Adrenal Cortex:
Addison disease
what it is
s/s
Hyposecretion of adrenocortical hormones
(decrease Aldosterone and cortisol)
Fatigue, orthostatic hypotension, syncope, hypoglycemia, hyponatremia, increase K
Adrenal Cortex:
Conn disease
what it is
s/s
Hyperaldosteronism
Hypertension, myalgias, weakness, chronic headaches, increase Na, decrease K
(opposite of Addison)
Adrenal Cortex:
Hypersecretion of adrenal androgens and estrogens
Feminization: happens to males
Virilization: happens to females
Adrenal Medulla:
Catecholamine hypersecretion
can cause (2)
s/s
(NE, Epi)
Chromaffin cell tumor
Pheochromocytoma
Secretions on a continuous or episodic basis
Hypertension, headaches, sweating, tachycardia, tachypnea, anxiety, chest pain
