Endocrine System

endocrine system - review

• secretes hormones as chemical messengers that target receptors

• the endocrine system causes the negative feedback systems

• these hormones chemical structures can be

  • peptide

  • steroid

• once they have been used they are excreted by the kidneys

endocrine system - where hormones are excreted from

• pituitary gland

• adrenal glands

• thyroid gland and parathyroid glands

• pancreas

• gonads

• pineal gland

• thymus

• local hormones

location of endocrine glands

sources of major hormones and primary effects

there are anterior and posterior lobes of the pituitary glands

• adenohypophysis: anterior lobe

• neurohypophysis

hormone release

• most often controlled by negative feedback mechanisms

  • endorine and nervous systems work tg to regulate metabolic activities

  • complex system for some hormones

  • secretion may be controlled by more than one mechanism

    • hypothalamus and pituitary working tg to get the hormone released

  • some hormones work antagonistically

    • some hormones work against eachother

      • ex: insulin and cortisol

  • rate and timing of secretion may vary

    • ex: menstral cycle - estrogen and prostoglandin released largely once a month

    • cyclic patterns

negative feeback loop

A negative feedback loop acts as a system's internal stabilizer by working to reverse any changes away from a desired baseline. When a disturbance occurs—such as a spike in body temperature or a drop in a home's thermostat reading—specialized sensors detect the shift and alert a central control mechanism. This controller immediately triggers corrective actions, or effectors, designed to counter the change and bring conditions back to normal. Once the system successfully returns to its optimal set point, the corrective process automatically shuts off, preventing overcorrection and successfully maintaining a steady, balanced state known as homeostasis.

negative feedback loop - decreasing blood sugar

Lowering High Blood Sugar

1. Stimulus: You eat food, carbohydrates break down, and blood glucose rises above normal levels.

2. Detection: Beta cells in the pancreas sense the elevated glucose in the blood.

3. Release: The pancreas secretes insulin into the bloodstream.

4. Transport: Insulin travels through the body and binds to receptors on cell membranes (like a key opening a lock).

5. Uptake:

• Muscle and fat cells open up gateways to pull glucose out of the blood for energy.

• The liver absorbs glucose and converts it into stored glycogen.

6. Correction: Blood glucose levels drop back down to the normal baseline.

7. Shutoff: The pancreas senses the normal glucose level and stops releasing insulin (the negative feedback loop closes).

negative feedback loop - increased blood sugar

Step-by-Step: Raising Low Blood Sugar

1. Stimulus: You skip a meal or exercise heavily, causing blood glucose to drop below normal levels.

2. Detection: Alpha cells in the pancreas sense the low glucose levels.

3. Release: The pancreas secretes glucagon into the bloodstream.

4. Target: Glucagon travels through the blood and targets the liver.

5. Conversion: The liver breaks down glycogen back into usable glucose molecules (glycogenolysis).

6. Release: The liver pumps this freshly freed glucose into the bloodstream.

7. Correction: Blood glucose levels rise back up to the normal baseline.

8. Shutoff: The pancreas senses the restored glucose levels and stops releasing glucagon (the negative feedback loop closes).

endocrie disorders

• all disorders reflect impared control/feedback

  • manifestation of hormonal disorders reflect the action of the hormone

    • ex: lack of insulin → gonna cause high blood sugar

      • the point of insulin is to decrease blood sugar

• excess hormone levels

  • tumor produces high levels

  • excretion by liver or kidney is impaired

    • body cant excrete it

  • congenital condition producess excess hormone

• deficit of hormone or reduced effects

  • tumor produces too little hormone or it could be pressing on the gland causing it to not be able to release it

  • inadequate tissue receptors present

    • might not be as sensitive to the hormone coming in

  • antagonistic hormone production is increased

  • malnutrition

  • atrophy, surgical removal of gland

  • congenital deficit - present at birth

diagnostic tests

• blood tests

  • check serum hormone levels

  • radioimmunoassay

  • immunochemical methods

• urine tests

• stimulation or suppression tests

• scans, ultrasounds, MRI

• biopsy

treatment

• deficit may be treated with replacement therapy

• excessive secretion may be treated with

  • medications

  • surgery

  • radiation

insulin and diabetes mellitus

• diabetes mellitus: basic problem is inadequate insulin effects in receptor tissues

  • deficit of insulin secretions

  • production of insulin antagonists

  • Diabetes results in abnormal carbohydrate, protein, and fat metabolism.

    • Due to glucose being stuck in the blood stream so now they have to find something else to give energy

      • without insulin these can help for short term but over time its going to be problomatic

• some tissues can transport glucose in the absence of insulin:

  • CNS, kidney, myocardium, gut, and skeletal muscle

    • skeletal muscle can partially meet tissue needs without insulin

type 1 diabetes

• deficit of insulin secretion

• autoimmune destruction of beta cells in pancreas

  • beta cells secrete insulin so when they are destroyed insulin isnt getting secreted

    • insulin dependent diabetes

• insulin replacement required

• acute onset in children and adolescents

• not linked to obesity

• genetic factors may play a role

type 2 diabetes

• deficit of insulin secretion or too much production of insulin antagonist

• non-insulin-dependent

  • make insulin but might not be enough

  • insulin typically isnt give to these people and oral hypoglucemic medications may be used instead

    • this med only works for people with type 2

• caused by decreased production of insulin and/or increased resistance by body cells to insulin

• onset is slow and insidious and usually in 50+ age (age is decreasing throughout the years)

• associated with obesity

• component of metabolic syndrome

• increasing incidence in teens and young adults

metabolic syndrome

• citeria

  • men: abdominal girth > 40in

  • women: abdominal girth > 35in

  • elevated triglycerides > 150 mg/dl

  • reduced HDL cholesterol < 50 mg/dl

    • good cholesterol

  • increased BP > 130/85 mmHG

  • hyperglycemia fasting BS > 100 mg/dl

• presence of 3 out of 5 is the diagnostic criteria for diagnosis

• this is obesity related

  • this is stuff that is modifiable

• this doesnt mean you automatically have type 2 but youre at high risk and on track to have it

general manifestations of DM

• insulin deficit results in decreased transportation and use of glucose in many cells

  • polyphagia

    • increase in hunger

  • fatigue

    • brain can only bring in so much glucose without the help of insulin

• too much glucose in the blood stream and isnt being put in the cells to use due to the decrease in insuline

  • insulin brings glucose to cells

• blood glucose levels rise - hyperglycemia

• excess glucose in urine - glucosuria

  • dehydration results from hyperosmolar filtrate

  • polyuria

    • h20 is going to follow the glucose causing decrease in h20 causing an increase in thirst

  • polydipsia

    • an abnormal, persistent and unquenchable feeling of extreme thirst that leads to excessive fluid intake

high glucose levels

• hyperglycemia

low glucose levels

• hypoglycemia

polyuria

abnormally large volume of urine

polydipsia

feeling of thirst

glucosuria

glucose in the urine

fasting blood glucose level

• 70-100 is normal

glucose tolerance test

• pt will be fasting before coming in and will drink 25 grams of a sugar drink in the dr office and we monitor their blood sugars after time (usually 1 hr sometimes 3 hrs long)

  • they want your glucose number to be less than a certain number to say that your body is trying to decrease glucose

glycosylated hemoglobin test (HbA1c)

• clinical and subclinical diabetes

• monitor glucose levels over several months

  • monitor for 90-120 days (this is how long rbcs live for)

• look at a rbc and cut it in half and then count the number of sugar molecules on a rbc

  • want it to be less than 7

  • tells us how well were managining our diabetes overtime

Diabetes - treatment principles

• maintenance of blood glucose levels in norm range

  • biggest thing: want to maintain for that specific person

  • helps to reduce complications

• diet and exercise (bigges ones to reduce risk for type 2 - when exersizing your body is using glucose)

  • exercise reduces blood glucose as skeletal muscle uses glucose

  • glucose within vessels is damaging which is why we need to manage

• oral medication

  • increase insulin secretion

  • reduce blood glucose levels

• insulin replacement

  • required for type 1 not always for type 2

T1D - metabolic changes

• catabolism (breaking down) of fats and proteins

  • excessive amts of fatty acids and metabolites

  • ketones in the blood

  • fats and proteins are breaking down and cause keto acids to be excreted making us have ketones in the blood

    • bicarb will try to help out so we will have a decreased serum bicarb bc they are being used up

• ketonuria

  • decreased serum bicab; decrease in pH of body fluids

  • ketoacids excreted in urine

    • tells us we have decompensated metabolic acidosis cause nothing is stoping the ketones and it has made it all the way to the urine

• decompensated metabolic acidosis

if the body doesnt have insulin to move the glucose, our bodys have to figure out how to make energy

T1D - complications

• complications are directly related to duration and extent of abnormal blood glucose levels

• many factors lead to fluctuations in serum glucose levels

  • variations in diet and alc use

    • basically glucose and carbs which can increase your blood glucose

  • change in physical activity

    • body is demanding more glucose be used

  • infection

    • body is demanding more glucose be used

  • vomiting

    • not keeping glucose in

• complications may be acute or chronic

diabetes - acute complications

• hypoglucemia (insulin shock)

• diabetic ketoacidosis

• HHNK or HHNC

• Mobilization and use of lipids to meet cellular needs result in production of ketoacids

  • Not enough insulin to bring in glucose so now we need to break down something else to get the energy but it will create a productions of keto acids

• May be initiated by infection or stress

  • Body demands more glucose and corticosol gets secreated when stressed or infection which is an antagonist of insulin

• May result from error in dosage, infection, change in diet, alcohol intake, or exercise

hypoglycemia (insulin shock)

• more common with insulin replacement treatment

  • more common in T1D

• can occur due to excess oral hypoglycemic drugs

insulin shock

• excess insulin in circulation

  • glucose deficit in blood (decrease of glucose in blood)

    • can be life threatening or cause brain damage if untreated

  • seen in

    • often following strenuous exercise

    • dosage error

    • vomiting

      • nutrients and glucose not keeping in

    • skipping meal after taking insulin

hyoglycemic shock: signs and symptoms

• disorientation and change in behavior

  • brain isnt getting enough glucose to function

• may appear impaired

• anxiety or decreased responsiveness

  • brain isnt getting enough glucose to function

• decreased blood glucose

  • initially might be high bc SNS has been kicked in

• decreased bp and increased hr

• decreasing level of consciousness

  • NOTE: immediate administration of glucose is required to prevent brain damage

diabetic ketoacidosis

• occurs in insulin dependent clients

• more commonly seen in T1D

• result of insufficent insulin in blood

• high blood glucose levels

• 300-600 range

diabetic ketoacidosis - signs and symptoms

• dehydration

  • thirst, dry , rough oral mucosa

  • warm, dry skin

• rapid, deep respiration - acetone breath

  • fruity smell and is strong (body is trying to get rid of the acid so its trying to breath it off)

  • kussmals breathing

  • lethargy, decreased responsiveness

• metabolic acidosis

  • may lead to loss of conciousness or coma

• electrolyte imbalances (low sodium - peeing out so much water, high potassium)

  • abdominal cramps, nausea, vomiting; lethargy weakness

effects of insulin deficit

acute complications: HHNK (hyperglucemic hyperosmolar non-ketoic)

• occurs in type 2 diabetes

• insidious (comes on slowly) in onset and diagnosis may be missed

• often occurs in older clients and assumed to be cognitive impairment

• results in severe dehydration and electrolyte imbalances

HHNK manifestations

• we have enough insulin present where ketones arent produced but if long term the body may create ketones

• hyperglucemia

• severe dehydration - so much glucose within the blood stream so the tissues are dumping fluid into blood stream

  • increased hematocrit

  • loss of turgor etc

  • increased hr and resperations

• 700-1000 glucose

• glucose has a high pulling pressure and is trying to pull in more water to even out the concentration of the blood

  • now we have so much water in the vasculature this is why we pee so much

• electrolyte embalances result in:

  • neurological deficits

  • muscle weakness

  • difficulties with speech

  • abnormal reflexes

HHNK vs DKA

DKA

• your blood glucose is extremely high but your body cant create insulin or there is a really really tiny amt

  • this causes your body to then break down other things like lipid and proteins to get energy and that causes ketoacid to accumulate causing ketones

• this is typically seen in children and help diagnose them with T1D

HHNK

• your blood glucose is extremely high but your body cant create enough insulin to support the glucose

  • you are still making insulin but it just isnt enough

  • it is enough insulin tho to not make your body break down other nutrients to get energy but isnt enough to bring down glucose in the blood

• typically seen in type 2 and helps diagnose someone with type 2

chronic complications of diabietes

• vascular problems

• microangiopathy

• macroangiopathy

• infections

• cataracts

• pregnancy issues

• Dawn Phenomenon

• Somogyi Effect

vascular problems - chronic comp

• increased incidence of atherosclerosis

• changes may occur in small and large arteries

microangiopathy - chronic comp

microangiopathy: changes in microcirculation

• obstruction or rupture of small capillaries and arteries

  • tissue necrosis and loss of func

  • neuropathy and loss of sensation

  • retinopathy - leading cause of blindness

  • chronic renal failure - degeneration in glomeruli of kidney

macroangiopathy - chonic comps

• macroangiopathy: affects large arteries

  • result of abnormal lipid levels

    • high incidence of heart attacks, strokes, peripheral vascular disease

    • may result in ulcers on feet and legs - slow healing

    • frequent infections and gangrenous ulcers

    • amputation may be necessary

vascular problems with diabetes

infections

• common and often more severe in diabetics

• infections in feet and legs due to vascular and neurologic impairment

• fungal infections common

  • candida

  • vagina and or oral cavity

• UTI

• dental caries

• gingivitis and periodontitis

cataracts - chronic comps

• opcity of lens in eye

• related to abnormal mtabolism of glucose

pregnancy

• complications to both mother and fetus may occur

• increased incidence of spontaneous abortions

• infants born to diabetic mothers

  • increased size and weight for date

  • may experience hypoglycemia in first hours postnatally

potential comps of diabetes mellitus

Dawn Phenomenon vs. Somogyi Effect

parathyroid hormone and calcium - hypoparathyroidism

• leads to hypocalcemia

  • weak cardiac muscle contractions

  • increased excitability of nerves - spontaneous contractions of skeletal muscle

• causes

  • tumor congenital lack of parathyroid

  • surgery or radiation in neck region

  • autoimmune disease

negative feedback loop of calcium

normal control and feedback of calcium

parathyroid hormone and calcium - hyperparathyroidism

• results in hypercalcemia

  • forceful cardiac contractions

  • osteoporosis

  • predisposition to kidney stones

• causes

  • tumor

  • secondary to renal failure

  • paraneoplastic syndrome

common effects of parathyroid hormone imbalence

pituitary hormones

• adenomas are the most common cause of pituitary disorders

• effect of mass

  • may cause pressure in the skull

    • headaches, seizures, drowsiness, visual deficits

• effect on hormone secretion

  • dependent on cells and location involved

  • may cause excessive or decreased release of hormones

growth hormone (GH) children

• dwarfism

  • deficit in growth hormone production/release

• gigantism

  • excessive GH prior to puberty and fusion of epiphysis

Growth hormone (GH) adult

• agromegaly

  • excess GH secretion in adults

  • often associated with adenoma

  • bones become broader and heavier

  • soft tissue grows

    • enlarged hands and feet; change in facial features

antidiueretic hormone (ADH) - diabetes insipidus

• diabetes insipidus: deficit of ADH

  • adenoma

  • may originate in the neurohypophysis

    • head injury or surgery

    • possible genetic problem

    • replacement treatment required

• 
  

ADH - inapproprite ADH syndrome

• excess ADH

  • may be temp, triggered by stress, may be secreted by an ectopic source such as a tumor

  • treatment: diuretics and sodium supplements

hypothalamus-pituitary-thyroid gland feedback

hypothalamus-pituitary-thyroid gland negative feedback - made easy

thyroid disorder - goiter

• enlargement of thyroid gland

  • endemic goiter

  • goitrogens

  • toxic goiter

endemic goiter

hypothyroid condition in regions with low iodine levels in soil and food

goitrogens

foods that contain elements to block synthesis of t3 and t4

toxic goiter

results from hyperactivity of thyroid gland

Thyroid Disorders: Hyperthyroidism - graves disease

• related to autoimmune factor

• hypermetabolism and increased stimulation of SNS

  • increased body temp

  • sweating

  • soft silky hair and skin

  • reduced BMI

  • insomnia

  • hyperactivity

    • toxic goiter

Thyroid Disorders: Hyperthyroidism - exophthalmos

• presence of protruding staring eyes, decreased blink and eye movement

• result of increased tissue mass in orbit

• may result in visual impairment

hypothyroidism

• iodine deficint

• hashimoto thyroiditis

  • autoimmune disorder

  • tumor

  • surgical removal or treatment of gland

  • cretinism

    • results in short stature and severe cognitive deficits

    • untreated congenital hypothyroidism

    • may be related to iodine deficiency during pregnancy

hypothyroidism manifestations

• goiter if cause is endemic iodine deficiency

• intolerance to cold

• increased BMI

• lethargy and fatigue

• decreased appetitie

• myxedema in severe untreated hypothyroidism

  • non pitting edema in face, thickened tongue

  • myxedema coma: acute hypotension, hypoglycemia, and hypothermia results in loss of consciousness, life-threatening if untreated

comparison of hypothyroidism and hyperthyroidism

adrenal glands

• adrenal medulla

  • pheochromocytoma

    • benign tumor of the adrenal medulla - secretes epinephrine, nonepinephrine, and possibly other substances

    • occasionally multiple tumors

    • headache, heart palpations, sweating, intermittent or constant anxiety

adrenal glands - adrenal cortex - cushing syndrome

• caused by an excessive level of glucocorticoids - possible result of

  • adrenal adenoma

  • pituitary adenoma

  • ectopic carcinoma

  • latrogenic conditions

  • substance abuse

cushing syndrome - changes

• change in persons appearance

  • round face with ruddy color

  • truncal obesity with fat pad between scapulae

  • thin limbs

  • thin hair

  • fragile skin, purpal striae

• retention of sodium and water

• suppression of the immune response

• stimulation of erythrocyte production

• emotional lability and euphoria

• increased catabolism of bone and protein

• delayed healing

• increased insulin resistance and possible glucose intolerance

addison disease

• deficiency of adrenocorticoid secretions

• autoimmune reaction is a common cause

• gland may be destroyed by hemorrhage or infection

• manifestations

  • decreased blood glucose levels

  • inadequate stress response

  • fatigue

  • weight loss; frequent infections

  • low serum sodium concentration

    • decreased blood volume

    • hypotension

    • high potassium levels

Comparison of Addison Disease with Cushing Syndrome